Evidence Report/Technology Assessment 

Number 104 

Celiac Disease 

Prepared for: 

Agency for Healthcare Research and Quality 

U.S. Department of Health and Human Services 

540 Gaither Road 

Rockville, MD 20850 

www.ahrq.gov 

Contract No. 290-02-0021 

Prepared by: 

University of Ottawa Evidence-based Practice Center, University of Ottawa, Ottawa, Canada 

Co-directors: David Moher, PhD and Howard M. Schachter, PhD 

Investigators

Alaa Rostom,* MD, MSc, FRCPC 

Catherine Dubé,* MD, MSc, FRCPC 

Ann Cranney,*†

 MD, MSc, FRCPC 

Navaaz Saloojee,* MD, FRCPC 

Richmond Sy,* MD, FRCPC 

Chantelle Garritty, BA, DCS 

Margaret Sampson, MLIS 

Li Zhang, MLIS 

Fatemeh Yazdi, MSc 

Vasil Mamaladze, MD, PhD 

Irene Pan, MSc 

Joanne McNeil,* RN 

David Moher, PhD 

David Mack,* MD, FRCPC 

Dilip Patel,* MD, FRCPC 

Chalmers Research Group; *Gastrointestinal Clinical Research Unit; †

Division of Rheumatology 

AHRQ Publication No. 04-E029-2 

September 2004 

 
 

This report may be used, in whole or in part, as the basis for development of clinical practice 

guidelines and other quality enhancement tools, or a basis for reimbursement and coverage 

policies. AHRQ or U.S. Department of Health and Human Services endorsement of such 

derivative products may not be stated or implied. 

AHRQ is the lead Federal agency charged with supporting research designed to improve the 

quality of health care, reduce its cost, address patient safety and medical errors, and broaden access 

to essential services. AHRQ sponsors and conducts research that provides evidence-based 

information on health care outcomes; quality; and cost, use, and access. The information helps 

health care decisionmakers—patients and clinicians, health system leaders, and policymakers—

make more informed decisions and improve the quality of health care services. 
This document is in the public domain and may be used and reprinted without permission except 

those copyrighted materials noted for which further reproduction is prohibited without the 

specific permission of copyright holders. 

Suggested Citation: 

Rostom A, Dubé C, Cranney A, Saloojee N, Sy R, Garritty C, Sampson M, Zhang L, Yazdi F, 

Mamaladze V, Pan I, McNeil J, Moher D, Mack D, Patel D. Celiac Disease. Evidence

Report/Technology Assessment No. 104. (Prepared by the University of Ottawa Evidence-based 

Practice Center, under Contract No. 290-02-0021.) AHRQ Publication No. 04-E029-2. 

Rockville, MD: Agency for Healthcare Research and Quality. September 2004. 

ii
Preface 

The Agency for Healthcare Research and Quality (AHRQ), through its Evidence-Based 

Practice Centers (EPCs), sponsors the development of evidence reports and technology 

assessments to assist public- and private-sector organizations in their efforts to improve the 

quality of health care in the United States. This report on Celiac Disease was requested and 

funded by the Office of Medical Applications of Research, National Institutes of Health (NIH) 

for the Consensus Development Conference on Celiac Disease as well as the National Institute of 

Diabetes and Digestive and Kidney Diseases, NIH. Marian D. James, Ph.D., served as 

AHRQ’s Task Order Officer in charge of overseeing the report development process. The 

reports and assessments provide organizations with comprehensive, science-based information 

on common, costly medical conditions and new health care technologies. The EPCs 

systematically review the relevant scientific literature on topics assigned to them by AHRQ and 

conduct additional analyses when appropriate prior to developing their reports and assessments. 

To bring the broadest range of experts into the development of evidence reports and health 

technology assessments, AHRQ encourages the EPCs to form partnerships and enter into 

collaborations with other medical and research organizations. The EPCs work with these partner 

organizations to ensure that the evidence reports and technology assessments they produce will 

become building blocks for health care quality improvement projects throughout the Nation. The 

reports undergo peer review prior to their release. 

AHRQ expects that the EPC evidence reports and technology assessments will inform 

individual health plans, providers, and purchasers as well as the healthcare system as a whole by 

providing important information to help improve health care quality. 

We welcome written comments on this evidence report. They may be sent to: Director, 

Center for Outcomes and Evidence, Agency for Healthcare Research and Quality, 540 Gaither 

Road, Rockville, MD 20850. Questions regarding this report should be sent to 

epc@ahrq.gov. 

Jean Slutsky, P.A., M.S.P.H. 

Director, Center for Outcomes and 

Evidence 

Agency for Healthcare Research and Quality 

Carolyn M. Clancy, M.D. 

Director

Agency for Healthcare Research and Quality 

Barnett S. Kramer, M.D., M.P.H. 

Director

Office of Medical Applications 

 of Research, NIH 

Allen M. Spiegel, M.D. 

Director

National Institute of Diabetes and Digestive and 

 Kidney Diseases, NIH

The authors of this report are responsible for its content. Statements in the report should not 

be construed as endorsement by the Agency for Healthcare Research and Quality or the U.S. 

Department of Health and Human Services of a particular drug, device, test, treatment, or 

other clinical service. 

iii
Acknowledgments 

The authors would like to thank several individuals for their support of the present project: 

Keith O'Rourke, who helped with the statistical analysis; Karen Patrias, who helped with 

conducting the literature search; Gabriela Lewin, who assisted with the quality assessment; and 

Christine Murray and Isabella Steffensen, who assisted in the editing of the report and the 

generation of evidence tables. 

Author Contribution 

Dr. Alaa Rostom was the lead investigator. He was involved in all aspects of the study 

design, management, planning, analysis and write-up, including article screening, data 

extraction, quality assessment, statistical analysis, and report write-up. Drs. Catherine Dubé and 

Ann Cranney were the second investigators. Dr. Catherine Dubé was involved in all aspects of 

study design, and planning and organization, including task management, article screening, data 

extraction, and quality assessment. She was the lead writer of Celiac 2 and 3. Dr. Ann Cranney 

was involved in all aspects of study design and planning, including article screening, data 

extraction, and quality assessment. She was the lead writer of Celiac 4, and oversaw the 

screening and data extraction for Celiac 3, 4, and 5. Dr. Navaaz Saloojee was involved in study 

planning, article screening, data extraction, and quality assessment, and was the lead writer of 

Celiac 5. Dr. Richmond Sy was involved in study planning, article screening, data extraction, 

and contributed to the writing of Celiac 4. Drs. David Mack and Dilip Patel were involved in 

study planning and article screening, in addition to being content experts in pediatric and adult 

celiac disease, respectively. They also reviewed and advised on the report write-up. JoAnne 

McNeal was involved in article screening and data extraction for Celiac 1 (serology) and Celiac 

2 (prevalence). 

Dr. David Moher was involved in all aspects of study design, management, planning, 

analysis, and write-up. He was the methodological content expert and reviewed and advised on 

all report conduct and documents. Chantelle Garrity was involved in all aspects of project 

planning and management, including liaison with all key partners. She oversaw the screening 

progress, document retrieval, and assisted in report management, review and write-up. Margaret 

Sampson was the lead information specialist and was involved in all aspects of the search 

strategy/key word design and refinement, in association with the information specialists at the 

NLM. She was involved in all aspects of article database management, including article 

retrieval, set-up of the online computerized SRS article screening and extraction system, and the 

development and write-up of the QUOROM Flow. Li Zhang was the information specialist 

involved in all aspects of SRS system management, article retrieval, and implementation of the 

SRS system. Dr. Vasil Mamaladze and Fatemeh Yazdi performed the data extraction of Celiac 

1–serology and Celiac 2–prevalence. Irene Pan performed data extraction and quality 

assessment of Celiac 2–prevalence. 

iv
Structured Abstract 

Context. Celiac disease (CD) is a disorder of small bowel malabsorption. It is characterized by 

mucosal inflammation, villous atrophy and crypt hyperplasia that occur upon exposure to gluten, 

and clinical and histological improvement with withdrawal of gluten from the diet. The classical 

presentation of CD has now been shown to be less common than silent or atypical presentation, 

in which patients do not have intestinal symptoms. Untreated CD is associated with multiple 

important short- and long-term complications including nutritional derangements, anemia, 

reduced bone density, as well as intestinal lymphoma. In the vast majority of patients, CD is 

effectively treated with dietary modifications that eliminate gluten. Mounting evidence suggests 

that CD is actually considerably more common than previously believed and, therefore, this 

disorder warrants consideration for screening of at-risk patients, as well as possibly the general 

population. 

Objectives. To conduct a comprehensive systematic review on five areas of CD: (1) sensitivity 

and specificity of serological tests; (2) prevalence and incidence of CD; (3) CD associated 

lymphoma; (4) consequences of testing for CD; and, (5) interventions for the promotion and 

monitoring of adherence to a gluten-free diet (GFD). 

Data Sources. Staff of the National Library of Medicine performed a series of searches in 

support of the literature review of CD. Searches were run in the MEDLINE® (1966 to Oct 

2003) and EMBASE (1974 to Dec 2003) databases for each of the five objectives and their 

respective sub-objectives separately. 

Study Selection. Study selection for each objective was performed using three levels of

screening with predetermined increasingly more strict criteria to ensure that all relevant articles

were captured. Following a calibration exercise, two reviewers independently screened all 

studies using a web-based system allowed automatic identification of review disagreements. 

These disagreements were resolved by consensus. 

Data Extraction. For each CD objective, a detailed and standardized data abstraction form was 

developed. For each objective, data abstraction was conducted by one reviewer and verified by 

another. The extracted data was further verified by one of the principal investigators. Quality 

assessments were performed using specific instruments for each of the included study types. 

Data Synthesis. The data obtained from this review fell into several broad categories, which 

correspond in large part to the individual study objectives. Data for the sensitivity and

specificity of each serological marker was considered separately, and studies were further 

divided according to the age group of the study population. Attempts were made to identify, 

explain, and minimize clinical and statistical heterogeneity in the included studies. A Pearson’s 

Chi Square with n-1 degrees of freedom, where n represents the number of included studies in an 

analysis, was calculated to assess statistical heterogeneity. Pooled estimates were only 

calculated if clinically and statistically appropriate. In situations where pooling was not 

performed, a qualitative systematic review was conducted. 

v
To produce clinically useful pooled statistics, a weighted mean of the overall sensitivity and 

specificity from the included studies was calculated, along with 95% confidence intervals (CIs). 

The pooled estimates for the sensitivity and specificity were compared with a summary receiver 

operating characteristic (ROC) curve, calculated for the same group of studies as a second check 

of the estimates. 

Results/Conclusions. This report has provided a systematic review of five broad areas (and 

corresponding sub-areas) of CD. Perhaps one of the most important findings of this report is the 

significance of how one chooses to define CD in the era of serological testing, and how this 

apparently clear-cut task has profound implications on all the results presented in this report. 

Specifically, can CD be diagnosed solely on the basis of serology? Is some degree of villous 

atrophy necessary for a diagnosis of CD. These questions have important implications 

downstream of the diagnosis as well. For example, do CD patients without symptoms or villous 

atrophy have the same risk of complications as those with villous atrophy. Is serological 

improvement on a GFD sufficient to reduce CD complications, or must there be documented 

histological improvement, and what degree of histological improvement is necessary? 

The results of the Celiac 1 objective suggest that in the era of EMA and tTG antibody testing, 

AGA antibody testing in both children and adults has a limited role. The sensitivity and 

specificity of EMA and tTG are quite high (over 95% for sensitivity, and close to 100% for 

specificity), as are their positive and negative predictive values; however, one has to be aware 

that the reported diagnostic parameters are taken from studies in which the prevalence of CD 

was, for the most part, much higher than that seen in usual clinical practice. The positive 

predictive values reported for these tests will certainly not be as high as that reported when these 

tests are used to screen the general population. The bulk of the evidence on the diagnostic 

characteristics of these tests was derived from studies that defined CD as having at least some

degree of VA. 

HLA DQ2/DQ8 testing appears to be a useful adjunct in the diagnosis of CD. The test has 

high sensitivity (in excess of 90%-95%), however, since approximately 30% of the general 

population, and an even higher proportion of “high-risk” subjects (e.g., diabetics and family 

members) also carry these markers, the specificity of this test is not ideal. The greatest 

diagnostic utility of this test appears to be its negative predictive value. 

Biopsy itself, when used with a strict cut-off requiring villous atrophy, appears to have high 

specificity, but poor sensitivity. Using a lower grade cut-off clearly improves sensitivity, but 

because of the wide differential of causes of histological lesions similar to Marsh I to IIIa, the 

specificity suffers. The use of histomorphometric measures such as quantification of gamma 

delta positive intraepithelial lymphocytes (γδ+ IELs) are likely to allow for the use of lower 

grade cut-offs, while maintaining reasonable specificity. Ultimately, a trial utilizing multiple 

diagnostic tests in an attempt to capture as many CD patients in a clinically-relevant population 

as possible, along with a time dimension such as a response to a GFD or gluten challenge, is 

required to fully assess the diagnostic characteristics of biopsy alone. This type of study would 

be able to characterize the false-positive and false-negative rates, provided that all studied 

patients are followed forward in time. 

The included prevalence studies demonstrated important differences between the studies 

including, execution, tests for prevalence assessment, and patient sampling. Thus, results have to 

be interpreted in the light of some of the limitations that have been identified regarding the 

diagnostic performance of the tests for CD. Nonetheless, the results of this report suggest that 

vi
CD is a very common disorder with a prevalence in the general population that is likely close to 

1:100 (1%). Several high-risk groups with a prevalence of CD greater than that of the general 

population have been identified and include: those suspected of having CD; family members of 

CD patients; type I diabetics; and, those with iron-defiency anemia (IDA) or low bone mineral 

density (BMD). Additionally, the review identified many other high-risk groups, including those 

with Down Syndrome, short stature, and infertility, to name a few. Their inclusion was however, 

beyond the scope of this report 

The results of this report confirm that, apart from a few limitations, there is a strong 

association between CD and GI lymphoma. The report identified standard incidence ratios (SIR) 

for lymphoma that ranged from 4 to 40, and standard mortality ratios (SMR) that ranged from 11 

to 70. A diagnostic delay—in particular a diagnosis of CD in adulthood as apposed to in 

childhood—is associated with poorer outcomes. Fortunately, several studies suggest that 

adherence to a GFD reduces the risk of lymphoma in CD patients. 

The consequences of testing for CD in at-risk and symptomatic patients appears to be more 

straightforward, since these patients appear to be more compliant with a GFD and would be 

expected to benefit from this intervention. The data is less clear for asymptomatic screenidentified patients, particularly those who have truly silent CD and/or don’t have fully-developed 

villous atrophy. On the one hand the outcome of such patients has not been extensively studied, 

and on the other hand compliance with a GFD appears problematic, particularly for those 

diagnosed in adulthood. 

Finally, no specific interventions have been identified that promote adherence to a GFD, but 

education of patients and family members about CD and about the intricacies of a GFD, and 

participation in local celiac societies, has been shown to improve compliance. Although 

somewhat controversial, biopsy monitoring of adherence to a GFD appears to be important, since 

improvement in histological grade has been associated with improved BMD, IDA, and 

nutritional status. The serological markers appear to be adequate for detecting gross dietary 

indiscretion, and respond to a gluten challenge, but appear to have poor sensitivity for detecting 

lesser degrees of dietary indiscretion, and inadequately correlating with histological 

improvement at least in the short-term. It should, however, be noted, that we could not identify a 

controlled study that objectively determined the level of histological improvement that would be 

associated with improved outcomes, and this is an area for future study. Nonetheless, based on 

this report it would appear that follow-up biopsy, at least 1 year after a GFD in adults to 

document improvement of the histological grade, would be valuable. 

vii
Contents 

Evidence Report 

Chapter 1. Introduction ..................................................................................................................3 

Overview..................................................................................................................................... 3 

Definition of CD ......................................................................................................................... 4 

General Definitions................................................................................................................. 5 

Report Purpose and Target Population ....................................................................................... 6 

Methodological Considerations .................................................................................................. 6 

Chapter 2. Methods ........................................................................................................................9 

Overview..................................................................................................................................... 9 

Key Questions Addressed in This Report................................................................................... 9 

Study Criteria Used in this Review........................................................................................... 10

Histological........................................................................................................................... 10 

Populations............................................................................................................................ 11 

HLA DQ2/DQ8..................................................................................................................... 11 

Analytical Framework .............................................................................................................. 12 

Study Identification................................................................................................................... 13 

Search Strategy ..................................................................................................................... 13 

Study Selection and Eligibility Criteria ................................................................................ 14 

Data Abstraction ................................................................................................................... 17 

Quality Assessment............................................................................................................... 19 

Data Synthesis and Analysis................................................................................................. 19 

Chapter 3. Results .........................................................................................................................21 

Celiac 1: Sensitivity and Specificity of Tests for CD............................................................... 21 

Serology ................................................................................................................................ 21 

HLA DQ2/DQ8..................................................................................................................... 55 

Biopsy ................................................................................................................................... 65 

Quality Assessment............................................................................................................... 65 

Celiac 2: Incidence and Prevalence of CD ............................................................................... 66 

Incidence of CD in the General Population .......................................................................... 67 

Prevalence of CD in the General Population—Different Geographic and Racial/Ethnic 

Populations............................................................................................................................ 71 

Prevalence of CD in Patients with Suspected CD ................................................................ 79 

Prevalence of CD in with Type I Diabetes ........................................................................... 81 

Prevalence of CD in Relatives of Patients with CD ............................................................. 89 

Prevalence of CD in Patients with IDA ................................................................................ 92 

Prevalence of CD in Patients with Low Bone Mineral Density (BMD)............................... 95 

Quality Assessment............................................................................................................... 96 

Celiac 3: Risk of Lymphoma in CD ......................................................................................... 97 

Literature Search................................................................................................................... 97 

Measures of Risk................................................................................................................... 99 
Study Characteristics ............................................................................................................ 99 

Types of Lymphomas ........................................................................................................... 99

Incidence of Lymphoma and Related Mortality Data......................................................... 100 

Role of a GFD..................................................................................................................... 102 

Risk of Lymphoma Versus Symptoms ............................................................................... 102 

Impact of the Age at Diagnosis of CD................................................................................ 102 

Risk of Lymphoma in Refractory CD................................................................................. 103 

Quality Assessment............................................................................................................. 103 

Celiac 4: Consequences of Testing for CD............................................................................. 104 

Part A .................................................................................................................................. 104 

Part B .................................................................................................................................. 109 

Quality Assessment............................................................................................................. 117 

Celiac 5: Promoting or Monitoring Adherence to a GFD....................................................... 118 

Monitoring Adherence to a GFD ........................................................................................ 118 

Interventions to Promote Adherence to a GFD................................................................... 121 

Quality Assessment............................................................................................................. 122 

Chapter 4. Discussion.................................................................................................................123 

Celiac 1: Sensitivity and Specificity of Tests for CD............................................................. 123 

Serology .............................................................................................................................. 123 

HLA DQ2/DQ8................................................................................................................... 128 

Biopsy ................................................................................................................................. 129 

Celiac 2: Incidence and Prevalence of CD ............................................................................. 139 

Incidence in the General Population—Different Geographic and Racial/Ethnic Populations

............................................................................................................................................. 139 

Prevalence in the General Population—Different Geographic and Racial/Ethnic Populations

............................................................................................................................................. 140 

Prevalence of CD in Patients with Suspected CD .............................................................. 140 

Prevalence of CD in Patients with Type I Diabetes............................................................ 141 

Prevalence of CD in Relatives of Patients with CD ........................................................... 141 

Prevalence of CD in Patients with Anemia......................................................................... 142 

Prevalence of CD in Patients with Low BMD.................................................................... 142 

Celiac 3: Risk of Lymphoma in CD ....................................................................................... 143 

Celiac 4: Consequences of Testing for CD............................................................................. 146 

Expected Outcomes of Treatment of CD............................................................................ 148 

Fractures/BMD/Osteoporosis/Osteopenia .......................................................................... 149 

Mortality ............................................................................................................................. 150 

Celiac 5: Promoting or Monitoring Adherence to a GFD....................................................... 150 

Monitoring Adherence to a GFD ........................................................................................ 150 

Interventions to Promote Adherence to a GFD................................................................... 152 

Strength of the Body of Evidence........................................................................................... 153 

Celiac 1 ............................................................................................................................... 153 

Celiac 2 ............................................................................................................................... 154 

Celiac 3 ............................................................................................................................... 154 

Celiac 4 ............................................................................................................................... 154 
Celiac 5 ............................................................................................................................... 154 

Future Research...........................................................................................................................155 

Conclusion...................................................................................................................................156 

References and Included Studies ................................................................................................159 

Abbreviations and Acronyms......................................................................................................183 

Tables 

Table 1: Inclusion/exclusion criteria by level of screening ..........................................................16 

Table 2: Included studies for IgA-AGA in children .....................................................................23 

Table 3: Included studies for IgA-AGA in adults.........................................................................24 

Table 4: Included studies for IgA-AGA in studies including both children and adults................25 

Table 5: Included studies for IgG-AGA in adults.........................................................................27 

Table 6: Included studies for IgG-AGA in children .....................................................................28 

Table 7: Included studies for IgG-AGA in studies including both children and adults................29 

Table 8: Included studies for IgA-EMA-ME in adults .................................................................32 

Table 9: Included studies for IgA-EMA-ME in children..............................................................33 

Table 10: Included studies for IgA-EMA-ME in studies including both children and adults ......34 

Table 11: Included studies for IgG-EMA-ME in adults ...............................................................36 

Table 12: Included studies for IgG-EMA-ME in children............................................................36 

Table 13: Included studies for IgA-EMA-HU in adults................................................................37 

Table 14: Included studies for IgA-EMA-HU in children............................................................37 

Table 15: Included studies for IgA-EMA-HU in studies including both children and adults ......38 

Table 16: Included studies for IgA-tTG-GP in adults...................................................................41 

Table 17: Included studies for IgA-tTG-GP in children ...............................................................41 

Table 18: Included studies for IgA-tTG-GP in studies including both adults and children .........41 

Table 19: Included studies for IgG-tTG-GP in studies including both children and adults .........43 

Table 20: Included studies for IgG-tTG-HR in studies including both children and adults .........45 

Table 21: Included studies for IgA-tTG-HR in adults ..................................................................45 

Table 22: Included studies for IgA-tTG-HR in children...............................................................45 

Table 23: Included studies for IgA-tTG-HR in studies including both children and adults .........46 

Table 24: Included studies for combination IgA and IgG AGA, when either test is positive ......49 

Table 25: Included studies for combination IgA and IgG tTG-HR, when either test is positive..49 

Table 26: Included studies for combination IgA-AGA and IgG-EMA-HU, when either test is 

positive..........................................................................................................................49 

Table 27: Weighted pooled estimates with 95% CIs and heterogeneity identified ......................52 

Table 28: HLA studies with biopsied cases and controls..............................................................56 

Table 29: Prevalence/frequency of HLA DQ2 and HLA DQ8 in prevalence and mixed-design 

studies, and in case-control studies with HLA DQ8 data.............................................59 

Table 30: Sensitivity/specificity (calculated) for HLA DQ2 in case-control studies ...................60 

Table 31: Sensitivity/specificity (calculated) for HLA DQ2 in mixed-design studies .................62 

Table 32: Sensitivity/specificity (calculated) for HLA DQ8 ........................................................63 

Table 33: Sensitivity/specificity (calculated) for HLA DQ2 or DQ8 ...........................................64 

Table 34: Included studies of incidence of CD in the general population....................................68 

Table 35: Prevalence of CD by country........................................................................................73
Table 36: Prevalence of CD by serological screening test............................................................76 

Table 37: Prevalence of CD by statistical percentiles...................................................................77 

Table 38: Included studies for prevalence of CD in patients with suspected CD.........................81 

Table 39: Included studies of prevalence of CD in type I diabetes ..............................................84 

Table 40: Summary of prevalence of CD in type I diabetes by age groups and screening test....88 

Table 41: Prevalence of CD in relatives of CD patients ...............................................................91 

Table 42: Included studies of CD in adult patients with anemia ..................................................93 

Table 43: Summary of prevalence of CD in adult patients with anemia by population and 

screening test ................................................................................................................95 

Table 44: Prevalence of CD in patients with low BMD ...............................................................96 

Table 45: Included studies for risk of lymphoma in CD...............................................................98 

Table 46: Results of study assessing γδ+ IELs in patients with and without CD .......................132 

Table 47: Results of study assessing density of γδ+ IELs in patients with untreated CD, treated 

CD and control patients ..............................................................................................133 

Table 48: Results of study comparing density of γδ+ IELs in patients with confirmed CD, those 

undergoing investigation for CD, and control subjects ..............................................133 

Table 49: Results of study comparing IEL density and villous/crypt ratio in patients with a 

suspicion of CD, and 59 biopsy-negative controls with dyspepsia ............................134 

Table 50: Results of study assessing IEL density in routinely stained specimens compared with 

specimens stained with the CD3 antibody..................................................................134 

Table 51: Results of study comparing IEL density and villous distribution among patients 

suspected of CD..........................................................................................................135 

Table 52: Results of study assessing patients with suspected CD and Marsh I or II, before and 

after a GFD .................................................................................................................137

Figures 

Figure 1: Analytic framework.......................................................................................................12 

Figure 2: IgA-AGA in children with CD ......................................................................................25 

Figure 3: IgA-AGA in adults with CD..........................................................................................26

Figure 4: IgA-AGA in adults and children with CD.....................................................................26 

Figure 5: IgG-AGA in adults with CD..........................................................................................29

Figure 6: IgG-AGA in children with CD ......................................................................................30 

Figure 7: IgG-AGA in children and adults with CD.....................................................................30 

Figure 8: IgA-EMA-ME in adults with CD ..................................................................................34 

Figure 9: IgA-EMA-ME in children with CD...............................................................................35 

Figure 10: IgA-EMA-ME in adults and children with CD ...........................................................35 

Figure 11: IgA-EMA-HU in adults with CD ................................................................................38 

Figure 12: IgA-EMA-HU in children with CD.............................................................................39 

Figure 13: IgA-EMA-HU in adults and children with CD............................................................39 

Figure 14: IgA-tTG-GP in adults with CD ...................................................................................42 

Figure 15: IgA-tTG-GP in children with CD................................................................................42 

Figure 16: IgA-tTG-GP in adults and children with CD...............................................................43 

Figure 17: IgG-tTG-GP in adults with CD ...................................................................................44 

Figure 18: IgA-tTG-HR in adults with CD ...................................................................................46 
Figure 19: IgA-tTG-HR in children with CD ...............................................................................47 

Figure 20: IgA-tTG-HR in adults and children with CD ..............................................................47 

Figure 21: PPV and prevalence from individual studies...............................................................53 

Figure 22: NPV and prevalence from individual studies ..............................................................53 

Figure 23: PPV based on the pooled estimates of sensitivity and specificity...............................54 

Figure 24: HLA DQ2 ....................................................................................................................64 

Figure 25: HLA DQ2 and DQ8.....................................................................................................65 

Figure 26: Frequency distribution of prevalence of CD by serology among included studies.....77 

Figure 27: Frequency distribution of prevalence of CD by biopsy among included studies........78 

Figure 28: Prevalence of CD by country.......................................................................................78

Figure 29: General population prevalence in relation to sample size ...........................................79 

Figure 30: Prevalence of CD in diabetes by study size.................................................................89 

Figure 31: PPV based on pooled estimates of sensitivity and specificity...................................147 

Appendixes 

Appendix A: Histological Data 

Appendix B: Search Strategies 

Appendix C: Data Assessment and Data Abstraction Forms 

Appendix D: Quality Assessment Forms 

Appendix E: Summary ROC Curves 

Appendix F: Modified QUOROM Flow Chart 

Appendix G: Raw Pooled Data 

Appendix H: Biopsy Results 

Appendix I: Evidence Tables 

Appendix J: Quality Assessment 

Appendix K: Additional Acknowledgments 

Appendix L: List of Excluded Studies 

Appendixes and Evidence Tables are provided electronically at 

http://www.ahrq.gov/clinic/tp/celiactp.htm 
Introduction

Celiac disease (CD) is a disorder of small bowel

malabsorption. It is characterized by mucosal

inflammation, villous atrophy, and crypt

hyperplasia, which occur upon exposure to

gluten, and clinical and histological improvement

with withdrawal of gluten from the diet.1-4 CD—

also referred to as celiac sprue, gluten-sensitive

enteropathy, non-tropical sprue, in addition to a

host of other names—is thought to result from

the activation of both a cell-mediated (T-cell) and

humoral (B-cell) immune response upon exposure

to the glutens (prolamins and glutenins) of wheat,

barley, rye, and oats, in a genetically susceptible

person.5,6 Genetic susceptibility is suggested by a

high concordance among monozygotic twins of

close to 70 percent,7 and an association with

certain type II human leukocyte antigens

(HLA).8,9 HLA DQ2 is found in up to 95

percent of CD patients, while most of the

remaining patients have HLA DQ8.8-10 However,

there is only a 30 percent HLA concordance

among siblings, suggesting that other genetic

factors are also at play.11 More recent evidence

suggests that the presence of auto-antibodies to a

connective tissue element surrounding smooth

muscle called endomysium is highly specific for

CD. The target of this autoantibody is now

known to be an enzyme called tissue

transglutaminase (tTG). This enzyme may play a

prominent role in the pathogenesis of CD by

modifying gliadin, resulting in a greater

proliferative response of gliadin specific T-cells,

which contributes to mucosal inflammation and

further B-cell activation.5,6,12,13

CD appears to represent a spectrum of clinical

features and presentations. Although “classical”

CD (i.e., fully developed gluten-induced villous

atrophy and classical features of intestinal

malabsorption) is most commonly described, it

appears that most patients have atypical CD (i.e.,

fully developed gluten-induced villous atrophy

found in the setting of another presentation such

as iron deficiency, osteoporosis, short stature, or

infertility) or silent CD (i.e., fully developed

gluten-induced villous atrophy discovered in an

asymptomatic patient by serologic screening or

perhaps an endoscopy for another reason). Other

authors describe a latent form of CD that is

characterized by a previous diagnosis that

responded to a gluten-free diet (GFD) and

retained a normal mucosal histology upon later

introduction of gluten. Latent CD can also

represent patients with currently normal intestinal

mucosa who will subsequently develop glutensensitive enteropathy.13,14

The true prevalence of CD is difficult to

estimate because of the variable presentation of

the disease, particularly since many patients can

have little or no symptoms. With this limitation

in mind, the prevalence of the disease is highest in

Celtic populations where estimates of 1:300 to

1:122 have been described. The prevalence of

CD in North America has been estimated to be

1:3000, but a recent American study found the

prevalence among the general not-at-risk

population to be 1:105, while the prevalence in

at-risk groups such as first-degree relatives of CD

patients was 1:22, suggesting that CD is greatly

under diagnosed. CD can affect persons of many

ethnic backgrounds, but appears to rarely affect

persons of purely Chinese, Japanese, or AfroCaribbean decent.13

The diagnosis of CD in adults is classically

made on the basis of clinical suspicion—that is,

recognizing atypical presentations such as isolated

iron deficiency, combined iron and folate

deficiency, and osteoporosis—compatible with a

duodenal biopsy while taking a gluten-containing

diet, followed by clinical and histological

improvement following commencement of a

GFD.2,4 However, several serologic markers have

become available that have altered the classic

Evidence Report/Technology Assessment

Number 104

Celiac Disease

Summary

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES • Public Health Service

Agency for Healthcare Research and Quality
2

diagnostic pathway. The sensitivity of IgA anti-gliadin

antibodies (AGA) is reported to range from 70 to 85 percent,

whereas the specificity ranges from 70 to 90 percent. IgA antiendomysial (EMA) and anti-tissue transglutaminase (tTG)

antibodies have sensitivities in excess of 90 percent and

specificities of over 95 percent.14 Significant variability seems to

exist in the reported values among the different studies, and

these IgA-based tests can be negative in IgA-deficient patients,

accounting for about 3 percent of CD cases.

The sensitivity and specificity of the anti-EMA and anti-tTG

antibodies, along with the perceived under diagnosis of CD,

has led to suggestions of using these tests for population

screening. Aside from the recognized influence of CD

prevalence on the predictive value of a serologic test result, little

consensus exists regarding the value of population screening.

Furthermore, specific questions regarding clinically important

outcomes resulting from screening remain unclear. In

particular, little data is available on adherence to a GFD in

asymptomatic CD patients detected by screening. 

The major complications of CD include intestinal and

extraintestinal malignancies, ulcerative jejunoileitis, and

collagenous sprue. Unlike most gastrointestinal (GI)

lymphomas that are typically of B-cell origin, lymphomas

associated with CD appear to be most commonly of T-cell

origin. Unfortunately, the prognoses for patients with CDassociated T-cell lymphomas, ulcerative jejunoileitis, and

collagenous sprue, appear grim. It is widely believed that strict

adherence to a GFD reduces the risk of these complications. It

is suggested that by 5 years of dietary adherence the risk of

lymphoma in CD patients approaches that of the general

population.14

The challenge of CD remains to determine which patient

populations should be screened, the best means of screening,

and whether early detection of patients with CD leads to

improved patient outcomes. For patient outcomes to improve

as a result of screening, the degree to which “positively”

screened individuals, particularly those who were

asymptomatic, adhere to the stringent GFD, needs to be

determined.

Methods

We completed a series of systematic reviews on five areas of

CD: (1) sensitivity and specificity of serological tests; (2)

prevalence and incidence of CD; (3) CD-associated lymphoma;

(4) consequences of testing for CD; and (5) interventions for

the promotion and monitoring of adherence to a gluten-free

diet (GFD). Staff at the National Library of Medicine

performed a series of searches in support of the literature review

of CD. Searches were run in the MEDLINE® (1966 to Oct

2003) and EMBASE (1974 to Dec 2003) databases for each of

the five objectives and their respective sub-objectives separately.

Furthermore, for the 4th and 5th objectives, PsycINFO (1840

forward), AGRICOLA (1970 forward), CAB (1972 forward),

and Sociological Abstracts (1963 forward) database searches

were run in December 2003. Study selection for each objective

was performed using three levels of screening with

predetermined increasingly more strict criteria to ensure that all

relevant articles were captured. Following a calibration exercise,

two reviewers independently screened all studies using a Webbased system that allowed automatic identification of review

disagreements. These disagreements were resolved by

consensus. For each CD objective, a detailed and standardized

data abstraction form was developed. For each objective, data

abstraction was conducted by one reviewer and verified by

another. The extracted data was further verified by one of the

principal investigators. Quality assessments were performed

using specific instruments for each of the included study types.

The data obtained from this review fell into several broad

categories, which correspond in large part to the individual

study objectives. Data for the sensitivity and specificity of each

serological marker was considered separately, and studies were

further divided according to the age group of the study

population. Attempts were made to identify, explain, and

minimize clinical and statistical heterogeneity in the included

studies. A Pearson’s Chi Square with n-1 degrees of freedom,

where n represents the number of included studies in an

analysis, was calculated to assess statistical heterogeneity.

Pooled estimates were only calculated, if clinically and

statistically appropriate. In situations where pooling was not

performed, a qualitative systematic review was conducted.

To produce clinically useful pooled statistics, a weighted

mean of the overall sensitivity and specificity from the included

studies was calculated, along with 95 percent confidence

intervals (CIs). The pooled estimates for the sensitivity and

specificity were compared with a summary receiver operating

characteristic (ROC) curve, calculated for the same group of

studies as a second check of the estimates.

Results and Discussion

Perhaps one of the most important findings of this report is

the significance of how one chooses to define CD in the era of

serological testing, and how this apparently clear-cut task has

profound implications on all the results presented in this

report. Specifically, can CD be diagnosed solely on the basis of

serology? Is some degree of villous atrophy necessary for a

diagnosis of CD? These questions have important implications

downstream of the diagnosis as well. For example, do CD

patients without symptoms or villous atrophy have the same

risk of complications as those with villous atrophy? Is

serological improvement on a GFD sufficient to reduce CD

complications, or Must there be documented histological

improvement? What degree of histological improvement is

necessary?

Out of 3,982 citations identified by the search strategy for

the Celiac 1 objective, 60 studies fulfilled the level 3 inclusion

criteria. Overall, the quality of the diagnostic studies assessed in

the Celiac 1 objective was quite good, due largely to our

stringent inclusion criteria. However, 59 percent of the
included studies reported using a selected patient population

that may not be representative of a clinically relevant

population. This is likely related to study design. In addition,

only 11 percent of the studies reported on whether the

reference test was reported without knowledge of the index test.

However, we felt that this was not a major threat to the validity

of the studies. 

Two other factors that affect the interpretation of these

results, are (1) the threshold effects for determining the

positivity of a serological test and (2) the high prevalence of

CD in these studies (see above). With these considerations in

mind, the overall strength of the evidence is quite good.

To minimize clinical and statistical heterogeneity, the

included articles of a particular antibody test were divided into

groups by age of the included population (adults, children,

mixed), the study design (case control, or relevant clinical

population/cohort), by antibody type (IgA or IgG), and by test

methodology (e.g., monkey esophagus [ME] or human

umbilical cord [HUC]). Within these groups, further

differences in study population, country of origin, and biopsy

definitions (especially whether or not mild grades without

villous atrophy were included) were assessed systematically.

Studies that reported using the ESPGAN criteria for the

diagnosis of CD were categorized as including patients with

some degree of villous atrophy. Other potential causes of

heterogeneity, such as the cut-offs used to define a positive test,

were assessed. The results of the Celiac 1 objective suggest that

in the era of EMA and tTG antibody testing, AGA antibody

testing in both children and adults has a limited role. The

sensitivity and specificity of EMA and tTG are quite high (over

95 percent for sensitivity, and close to 100 percent for

specificity), as are their positive and negative predictive values;

however, the reported diagnostic parameters are taken from

studies in which the prevalence of CD was, for the most part,

much higher than that seen in usual clinical practice. The

positive predictive values reported for these tests will certainly

not be as high as that reported when these tests are used to

screen the general population. The bulk of the evidence on the

diagnostic characteristics of these tests was derived from studies

that defined CD as having at least some degree of villous

atrophy. 

HLA DQ2/DQ8 testing appears to be a useful adjunct in

the diagnosis of CD. The test has high sensitivity (in excess of

90 to 95 percent); however, since approximately 30 percent of

the general population, and an even higher proportion of

“high-risk” subjects (e.g., diabetics and family members) also

carry these markers, the specificity of this test is not ideal. The

greatest diagnostic utility of this test appears to be its negative

predictive value.

Biopsy itself, when used with a strict cut-off requiring villous

atrophy, appears to have high specificity, but poor sensitivity.

Using a lower grade cut-off clearly improves sensitivity, but

because of the wide differential of causes of histological lesions

similar to Marsh I to IIIa, the specificity suffers. The use of

histomorphometric measures such as quantification of gamma

delta positive intraepithelial lymphocytes (gd+ IELs) are likely

to allow for the use of lower grade cut-offs, while maintaining

reasonable specificity. Ultimately, a trial utilizing multiple

diagnostic tests in an attempt to capture as many CD patients

in a clinically relevant population as possible, along with a time

dimension such as a response to a GFD or gluten challenge, is

required to fully assess the diagnostic characteristics of biopsy

alone. This type of study would be able to characterize the

false-positive and false-negative rates, provided that all studied

patients are followed forward in time.

The literature search yielded 2,116 references to address the

Celiac 2 objective. Studies were included if they reported the

prevalence and/or incidence of CD in the following groups: (1)

general populations from North America or Western Europe;

(2) first-degree relatives of patients with CD; (3) patients with

type 1 diabetes; (4) patients being investigated for anemia; (5)

patients with osteoporosis or osteopenia; and (6) patients with

suspected CD on the basis of their clinical presentations. We

did not use any geographic restriction for the studies of

populations at risk (first-degree relatives and type 1 diabetics) or

of associated clinical presentations (suspected CD, anemia, or

metabolic bone disease). Studies of prevalence or incidence

that used AGA tests conducted prior to 1990 were excluded

after discussion with AHRQ because of potential problems

with the reliability of older AGA assays. One hundred and

nineteen studies were included. 

The overall quality of reports of the included studies in the

Celiac 2 objective was found to be marginal to fair. For

example, most of the studies did not report on whether the

patients were consecutively enrolled, a factor that could

contribute to selection bias. However, setting aside the quality

of individual studies, from a policy perspective, the strength of

the evidence is fairly good in that the study populations were

selected to reflect that of a North American/Western European

descent, that should reflect the demographics of the U.S.

population.

The crude incidence of CD in adults varied from lows of

1.27 in Denmark15 and 3.08 in England,16 to a high of 17.2

cases per 100,000 patient years in Finland,17 where specific

efforts had been untaken to encourage screening for CD (see

Table 34). The crude incidence of CD in children age 0 to 15

years varied from 2.15 to 51 cases per 100,000 patient years.18-

20,21,16,22 When reported, the relative risk (RR) of CD was

greatest for the 0- to 2-year age group, as well as for women,

and varied from 32.26 to 42.4 18,19,22 and from 1.9 to 3.34, 23,18,20

respectively. The cumulative incidence at age 5, when reported,

varied between 0.089 and 9 cases per 1,000 live births.23,24,25,26

The included prevalence studies demonstrated important

differences between the studies including execution, tests for

prevalence assessment, and patient sampling. Thus, results have

to be interpreted in light of some of the limitations that have

been identified regarding the diagnostic performance of the

tests for CD. Nonetheless, the results of this report suggest that

3
4

CD is a very common disorder with a prevalence in the general

population that is likely close to 1:100 (1 percent). Several

high-risk groups with a prevalence of CD greater than that of

the general population have been identified and include: (1)

those suspected of having CD; (2) family members of CD

patients; (3) type I diabetics; and (4) those with iron-defiency

anemia (IDA) or low bone mineral density (BMD).

Additionally, the review identified many other high-risk groups,

including those with Down Syndrome, short stature, and

infertility, to name a few. Their inclusion was, however,

beyond the scope of this report.

Out of 379 references resulting from the literature search on

CD and lymphoma, our third objective, eight cohort studies

and one case-control study were selected for data extraction.

The studies included in the Celiac 3 objective were found,

overall, to be of good quality. Again, the overall strength of the

evidence is due largely to the stringent inclusion criteria, such

as the requirement for the reporting of standardized rates for

the outcomes based on rates from the local general population,

and the overall good quality of the included studies.

Out of 1,199 citations that were identified by the search

strategy for the Celiac 4 objective, 35 articles satisfied the

screening criteria. The majority of studies included in this

objective were single group “before–after” studies, although

some also had a comparative healthy control group. We could

not identify any quality instruments for this type of study

design and, in general, this type of study is considered weak,

particularly in the absence of a control group. Overall,

however, the strength of the evidence for this objective is fair to

good and suggests that the results can be used for policy

decisions with the understanding that this area of CD research

is still relatively new and requires further high-quality studies.

The results of this report confirm that, apart from a few

limitations, there is a strong association between CD and GI

lymphoma. The report identified standard incidence ratios

(SIR) for lymphoma that ranged from 4 to 40, and standard

mortality ratios (SMR) that ranged from 11 to 70. A

diagnostic delay—and possibly a diagnosis of CD in adulthood

as opposed to in childhood—may be associated with poorer

outcomes. Fortunately, several studies suggest that adherence to

a GFD reduces the risk of lymphoma in CD patients. 

The consequences of testing for CD in at-risk and

symptomatic patients appears to be more straightforward, since

these patients appear to be more compliant with a GFD and

would be expected to benefit from this intervention. The data

are less clear for asymptomatic screen-identified patients,

particularly those who have truly silent CD and/or don’t have

fully developed villous atrophy. On the one hand, the outcome

of such patients has not been extensively studied; on the other

hand, compliance with a GFD appears problematic,

particularly for those diagnosed in adulthood.

Out of 502 citations identified by the search strategy for the

Celiac 5 objective, 20 studies met level 3 inclusion criteria. The

majority of studies in this objective were also of a “before–after”

design. However, in this setting, this design may not pose a

major limitation, since the purpose of the study is to assess the

change in serology and histology after introduction of a GFD.

In this regard, the strength of the evidence for monitoring

adherence to a GFD is fairly good. However, there is almost a

complete absence of studies of interventions for the promotion

of adherence to a GFD.

No specific interventions have been identified that promote

adherence to a GFD, but education of patients and family

members about CD and about the intricacies of a GFD, and

participation in local celiac societies, has been shown to

improve compliance. Although somewhat controversial, biopsy

monitoring of adherence to a GFD appears to be important,

since improvement in histological grade has been associated

with improved BMD, IDA, and nutritional status. The

serological markers appear to be adequate for detecting gross

dietary indiscretion and respond to a gluten challenge, but

appear to have poor sensitivity for detecting lesser degrees of

dietary indiscretion and inadequately correlate with histological

improvement, at least in the short-term. Children, on the other

hand, show more rapid and complete histological improvement

on a GFD. Therefore, monitoring adherence using serology is

reasonable in this age group. It should, however, be noted, that

we could not identify a controlled study that objectively

determined the level of histological improvement that would be

associated with improved outcomes; this is an area for future

study. Nonetheless, based on this report it would appear that

followup biopsy at least 1 year after a GFD in adults to

document improvement of the histological grade would be

valuable.

This review has allowed us to identify several areas in need of

future research. Perhaps the most important of these is a need

for the development of a consensus on the definition of CD in

the era of advanced serological testing. As discussed in the

report, this distinction of what one calls CD has profound

implications for each of the requested task order objectives. Do

screen-positive patients without villous atrophy have CD?

Certainly, the preliminary evidence suggests that this is the

situation in many cases. However, what is required is a new

definition of a gold standard for the diagnosis of CD. This

new gold standard may include a combination of serology,

biopsy, and HLA testing. Such a gold standard, when used in

studies with a time dimension (e.g., response to a GFD or

gluten challenge; extended followup), would help answer some

of the uncertainties identified in this report including: the real

performance of the serological tests when low-grade lesions are

considered CD; the diagnostic performance of biopsy alone;

the outcomes of patients with these low-grade lesions; and

those that would be “missed” using current screening strategies.

Even in the absence of a new gold standard, we could not

identify a well-conducted study of the diagnostic performance

of the various serological markers when applied to an average

population (i.e., one with a prevalence of CD in keeping with

the range identified for average risk), with the entire cohort
being investigated equally (i.e., all are biopsied). Such a study

would at least be able to shed light on the performance of these

tests in average-risk patients, and since all patients are biopsied,

the relationship of histology to serology could be further

assessed.

On a similar theme, we have identified multiple studies that

suggest the importance of histological improvement on a GFD.

This is a controversial area because in common clinical practice

clinicians are moving away from routine followup biopsy. It

seems reasonable to believe that improvement in clinical

parameters with loss of serological markers is adequate evidence

of response to a GFD. In children, this issue may be less

important since histological improvement is much more rapid

and complete than in adults, and correlation with serology

seems better. However, we have identified multiple studies in

adults that suggest poor correlation between serology and

improvement of histology on a GFD, and other studies that

suggest that serology is useful for detecting gross dietary

indiscretion, but not minor occurrences. Therefore, the

questions that arise are What constitutes adequate

improvement on a GFD?, and What are the criteria to define

this improvement? Based on the lymphoma literature that

suggests that this malignancy may arise from chronic antigenic

stimulation and immune activation, what are the outcomes of

adults with clinical improvement, yet persistent histological

abnormalities? Are some histological features, such as reduction

of mucosal lymphocytes, more important markers of

improvement and possibly prognosis than other features such as

villous height?

Availability of the Full Report

The full evidence report from which this summary was taken

was prepared for the Agency for Healthcare Research and

Quality (AHRQ) by the University of Ottawa Evidence-based

Practice Center, under Contract No. 290-02-0021. It is

expected to be available in July 2004. At that time, printed

copies may be obtained free of charge from the AHRQ

Publications Clearinghouse by calling 800-358-9295.

Requesters should ask for Evidence Report/Technology

Assessment No. 104, Celiac Disease. In addition, Internet users

will be able to access the report and this summary online

through AHRQ’s Web site at www.ahrq.gov.

Suggested Citation

Rostom A, Dubé C, Cranney A, Saloojee N, Sy R, Garritty

C, Sampson M, Zhang L, Yazdi F, Mamaladze V, Pan I,

McNeil J, Moher D, Mack D, Patel D. Celiac Disease.

Summary, Evidence Report/Technology Assessment No. 104.

(Prepared by the University of Ottawa Evidence-based Practice

Center, under Contract No. 290-02-0021.) AHRQ Publication

No. 04-E029-1. Rockville, MD: Agency for Healthcare

Research and Quality. June 2004.

References

1. Marsh MN. Gluten, major histocompatibility complex, and the small

intestine: A molecular and immunobiologic approach to the spectrum

of gluten sensitivity (‘celiac sprue’). Gastroenterology

1992;102(1):330-54.

2. McNeish AS, Harms HK, Rey J, Shmerling DH, Visakorpi JK,

Walker-Smith JA. The diagnosis of coeliac disease. A commentary on

the current practices of members of the European Society for

Paediatric Gastroenterology and Nutrition (ESPGAN). Archives of

Disease in Childhood 1979;54(10):783-6.

3. Oberhuber G, Granditsch G, Vogelsang H. The histopathology of

coeliac disease: time for a standardized report scheme for pathologists.

European Journal of Gastroenterology & Hepatology

1999;11(10):1185-94.

4. Walker-Smith JA, Guandalini S, Schmitz J, Shmerling DH, Visakorpi

JK. Revised criteria for diagnosis of coeliac disease. Arch Dis Child

1990;65(8):909-11.

5. van de WY, Kooy Y, van Veelen P, Vader W, Koning F, Pena S. Coeliac

disease: it takes three to tango! Gut 2000;46(5):734-7.

6. Papadopoulos GK, Wijmenga C, Koning F. Interplay between genetics

and the environment in the development of celiac disease: perspectives

for a healthy life. Journal of Clinical Investigation 2001;108(9):1261-

6.

7. Sollid LM, McAdam SN, Molberg O, Quarsten H, Arentz-Hansen H,

Louka AS, et al. Genes and environment in celiac disease. Acta

Odontologica Scandinavica 2001;59(3):183-6.

8. Sollid LM, Markussen G, Ek J, Gjerde H, Vartdal F, Thorsby E.

Evidence for a primary association of celiac disease to a particular

HLA-DQ alpha/beta heterodimer. Journal of Experimental Medicine

1989;169(1):345-50.

9. Ploski R, Ek J, Thorsby E, Sollid LM. On the HLA-DQ(alpha

1*0501, beta 1*0201)-associated susceptibility in celiac disease: a

possible gene dosage effect of DQB1*0201. Tissue Antigens

1993;41(4):173-7.

10. Ploski R, Ascher H, Sollid LM. HLA genotypes and the increased

incidence of coeliac disease in Sweden. Scand J Gastroenterol

1996;31(11):1092-7.

11. Holopainen P, Mustalahti K, Uimari P, Collin P, Maki M, Partanen J.

Candidate gene regions and genetic heterogeneity in gluten sensitivity.

Gut 2001;48(5):696-701.

12. Kagnoff MF. Celiac disease pathogenesis: the plot thickens.

Gastroenterology 2002;123(3):939-43.

13. Feldman M, Friedman LS, Sleisenger MH. Sleisenger and Fordtran’s

Gastrointestinal and Liver Disease. 7th edition W.B. Saunders; 2003.

14. Fasano A, Catassi C. Current approaches to diagnosis and treatment

of celiac disease: an evolving spectrum. Gastroenterology

2001;120(3):636-51.

15. Bode S, Gudmand-Hoyer E. Incidence and prevalence of adult coeliac

disease within a defined geographic area in Denmark. Scand J

Gastroenterol 1996;31(7):694-9.

16. Hawkes ND, Swift GL, Smith PM, Jenkins HR. Incidence and

presentation of coeliac disease in South Glamorgan. Eur J

Gastroenterol Hepatol 2000;12(3):345-9.

17. Collin P, Reunala T, Rasmussen M, Kyronpalo S, Pehkonen E,

Laippala P, et al. High incidence and prevalence of adult coeliac

disease. Augmented diagnostic approach. Scand J Gastroenterol

1997;32(11):1129-33.

18. Ivarsson A, Persson LA, Nystrom L, Ascher H, Cavell B, Danielsson

L, et al. Epidemic of coeliac disease in Swedish children. Acta Paediatr

2000;89(2):165-71.

5
19. Maki M, Holm K. Incidence and prevalence of coeliac disease in

Tampere. Coeliac disease is not disappearing. Acta Paediatrica

Scandinavica 1990;79(10):980-2.

20. Ivarsson A, Persson LA, Nystrom L, Hernell O. The Swedish coeliac

disease epidemic with a prevailing twofold higher risk in girls

compared to boys may reflect gender specific risk factors. Eur J

Epidemiol 2003;18(7):677-84.

21. Maki M, Kallonen K, Lahdeaho ML, Visakorpi JK. Changing pattern

of childhood coeliac disease in Finland. Acta Paediatrica Scandinavica

1988;77(3):408-12.

22. Lopez-Rodriguez MJ, Canal Macias ML, Lavado Garcia JM, Sanchez

BM, Robledo AP, Pedrera Zamorano JD. Epidemiological changes in

diagnosed coeliac disease in a population of Spanish children. Acta

Paediatr 2003;92(2):165-9.

23. Hoffenberg EJ, MacKenzie T, Barriga KJ, Eisenbarth GS, Bao F, Haas

JE, et al. A prospective study of the incidence of childhood celiac

disease. J Pediatr 2003;143(3):308-14.

24. Weile B, Krasilnikoff PA. Extremely low incidence rates of celiac

disease in the Danish population of children. J Clin Epidemiol

1993;46(7):661-4.

25. Corrao G, Usai P, Galatola G, Ansaldi N, Meini A, Pelli MA, et al.

Estimating the incidence of coeliac disease with capture-recapture

methods within four geographic areas in Italy. J Epidemiol

Community Health 1996;50(3):299-305.

26. Magazzu G, Bottaro G, Cataldo F, Iacono G, Di Donato F, Patane R,

et al. Increasing incidence of childhood celiac disease in Sicily: results

of a multicenter study. Acta Paediatr 1994;83(10):1065-9.

www.ahrq.gov

AHRQ Pub. No. 04-E029-1

June 2004

ISSN 1530-440X
 

Evidence Report
 

Note: Appendixes and Evidence Tables are provided electronically at 

http://www.ahrq.gov/clinic/tp/celiactp.htm 

 3 

Chapter 1. Introduction 

Overview 

Celiac disease (CD) is a disorder of small bowel malabsorption. It is characterized by 

mucosal inflammation, villous atrophy and crypt hyperplasia, which occur upon exposure to 

gluten, and clinical and histological improvement with withdrawal of gluten from the diet.1-4 

CD—also referred to as celiac sprue, gluten-sensitive enteropathy, non-tropical sprue, in 

addition to a host of other names—is thought to result from the activation of both a cellmediated (T-cell) and humoral (B-cell) immune response upon exposure to the glutens 

(prolamins and glutenins) of wheat, barley, rye, and oats, in a genetically susceptible 

person.5,6 Genetic susceptibility is suggested by a high concordance among monozygotic 

twins of close to 70 percent,7

 and an association with certain type II human leukocyte antigens 

(HLA).8,9 HLA DQ2 is found in up to 95 percent of CD patients, while most of the remaining 

patients have HLA DQ8.8-10 However, there is only a 30 percent HLA concordance among 

siblings, suggesting that other genetic factors are also at play.11 More recent evidence 

suggests that the presence of auto-antibodies to a connective tissue element surrounding 

smooth muscle called endomysium is highly specific for CD. The target of this autoantibody 

is now known to be an enzyme called tissue transglutaminase (tTG). This enzyme may play a 

prominent role in the pathogenesis of CD by modifying gliadin, resulting in a greater 

proliferative response of gliadin specific T-cells, which contributes to mucosal inflammation 

and further B-cell activation.5,6,12,13

CD appears to represent a spectrum of clinical features and presentations. Although 

“classical” CD (i.e., fully developed gluten-induced villous atrophy and classical features of 

intestinal malabsorption) is most commonly described, it appears that most patients have 

atypical CD (i.e., fully developed gluten-induced villous atrophy found in the setting of 

another presentation such as iron deficiency, osteoporosis, short stature, or infertility) or silent 

CD (i.e., fully developed gluten-induced villous atrophy discovered in an asymptomatic 

patient by serologic screening or perhaps an endoscopy for another reason). Other authors 

describe a latent form of CD that is characterized by a previous diagnosis that responded to a 

gluten-free diet (GFD) and retained a normal mucosal histology upon later introduction of 

gluten. Latent CD can also represent patients with currently normal intestinal mucosa who 

will subsequently develop gluten-sensitive enteropathy.13,14

The true prevalence of CD is difficult to estimate because of the variable presentation of 

the disease, particularly since many patients can have little or no symptoms. With this 

limitation in mind, the prevalence of the disease is highest in Celtic populations where 

estimates of 1:300 to 1:122 have been described. The prevalence of CD in North America has 

been estimated to be 1:3000, but a recent American study found the prevalence among the 

general not-at-risk population to be 1:105, while the prevalence in at-risk groups such as firstdegree relatives of CD patients was 1:22, suggesting that CD is greatly under-diagnosed. CD 

can affect persons of many ethnic backgrounds, but appears to rarely affect persons of purely 

Chinese, Japanese, or Afro-Caribbean decent.13
4

The diagnosis of CD in adults is classically made on the basis of clinical suspicion—that 

is, recognizing atypical presentations such as isolated iron deficiency, combined iron and 

folate deficiency, and osteoporosis—compatible with a duodenal biopsy while taking a 

gluten-containing diet, followed by clinical and histological improvement following 

commencement of a GFD.2,4 However, several serologic markers have become available 

which have altered the classic diagnostic pathway. The sensitivity of IgA anti-gliadin 

antibodies (AGA) is reported to range from 70 to 85 percent, whereas the specificity ranges 

from 70 to 90 percent. IgA anti-endomysial (EMA) and anti-tissue transglutaminase (tTG) 

antibodies have sensitivities in excess of 90 percent and specificities of over 95 percent.14 

Significant variability seems to exist in the reported values among the different studies, and 

these IgA-based tests can be negative in IgA-deficient patients, accounting for about 3 percent 

of CD cases. 

The sensitivity and specificity of the anti-EMA and anti-tTG antibodies, along with the 

perceived under diagnosis of CD, has led to suggestions of using these tests for population 

screening. Aside from the recognized influence of CD prevalence on the predictive value of a 

serologic test result, little consensus exists regarding the value of population screening. 

Furthermore, specific questions regarding clinically important outcomes resulting from 

screening remain unclear. In particular, little data is available on adherence to a GFD in 

asymptomatic CD patients detected by screening. 

The major complications of CD include intestinal and extraintestinal malignancies, 

ulcerative jejunoileitis, and collagenous sprue. Unlike most gastrointestinal (GI) lymphomas 

that are typically of B-cell origin, lymphomas associated with CD appear to be most 

commonly of T-cell origin. Unfortunately, the prognoses for patients with CD-associated Tcell lymphomas, ulcerative jejunoileitis and collagenous sprue, appear grim. It is widely 

believed that strict adherence to a GFD reduces the risk of these complications. It is 

suggested that by 5 years of dietary adherence the risk of lymphoma in CD patients 

approaches that of the general population.14

The challenge of CD remains to determine which patient populations should be screened, 

the best means of screening, and whether early detection of patients with CD leads to 

improved patient outcomes. For patient outcomes to improve as a result of screening, the 

degree to which “positively” screened individuals, particularly those who were asymptomatic, 

adhere to the stringent GFD, needs to be determined. 

Definition of CD 

As briefly described in the Overview, CD can take on a variety of forms. Paramount to 

the conduct of this review and subsequent interpretation of the literature is the identification 

of clear definitions of the many faces of CD. Implicit to a definition of CD (with a few 

exceptions that are detailed below) is the concept that the clinical and the small intestinal 

pathological features are present in patients who consume a gluten-containing diet, normalize 

with the introduction of a GFD, and recur with the re-introduction of dietary gluten.2,4 The 

historical tendency to rely on biopsy features as part of the definition of CD, creates 

difficulties (as discussed below) in accurately addressing the sensitivity and specificity of 

biopsy for the diagnosis of CD, and in assessing the sensitivity and specificity of the serologic 
5

markers, if different studies use different criteria to define CD. For the purpose of this 

review, the following definitions have been used. 

General Definitions 

1) Classical CD. The most commonly described form. It describes patients with the 

classical features of intestinal malabsorption who have fully developed gluten-induced 

villous atrophy and the other classic histological features. These patients present because 

of GI symptoms, and are identified as CD sufferers through the investigation of these 

symptoms. This group can also be said to have symptomatic CD. 

2) Atypical CD. Appears to be one of the most common forms. These patients generally 

have little to no GI symptoms, but seek medical attention because of another reason such 

as iron deficiency, osteoporosis, short stature, or infertility. These patients generally have 

fully developed gluten-induced villous atrophy. Because these patients are 

“asymptomatic” from the GI perspective, if their atypical CD feature is not recognized, 

they may be difficult or impossible to distinguish from “true” silent (asymptomatic) CD 

patients. 

3) Silent CD. A very common form of CD. Refers to patients who are asymptomatic but are 

discovered to have fully developed gluten-induced villous atrophy after having undergone 

serologic screening or perhaps an endoscopy and biopsy for another reason. These 

patients are clinically silent, in that they do not manifest any clear GI symptoms or 

associated atypical features of CD such as iron deficiency or osteoporosis. These patients 

can be confused with atypical CD if their atypical features are not recognized in an early 

stage. As well, Fasano et al.15 have shown that many of these patients do not manifest 

fully developed villous atrophy. 

4) Latent CD. Represents patients with a previous diagnosis of CD that responded to a GFD 

and who retain a normal mucosal histology upon later re-introduction of gluten. Latent 

CD can also represent patients with currently normal intestinal mucosa who will 

subsequently develop gluten-sensitive enteropathy. 

5) Refractory CD. For the purpose of this review, patients with refractory CD are patients 

with true CD and villous atrophy (i.e., not a misdiagnosis) who do not, or no longer, 

respond to a GFD. Although the most common reason for failure to respond to a GFD is 

dietary indiscretion or unknown exposure to gluten, refractory CD also occurs in patients 

on a GFD who have developed a complication such as ulcerative-jejunoileitis, or 

enteropathy-associated lymphoma. Patients with refractory CD do not necessarily have 

positive serology for CD. Refractory CD was reviewed in the context of the requested 

objectives. 

In order to utilize the above definitions, there needs to be clear and valid histological 

criteria for the diagnosis of CD. The histological patterns, particularly the more mild lesions, 

are not specific for CD and can be seen in a variety of other disorders (Table 1, Appendix A). 
6

To help standardize the histological criteria for the diagnosis of CD, several scoring systems 

have been developed. The classic Marsh criteria,1

 and its modification by Rostami,16 are 

presented in Table 2 (Appendix A). The revised ESPGAN criteria4

 use histological, 

serological and clinical criteria (Table 3, Appendix A). 

Report Purpose and Target Population

The purpose of this report is to systematically review the available CD literature in order 

to provide organized evidence relating to a number of objectives put forth by the AHRQ. The 

findings of the report are intended to assist an assembled group of American and world 

experts in the field of CD in the development of a National Institute of Health (NIH) 

Consensus Development Conference Guidelines sponsored by AHRQ and OMAR. 

Methodological Considerations 

At first glance, the determination of the sensitivity and specificity of the various 

diagnostic modalities for CD seems straightforward. There are a multitude of studies that 

have assessed the diagnostic characteristics of each of the serological markers using a variety 

of different laboratory methods. However, these studies are remarkably heterogeneous on a 

number of levels. 

For example, there appears to be notable heterogeneity in the actual definition of CD, an 

issue that has important consequences on all of the task order objectives. Central to the 

classic definition of CD is the recognition that biopsy is the gold standard for diagnosis. 

However, it has become clear over the years that the majority of patients with CD do not have 

the classically described features of intestinal malabsorption, and that a large proportion of 

patients do not have the classic flat mucosa (sub-total or total villous atrophy). To further aid 

in the diagnosis of CD, multiple authors have devised and modified histological criteria to 

grade the mucosal lesions of patients with CD. But still at issue is the broad differential of 

disorders that can cause villous atrophy, particularly the milder histological grades. To help 

address this issue, others have attempted to address specific features of the biopsy, such as the 

number of intraepithelial lymphocytes (IELs), the number of gamma delta positive (γδ+) IELs 

and other lymphocyte subtypes, as well as the localization of IELs towards the villous tip, just 

to name a few. 

The serological screening studies, together with the recognition that a low-grade 

histological lesion can be consistent with CD, have helped bring to light the concept of a 

spectrum of CD and the so-called “celiac iceberg.” In brief, it is recognized that classic CD 

with the typical symptoms of malabsorption and a fully developed mucosal lesion represents a 

small proportion of patients. The majority of patients are asymptomatic and are classified as 

having either atypical CD, silent CD, or less commonly latent CD. Some authors question 

whether most, if not all cases of silent CD, are in fact atypical CD, although the associated 

consequence of this has not been recognized. To further complicate the issue, Fasano15 has 

clearly characterized patients with silent CD without fully developed mucosal lesions, and 

found that only 34 percent of the patients had subtotal or total villous atrophy. 

It should be recognized that the majority of studies assessing the diagnostic characteristics 

of the serological markers have defined CD by a biopsy with Marsh III or modified IIIa 
7

lesions or greater. These studies have reported a high sensitivity and specificity for these 

tests, particularly for the anti-EMA and anti-tTG antibody tests. However, some studies have 

looked at the characteristics of these tests in lower-grade lesions, and have found that while 

100 percent of patients with Marsh IIIc histology show antibodies to endomysium, only 60 

percent of patients with Marsh IIIa histology have anti-EMA antibodies.17,18 Furthermore, it 

is apparent that serological markers can be used to monitor adherence to a GFD; for example, 

EMA and tTG antibodies fall to normal or non-diagnostic levels on a GFD, but the correlation 

with improvement of villous height is not as clear-cut. Finally, with the discovery by Sollid et 

al.8

 and others, that over 95 percent of patients with CD have HLA DQ2 and most of the 

remainder having HLA DQ8, it became hopeful that a reliable confirmatory test based on 

HLA typing would be available. Unfortunately, up to 40 percent of the general population 

and a much higher proportion of those with autoimmune disorders such as type I diabetes also 

have HLA DQ2 and/or HLA DQ8. Therefore, the specificity of this test can be quite low, 

making its positive predictive value relatively low. It is also becoming apparent that HLA 

DQ2/8 may not be the true risk-genes, and researchers are actively studying other candidate 

genes that may be associated with DQ2/8, or in patients without DQ2/8, other genes 

altogether. 

The preceding overview was presented to simply illustrate the complexity involved in 

separately assessing the sensitivity and specificity of the serological markers, HLA typing, 

and biopsy itself, in the diagnosis of CD. Over time, the status of the biopsy as the gold 

standard for the diagnosis of CD has been eroded. Yet at the same time, most of what we 

know about the sensitivity and specificity of serological markers and HLA typing rely on 

biopsy as the gold standard. Therefore, one is locked in a circular argument of how best to 

choose the gold standard test(s), when each has important shortcomings and is dependent on 

another to define its own diagnostic characteristics. The major problem in accurately 

evaluating the diagnostic characteristics of these tests, is the issue of identifying all possible 

CD patients in a general screened population to use as a benchmark. Serology would be the 

most convenient strategy, but appears to loose sensitivity in patients with low-grade lesions. 

Screening a general population with biopsy has significant practical/cost issues, as well as 

potential ethical problems; however, if such a study was performed along with measuring the 

serological and HLA status of patients, this would allow for identification of Marsh I or II 

lesions that would need to be characterized further. HLA DQ2/8-negative patients could 

likely be excluded from having CD. But those patients with Marsh I-II lesions would have to 

be followed, whether or not they were serology positive or HLA DQ2/8 positive, to see if CD 

develops; alternatively, they could be tested with a GFD and subsequently rechallenged to see 

whether they truly have CD. Only in this way can the true sensitivity of biopsy be 

determined. Using this multi-test gold standard with follow-up of equivocal cases, would also 

be the best way of assessing the sensitivity and specificity of serology markers and HLA 

DQ2/DQ8 typing. 

Finally, a question which needs to be addressed is: “What are the implications of 

identifying a truly asymptomatic individual, for example with serological screening, who has 

no other obvious complications such as iron deficiency or osteoporosis, and is then found to 

have a Marsh I or II lesion?” This returns the circular argument back to “What is truly 

CD?”—a question that is beyond the scope of this review. 

Note: Appendixes and Evidence Tables are provided electronically at 

http://www.ahrq.gov/clinic/tp/celiactp.htm 

 9 

Chapter 2. Methods 

Overview 

The UO-EPC’s evidence report on CD is based on a systematic review of the scientificmedical literature to identify, and synthesize the results from studies addressing the key 

questions put forth by the AHRQ. The Celiac Review Team, together with content experts, 

identified specific issues integral to the review. A Technical Expert Panel (TEP) refined the 

research questions, as well as highlighted key variables requiring consideration in the evidence 

synthesis. Evidence tables presenting the key study characteristics and results were developed. 

Summary tables were derived from the evidence tables. The methodological quality of reports of 

the included studies was appraised, and individual study results were summarized. For some 

objectives a narrative interpretation of the literature was provided. 

Key Questions Addressed in This Report 

The AHRQ task order requested answers to the questions outlined below: 

1) Objective 1 – Sensitivity and specificity of tests for CD (Celiac 1) 

a) What is the sensitivity and specificity of the following tests for CD: 

i) AGA; 

ii) EMA; 

iii) human tTG lgA antibodies; 

iv) HLA (DQ2/DQ8); 

v) duodenal/jejunal biopsy (see section below on celiac definition) 

b) Do sensitivity and specificity vary in different target populations (e.g., symptomatic vs. 

asymptomatic; geographic populations)? 

2) Objective 2 – Prevalence and incidence of CD (Celiac 2) 

a) What is the prevalence and incidence of symptomatic and “clinically silent” CD in: 

i) the general population; 

ii) high-risk populations: 

(1) family member of patient with CD; 

(2) type 1 diabetes mellitus; 

(3) iron deficiency anemia (IDA); 

(4) osteoporosis? 

b) How does prevalence and incidence in the general population vary in different 

geographic and racial/ethnic populations? 

3) Objective 3 – Celiac associated lymphoma (Celiac 3) 
10

a) What is the association between CD and GI lymphoma? 

i) What is the cumulative risk of developing GI lymphoma in patients with CD? 

ii) Does the cumulative risk vary with clinical presentation? 

4) Objective 4 – Expected consequences of testing for CD (Celiac 4) 

a) What are the expected consequences of testing for CD in the following populations: 

i) patients with symptoms suggestive of CD; 

ii) asymptomatic, at-risk populations (affected family members, patients with type 1 

diabetes); 

iii) the general population? 

b) “Consequences” include: 

i) false-positive results; 

ii) follow-up testing; 

iii) invasive procedures (biopsies); 

iv) cases diagnosed; 

v) patients complying with treatment; and 

vi) response to treatment. 

5) Objective 5 – Promoting or monitoring adherence to a GFD (Celiac 5) 

a) What interventions are effective for promoting or monitoring adherence to a GFD? 

Study Criteria Used in this Review 

Histological 

From the preceding discussion in the methodological consideration section it is clear that 

current histological criteria using a cut-off grade to define CD have important shortcomings. We 

therefore adopted an open histological definition of CD when selecting a study for inclusion, as 

long as the authors’ explicitly stated or described the criteria used to define CD (see inclusion 

criteria below). However, with the help of the TEP, we defined a “standard” histological 

definition of CD as a biopsy grade showing a modified Marsh IIIa or greater. This definition 

was NOT used as an inclusion/exclusion criterion, but simply to frame our results and to allow 

for the evaluation of the effect of different histological criteria on the performance of the various 

CD tests. 

The choice of biopsy criteria and/or histological grade “cut-off” used to define CD has 

important implications for the interpretation of the studies of serology, HLA, and biopsy. It is 

recognized that some patients with CD may have Marsh I or II lesions, and by definition patients 

with latent CD have Marsh 0 lesions. However, as emphasized by Marsh,1

 and as is discussed 

further below, in order to correctly interpret these early lesions, prospective follow-up studies are 

required, and an individual patient follow-up and documented response to gluten withdrawal 

would be required to firmly establish the diagnosis of CD. 
11

The practical importance of the histological definition is evident from our preliminary review 

of articles that demonstrated considerable heterogeneity in the histological criteria used within 

the studies to define CD. Some used strict definitions, whereas, others accepted milder grade 

lesions. Furthermore, since the existence of latent CD and some silent CD without fully 

developed histology is now recognized, a study that aims to assess the sensitivity and specificity 

of biopsy itself in CD needs to use a design that incorporates the most sensitive and specific 

serologic and HLA tests available. The biopsy and serology should be performed 

simultaneously, with patients having discordant test results being further evaluated. Those with 

normal biopsy and positive serology would have to be followed over time to see if they have a 

latent form of CD. Conversely, patients with positive biopsies and normal serology would have 

to demonstrate improvement in histology on a GFD, and ideally, certification of relapse by 

biopsy with reintroduction of gluten. This type of study design was sought in order to address 

the objective of the sensitivity and specificity of biopsy. 

Populations 

1) Unselected general population. The unselected general population implies a representative 

sample of a given population, such as a random sample of healthy blood donors or healthy 

school children. Some unselected populations are better than others for determining the true 

prevalence or incidence of CD. For example, blood donors are required to have normal 

hemoglobin and no iron deficiency, and therefore may underestimate the true numbers of 

patients with CD. 

2) Suspected CD. Patients with suspected CD include patients with GI symptoms, such as 

diarrhea or symptomatic malabsorption, who are being investigated for the possibility of CD. 

These patients are typically undergoing other investigations in addition to being worked-up 

for CD. 

3) High-risk populations. High-risk populations include populations with an expectedly higher 

prevalence of CD. Such populations include asymptomatic family members of patients with 

CD, patients with type I diabetes where identified CD would likely be silent or latent, and 

populations such as those with iron deficiency or osteoporosis where identified CD would be 

in the atypical CD classification. 

HLA DQ2/DQ8 

The HLA DQ2 haplotype represents the occurrence of HLA class II heterodimer alleles 

DQA1*0501 and DQB1*0201. These typically occur in a cis position as HLA DR3-DQ2 or in a 

trans position as HLA DR5/DR7-DQ2. The HLA DQ8 haplotype DQA1*0301/DQB1*302 

typically occurs in association with DR4. 
12

Analytical Framework 

The analytical framework is presented in Figure 1. In this framework, we wanted to 

represent the diagnostic pathways and the potential outcomes of testing various populations for 

CD. Each step of the pathway represents a portion of this systematic review, starting with the 

identification of the populations of interest, their diagnostic pathways, and ultimately the clinical 

outcomes, as well as consequences of testing. 

Figure 1: Analytic framework 

Celiac disease

Latent Classic Atypical Silent

Diagnostic 

testing 

Asymptomatic general 

population 

Asymptomatic population at 

elevated risk of CD 

Symptoms suggestive of 

CD 

Asymptomatic with CD 

associated feature 

Diagnostic 

screening 

True negative False negative True positive False positive 

Gluten-free diet 

Monitoring 

adherence 

Promoting 

adherence 

Compliant Non-compliant

Clinical outcomes 

Negative Positive 

Repeat testing Repeat testing 

Clinical outcomes Clinical outcomes 

Missed diagnosis Wrong diagnosis 

Celiac 

excluded 

Celiac 

excluded 

Gluten-free diet 
13

Study Identification 

Although the objectives of this task order are contained within a request for a single evidence 

report, we conducted five separate reviews, from the literature search onwards, as the objectives 

of this mandate were more orthogonal than overlapping. 

Search Strategy 

A series of searches were performed by National Library of Medicine staff in support of the 

literature review for CD. Strategies were developed using the guidelines supplied by the UOEPC, and were divided into the five questions posed by AHRQ. All searches were limited to 

human studies published in English language journal articles. The specific strategies used for 

each search are located in Appendix B. 

1. What is the sensitivity and specificity of the following tests for CD: 

a. EMA 

b. human tTG IgA antibodies 

c. AGA 

d. HLA DQ2/DQ8 

e. small bowel biopsy 

Searches were run in the MEDLINE® and EMBASE databases for each of the five tests. 

With the exception of the search for small bowel biopsy, a reference to CD or its synonyms was 

not a requirement for retrieval in order to obtain the widest possible information on these tests. 

Because of their complexity, a separate search was run for each test, then the results combined 

into one Pro-Cite file and duplicates eliminated. Individual case reports and letters to the editor 

were also removed. 

The MEDLINE® searches were run in October 2003 for the year 1966 forward and yielded a 

total of 2885 citations, with a follow-up search for HLA DQ2 and DQ8 performed in November 

2003 that yielded an additional 390 citations. The EMBASE searches were run in December 

2003 for the year 1974 forward and yielded a total of 1,046 citations after duplicates to 

MEDLINE® were removed. 

2. What is the prevalence and incidence of symptomatic and clinically silent CD in the 

general population and in the following identified high-risk populations: 

a. patients with an affected family member 

b. type 1 diabetes mellitus 

c. IDA 

d. osteoporosis 

Searches were run in the MEDLINE® and EMBASE databases. The MEDLINE® search 

was performed in October 2003 for the year 1966 forward and retrieved a total of 1,584 citations. 

The EMBASE search was run in December 2003 for the year 1974 forward and yielded 467 

citations after duplicates to the MEDLINE® retrieval were removed. Individual case reports and 

letters to the editor were also removed from both searches. 

3. What is the association between CD and GI lymphoma? 
14

Searches were run in the MEDLINE® and EMBASE databases. The MEDLINE® search 

was performed in October 2003 for the year 1966 forward and retrieved a total of 230 citations. 

The EMBASE search was run in December 2003 for the year 1974 forward and yielded 97 

citations after duplicates to the MEDLINE® retrieval were removed. Individual case reports and 

letters to the editor were also removed from both searches. 

4. What are the expected consequences of testing for CD in the following populations: 

a. patients with symptoms suggestive of CD 

b. asymptomatic, at-risk populations 

c. general population 

Searches were run in the MEDLINE®, EMBASE, PsycINFO, AGRICOLA, CAB, and 

Sociological Abstracts databases. In order to obtain the widest possible retrieval, all articles on 

screening for celiac and its synonyms were included, not just those discussing consequences. 

The MEDLINE® search was performed in October 2003 for the year 1966 forward and 

retrieved a total of 917 citations. The EMBASE (1974 forward), PsycINFO (1840 forward), 

AGRICOLA (1970 forward), CAB (1972 forward), and Sociological Abstracts (1963 forward) 

database searches were run in December 2003 and yielded a combined total of 204 citations after 

duplicates to the MEDLINE® retrieval were removed. Individual case reports and letters to the 

editor were also removed from both searches. 

5. What interventions are effective for promoting or monitoring adherence to a GFD? 

Searches were run in the MEDLINE®, EMBASE, PsycINFO, AGRICOLA, CAB, and 

Sociological Abstracts databases. Because of the small number of citations retrieved, a few 

selected articles discussing adherence to dietary limitations for other conditions were included. 

The MEDLINE® search was performed in October 2003 for the year 1966 forward and retrieved 

a total of 152 citations. The EMBASE (1974 forward), PsycINFO (1840 forward), AGRICOLA 

(1970 forward), CAB (1972 forward), and Sociological Abstracts (1963 forward) database 

searches were run in December 2003 and yielded a combined total of 168 citations after 

duplicates to the MEDLINE® retrieval were removed. Individual case reports and letters to the 

editor were also removed from both searches. 

Some citations fulfilled the criteria of more than one celiac objective. Duplicates within each 

celiac objective were electronically removed. The obtained citations were uploaded into an 

internal web-based review system (SRS) for online collaborative citation screening and 

abstraction. Articles passing the first level screen were retrieved in full for further screening (see 

below). 

Reference lists of included studies, book chapters, and narrative or systematic reviews 

retrieved after having passed the first level of relevance screening, were manually searched to 

identify additional unique references. Through contact with content experts, and the TEP, 

attempts were made to identify other studies not identified by the search. 

Study Selection and Eligibility Criteria 

Study selection was performed using three levels of screening with increasingly more strict 

criteria to ensure that all relevant articles were captured (Table 1). Each celiac objective had its 

own selection criteria for each level of screening and, as discussed previously, each celiac 

objective was treated as a separate sub-review. Following a calibration exercise, two reviewers 
15

independently screened all studies using the SRS web-based system. This system allows 

automatic identification of review disagreements. Any disagreements were resolved by the two 

reviewers by consensus; rarely, a third reviewer was used to break an impasse. The specific 

screening questions for each screen level are included in Appendix C. 

Level 1 broad screening. Level 1 screening was used to identify any potentially relevant 

citation, based on review of the title, abstract and key words. For each objective, the SRS system 

displayed the corresponding task order questions alongside the citation details. Reviewers 

answered a broad question of whether the citation potentially related to the current objective. 

Furthermore, the SRS system was set-up in such a way that articles which were identified in one 

celiac objective silo, that could also be relevant to another objective, could be identified and 

moved/copied to the other silo. The review team was divided up so that two members could be 

simultaneously reviewing each objective. 

Level 2 refined screening. Potentially relevant articles identified at level 1 were obtained in full 

for level 2 screening. Again, using the SRS system with the actual articles on hand, reviewers 

selected articles that related to each of the specific objectives. The reviewers were asked to err 

on the side of inclusion for this level, and to classify articles as “original” or “review”. Original 

articles meeting level 2 inclusion also had basic demographic data—such as screening test used, 

celiac definition, and study population identified—recorded into the SRS system.

Level 3 final screening. Level 3 screening identified articles that specifically allowed for the 

answering of the task order questions. These articles fulfilled the final inclusion/exclusion 

criteria, allowed actual extraction of the required data, and did not have fatal methodological 

flaws.
16

Table 1: Inclusion/exclusion criteria by level of screening 

Objective Level Inclusion Exclusion 

1 Any article reporting sensitivity/specificity 

of AGA, EMA, tTG, HLA DQ2/DQ8, or 

biopsy. 

Clearly unrelated citation. 

2 For serology and HLA – articles where 

sensitivity and specificity could be 

extracted. 

For biopsy – articles were included if 

some measure of diagnostic utility could 

be obtained. 

Celiac 1 

3 Articles that allowed determination of 

sensitivity or specificity for all tests were 

included. 

• Articles with major 

methodological flaws excluded 

• Control group did not have gold 

standard test (biopsy) applied 

• No description of biopsy criteria 

given 

• Celiac group known to be 

positive for test under evaluation 

• Control group known to be 

negative for the test under 

evaluation 

• Control groups included patients 

with Marsh I or II biopsy lesions 

• AGA test performed without 

commercial ELISA kit or before 

1990 

1 Any potential citation of prevalence or 

incidence of CD in general and high-risk 

populations or association of CD with 

other disorders 

Clearly unrelated citation. 

2 Citations limited to those that gave 

evidence of the prevalence or incidence 

of CD in the general population or the 

AHRQ identified high-risk populations 

(e.g., diabetes, relatives, iron deficiency, 

osteoporosis). 

Countries: North America, western 

Europe, Australia, New Zealand. 

Any studies of other CD-associated 

disorders not identified by the task 

order. 

Citations of the prevalence of 

specific disorders in patients with 

celiac (i.e., reverse of the 

inclusion). 

Any other country. 

Celiac 2 

3 Incidence and/or prevalence could be 

extracted from the article. 

Serious methodological flaws: 

• patients identified by surveys, 

through solicitation of celiac 

societies 

• incidence studies without a 

population density denominator
17

Table 1 (cont’d): Inclusion/exclusion criteria by level of screening 

Objective Level Inclusion Exclusion 

1 Any potential citation of the association, 

prevalence or risk of lymphoma in CD, 

including articles on outcome of refractory 

sprue and ulcerative jejunoileitis. 

Clearly unrelated citation. 

2 Measure of risk or prevalence/incidence 

of lymphoma in a population with CD. 

Prevalence of CD in a population of 

lymphoma. 

Case reports and non-comparative 

case series. 

Celiac 3 

3 Extractable prevalence, incidence, or 

cumulative risk of lymphoma in CD. 

Clonality of lymphocytes in 

ulcerative jejunoileitis-ileitis not 

determined or stated (as per TEP). 

Serious methodological flaw. 

1 Any potential citation of possible 

consequences of testing for CD. 

Clearly unrelated citation. 

2 Consequences extractable from article. 

Celiac 4 

3 Consequences limited to the AHRQ list. Consequences obtainable from the 

other celiac objective sub-review – 

i.e., false positive and negative 

results, etc. 

1 Any potential citation of interventions for 

the monitoring or promotion of 

adherence. 

Clearly unrelated citation. 

2 Studies of monitoring adherence were 

included if they assessed monitoring, by 

biopsy, serology (AGA publication date 

1990 or later, EMA, tTG), or both. 

Any promotion intervention. 

Serology prior to 1990. 

Celiac 5 

3 Data from article could be extracted. 

Data included follow-up by biopsy alone 

or serology with biopsy confirmation. 

Articles assessing adherence 

through the measures of intestinal 

permeability. 

Studies that reported changes in 

mean serological titers with a GFD 

or gluten challenge, but did not 

address the potential usefulness of 

a serologic test to assess 

compliance. 

Important articles answering a stated objective but not meeting inclusion criteria (i.e., 

containing potential threats to internal validity), were presented and discussed in the discussion 

section. 

Data Abstraction 

For each objective, a detailed and standardized data abstraction form was developed with the 

assistance of content experts and the TEP panel. The data abstraction forms included baseline 

study characteristics as well as questions allowing for the abstraction of all relevant study results 

and characteristics. The electronic data extraction forms began with basic study and patient 
18

demographic questions that were common across the five sub-review forms. These included 

reviewer name, author name, publication year, publication type, study design type, and basic 

study population demographics such as race, age, gender, and type of CD population. The 

extraction forms then moved to specific questions geared at extracting data to answer the 

respective objective’s questions. The individual data abstraction forms are included in Appendix 

C. 

Celiac 1 (sensitivity and specificity) data abstraction form. Separate data abstraction forms 

were developed for serology, HLA, and the biopsy sub-questions. Two-by-two tables were used 

to abstract data on sensitivity and specificity, and to determine positive and negative predictive 

values and the prevalence of CD in the tested population. The biopsy studies were quite 

heterogeneous, and did not allow for direct numeric extraction of data.

Celiac 2 (prevalence and incidence) data abstraction form. For this objective, the data 

extraction form included questions for detailing the screened study population, the number of 

individuals screened, the number of CD cases identified and how CD was confirmed. For 

incidence studies, the comparison population and time period were recorded. 

Celiac 3 (lymphoma) data abstraction form. In addition to the basic demographic, and study 

design data, the extraction form contained fields for the extraction of risk data linking GI 

lymphoma to CD. Types of data sought were prevalence and incidence of lymphoma in CD in 

the setting of comparison data from a control population. Fields for extracting standardized 

incidence, morbidity, and mortality ratios were included. 

Celiac 4 (consequences of screening) data abstraction form. The extraction forms for this 

objective included text fields to detail the consequences of testing for CD. The form contained 

fields that identified the specific consequence of testing which was addressed by the study, as 

well as a data field to report the study findings. The general field approach was chosen to allow 

extraction of the expected varied data for this objective. 

Celiac 5 (monitoring and promoting adherence) data abstraction form. For this objective, 

standard demographic data was collected, as well as the methods used to monitor adherence to a 

GFD, the response of those measures to the diet, and the correlation of serological methods with 

biopsy findings. Space was provided to detail the sensitivity and specificity of the monitoring 

method when that data was available. For the objective of promoting adherence to a GFD, a 

text-based form was used to allow the extractor to describe the intervention and the results of its 

use. 

Electronic forms. The abstraction forms were developed in Microsoft Excel to allow for 

electronic data entry and recording, and to allow exporting the evidence table data into Microsoft 

Word. For each celiac objective, data abstraction was conducted by one reviewer and verified by 

another. The extracted data was further verified by one of the principal investigators. 
19

Quality Assessment 

The quality of reporting of diagnostic test studies was assessed using the QUADAS tool.19 

This tool is the first to be published that allows for the assessment of the quality of studies of 

diagnostic tests. The instrument was developed using a Delphi procedure. The Delphi panel 

consisted of nine experts in diagnostic research who refined an initial list of items in four rounds, 

after which agreement was reached on the items to be included in the tool. The QUADAS tool 

consists of 14 questions that are answered “yes,” “no,” or “unsure.” The tool addresses the items 

individually and does not incorporate an overall quality score (Appendix D). 

Cohort and case-control study reports were assessed using the Newcastle-Ottawa scale 

(NOS; Appendix D). The NOS is an ongoing collaboration between the Universities of 

Newcastle, Australia and Ottawa, Canada. It was developed to assess the quality of nonrandomized studies with its design, content and ease-of-use directed to the task of incorporating 

the quality assessments in the interpretation of meta-analytic results. A “star system” has been 

developed in which a study is judged on three broad perspectives: the selection of the study 

groups; the comparability of the groups; and the ascertainment of either the exposure or outcome 

of interest for case-control or cohort studies, respectively. The goal of this project is to develop 

an instrument that provides an easy and convenient tool for quality assessment of nonrandomized studies for use in a systematic review. 

The inter- and intra-rater reliability of the NOS have been established. The face content 

validity of the NOS has been reviewed based on a critical review of the items by several experts 

in the field, who evaluated its clarity and completeness for the specific task of assessing the 

quality of studies to be used in a meta-analysis. Furthermore, the validity of the NOS criteria has 

been established by comparisons to more comprehensive but cumbersome scales. An assessment 

plan is being formulated for evaluating its construct validity, with consideration of the theoretical 

relationship of the NOS to external criteria and the internal structure of the NOS components.20

Quality assessments of cross-sectional reports were assessed using a 19-item instrument 

adapted from Ophthalmology (Appendix D).21

We did not conduct any sensitivity analysis of quality assessments on the observational 

studies, as there is little by way of guidance to suggest what a poor quality study score would be 

based on for these assessment instruments. 

One reviewer assessed the quality of an entire celiac objective to maintain internal 

consistency. Quality assessment was not performed under masked conditions. 

Data Synthesis and Analysis 

The data obtained from this review fell into several broad categories, which correspond in 

large part to the individual study objectives. These will be addressed in turn. 

Data for the sensitivity and specificity of each serological marker was considered separately. 

In addition, studies were subdivided by the population age group (adults, children, mixed 

population), and by study design (case control, relevant clinical population/cohort). 

Attempts were made to identify, explain, and minimize clinical and statistical heterogeneity 

in the included studies. Heterogeneity was assessed graphically by plotting receiver operator 

(ROC) curves for each of the included studies in a given analysis. A Pearson’s Chi Square with 
20

n-1 degrees of freedom, where n represents the number of included studies in an analysis was 

calculated to assess statistical heterogeneity. 

Pooled estimates were only calculated if clinically and statistically appropriate. In situations 

where pooling was not performed, a narrative systematic review was conducted. 

There are several potential ways to pool the results of studies of diagnostic tests, each having 

both advantages and disadvantages. The simplest and most intuitive is to simply perform a 

weighted mean of the sensitivity and specificity for the studies in question. This method 

provides a pooled estimate that is easy to interpret by clinicians. Several other techniques 

involve the pooling of diagnostic odds ratios or likelihood ratios. These methods have the 

distinct disadvantage of difficulty in interpretation, and the inability to derive a pooled sensitivity 

or specificity from the resulting estimates. Lastly, one can use one of several methods to 

produce a summary ROC curve. The method described by Littenberg and Moses,22,23 has the 

advantage of being able to produce a summary curve while taking into account a threshold effect. 

This can occur when different studies use different thresholds to define a positive test, or even 

from differences in labs using the same cut-off. To interpret summary ROC curves it is 

necessary to know the sensitivity or specificity of the test in question in the population in which 

it will be applied. Since neither of these values is estimable without conducting yet another 

diagnostic accuracy study for the given population, the clinical usefulness of using this method 

alone is limited.24,25

In order to produce clinically useful pooled statistics, we calculated a weighted mean of the 

sensitivity and specificity from those of the included study. For both sensitivity and specificity, 

this pooling relies on the assumption that the test statistic is the same in all of the included 

studies. For each pooled estimate, a 95% confidence interval (CI) was calculated using both a 

fixed and random effects model. The results of which were compared as a further test for 

heterogeneity. The pooled estimates for the sensitivity and specificity were also compared with 

a summary ROC curve calculated for the same group of studies as a second check of the 

estimates (summary ROC Curves are included in Appendix E). 

The prevalence and incidence data from the Celiac 2 objective, and the CD-lymphoma data 

from the Celiac 3 objective, were anticipated to be quite heterogeneous considering the different, 

countries, age groups, and risk characteristics of the studied patients. Attempts were made to 

group studies of prevalence by age group, study population, and serological screening method. 

If the grouped studies did not show evidence of heterogeneity, pooled estimates of the 

prevalence were produced for that group of studies, otherwise a descriptive presentation of the 

data with a qualitative systematic review was conducted. Likewise, the outcome measures of the 

Celiac objectives 4 and 5 were presented in a qualitative systematic review, except in cases 

where it was possible to pool the sensitivity and specificity data as measures of monitoring of 

patients at various stages of recovery on a GFD. 
Note: Appendixes and Evidence Tables are provided electronically at 

http://www.ahrq.gov/clinic/tp/celiactp.htm 

 21 

Chapter 3. Results 

Celiac 1: Sensitivity and Specificity of Tests for CD 

Serology 

Out of 3,982 citations identified by the search strategy for the Celiac 1 objective, 907 met 

level 2 screening criteria. Of these, 204 diagnostic test studies of one or more of the serological 

markers of interest (AGA, EMA, tTG) were identified. Sixty studies fulfilled the level 3 

inclusion criteria (Appendix F; Evidence Table 1, Appendix I).26-85 The most common reasons 

for failing level 3 inclusions were AGA studies conducted before 1990, studies utilizing an 

improper or an unbiopsied control group, or studies that did not give any description of the 

biopsy criteria defining CD. Five pairs of duplicate publications were 

identified.27,28,45,46,58,65,73,74,84,86 Out of each duplicate pair, the study with the most complete data 

was abstracted,27,45,46,58,74 bringing the total of included unique studies to 55. The majority of 

these studies assessed more than one serological marker, and some studied more than one age 

group. Of the included articles, 20 were conducted in or included an adult population, 33 were 

conducted in a population of children, and eight in a mixed population of adults and children of 

varying proportions. The statements in this section that relate to mixed studies or studies in 

children and adults refer to these eight studies, and not to a sample that we pooled from different 

studies. 

To minimize clinical and statistical heterogeneity, the included articles of a particular 

antibody test were divided into groups by age of the included population (adults, children, 

mixed), the study design (case control, or relevant clinical population/cohort), by antibody type 

(IgA or IgG), and by test methodology (e.g., monkey esophagus [ME] or human umbilical cord 

[HUC]). Within these groups, further differences in study population, country of origin, and 

biopsy definitions (especially whether or not mild grades without villous atrophy were included) 

were assessed systematically. Studies that reported using the ESPGAN criteria for the diagnosis 

of CD were categorized as including patients with some degree of villous atrophy. Other 

potential causes of heterogeneity such as the cut-offs used to define a positive test were assessed. 

Two articles were identified that assessed the diagnostic value of various antibodies in 

children64 and in mixed-age populations40 with IgA deficiency. As well, one study enrolled 

biopsy-proven CD patients who were known to be EMA negative.66 These studies were 

considered separately from the others. Studies of using antibodies in combination were also 

assessed separately. 

Pooled statistical estimates (with 95% CIs) are provided for studies without clinical and 

statistical heterogeneity, and summary ROC curves for the studied antibodies are provided in 

Appendix E. Sensitivity analyses by study design did not show a significant difference except 

for the analysis of IgA-tTG-guinea pig (GP) in adults. Therefore, apart from studies of IgA-tTGGP in adults, pooled estimates, when available, included data from both study designs. 
22

AGA. The diagnostic characteristics of IgA were assessed in 35 studies and the diagnostic 

characteristics of IgG-AGA were assessed in 30 studies. Of the 35 IgA-AGA studies, 11 were 

conducted in an adult population,30,33,45,50,54,61-63,71,77,80 21 in a population of children, 

26,27,29,31,34,36,38,42,43,50,52,56,59,60,64,67,68,83,85,87,88 and five in a mixed population.27,37,40,74,75

Of the 30 IgG-AGA studies, seven were conducted in an adult population,30,33,54,62,63,71,80 19 

were conducted in population of children,26,27,29,31,34,36,38,42,43,50,52,58,59,64,66,68,69,83,85 and five in a 

mixed population.27,37,40,74,75 Some studies provided data for more than one age group. 

Some studies only provided summary statistics without the raw two-by-two table 

results,33,34,54,58,59,69 however, the raw data was calculated from the presented sensitivity and 

specificity, and from the group sizes. 

One study66 was conducted in CD patients who were known to be IgA-EMA negative, and 

was not included in the main analysis. In this study of children, the sensitivity for IgA-AGA was 

22% and the sensitivity for IgG-AGA was 33%, whereas, the specificity for IgA-AGA was 67% 

and the specificity for IgG-AGA was 58%; these values are considerably lower than those 

reported in other studies. Another two studies were conducted in patients with IgA 

deficiency.40,64 The first demonstrated a sensitivity of 0% using IgA-AGA, but a sensitivity and 

specificity of 100% using IgG-AGA,40 whereas the second showed a sensitivity of 0% with IgAAGA, but a sensitivity of 100% and a specificity of 80% using IgG-AGA. 

Despite clinical subdivision of the identified studies, significant heterogeneity was identified 

for each of the pooled AGA subgroup results (Tables 2 to 7). Heterogeneity can be visualized 

graphically in the ROC curves (Figures 2 to 4) and suggests that the heterogeneity is in part 

related to a serological test cut-off threshold effect. As well, two studies included CD patients 

with less than a Marsh IIIa grade;37,45 these studies had lower than average sensitivities (61% and 

67% for IgA-AGA) then that reported in other studies. The remaining heterogeneity likely 

represents a combination of the effects of different test kits, inter-lab variability, and differences 

in the study groups. For example, within the child population, two of the outlier studies were 

conducted in Turkey,26,85 although apparently using standard methodology. Therefore, overall 

pooled estimates do not represent true summary statistics in these situations. 

IgA-AGA. Despite the apparent heterogeneity, one can make some broad statements regarding 

the diagnostic value of AGA antibodies. IgA-AGA appears to offer fair to good performance in 

children (Table 2; Figure 2).26,27,29,31,34,36,38,42,43,50,52,58,59,64,66,68,69,83,85 Ten of the 19 studies 

demonstrated a sensitivity of IgA-AGA of greater than 80%, and six of the studies demonstrated 

a sensitivity of greater than 90%. However, nine studies demonstrated sensitivities of less than 

80%. The specificity was greater than 80% in 15 of the 19 studies, and greater than 90% in 11 

studies. Only four studies showed a specificity of less than 80%. 

Ten studies assessed IgA-AGA in adults (Table 3; Figure 3).30,33,54,62,63,71,80 Five of the ten 

studies demonstrated sensitivities greater than 80%, and three of the studies demonstrated 

sensitivities of greater than 90%. However, four studies demonstrated sensitivities of less than 

65%. The specificity was greater than 80% in eight studies and greater than 90% in three. Five 

studies had specificities between 80% and 90%, and only two studies had specificities less than 

80%. 

Among the studies that assessed IgA-AGA in a mixed population of adults and 

children,27,37,74,75 two demonstrated poor sensitivities of less than 70% but with specificities 

between 90% and 92%, one demonstrated a sensitivity of 85% and a specificity of 85%, and the 

last demonstrated a sensitivity of 91% and a specificity of 98% (Table 4; Figure 4). 
23

Table 2: Included studies for IgA-AGA in children 

Author, year; 

country Study type Biopsy criteria Sens Spec PPV NPV Prev 

Picarelli, 

2000; Italy 

Case-control ESPGAN 22.2* 66.7* 50* 36.3* 0.60* 

Gaetano, 

1997; Italy 

Case-control ESPGAN 92 68 85.2 80.9 0.67 

Carroccio, 

1993; Italy 

Case-control Biopsies confirmed at diagnosis, 

on GFD, and rechallenge 

(severity grade - not reported) 

68 91.7 86.1 79.7 0.43 

Hansson, 

2000; Sweden 

Case-control ESPGAN 95.5 73.9 77.8 94.4 0.49 

Berger, 1996; 

Switzerland 

Case-control ESPGAN revised with complete 

villous atrophy 

76 67 74 59 0.55 

Lerner, 1994; 

USA, Israel 

Case-control Criteria of Townley modified by 

Ingkaran 

52 94 87 74 0.52 

Bahia, 2001; 

Brazil 

Relevant clinical 

population 

Severe villous atrophy 95.5 95.6 91.3 97.9 0.31 

Russo, 1999; 

Canada 

Relevant clinical 

population 

ESPGAN 83.3 84.5 64.5 93.8 0.25 

Bode, 1993; 

Denmark 

Relevant clinical 

population 

ESPGAN 64 99 90 97 0.07 

Poddar, 2002; 

India 

Relevant clinical 

population 

ESPGAN (villous atrophy and 

unequivocal response to GFD) 

94 91.5 92 93.5 0.52 

Ascher, 1996; 

Sweden 

Relevant clinical 

population 

ESPGAN 100 94.4 95.7 100 0.55 

Lindberg, 

1985; Sweden 

Relevant clinical 

population 

ESPGAN; Alexander grading 88 88 0.31 

Altuntas, 

1998; Turkey 

Relevant clinical 

population 

Subtotal or total villous atrophy, 

crypt hyperplasia, increased IEL 

23 90 75 48 0.55 

Artan, 1998; 

Turkey 

Relevant clinical 

population 

ESPGAN ; 58 51 42.4 66.7 0.38 

Rich, 1990; 

USA 

Relevant clinical 

population 

Not recorded - state "severe" 

lesion 

53 93 72.7 85.7 0.25 

Gonczi, 1991; 

Australia 

Relevant clinical 

population (184 

children with 

suspected CD) 

ESPGAN no details on biopsy 

findings 

95 92.4 76 98.6 0.20 

Wolters, 

2002; 

Netherlands 

Relevant clinical 

population (identified 

retrospectively) 

Subtotal villous atrophy with crypt 

hyperplasia 

83 86 81 81 0.51 

Lindquist, 

1993; Sweden 

Relevant clinical 

population (suspected 

celiac) 

ESPGAN; subtotal or partial 

villous atrophy 

86.5 92.7 93.7 85 0.55 

Chirdo, 1999; 

Argentina 

Relevant clinical trial Total or subtotal villous atrophy 75 87.1 84 80 0.47 

Chartrand, 

1997; Canada 

Relevant clinical 

population 

ESPGAN - with flat mucosal 

biopsy 

80 92 67 96 0.17 

Meini, 1996; 

Italy 

Relevant clinical 

population 

Partial villous atrophy or total 

villous atrophy 

0 100 0 91.7 0.08 

*30 IgA-EMA-negative patients suspected of CD; 9 of 18 CD patients IgA deficient 
24

Table 3: Included studies for IgA-AGA in adults 

Author, year; 

country Study type Biopsy criteria Sens Spec PPV NPV 

Prev 

(%) 

SateganaGuidetti, 

1995; Italy 

Case-control Roy-Choudhury criteria; 

partial or total villous 

atrophy 

55 100 100 55.9 35.0 

Dahele, 2001; 

Scotland 

Case-control Included 6 with IEL, rest 

partial villous atrophy or 

greater 

61 86 88.5 42.7 43.6 

Bode, 1994; 

Denmark 

Relevant 

clinical 

population 

Crypt hyperplasia, villous 

atrophy and increase 

inflammatory cells 

46 98 75 92 25.7 

Kaukinen, 

2000; Finland 

Relevant 

clinical 

population 

Villous height to crypt 

ratio <2.0; IEL and HLA 

also tested 

83 45 75 92 57.0 

Maki, 1991; 

Finland 

Relevant 

clinical 

population 

Severe pathology with 

crypt hyperplasia to total 

villous atrophy; mild 

changes considered 

normal 

30.8 87.2 22.2 91.3 14.8 

McMillan, 

1991; Ireland 

Relevant 

clinical 

population 

Revised ESPGAN 100 100 100 100 31.5 

Bardella, 

2001; Italy 

Relevant 

clinical 

population 

Marsh; no grade 

reported 

95 89 76 98 33.3 

Gonczi, 1991; 

Australia 

Relevant 

clinical 

population 

(184 children 

with 

suspected 

CD) 

ESPGAN no details on 

biopsy findings 

92 88.2 85.2 93.8 45.8 

Valdimarsson, 

1996; Sweden 

Relevant 

clinical 

population+ 

a few 

dypeptic 

controls 

Alexander's 

classification; partial or 

subtotal villous atrophy 

79 70 28 96 36.8 

Vogelsang, 

1995; Austria 

Relevant 

study 

population 

Modified ESPGAN; flat 

mucosa; crypt 

hyperplasia raised IELs 

81.6 83 81.6 83 48.0 
25

Table 4: Included studies for IgA-AGA in studies including both children and adults 

Author, year; 

country Study type Biopsy criteria Notes Sens Spec PPV NPV Prev 

Cataldo, 

2000; Italy 

Case-control Original & 

revised criteria? 

20 IgA-deficient 

CD vs healthy 

IgA-deficient 

non-CD 

0 100 0 33.3 0.7 

Sulkanen, 

1998; Finland 

Case-control ESPGAN 84.5 81.6 75.2 89 0.4 

Ascher, 1996; 

Sweden 

Relevant 

clinical 

population 

ESPGAN 90.9 98.5 98 92.7 0.5 

Carroccio, 

2002; Italy 

Relevant 

clinical 

population 

Marsh, broken 

down by 

criteria; CD was 

diagnosed as 

enlarged crypts 

and/or villous 

atrophy-with 

normalization 

on GFD 

 67 90 86 75 0.5 

Tesei, 2003; 

Argentina 

Relevant 

clinical 

population 

Marsh II to IV - 

with 

confirmation 

 64 92 92 64 0.6 

Figure 2: IgA-AGA in children with CD 

IgA AGA in Children

0

10

20

30

40

50

60

70

80

90

100

0 10 20 30 40 50 60 70 80 90 100

1-Specificity

Sensitivity

Case Control

Cohort

Altuntas, 1998

Rich, 1990 Artan, 1998

Lerner, 1994
26

Figure 3: IgA-AGA in adults with CD 

AGA - IgA in Adults

0

10

20

30

40

50

60

70

80

90

100

0 10 20 30 40 50 60 70 80 90 100

1- Specificity

Sensitivity

Case Control

Cohort

Kaukinen, 2000

Sategana-Guidetti, 1995

Dahele, 2001

Bode, 1994

Maki, 1991

Figure 4: IgA-AGA in adults and children with CD 

IgA AGA in Studies of Adults

and Children

50

60

70

80

90

100

0 10 20 30 40 50

1-Specificity

Sensitivity

Case Control

Cohort

Tesei, 2003

Carroccio, 2002

Ascher, 1996

Sulkanen, 1998

IgG-AGA. The seven studies of IgG-AGA in adults demonstrated considerably greater 

heterogeneity.30,33,54,62,63,71,80 The sensitivity ranged from 17% to 100%, with little study 

grouping. However, there was less variation in the reported specificities. Five of the seven 

studies demonstrated specificities greater than 80%, whereas, the remaining two studies had 

specificities of greater than 70%. (Table 5; Figure 5) 
27

In contrast, among the 17 analyzed studies (non-IgA deficient) of IgG-AGA conducted in 

children,26,27,29,31,34,36,38,42,43,50,52,58,59,68,69,83,85 there seemed to be greater variability in the 

specificity than in the sensitivity (Table 6; Figure 6). Fifteen of the 17 studies demonstrated 

sensitivities that were greater than 80%, and six demonstrated sensitivities greater than 90%. 

Only two studies showed a sensitivity of less than 80%. In contrast, with regards to specificity, 

two groupings of studies become apparent. The first group consists of 11 studies, all of which 

had specificities greater than 79%, and except for one study, had sensitivities that were greater 

than 80%. In contrast, the second group of six studies all had specificities below 70%, and with 

the exception of one study, had sensitivities greater than 80%. (Tables and figures) 

Four studies looked at IgG-AGA in a non-IgA-deficient mixed population of adults and 

children.27,37,74,75 Two of these demonstrated sensitivities greater than 80%, one showed a 

sensitivity of 84%, whereas the second had a sensitivity of 96%. However, only the first study 

had specificity greater than 80%. In total, three of the four studies had specificities less than 

80% (Table 7; Figure 7). 

Table 5: Included studies for IgG-AGA in adults 

Author, year, 

country Study type Biopsy criteria Sens Spec PPV NPV 

Prev 

(%) 

SateganaGuidetti, 

1995; Italy 

Case-control Roy-Choudhury 

criteria; partial or 

total villous atrophy 

78 80.7 87.6 67.6 56.7 

Bode, 1994; 

Denmark 

Relevant 

clinical 

population 

Crypt hyperplasia, 

villous atrophy and 

increase 

inflammatory cells 

62 97 73 94 34.8 

Kaukinen, 

2000; Finland 

Relevant 

clinical 

population 

Villous height to 

crypt ration <2.0; 

IEL and HLA also 

tested 

17 86 14 93.5 15.1 

Maki, 1991; 

Finland 

Relevant 

clinical 

population 

Severe pathology 

with crypt 

hyperplasia to total 

villous atrophy; mild 

changes 

considered normal 

46.2 89 33.3 93.3 14.8 

McMillan, 

1991; Ireland 

Relevant 

clinical 

population 

Revised ESPGAN 57 85 64 81 28.1 

Gonczi, 1991; 

Australia 

Relevant 

clinical 

population 

(184 

children with 

suspected 

CD) 

ESPGAN no details 

on biopsy findings 

100 69.7 69.4 100 61.0 

Vogelsang, 

1995; Austria 

Relevant 

study 

population 

Modified ESPGAN; 

flat mucosa; crypt 

hyperplasia raised 

IELs 

73.5 73.6 72 75 49.0 
28

Table 6: Included studies for IgG-AGA in children 

Author, year; 

country Study type Biopsy criteria Sens Spec PPV NPV Prev 

Picarelli, 

2000; Italy 

Case-control ESPGAN 33.3 58.3 54.5 36.8 0.60 

Gaetano, 

1997; Italy 

Case-control ESPGAN 100 36 75.7 100 0.67 

Carroccio, 

1993; Italy 

Case-control Biopsies confirmed at 

diagnosis, on GFD, 

and rechallenge 

(severity grade – not 

recorded) 

88.9 46.7 55.6 84.8 0.43 

Hansson, 

2000; 

Sweden 

Case-control ESPGAN 81.8 82.6 81.8 82.6 0.49 

Berger, 1996; 

Switzerland 

Case-control ESPGAN revised with 

complete villous 

atrophy 

69 59 68 53 0.55 

Lerner, 1994; 

U.S.A, Israel 

Case-control Criteria of Townley 

modified by Ingkaran 

88 92 88 92 0.52 

Bahia, 2001; 

Brazil 

Relevant clinical 

population 

Severe villous atrophy 90.9 97.8 95.2 95.7 0.32 

Russo, 1999; 

Canada 

Relevant clinical 

population 

ESPGAN 83.3 85.9 66.7 93.8 0.25 

Bode, 1993; 

Denmark 

Relevant clinical 

population

ESPGAN 71 99 100 98 0.07 

Ascher, 1996; 

Sweden 

Relevant clinical 

population

ESPGAN 100 66.7 75.6 100 0.55 

Lindberg, 

1985; 

Sweden 

Relevant clinical 

population

ESPGAN; Alexander 

or Perea et al. 

93 89 93.1 88.6 0.31 

Altuntas, 

1998; Turkey 

Relevant clinical 

population

Subtotal or total 

villous atrophy, crypt 

hyperplasia, 

increased IEL 

100 0 55 0 0.55 

Artan, 1998; 

Turkey 

Relevant clinical 

population

ESPGAN 83 59 55.6 85.2 0.38 

Rich, 1990; 

USA 

Relevant clinical 

population

Not reported - state 

"severe" lesion 

100 58 44 100 0.25 

Gonczi, 1991; 

Australia 

Relevant clinical 

population (184 

children with 

suspected CD) 

ESPGAN no details 

on biopsy findings 

100 92.4 76.9 100 0.20 

Wolters, 

2002; 

Netherlands 

Relevant clinical 

population 

(identified 

retrospectively) 

Subtotal villous 

atrophy with crypt 

hyperplasia 

83 80 86 82 0.51 

Chirdo, 1999; 

Argentina 

Relevant clinical 

trial 

Total or subtotal 

villous atrophy 

85.7 80.6 80 86 0.47 

Chartrand, 

1997; Canada 

Relevant clinical 

population 

ESPGAN - with flat 

mucosal biopsy 

83 79 45 96 0.17 

Meini, 1996; 

Italy 

Relevant clinical 

population 

Partial villous atrophy 

or total villous atrophy 

100 80 31.2 100 0.08 
29

Table 7: Included studies for IgG-AGA in studies including both children and adults 

Author, year; 

country Study type Biopsy criteria Notes Sens Spec PPV NPV Prev 

Cataldo, 

2000; Italy 

Case-control Original and revised 

criteria? 

20 IgA-deficient 

CD vs healthy 

IgA-deficient 

non-CD 

100 100 100 100 0.7 

Sulkanen, 

1998; Finland 

Case-control ESPGAN 69 73.4 63 78.3 0.4 

Ascher, 1996; 

Sweden 

Relevant 

clinical 

population 

ESPGAN 96.4 69.2 72.6 95.7 0.5 

Carroccio, 

2002; Italy 

Relevant 

clinical 

population 

Marsh-broke down 

by criteria; CD was 

diagnosed as 

enlarged crypts 

and/or villous 

atrophy - with 

normalization on 

GFD 

 76 75 73.4 77.3 0.5 

Tesei, 2003; 

Argentina 

Relevant 

clinical 

population 

Marsh II to IV - with 

confirmation 

 84 86 89 79 0.6 

Figure 5: IgG-AGA in adults with CD 

AGA - IgG In Adults

0

10

20

30

40

50

60

70

80

90

100

0 10 20 30 40 50 60 70 80 90 100

1- Specificity

Sensitivity

Case Control

Cohort

Kaukinen, 2000

maki, 1991

Gonczi, 1991
30

Figure 6: IgG-AGA in children with CD 

IgG AGA in Children

0

10

20

30

40

50

60

70

80

90

100

0 10 20 30 40 50 60 70 80 90 100

1-Specifity

Sensitivity

Case Control

Cohort

Bottaro, 1997

Carroccio, 1993

Berger, 1996

Artan, 1998

Altuntas, 1998 Rich, 1990

Figure 7: IgG-AGA in children and adults with CD 

IgG AGA - in Studies including Children

and Adults

50

60

70

80

90

100

0 10 20 30 40 50

1-Specificity

Sensitivity

Case Control

Cohort

Sulkanen, 1998

Carroccio, 2002

Tesei, 2003

Ascher, 1996
31

EMA 

EMA—ME. The diagnostic characteristics of IgA-EMA-ME were assessed in 35 studies, and the 

diagnostic characteristics of IgG-EMA-ME were assessed in three studies. Of these included 

studies, 11 IgA-EMA-ME studies were conducted in adults,30,32,39,51,57,63,71,77,78,80,81 17 in 

children,27,35,36,38,41,44,46,51,52,55,56,58,60,69,79,82,83 and five in a mixed population.27,37,40,47,75 Some 

studies provided data for more than one age group. One study in children provided data on two 

different populations (including different control groups).55 IgG-EMA-ME was assesed in one 

adult population,63 one child population,66 but not in any of the mixed-population studies. 

One study was conducted in a population of known CD patients who had previously tested 

negative for EMA. In this study, the sensitivity and specificity of IgG EMA-ME were both 

100%;66 the performance of IgA-EMA was not reported. Another study that included CD 

patients with less than a Marsh IIIa grade,37 demonstrated a sensitivity of 88%. Some studies 

only provided summary statistics without the raw two-by-two table results,46,58,69 however, the 

raw data was abstracted based on the reported sensitivity and specificity, and the group sizes. 

IgA-EMA-ME. Among the 11 studies of IgA-EMA-ME conducted in 

adults,30,32,39,51,57,63,71,77,78,80,81 the specificity of the test was 100% in all except one, which 

showed a specificity of 97.2% (Table 8; Figure 8). The sensitivity of the test showed some slight 

variation among the studies. One outlier study demonstrated a sensitivity of only 74%;77

however, the authors found that in the remaining five of 19 CD patients who tested negative for 

EMA, three were IgA deficient. If these patients were excluded, the sensitivity rose to 88%. 

The authors also go on to say that they seem to have a high proportion of IgA-deficient subjects 

in their referral base. The remaining ten studies showed sensitivities of 89% or greater. In fact, 

five studies showed a sensitivity of 100%, one a sensitivity of 99%, and another a sensitivity of 

97%. In all, eight out of the 11 showed a sensitivity of 95% or greater, matching the very high 

specificity of this test. There was no statistical heterogeneity for this analysis. The pooled 

estimates for the sensitivity and specificity along with their 95% CI values were 97% (95% CI: 

95.7-98.5) and 99.6% (95% CI: 98.8-99.9), respectively. 

Among the 18 studies that assessed IgA-EMA-ME in 

children,27,35,36,38,41,44,46,51,52,55,56,58,60,69,79,82,83 all but one outlier69 were grouped together, and the 

sensitivities and specificities were both greater than 89% (Table 9; Figure 9). The outlier study 

demonstrated a sensitivity of only 74%, and also demonstrated low sensitivity for IgA-EMA-HU 

(see below).69 The authors comment on the difficulties of interpretating immunofluorescence 

data as a likely explanation. Ten studies showed sensitivities greater than 95%, and except for 

one study with a sensitivity of 89%, the remaining seven studies had sensitivities between 90% 

and 95%. All these studies demonstrated specificities of 89% or greater, 16 had specificities 

greater than 90%, and 14 had specificities greater than 96%. There was no evidence of statistical 

heterogeneity in this analysis. The pooled sensitivity and specificity was 96.1% (95% CI: 94.4-

97.3) and 97.4% (95% CI: 96.3-98.2), respectively. 

Among the four studies in a mixed-age population that assessed IgA-EMA-ME,27,37,47,75 all 

showed specificities of greater than 98% (Table 10; Figure 10). However, these studies showed 

some variation in the reported sensitivities. One study reported a very low sensitivity of 75%.47 

Two other studies showed a sensitivity of 86% and 88%, respectively, whereas the last showed a 

sensitivity of 98%. 
32

Table 8: Included studies for IgA-EMA-ME in adults 

Author, year; 

country Study type Biopsy criteria Sens Spec PPV NPV 

Prev 

(%) 

Hallstrom, 

1989; Finland 

Case-control Flat mucosa 90.6 100 100 88.9 51.8 

Biagi, 2001; 

Italy 

Case-control Partial villous atrophy or 

greater 

94.6 100 100 94.5 49.1 

Ladinser, 

1994; Italy 

Case-control Revised ESPGAN 100 100.0 100 100 21.1 

SateganaGuidetti, 1995; 

Italy 

Case-control Roy-Choudhury criteria; partial 

or total villous atrophy 

100 100 100 100 63.7 

Valentini, 

1994; Italy 

Case-control Partial villous atrophy or 

greater 

99 100 100 96.7 76.2 

Volta, 1995; 

Italy 

Case-control Roy-Choudhury criteria 95 100 100 97.1 35.6 

Carroccio, 

2002; Italy 

Relevant clinical 

population 

Ferguson and Murray; partial 

or total villous atrophy 

100 100 100 100 11.6 

McMillan, 

1991; Ireland 

Relevant clinical 

population

Revised ESPGAN 89.2 100 100 95.3 28.1 

Bardella, 

2001; Italy 

Relevant clinical 

population

Marsh 100 97.2 93 100 28.7 

Valdimarsson, 

1996; Sweden 

Relevant clinical 

population+ a few 

dypeptic controls 

Alexander's classification; 

partial or subtotal villous 

atrophy 

74 100 100 96 9.7 

Vogelsang, 

1995; Austria 

Relevant study 

population 

Modified ESPGAN; flat 

mucosa; crypt hyperplasia 

raised IELs 

100 100 100 100 48.0 
33

Table 9: Included studies for IgA-EMA-ME in children 

Author, year; 

country Study type Biopsy criteria Sens Spec PPV NPV Prev 

Chirdo, 2000; 

Argentina 

Case-control ESPGAN 92.4 100 100 85.2 0.7 

Kolho, 1997; 

Finland 

Case-control Revised ESPGAN 95 100 100 97 0.3 

Kolho, 1997; 

Finland 

Case-control Revised ESPGAN 100 100 100 100 0.5 

Whelan, 1996; 

Ireland 

Case-control Subtotal villous 

atrophy 

100 100 100 100 0.4 

Bonamico, 2001; 

Italy 

Case-control ESPGAN 95.1 98.2 90 44.3 0.5 

Gaetano, 1997; 

Italy 

Case-control ESPGAN 96 96 97.9 92.3 0.7 

Carroccio, 1993; 

Italy 

Case-control Biopsies confirmed at 

diagnosis, on GFD, 

and rechallenge 

(severity grade - not 

reported) 

100 96.7 95.7 100 0.4 

Di Leo, 2003; 

Italy 

Case-control ESPGAN 100 96.5 93.5 100 0.4 

Vitoria, 2001; 

Italy 

Case-control Subtotal villous 

atrophy 

100 100 100 100 0.6 

Hansson, 2000; 

Sweden 

Case-control ESPGAN 95.5 100 100 95.8 0.5 

Lerner, 1994; 

USA, Israel 

Case-control Criteria of Townley 

modified by Ingkaran 

97 98 97 98 0.5 

Hallstrom, 1989; 

Finland 

Case-control Flat mucosa 100 100 100 100 0.4 

Chan, 2001; 

Canada 

Relevant clinical 

population 

Villous atrophy, crypt 

hyperplasia, 

increased 

lymphocytes 

89 97 80 98 0.1 

Russo, 1999; 

Canada 

Relevant clinical 

population 

ESPGAN 75 88.7 69.2 91.3 0.3 

Ascher, 1996; 

Sweden 

Relevant clinical 

population 

ESPGAN 95.4 100 100 94.7 0.6 

Wolters, 2002; 

Netherlands 

Relevant clinical 

population 

(identified 

retrospectively) 

Subtotal villous 

atrophy with crypt 

hyperplasia 

92 90 90.5 92 0.5 

Lindquist,1993; 

Sweden 

Relevant clinical 

population 

(suspected CD) 

ESPGAN; subtotal or 

partial villous atrophy 

98.1 92.7 94.4 97.5 0.6 

Kumar, 1989; 

USA, Israel 

Relevant clinical 

population and 

control cases 

ESPGAN + Townley 96.0 89.0 87.0 96.7 0.2 
34

Table 10: Included studies for IgA-EMA-ME in studies including both children and adults 

Author, 

year; 

country Study type Biopsy criteria Notes Sens Spec PPV NPV Prev 

Cataldo, 

2000; 

Italy 

Casecontrol Original & revised 

criteria? 

20 IgAdeficient CD 

vs healthy 

IgA-deficient 

non-CD 

0 100 0 33.3 0.7 

Dickey, 

2001; 

Northern 

Ireland 

Casecontrol Villous atrophy 75.3 98.3 98.2 76 0.6 

Ascher, 

1996; 

Sweden 

Relevant 

clinical 

population 

ESPGAN 98.2 100 100 98.5 0.5 

Carroccio 

2002; 

Italy 

Relevant 

clinical 

population 

Marsh - broke 

down by criteria; 

CD was diagnosed 

as enlarged crypts 

and/or villous 

atrophy - with 

normalization on a 

GFD 

 88 99 98.7 90 0.5 

Tesei, 

2003; 

Argentina 

Relevant 

clinical 

population 

Marsh II to IV - 

with confirmation 

 86 100 100 83 0.6 

Figure 8: IgA-EMA-ME in adults with CD 

IgA EMA - Monkey Esophagus in Adults

50

60

70

80

90

100

0 10 20 30 40 50

1- Specificity

Sensitivity

Case Control

Cohort

Valdimarsson, 1996
35

Figure 9: IgA-EMA-ME in children with CD 

IgA EMA Monkey Esophagus

in Children

50

60

70

80

90

100

0 10 20 30 40 50

1-Specificity

Sensitivity

Case Control

Cohort

Russo, 1999

Figure 10: IgA-EMA-ME in adults and children with CD 

IgA EMA - Monkey Esophagus

in Studies including Children and Adults

50

60

70

80

90

100

0 10 20 30 40 50

1-Specificity

Sensitivity

Case Control

Cohort

Dickey, 2001

IgG-EMA-ME. Only two studies meeting our inclusion criteria assessed IgG-EMA-ME, one in 

adults (Table 11),63 and one in children (Table 12).66 In the single adult study,63 the sensitivity of 

the test was found to be 39%, whereas, the specificity was 98%. In a case-control study design, 

Picarelli et al. studied 30 IgA-EMA-negative children suspected of having CD.66 Of these 30 

children, 18 were subsequently found to have CD by duodenal biopsy and nine of the 18 were 
36

found to be IgA deficient. In this highly selected population, the reported sensitivity and 

specificity of IgG-EMA-ME were both 100%.

Table 11: Included studies for IgG-EMA-ME in adults 

Author, 

year; 

country Study type Biopsy criteria Sens Spec PPV NPV 

Prev 

(%) 

McMillan, 

1991; 

Ireland 

Relevant clinical 

population 

Revised ESPGAN 39 98.3 92 78 13.5 

Table 12: Included studies for IgG-EMA-ME in children 

Author, 

year; 

country Study type 

Biopsy 

criteria Notes Sens Spec PPV NPV Prev 

Picarelli, 

2000; 

Italy 

Case-control ESPGAN 30 IgA-EMA 

neg. pts 

suspected of 

CD; 9/18 CD 

patients IgA 

deficient 

100 100 100 100 0.1 

EMA—HU. IgA-EMA-HU was assessed in 13 studies. Six of these studies were conducted in 

adults,45,49,54,57,61,70,89 five in children,36,53,55,69,70 and two in a mixed population.72,74 One study 

provided summary statistics without the raw two-by-two table results,69 however the raw data 

was calculated from the reported sensitivity and specificity and the group numbers. One study 

provided data on two different populations (including different control groups).55

IgG-EMA-HU was not assessed in any of the studies meeting our inclusion criteria. 

Two studies included CD patients (both adult and children) with less than a Marsh IIIa grade, 

and reported IgA-EMA-HU sensitivities of 87% and 100%.45

70

IgA-EMA-HU. Six studies in adults assessed IgA-EMA-HU (Table 13; Figure 11).45,49,54,57,61,70,89 

In all six, the specificity was reported to be 100%. There was, however, variability in the 

reported sensitivities, which ranged from 87% to 100%. Three studies demonstrated sensitivities 

between 87% and 89%, two between 90% and 95% and one showing a sensitivity of 100%. 

There was no observed statistical heterogeneity for this analysis. The pooled sensitivity and 

specificity was found to be 90.2% (95% CI: 85.9-93.4) and 100% (95% CI: 99.1-100), 

respectively. 

Five studies with six separate child populations assessed IgA-EMA-HU (Table 14; Figure 

12).36,53,55,69,70 Four of the six studies were grouped together and revealed sensitivities between 

94% and 100%, and specificities of 100%. Of the two outliers,90 one showed a sensitivity of 

100% and a specificity of 77%. The other study,69 was an outlier in other analyses, and 

demonstrated a sensitivity of 46% and a specificity of 96%. The authors comment on difficulties 

of interpretation of the immunofluorescence as a likely explanation. After accounting for this 

study, there was no statistical heterogeneity documented for sensitivity. The pooled sensitivity 

for this analysis was 96.9% (95% CI: 93.5-98.6). A pooled specificity for this analysis was not 

calculated, but is likely close to 100% given that four of the five grouped studies demonstrated a 

specificity of 100%. 
37

Two studies assessed IgA-EMA-HU in a mixed-age population (Table 15; Figure 13).72,74 In 

both these studies, the specificity was 100% (95% CI: 97.5-100) and the sensitivity 93% (95% 

CI: 88.1-95.4). 

Table 13: Included studies for IgA-EMA-HU in adults 

Table 14: Included studies for IgA-EMA-HU in children 

Author, 

year; 

country Study type Biopsy criteria Sens Spec PPV NPV 

Prev 

(%) 

Gillbert, 

2000; 

Canada 

Case-control Mild, moderate, 

severe villous atrophy 

100 100 100 100 33.3 

Ladinser, 

1994; Italy 

Case-control Revised ESPGAN 90 100 100 98 18.9 

Salmaso, 

2001; Italy 

Case-control Grades I-IV Marsh 

with response to a 

GFD 

87 100 100 95.1 24.7 

Volta, 

1995; Italy 

Case-control Roy-Choudhury 

criteria 

95 100 100 97.1 35.6 

Dahele, 

2001; 

Scotland 

Case-control Included 6 with IEL, 

rest partial villous 

atrophy or greater 

87 100 100 81.3 55.3 

Kaukinen, 

2000; 

Finland 

Relevant 

clinical 

population 

Villous height to crypt 

ration <2.0; IEL and 

HLA also tested 

88.9 100 100 98.9 7.6 

Author, 

year; 

country Study type Biopsy criteria Sens Spec PPV NPV Prev 

Kolho, 

1997; 

Finland 

Case-control Revised ESPGAN 95 100 100 97 0.3 

Kolho, 

1997; 

Finland 

Case-control Revised ESPGAN 100 100 100 100 0.5 

Gaetano, 

1997; Italy 

Case-control ESPGAN 94 100 100 89.2 0.7 

Salmaso, 

2001; Italy 

Case-control Grades I-IV Marsh 

with response to 

GFD 

100 100 100 100 0.6 

Russo, 

1999; 

Canada 

Relevant 

clinical 

population 

ESPGAN 45.8 95.8 78.6 84 0.3 

Iltanen, 

1999 

Finland 

Relevant 

clinical 

population 

ESPGAN - CD 

confirmed at followup 

100 77.1 60.1 100 0.3 
38

Table 15: Included studies for IgA-EMA-HU in studies including both children and adults 

Figure 11: IgA-EMA-HU in adults with CD 

IgA EMA Human Umbilical Cord in Adults

50

60

70

80

90

100

0 10 20 30 40 50

1-Specificity

Sensitivity

Case Control

Cohort

Author, 

year; 

country Study type Biopsy criteria Sens Spec PPV NPV Prev 

Sblaterro, 

2000; 

Italy 

Case-control ESPGAN 93 100 100 80 0.8 

Sulkanen, 

1998; 

Finland 

Case-control ESPGAN 92.6 99.5 99.2 94.9 0.4 
39

Figure 12: IgA-EMA-HU in children with CD 

IgA EMA Human Umbilical Cord

in Children

40

50

60

70

80

90

100

0 10 20 30 40 50

1-Specificity

Sensitivity

Case Control

Cohort

Iltanen, 1999

Russo, 1999

Figure 13: IgA-EMA-HU in adults and children with CD 

IgA EMA - Human Umbilical Cord

in Studies Including Children and Adults

50

60

70

80

90

100

0 10 20 30 40 50

1-Specificity

Sensitivity

Case Control
40

tTG antibodies 

tTG—GP liver. The diagnostic characteristics of IgA-tTG-GP were assessed by ELISA in nine 

studies, and the diagnostic characteristics IgG-tTG-GP assessed by ELISA in three studies. Of 

the IgA-tTG–GP studies, five were conducted in adults,30,32,39,45,70 five in children,35,41,52,70,83 and 

four in a mixed population.47,72,74,76 One study provided separate data for more than one age 

group.70

Of the IgG-tTG-GP studies that met the inclusion criteria, none were in adults or children, 

although two studies were in a mixed population.72,76

Two studies included CD patients with less than a Marsh IIIa grade.45,70 These studies 

demonstrated sensitivities of 81% and 95% for IgA-tTG-GP. 

IgA-tTG-GP. In the analysis of IgA-tTG-GP in adults, five studies grouped themselves by study 

design.30,32,39,45,70 The two cohort studies (relevant clinical population)30,39 both showed 

sensitivities of 100%, and specificities of 92% and 98%, respectively. On the other hand, the 

three case-control studies32,45,70 demonstrated high specificities (97% to 98%), but sensitivities of 

only 81% to 88% (Table 16; Figure 14). This analysis did not show statistical heterogeneity, but 

the differences by study design were striking, so a pooled estimate for sensitivity was not 

performed. The pooled specificity was 95.3% (95% CI: 92.5-98.1). 

The analysis of IgA-tTG-GP in children showed very little variability in either the sensitivity, 

or specificity (Table 17; Figure 15). Among these five studies,35,41,52,70,83 the sensitivities ranged 

from 89% to 96%. The specificities were all greater than 92%, with three studies showing 

specificities greater than 96%,41,52,83 and two studies having a sensitivity of 100%.35,70 The 

pooled estimates of the sensitivity and specificity were 93.1% (95% CI: 88.8-95.9) and 96.3% 

(95% CI: 93.1-98.0), respectively (Table 17; Figure 15) 

Among the studies of mixed-age groups,47,72,74,76 there was one outlier study with a 

sensitivity of only 84% but a specificity of 100% (Table 18).72 The specificities of the remaining 

studies were all greater than 94% (Table 18; Figure 16), and the sensitivities were between 92% 

and 95%. Heterogeneity was detected in the estimates of sensitivity, but not for specificity. The 

pooled specificity was 95.4% (95% CI: 92.7-97.2). 
41

Table 16: Included studies for IgA-tTG-GP in adults

Author, 

year; 

country Study type Biopsy criteria Sens Spec PPV NPV 

Prev 

(%) 

Biagi, 

2001; Italy 

Case-control Partial villous atrophy or 

greater 

87.5 98.1 98 87.1 46.3 

Salmaso, 

2001; Italy 

Case-control Grades I-IV Marsh with 

response to a GFD 

87 97 90.9 94.9 27.2 

Dahele, 

2001; 

Scotland 

Case-control Included 6 with IEL, rest 

partial villous atrophy or 

greater 

81 97 97.9 74.1 52.5 

Carroccio, 

2002; Italy 

Relevant 

clinical 

population 

Ferguson and Murray; 

partial or total villous 

atrophy 

100 92 60 100 18.8 

Bardella, 

2001; Italy 

Relevant 

clinical 

population 

Marsh 100 98.2 83.3 100 10.0 

Table 17: Included studies for IgA-tTG-GP in children

Author, 

country; 

year Study type Biopsy criteria Sens Spec PPV NPV Prev 

Bonamico, 

2001; Italy 

Case-control ESPGAN 90.3 100 100 30.3 0.5 

Salmaso, 

2001; Italy 

Case-control Grades I-IV Marsh with 

response to a GFD 

95 100 100 94.1 0.6 

Hansson, 

2000; 

Sweden 

Case-control ESPGAN 90.9 95.7 95.2 91.7 0.5 

Chan, 

2001; 

Canada 

Relevant 

clinical 

population 

Villous atrophy, crypt 

hyperplasia, increase 

lymphocytes 

89 94 67 98 0.1 

Wolters, 

2002; 

Netherlands 

Relevant 

clinical 

population 

(identified 

retrospectively) 

Subtotal villous atrophy 

with crypt hyperplasia 

96 92 92.6 95.7 0.5 

Table 18: Included studies for IgA-tTG-GP in studies including both adults and children

Author, 

year, 

country Study type Biopsy criteria Sens Spec PPV NPV Prev 

Dickey, 

2001; 

Northern 

Ireland 

Case-control Villous atrophy 93.2 96.6 97.1 91.8 0.6 

Sblaterro, 

2000; Italy 

Case-control ESPGAN 84 100 100 62.5 0.8 

Sulkanen, 

1998; 

Finland 

Case-control ESPGAN 95 93.7 90.8 96.5 0.4 

Troncone, 

1999; Italy 

Relevant 

clinical 

population 

ESPGAN 91.7 98 98 94 0.4 
42

Figure 14: IgA-tTG-GP in adults with CD 

IgA tTg Guinea Pig in Adults

50

60

70

80

90

100

0 10 20 30 40 50

1-Specificity

Sensitivity

Case Control

Cohort

Dahele, 2001

salmaso, 2001

Biagi, 2001

Figure 15: IgA-tTG-GP in children with CD 

IgA tTG Guinea Pig In Children

50

60

70

80

90

100

0 10 20 30 40 50

1-Specificity

Sensitivity

Case Control

Cohort
43

Figure 16: IgA-tTG-GP in adults and children with CD 

IgA tTg - Guinea Pig - In Studies

Including Children and Adults

50

60

70

80

90

100

0 10 20 30 40 50

1-Specificity

Sensitivity

Case Control

Cohort

Sblaterro, 2000

IgG-tTG-GP. Two studies in a mixed-age population assessed IgG-tTG- GP (Table 19; Figure 

17).72,76 The specificities in both studies were greater than 98%, but the sensitivities were 23% 

and 62%, respectively. 

Table 19: Included studies for IgG-tTG-GP in studies including both children and adults

Author, 

year; 

country Study type Biopsy criteria Sens Spec PPV NPV Prev 

Sblaterro, 

2000; Italy 

Case-control ESPGAN 61.5 100 100 44.4 0.8 

Troncone, 

1999; Italy 

Relevant 

clinical 

population 

ESPGAN 23 98 92 63 0.4 
44

Figure 17: IgG-tTG-GP in adults with CD 

IgG tTG in Studies Including Children and Adults

0

10

20

30

40

50

60

70

80

90

100

0 10 20 30 40 50

1-Specificity

Sensitivit

y

Case Control -

Guinea Pig

Cohort -

Guinea Pig

Case Control -

Human

Recombinant Troncone, 1999

tTG – human recombinant (HR) 

IgG-tTG-HR. The diagnostic characteristics of IgA-tTG-HR were assessed by ELISA in ten 

studies, and the diagnostic characteristics IgG-tTG-HR were assessed by ELISA in two studies. 

Of the IgA-tTG-HR studies, three were conducted in adults,39,49,54 three in children,52,79,83 and 

three in a mixed population.40,72,75

Of the IgG-tTG-HR studies, two were conducted in a mixed population (Table 20),40,72 but 

none were conducted in adults or children. One study was conducted in IgA-deficient patients 

and is described below.40

Two studies included CD patients with less than a Marsh IIIa grade.45,70 These studies 

demonstrated sensitivities of 81% and 95% for IgA-tTG-GP. 

One study was conducted in a mixed-age population of patients with known IgA 

deficiency.40 In this study, the sensitivity of IgA-tTG–HR was 0%, wheras, the sensitivities and 

specificities of IgG-tTG-HR were 100% and 80%, respectively. 
45

Table 20: Included studies for IgG-tTG-HR in studies including both children and adults

Author, 

year; 

country Study type 

Biopsy 

criteria Notes Sens Spec PPV NPV Prev 

Cataldo, 

2000; Italy 

Casecontrol Original & 

revised 

criteria? 

20 IgA-deficient CD 

vs healthy IgAdeficient non-CD 

100 80 90.1 100 0.7 

Sblaterro, 

2000; Italy 

Casecontrol ESPGAN 67.6 100 100 48.7 0.8 

IgA-tTG-HR. Three studies assessed IgA-tTG-HR in an adult population (Table 21; Figure 

18).39,49,54 There was very little variability in the reported values for the sensitivities and 

specificities. The sensitivities were 100% in two studies, and 95% in the other. The specificities 

were 100% in two studies, and 97% in another. The pooled estimates of the sensitivity and 

specificity were 98.1% (95% CI: 90.1%-99.7%) and 98.0% (95% CI: 95.8-99.1), respectively. 

Among the three studies in children (Table 22; Figure 19),52,79,83 the sensitivities were 96% in 

two studies and 95% in one. The specificities were 100% in two studies, and 96% in one. The 

pooled estimates of the sensitivity and specificity were 95.7% (95% CI: 90.3-98.1) and 99.0% 

(95% CI: 94.6-99.8), respectively. 

Only two studies assessed the IgA-tTG-HR in a mixed-age population without IgA 

deficiency (Table 23; Figure 20).72,75 The sensitivities and specificities were 92% and 100%, 

respectively, for the first study, and 91% and 96%, respectively, for the second. The pooled 

estimates of the sensitivity and specificity were 90.2% (95% CI: 86.4-93.0) and 95.4% (95% CI: 

91.5- 97.6), respectively. 

Overall, these studies demonstrated a specificity of close to 100% and sensitivity in the range 

of 90% to 96%. 

Table 21: Included studies for IgA-tTG-HR in adults

Author, 

year; 

country Study type Biopsy criteria Sens Spec PPV NPV 

Prev 

(%) 

Carroccio, 

2002; Italy 

Relevant 

clinical 

population 

Ferguson and Murray; partial or total 

villous atrophy 

100 97 80 100 14.5 

Gillbert, 

2000; Italy 

Case-control Mild, moderate, severe villous atrophy 95.2 100 95.2 100 31.7 

Kaukinen, 

2000; 

Finland 

Relevant 

clinical 

population 

Villous height to crypt ration <2.0; IEL 

and HLA also tested 

100 100 100 100 8.7 

Table 22: Included studies for IgA-tTG-HR in children

Author, year; 

country Study type Biopsy criteria Sens Spec PPV NPV Prev 

Vitoria, 2001; 

Italy 

Case-control Subtotal villous atrophy 95 100 100 93 0.6 

Hansson, 2000; 

Sweden 

Case-control ESPGAN 95.5 95.7 95.5 95.7 0.5 

Wolters, 2002; 

Netherlands 

Relevant 

clinical 

population 

(identified 

retrospectively) 

Subtotal villous atrophy 

with crypt hyperplasia 

96 100 100 96 0.5 
46

Table 23: Included studies for IgA-tTG-HR in studies including both children and adults

Author, 

year; 

country Study type 

Biopsy 

criteria Notes Sens Spec PPV NPV Prev 

Cataldo, 

2000; Italy 

Case-control Original & 

revised 

criteria? 

20 IgA deficient 

CD vs healthy 

IgA-deficient 

non-CD 

0 100 0 33.3 0.7 

Sblaterro, 

2000; Italy 

Case-control ESPGAN 91.5 100 100 76.9 0.8 

Tesei, 

2003; 

Argentina 

Relevant 

clinical 

population 

Marsh II to IV 

- with 

confirmation 

 91 96 97 87 0.6 

Figure 18: IgA-tTG-HR in adults with CD 

IgA tTg - Human Recombinant in Adults

50

60

70

80

90

100

0 10 20 30 40 50

1-specificity

Sensitivity

Case Control

Cohort
47

Figure 19: IgA-tTG-HR in children with CD 

IgA tTG Human Recombinant in Children

50

60

70

80

90

100

0 10 20 30 40 50

1-Specificity

Sensitivity

Case Control

Cohort

Figure 20: IgA-tTG-HR in adults and children with CD 

IgA tTG - Human Recombinant in

Studies Including Children and Adults

50

60

70

80

90

100

0 10 20 30 40 50

1-Specificity

Sensitivity

Case Control

Cohort

IgG-tTG-HR, IgA deficient. Only one study of IgG-tTG-HR, conducted in an IgA-deficient 

population, was identified.72 In this study, the sensitivity and specificity of IgG-tTG-HR was 

68% and 100%, respectively. 
48

Mixed-antibody combinations. Several studies were identified that tested different antibodies 

in combination. Six studies in children assessed the use of IgA- and IgG-AGA (Table 

24).34,42,48,50,59,85 When either of these tests were positive, the resulting sensitivities ranged from 

83% to 100%, and the specificities ranged from 71% to 99%. One study, that apparently used 

similar methodologies, had the lowest sensitivity (83%) and specificity (36%) of the group.85 

When the same authors tested the antibodies under the requirement of both tests being 

concordant, the sensitivity fell, as would be expected, to 50%, and the specificity rose to 67%.85 

Three adult studies were identified that used IgA- and IgG-AGA in an either/or protocol (Table 

24).33,50,78 As was observed in the studies of children, significant between-study differences 

existed, making pooled estimates inappropriate. Nonetheless, in these studies the sensitivity 

ranged from 77% to 100%, while the specificity ranged from 90% to 97%.

One study in a mixed-age population assessed the use of a combination of IgA- and IgGtTG-HR antibodies (Table 25).72 In this study, the sensitivity when either test was positive was 

98.5%, while the specificity remained high at 100%. Another study in children assessed the 

combination of IgA-AGA and IgA-EMA-HU when either test was positive, and found a 

sensitivity of 100% and a specificity of 73% (Table 26).69 This same study assessed the same 

antibodies under the situation where both tests needed to be concordant. In this circumstance, 

the sensitivity remained 100% and the specificity rose to 93%. 

In general, combining tests when either test is positive tended to improve sensitivity at the 

cost of specificity, while a requirement for the tests to be concordant tended to improve 

specificity. 
49

Table 24: Included studies for combination IgA and IgG AGA, when either test is positive

Author, 

year; 

country Study type Biopsy criteria Notes Sens Spec PPV NPV Prev 

Valentini, 

1994; Italy 

Case-control Partial villous atrophy 

or greater 

Adults 92 90 96.8 77.1 0.76 

Bode, 1994; 

Denmark 

Relevant clinical 

population 

Crypt hyperplasia, 

villous atrophy and 

increase inflammatory 

cells 

Adults 77 95 71 97 0.41 

Gonczi, 

1991; 

Australia 

Relevant clinical 

population (184 

children with 

suspected 

celiac) 

ESPGAN no details 

on biopsy findings 

Adults 100 97.1 96.2 100 0.44 

Bode, 1993; 

Denmark 

Relevant clinical 

population 

ESPGAN Children 86 99 92 99 0.1 

FalthMagnusson, 

1994; 

Sweden 

Relevant clinical 

population 

ESPGAN + Alexander 

grading IV, grade III 

to IV challenge 

Children 88.5 93.7 88.8 93.5 0.4 

Lindberg, 

1985; 

Sweden 

Relevant clinical 

population 

ESPGAN, Alexander 

grading 

Children 97 83 41.8 98.2 0.3 

Artan, 1998; 

Turkey 

Relevant clinical 

population 

ESPGAN Children: 

IgA AGA 

or IgG 

AGA 

83 36 44 77.8 0.3 

Gonczi, 

1991; 

Australia 

Relevant clinical 

population (184 

children with 

suspected CD) 

ESPGAN no details 

on biopsy findings 

Children 100 98.7 95.2 98.7 0.2 

Chartrand, 

1997; 

Canada 

Relevant clinical 

population 

ESPGAN – with flat 

mucosal biopsy 

Children 93 71 43 98 0.2 

Table 25: Included studies for combination IgA and IgG tTG-HR, when either test is positive

Author, 

year; 

country Study type Biopsy criteria Notes Sens Spec PPV NPV Prev 

Sblaterro, 

2000; Italy 

Case-control ESPGAN Adults and 

children 

98.5 100 100 95.2 0.8 

Table 26: Included studies for combination IgA-AGA and IgG-EMA-HU, when either test is positive

Author, year; 

country Study type Biopsy criteria Notes Sens Spec PPV NPV Prev 

Russo, 1999; 

Canada 

Relevant 

clinical 

population 

ESPGAN Children 100 73 57 82 0.3 
50

Prevalence of CD and the positive predictive value (PPV) and negative predictive value 

(NPV) of serology. The prevalence of CD in the tested populations is presented in Tables 2 to 

26 for the individual studies, and in Table 27 for the pooled estimate for the analysis groups.

The minimum prevalence of CD in individual study populations was greater than 25% in 

most of the studied analysis groups (i.e., IgA-AGA, IgG-AGA, etc), except for ten analysis 

groups where the minimum prevalence was between 9% and 12%. In all the analysis groups, the 

maximum prevalence ranged from 30% to as high as 70%. The pooled prevalence for the 

analysis groups was predominantly between 30% and 45%. 

In assessing the IgA-EMA and IgA-tTG analysis groups, the pooled prevalence ranged from 

33% to 46% except for the analysis of IgA-tTG-HR in adults, which showed a pooled prevalence 

of 16%. Figure 21 is a plot of the individual study prevalence versus the study’s PPV, and 

suggests that below a CD prevalence of about 35% to 40%, the PPV of these IgA-based tests 

tends to drop from about 90% to 100%, to about 80% or less. As expected, Figure 22 

demonstrates the reverse relationship, with the NPV being between 95% and 100% up to a CD 

prevalence of about 45%, and then dropping off. 
51 

Table 27: Weighted pooled estimates with 95% CIs and heterogeneity identified 

Analysis 

Sens 

L 95% 

CI: 

U 95% 

CI: Spec 

L 95% 

CI: 

U 95% 

CI: Prev 

L 95% 

CI: 

U 95% 

CI: PPV 

L 95% 

CI: 

U 95% 

CI: 

IgA-AGA–ADULT H H H H H H 0.358 0.332 0.385 H H H IgG-AGA–ADULT H H H H H H 0.367 0.335 0.401 H H H IgA-EMA-ME–ADULT 0.974 0.957 0.985 0.996 0.988 0.999 0.398 0.371 0.425 0.974 0.957 0.985 IgG-EMA-ME–ADULT (one study) 0.393 0.236 0.576 0.984 0.913 0.997 0.135 0.079 0.221 0.393 0.236 0.576 IgA-EMA-HU–ADULT 0.902 0.859 0.934 1.000 0.991 1.000 0.331 0.297 0.368 0.902 0.859 0.934 IgA-tTG-GP—ADULT 0.859 0.808 0.898 0.953 0.930 0.969 0.312 0.279 0.348 0.859 0.808 0.898 IgA-tTG-HR–ADULT 0.981 0.901 0.997 0.981 0.958 0.991 0.160 0.126 0.202 0.981 0.901 0.997 IgA-AGA–CHILD H H H H H H 0.363 0.341 0.385 H H H IgG-AGA–CHILD H H H H H H 0.437 0.413 0.462 H H H IgA-EMA-ME–CHILD 0.961 0.945 0.973 0.974 0.963 0.982 0.400 0.378 0.423 0.961 0.945 0.973 IgA-EMA-HU–CHILD 0.969 0.935 0.986 H H H 0.447 0.402 0.493 0.969 0.935 0.986 IgA-tTG-GP–CHILD 0.931 0.888 0.959 0.963 0.931 0.980 0.446 0.401 0.493 0.931 0.888 0.959 IgA-tTG-HR–CHILD 0.957 0.903 0.981 0.990 0.946 0.998 0.519 0.452 0.584 0.957 0.903 0.981 IgA-AGA–MIXED H H H H H H 0.415 0.386 0.444 H H H H = significant heterogeneity by Pearson’s Chi square 

Note: Appendixes and Evidence Tables are provided electronically at 

 

 

http://www.ahrq.gov/clinic/tp/celiactp.htm

 51
52

Table 27 (cont’d): Weighted pooled estimates with 95% CIs and heterogeneity identified 

Analysis 

Sens 

L 95% 

CI: 

U 95% 

CI: Spec 

L 95% 

CI: 

U 95% 

CI: Prev 

L 95% 

CI: 

U 95% 

CI: PPV 

L 95% 

CI: 

U 95% 

CI: 

IgG-AGA–MIXED H H H H H H 0.510 0.480 0.540 H H H IgA-EMA-ME–MIXED H H H 0.995 0.982 0.999 0.467 0.434 0.500 0.859 0.825 0.888 IgA-EMA-HU–MIXED 0.925 0.881 0.954 0.996 0.975 0.999 0.437 0.391 0.484 0.925 0.881 0.954 IgA-tTG-GP–MIXED H H H 0.954 0.927 0.972 0.463 0.425 0.501 0.913 0.877 0.939 IgG-tTG-GP–MIXED 0.451 0.363 0.543 0.988 0.935 0.998 0.265 0.208 0.331 0.451 0.363 0.543 IgA-tTG-HR–MIXED 0.902 0.864 0.930 0.954 0.915 0.976 0.573 0.530 0.616 0.902 0.864 0.930 IgG-tTG-HR–MIXED (one study) 0.677 0.556 0.778 1.000 0.839 1.000 0.518 0.413 0.621 0.677 0.556 0.778 H = significant heterogeneity by Pearson’s Chi square Note: see Appendix G for raw pooled data by antibody test 

 

 

 52 
 53

Figure 21: PPV and prevalence from individual studies 

PPV and Prevalence

0.3

0.4

0.5

0.6

0.7

0.8

0.9

1

1.1

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9

Prevalence

PPV

EMA adult

EMA Child

tTg Adult

tTg Child

Figure 22: NPV and prevalence from individual studies 

NPV vs Prevalence

0.3

0.4

0.5

0.6

0.7

0.8

0.9

1

1.1

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9

Prevalence

NPV

EMA adult

EMA Child

tTg Adult

tTg Child
 54

Figure 23: PPV based on the pooled estimates of sensitivity and specificity 

PPV Based on the Pooled Estimates of 

Sensitivity and Specificity

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

1

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1

Prevalence

PPV

IgA-EMA-HU-ADULT

IgA-tTG-GP-ADULT

IgA-tTG-HR-ADULT

IgA-EMA-ME-CHILD

IgA-tTG-GP-CHILD

IgA-tTG-HR-CHILD

IgA-EMA-HU-MIXED

IgA-tTG-HR-MIXED
 55

HLA DQ2/DQ8 

We identified 99 potentially relevant HLA articles that appeared to address HLA DQ2/DQ8 

in a CD population (Appendix F).8-11,15,53,54,62,91-100,100-177 These studies were not designed to 

determine the diagnostic utility of DQ2 or DQ8 per se. 

Of the identified studies, 54 allowed estimation of the prevalence, sensitivity or specificity of 

HLA DQ2/DQ8 in the studied population.8-10,15,53,54,93,100,109,120,134-177 In one study, DQ2 data 

could not be reliably extracted.169 The authors of one study9

 explicitly stated that the patients 

used were the same as in two of their other publications.8,93 In two other publications by the 

same authors,9,10 the patients appear to be different and the authors do not indicate that they used 

patients from a previous study. However, the possibility that these two studies9,10 share a subset 

of patients cannot be excluded. Another two studies addressing different topics but with 

extractable HLA data, also appeared to have used the same patients.53,136 In cases of duplicate 

publications, the studies with the greater number of patients were used.9,136

The study designs and strictness of CD diagnosis in these articles varied, as did the inclusion 

of a control group. Most of the CD cases were diagnosed based on the ESPGAN criteria, 

although in some studies CD was diagnosed based on serology and then in most cases later 

confirmed by biopsy.15,109,120,160,161,164,168,170,172,177 Nine of the studies were classified as crosssectional studies,169-177, 32 were case-control studies,8-10,53,100,120,134-159 and 12 were mixed crosssectional/case-control studies or could be considered as diagnostic cohort studies.15,54,109,160-168 

Four of the mixed design studies109,164,166,178 used screen-negative patients as the control group, 

whereas the rest used a control group that was separate from the screened population. The study 

populations were also variable. The case-control studies used known CD cases compared with 

variously defined CD negative controls. 

Seven studies used relatives of CD patients,158,161,164,166,169,172,177 four used a population with 

Down Syndrome,109,134,160,170 two used a population with type I diabetes,165,173 and one used a 

mixed group of patients with CD including some with Down’s and others with diabetes.173 The 

mixed-design/cohort studies used patients suspected of CD on clinical grounds or subjects who 

belonged to a high-risk group, such as type 1 diabetics or first-degree relatives of patients with 

CD. The remaining articles used a screened healthy population or another specific group. 

The articles with extractable data stated the frequency of HLA DQ2, and to a lesser extent 

the frequency of HLA DQ8, in their CD group. The cross-sectional studies did not include a 

control group. Only the frequency as a surrogate of sensitivity was available. None of the casecontrol or mixed-design studies calculated the sensitivity or specificity of HLA DQ2 or DQ8. 

However, these studies allowed us to derive estimates of these statistics from their results or 

tables. The considerable degree of clinical and methodological heterogeneity between the 

identified studies did no allow for statistical pooling of the results. 

Two studies fulfilled our inclusion requirement of both cases and control groups undergoing 

intestinal biopsy (Evidence Table 2, Appendix I; Table 28).136,152 The remaining studies had 

various control group types: unbiopsied, healthy controls, disease controls, or serology-negative 

controls. These studies provide useful information and are presented at the end of the HLA 

results section for reference. 

The study by Iltanen et al.,136 was conducted in a group of Finnish children to assess the 

density of gamma delta positive intraepithelial lymphocytes (γδ+ IELs) in: patients with CD by 

biopsy (ESPGAN); patients with suspected CD where the diagnosis was excluded by biopsy; 

and, in a group of biopsy-negative patients who underwent endoscopy for dyspepsia. The biopsy 
 56

aspect of this study is presented in its respective section. In this study, HLA DQ2 was found in 

19 of 21 (90.5%) of patients with CD as apposed to 29 out of 67 (29.9%) of the control patients. 

Elevated γδ+ IEL density was significantly associated with DQ2 positivity. The calculated 

diagnostic measures for this study are presented in Table 28. In this population, DQ2 

demonstrated a high sensitivity of 90.5% but a relatively modest specificity of only 70%, which 

is understandable given that the control population had a fairly high frequency of DQ2 positivity. 

The prevalence of CD in the study population was 1:4.2 (or 24%). The PPV was 49% and the 

NPV was 96%, suggesting that a negative DQ2 test result provides the greatest diagnostic 

information. 

Sacchetti et al.152 studied a group of Italian children suspected of having CD. Patients 

fulfilling the ESPGAN criteria were classified as having CD (n = 48 of 80), whereas, the 

remainder (n=32) were considered disease controls. The authors also used a second 

retrospectively defined group of known CD patients by ESPGAN criteria (n = 74), and a second 

group control of 180 unbiopsied healthy subjects. HLA DQ2 was determined in the CD group as 

a whole and in the two control groups, with the results presented in Table 28. In this study, the 

sensitivity of HLA DQ2 was 88.9% and the specificity was 81% for the comparison with the 

biopsied controls; the sensitivity of HLA DQ2 was 88.9% and the specificity was 73% for the 

comparison with the unbiopsied controls. Interestingly, in this study only 18.8% of the biopsynegative controls were positive for HLA DQ2, whereas, 26.7% of the unbiopsied controls were 

HLA DQ2 positive. This difference accounts for the higher specificity seen for HLA DQ2 in the 

comparison with the biopsy-negative control group as compared with the comparison with the 

healthy controls. The prevalence of CD in the studied population was also quite high in both 

portions of this study (79% for comparison with biopsied controls and 51% for the comparison 

with unbiopsied controls). As such the PPV and the NPV of HLA DQ2 in this study were 95% 

and 62%, respectively. The difference in prevalence between this and the Iltanen study accounts 

for the differences seen in the PPVs and NPVs. 

Table 28: HLA studies with biopsied cases and controls 

Author, 

year; 

country 

Prev 

of 

CD 

DQ2 

in CD 

DQ2 in 

controls Sensitivity Specificity PPV NPV CD population 

Iltanen, 

1999; 

Finland 

0.24 90.48 29.85 90% 70% 49% 96% Known CD 

versus biopsied 

controls 

0.79 86.89 18.75 87% 81% 95% 62% Known CD 

versus biopsied 

controls 

Sacchetti, 

1998; Italy 

0.51 86.89 26.72 87% 73% 77% 84% Versus 

unbiopsied 

healthy controls 
 57

HLA all study data. The following section presents the data of the HLA studies that failed to 

be included on the basis that the control groups were not assessed with the gold standard test for 

CD (biopsy). These studies collectively provide useful information on the diagnostic value of 

HLA testing, but have to be interpreted with caution.

The prevalence of DQ2 and DQ8 in these studies is presented in Table 29, while the results 

of the diagnostic value of HLA DQ2 and HLA DQ8 are presented in Tables 30 and 31. 

Unfortunately, none of these studies were actual studies of the diagnostic value of HLA DQ2 or 

HLA DQ8 for the diagnosis or screening of CD. However, as presented in the Tables, the crude 

data was abstracted and the diagnostic characteristics were calculated. Significant clinical and 

statistical heterogeneity existed between these studies, making arithmetic pooling of the studies 

unjustified. Figure 24 and Figure 25 represent the plotting of each study’s sensitivity (true 

positives) versus 1-specificity (false positives) to create a ROC presentation. The value of these 

figures lies in the global picture they represent regarding the results of each of the studies. 

Figure 24 demonstrates that the vast majority of the studies cluster together in a region where the 

sensitivity of HLA DQ2 is greater than 80%, with most studies lying above the 90% sensitivity 

mark. In contrast, these same studies have specificities in the range of 55% to 80%. Outlier 

studies are identified by author name. The best sensitivities and specificities were seen in two 

studies. The first, by Kaur et al.,163 was a study from India where only 4.6% of the control 

population was positive for HLA DQ2. The second study, by Tighe et al.,149 was conducted in a 

group of patients with CD and ethnically-matched control subjects from Rome, Italy. The 

prevalence of CD was quite high in the studied group (51%), and the frequency of HLA DQ2 in 

the control population of 12.2% was much lower than that observed in other Italian studies. 

The remaining outlier studies were divided into a low-sensitivity/high-specificity group 

(Group 1), and a high-sensitivity/low-specificity group (Group 2). In the first case, all the 

studies were conducted in a non-Western European population. In particular, the worst 

performance of HLA DQ2 occurred in a study from Chile,137 where the frequency of HLA DQ2 

was very low in both the patients with CD and the control subjects. It is important to note, 

however, that not all non-Western populations deviated from the main cluster of studies. For 

example, Catassi et al.120 found that 91% of Saharawi Arabs (Algeria) with CD carried HLA 

DQ2 compared with 38.9% of Saharawi controls. These values are similar to those seen in most 

Western populations. The second group all showed relatively poor specificity, although the 

sensitivity was preserved. As would be expected, the control groups of these studies were at 

high risk of having CD (relatives of CD158,164,166), or were a population with a known higher 

frequency of HLA DQ2 (individuals with diabetes161,165). As such, the high frequency of HLA 

DQ2 in these control populations makes the specificity of HLA DQ2 rather poor. 

The frequency of HLA DQ8 in Western European populations with CD varies from 

approximately 2.7% to 6% (Table 29). The frequency is slightly higher in studies from Italy, the 

UK, and France (5.6% to 8% of CD patients). The frequency of HLA DQ8 in a subset of 

patients who had HLA testing in a large American serology screening study for CD was 22%,15

which is quite a bit higher than that reported in the European studies. 

A small group of studies allowed the estimation of the sensitivity and specificity of having 

either HLA DQ2 or DQ8. The results of these studies are presented in Table 33 and Figure 25. 

As can be seen in the figure, these studies confer a wide variation. Clearly, the sensitivity of 

using this strategy is quite high and is likely close to 100% in Western populations. The study 

by Balas et al.,155 likely represents the closest to the truth, as this was a typical case-control 

design in patients with know CD compared with healthy controls. The Fasano et al. study15
 58

represents the largest study and gives similar results to those obtained by Balas et al., however, 

the higher frequency of HLA DQ8 in their control group compared with other studies is of 

concern. Once again, the remaining studies can be grouped into high-specificity/low-sensitivity 

(Group 1) and high-sensitivity/low-specificity (Group 2). As was the case for HLA DQ2, Group 

1 consists of two studies of non-Western populations, whereas, Group 2 represents studies with 

first-degree relatives and a study that used patients with diabetes as their control group. 
 59

Table 29: Prevalence/frequency of HLA DQ2 and HLA DQ8 in prevalence and mixed-design 

studies, and in case-control studies with HLA DQ8 data 

Author Year Country 

# of 

CD % DQ2 % DQ8 % DQ2/8 Population with CD 

Lewis 2000 USA 101 90.10 n/a n/a Confirmed cases 

among CD relatives 

Book 2001 USA 8 87.50 12.50 100 Down Syndrome 

Book 2003 USA 34 

n/a 

n/a 97.06 Affected 1st-degree 

relatives of CD sib. 

pairs 

Csizmadia 2000 Netherlands 10 100 20 n/a Down Syndrome 

Fasano 2003 USA 98 83.67 22.45 100 Screened large 

population only subset 

tested for HLA 

Iltamen 1999 Finland 5 100 n/a n/a Sjogren's syndrome 

Kaukinen 2000 Finland 6 100 n/a n/a Known CD 

Maki 2003 Finland 56 85.71 n/a n/a Screen of school-age 

children 

Mustalahti 2002 Finland 29 100 n/a n/a Relatives of CD or DH 

Catassi 2001 Algeria 79 91.3 n/a 95.6 Saharawi Arabs 

Lui 2002 Finland 260 96.92 2.69 99.62 Family members of 

celiacs 

Polvi 1996 Finland 45 100 n/a n/a Known CD 

Ploski / 

Sollid 

1996 Sweden 135 91.85 4.44 96.30 Known CD 

Popat 2002 Sweden 62 93.55 n/a n/a Known CD 

Larizza 2001 Italy 7 100 n/a n/a Children with 

autoimmune thyroid 

disease, EMA+biopsy 

Failla 1996 Italy 7 14.29 n/a n/a Down Syndrome (only 

7 CD cases) 

Farre 1999 Spain 60 93.33 n/a n/a 1st-degree relatives of 

celiacs 

Balas 1997 Spain 212 94.81 4.25 99.06 Known CD 

Zubillaga 2002 Spain 135 92.59 3.70 96.0 

(calc) 

Mostly CDs, some CD 

in subjects with Down 

Syndrome and 

subjects with diabetes 

France 92 86.96 6.52 93.48 

Italy 302 93.71 5.63 89.40 

Finland 100 91 5.00 96.00 

Norway/ 

Sweden 

326 91.41 5.21 96.63 

Uk 188 87.77 7.98 95.74 

Karell 2003 

Total 1008 93.71 5.95 93.95 

Known CD 

Kaur 2002 India 35 97.14 n/a n/a Known CD 

Neuhausen 2002 Israel 23 82.61 56.52 100 Bedouin Arabs 

Tuysuz 2001 Turkey 55 83.64 16.36 90.91 Children with known 

CD 

Bouguerra 1996 Tunisia 94 84.04 n/a n/a Known CD 

Sumnik 2000 Czech 15 80 66.67 100 Diabetics 

Perez-Bravo 1999 Chile 62 11.29 25.81 37.10 Chileans 

DH = dermatitis herpetiformis
 60

Table 30: Sensitivity/specificity (calculated) for HLA DQ2 in case-control studies 

Author, 

year; 

country 

Prev 

of CD % DQ2 in CD 

% DQ2 in 

Controls Sens Spec PPV NPV 

CD 

population 

Fine, 2000; 

USA 

0.06 88 (22/25) 31.24 

(134/429) 

0.88 0.69 0.14 0.99 Known CD 

Howell, 1995; 

UK 

0.38 91.21 (83/91) 23.18 (35/151) 0.91 0.77 0.7 0.94 Known CD

Michalski, 

1995; Ireland 

0.62 96.67 (87/90) 39.29 (22/56) 0.97 0.61 0.8 0.92 Known CD

Colonna, 

1990; Italy 

0.36 94.59 

(140/148) 

40.82 

(109/267) 

0.95 0.59 0.56 0.95 Known CD

Catassi, 

2001; Algeria 

0.37 91.1 (72/79) 38.9 (53/136) 

0.91 0.61 0.58 0.92 

Saharawi 

Arabs 

Congia, 

1991; Italy 

0.2 96 (24/25) 34 (34/100) 0.96 0.66 0.41 0.99 Known CD

Ferrante, 

1992; Italy 

0.48 88 (44/50) 16.36 (9/55) 0.88 0.84 0.83 0.88 Known CD

Mazzilli, 

1992; Italy 

0.5 92 (46/50) 18 (9/50) 0.92 0.82 0.84 0.91 Known CD

Tighe, 1992; 

Italy 

0.49 70.59 (39/43) 8.33 (5/41) 0.91 0.88 0.89 0.9 Known CD 

Castro, 1993; 

Italy 

0.38 80 (4/5) 37.5 (3/8) 0.8 0.63 0.57 0.83 Down 

Syndrome 

Lio, 1997; 

Italy 

0.45 100 (18/18) 63.64 (14/22) 1 0.36 0.56 1 Known CD 

Sacchetti, 

1998; Italy 

0.79 86.89 

(106/122) 

18.75 (6/32) 0.87 0.81 0.95 0.62 Known CD 

and 

biopsied 

controls 

Sacchetti, 

1998; Italy 

0.51 86.89 

(106/122) 

26.72 (31/116) 0.87 0.73 0.77 0.84 Healthy 

controls 

Iltamen, 

1999; Finland 

0.24 90.48 (19/21) 29.85 (20/67) 0.9 0.7 0.49 0.96 Known CD

Ploski/Sollid, 

1993; 

Sweden 

0.34 94.68 (89/94) 25.97 (47/181) 0.95 0.74 0.65 0.96 Known CD

Pattersson, 

1933; 

Sweden 

0.4 92.31 (60/65) 43.75 (42/96) 0.92 0.56 0.59 0.92 Known CD

Ploski/Sollid, 

1996; 

Sweden 

0.43 91.85 

(124/135) 

22.35 (40/179) 0.92 0.78 0.76 0.93 CD vs 

blood 

donors 

FernandezArquero, 

1995; Spain 

0.36 92 (92/100) 25.56 (46/180) 0.92 0.74 0.67 0.94 Known CD

Arranz, 1997; 

Spain 

0.5 92 (46/50) 24 (12/50) 0.92 0.76 0.79 0.9 Known CD

Balas, 1997; 

Spain 

0.22 94.81 

(201/212) 

29.25 

(217/742) 

0.95 0.71 0.48 0.98 Known CD
 61

Table 30 (cont’d): Sensitivity/specificity (calculated) for HLA DQ2 in case-control studies 

Author, 

year; 

country 

Prev 

of CD % DQ2 in CD 

% DQ2 in 

Controls Sens Spec PPV NPV 

CD 

population 

Ruiz Del 

Prado, 2001; 

Spain 

0.04 94.74 (36/38) 39.22 

(351/895) 

0.95 0.61 0.09 1 Known CD

Dijilali-Saiah, 

1994; France 

0.27 88.75 (71/80) 21.13 (45/213) 0.89 0.79 0.61 0.95 Known CD

Dijilali-Saiah, 

1998; France 

0.44 83.17 (84/101) 20 (26/130) 0.83 0.8 0.76 0.86 Known CD

Tighe, 1993; 

Israel 

0.51 90.7 (24/34) 12.2 (3/36) 0.71 0.92 0.89 0.77 Ashkenazi 

Jews, 

known CD 

Arnason, 

1994; Iceland 

0.13 84 (21/25) 36.36 (60/165) 0.84 0.64 0.26 0.96 Known CD

Boy, 1994; 

Sardinia 

0.5 96 (48/50) 32 (16/50) 0.96 0.68 0.75 0.94 Known CD

Congia, 

1994; 

Sardinia 

0.42 90.77 (59/65) 39.33 (35/89) 0.91 0.61 0.63 0.9 Known CD

Erkan, 1999; 

Turkey 

0.5 40 (12/30) 6.67 (2/30) 0.4 0.93 0.86 0.61 Known CD

Tumer, 2000; 

Turkey 

0.3 51.52 (17/33) 25.97 (20/77) 0.52 0.74 0.46 0.78 Turkish, 

known CD 

Tuysuz, 

2001; Turkey 

0.52 83.64 (46/55) 24 (12/50) 0.84 0.76 0.79 0.81 Turkish, 

known CD 

Perez-Bravo, 

1999; Chile 

0.33 11.29 (7/62) 2.42 (3/124) 0.11 0.98 0.7 0.69 Chilean 
 62

Table 31: Sensitivity/specificity (calculated) for HLA DQ2 in mixed-design studies 

Author, 

year; 

country 

Prev 

of CD 

% DQ2 in 

CD 

% DQ2 in 

controls Sens Spec PPV NPV CD population 

Book, 2001; 

USA 

0.09 87.50 

(7/8) 

15.58 

(12/77) 

0.88 0.84 0.37 0.98 

Down Syndrome 

Csizmadia, 

2000; 

Netherlands 

0.11 100 

(10/10) 

28 (25/90) 1.00 0.72 0.29 1.00 Down Syndrome 

Fasano, 

2003; USA 

0.52 83.67 

(82/98) 

42.39 

(39/92) 

0.84 0.58 0.68 0.77 9019 at risk, 4126 not 

at risk 

Larizza, 

2001; Italy 

0.08 100 (7/7) 34.62 

(27/78) 

1 0.65 0.21 1 Children with 

autoimmune thyroid 

disease, EMA+biopsy 

Polvi, 1996; 

Finland 

0.58 100 

(45/45) 

28.13 

(9/32) 

1 0.72 0.83 1 CD vs various 

controls 

Iltamen, 

1999; 

Finland 

0.15 100 (5/5) n/a 1 n/a n/a n/a Sjogren's syndrome 

Kaukinen, 

2000; 

Finland 

0.17 100 (6/6) n/a 1 n/a n/a n/a CD vs disease 

controls 

Lui, 2002; 

Finland 

0.52 96.92 

(252/260) 

57.38 

(136/237) 

0.97 0.43 0.65 0.93 Family members of 

celiacs 

(controls=unaffected 

family members) 

0.55 93.33 

(56/60) 

18 (9/50) 0.93 0.82 0.86 0.91 CD vs healthy 

controls 

Farre, 1999; 

Spain 

0.26 93.33(56/

60) 

63.91(108/

169) 

0.93 0.36 0.34 0.94 

CD vs relatives of CD 

Sumnik, 

2000; 

Czech 

0.07 80 

(12/15) 

49.46 

(92/186) 

0.8 0.51 0.12 0.97 Diabetes 

(control=EMA neg.) 

Kaur, 2002; 

India 

0.11 97.14 

(34/35) 

4.64 

(13/280) 

0.97 0.95 0.72 1 CD vs healthy 

controls 

Neuhausen, 

2002; Israel 

0.31 82.61 

(19/23) 

61.54 

(32/52) 

0.83 0.38 0.37 0.83 Bedouin Arabs (some 

cases and controls 

not biopsied) 
 63

Table 32: Sensitivity/specificity (calculated) for HLA DQ8 

Author, 

year; 

country 

Prev 

of CD 

DQ8 in 

CD 

DQ8 in 

controls Sens Spec PPV NPV CD population 

Csizmadia, 

2000; 

Netherlands 

0.11 20 (2/10) 20 (18/90) 0.20 0.80 0.10 0.90 Down Syndrome 

Fasano, 

2003; USA 

0.52 22.45 

(22/98) 

20.65 

(19/92) 

0.22 0.79 0.54 0.49 Screened at-risk and 

not-at-risk 

populations 

Lui, 2002; 

Finland 

0.52 2.69 

(7/260) 

10.55 

(25/237) 

0.03 0.89 0.22 0.46 Family members of 

CD patients 

(controls=unaffected 

family members) 

Ploski/Sollid

1996; 

Sweden 

0.43 4.44 

(6/135) 

25.14 

(45/179) 

0.04 0.75 0.12 0.51 Known CD 

Balas, 

1997; Spain 

0.22 4.25 

(9/212) 

16.85 

(125/742) 

0.04 0.83 0.07 0.75 Known CD 

Sumnik, 

2000; 

Czech 

0.07 66.67 

(10/15) 

65.59 

(122/186) 

0.67 0.34 0.08 0.93 Diabetes 

Neuhausen, 

2002; Israel 

0.31 56.52 

(13/23) 

25 (13/52) 0.57 0.75 0.5 0.8 Bedouin Arabs 

Tuysuz, 

2001; 

Turkey 

0.52 16.36 

(9/55) 

8 (4/50) 0.16 0.92 0.69 0.5 Turkish known CD 

PerezBravo, 

1999; Chile 

0.33 25.81 

(16/62) 

12.9 

(16/124) 

0.26 0.87 0.5 0.7 Chileans 
 64

Table 33: Sensitivity/specificity (calculated) for HLA DQ2 or DQ8 

Author; 

year; 

country 

Prev 

of CD 

DQ2 or 

DQ8 in 

CD 

DQ2 or 

DQ8 in 

controls Sens Spec PPV NPV Notes 

Fasano, 

2003; USA 

0.52 100 

(98/98) 

59.78 

(55/92) 

1 0.4 0.64 1 Screened at-risk and 

not-at-risk 

populations 

Catassi, 

2001; 

Algeria 

0.37 96.2 

(76/79) 

41.9 

(57/136) 

0.96 0.58 0.57 0.96 

Saharawi Arabs 

Lui, 2002; 

Finland 

0.52 99.62 

(259/260) 

67.93 

(161/237) 

1 0.32 0.62 0.99 Family members of 

CD 

(controls=unaffected 

family members) 

Balas, 

1997; Spain 

0.22 99.06 

(210/212) 

46.09 

(342/742) 

0.99 0.54 0.38 1 Known CD 

Sumnik, 

2000; 

Czech 

0.07 100 

(15/15) 

87.63 

(163/186) 

1 0.12 0.08 1 Diabetes 

Tuysuz, 

2001; 

Turkey 

0.52 90.91 

(50/55) 

32 (16/50) 0.91 0.68 0.76 0.87 Turkish Known CD 

Neuhausen, 

2002; Israel 

0.31 100 

(23/23) 

86.54 

(45/52) 

1 0.13 0.34 1 Bedouin Arabs 

PerezBravo, 

1999; Chile 

0.33 37.1 

(23/62) 

15.32 

(19/124) 

0.37 0.85 0.55 0.73 Chileans 

Figure 24: HLA DQ2 

HLA DQ2 

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

1

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1

1-specificity

Sensitivity

Case Control Studies

Cohort Studies

Perez-Bravo

Erkan

Tumer

Tighe, 1993

Lio

Tighe, 1992

Kaur

Sumnik Neuhausen

Lui

Castro

Farre
 65

Figure 25: HLA DQ2 and DQ8 

HLA DQ2 or 8

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

1

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1

1- Specificity

Sensitivity

Perez-Bravo

Neuhausen Balas Fasano Lui

Tuysuz

Sumnik

Biopsy 

Using epidemiologically appropriate eligibility criteria, our comprehensive literature search 

did not identify any studies that specifically addressed the question of the sensitivity or 

specificity of biopsy for the diagnosis of CD. 

However we sought to obtain indirect evidence regarding the diagnostic performance of 

biopsy as a test for CD. Some data was available from those studies identified for other review 

objectives, such as the cross-sectional screening studies, the HLA DQ2/8 studies, and studies of 

IELs. We also sought studies of follow-up of biopsy negative patients suspected of CD, and 

studies of silent and latent CD. The findings from these studies are presented in the Discussion 

and in Appendix H. 

Quality Assessment 

Overall, the quality of the diagnostic studies assessed in the Celiac 1 objective was quite 

good (Appendix J, Table 1). However, 59% of the studies reported using a selected patient 

population that may not be representative of a clinically relevant population. This is likely 

related to study design. Only 11% of the studies reported on whether the reference test was 

reported without knowledge of the index test. We felt that this was not a major threat to the 

validity of the studies. 
 66

Celiac 2: Incidence and Prevalence of CD 

The literature search yielded 2,116 references (Appendix F). A first-level screen of the titles, 

abstracts and keywords, for articles that related to the incidence or prevalence of CD, excluded 

1,506 references. Full-text versions of each of the 610 retained references were obtained and 

used for a second-level screen for articles, with a focus on the incidence and/or prevalence of 

CD. Review articles were also identified and kept for reference (n = 71). Three hundred and 

forty-eight out of the 610 references were excluded. The remaining 262 references were 

screened at a third level (Appendix F). Studies were included if they reported the prevalence 

and/or incidence of CD in the following groups: (1) general populations from North America or 

Western Europe; (2) first-degree relatives of patients with CD; (3) patients with type 1 diabetes; 

(4) patients being investigated for anemia; (5) patients with osteoporosis or osteopenia; (6) 

patients with suspected CD on the basis of their clinical presentations. We did not use any 

geographic restriction for the studies of populations at risk (first-degree relatives and type 1 

diabetics) or of associated clinical presentations (suspected CD, anemia, or metabolic bone 

disease). Studies of prevalence or incidence that used AGA tests conducted prior to 1990 were 

excluded after discussion with the AHRQ because of potential problems with the reliability of 

older AGA assays. Reports which were not sufficiently explicit for data extraction also had to be 

excluded.179-181

We defined incidence studies as those studies that reported the total number of new cases of 

CD for a given territory and period, over a unit of population density. Therefore, studies of 

incidence where there was no population denominator were excluded. When multiple studies of 

incidence of CD were available for a similar country or geographic area, the most recent and/or 

most encompassing was selected. In general, we excluded the studies whose observation periods 

pertained exclusively to a period prior to 1990. 

A total of 133 publications were selected. Of these, 14 publications were identified as 

duplicates on the basis that the same study population was reported on elsewhere, or as part of a 

larger cohort.122,182-194 The remaining 119 original studies on prevalence and/or incidence of CD 

in the populations of interest were included and their data abstracted. Of these included studies, 

42 assessed the prevalence and/or incidence of CD in a general population. Twelve of the 42 

reported on the incidence of CD,128,195-205 and 30 reported on the prevalence, either in the US 

(three studies206-208), Scandinavia (11 studies209-219), Italy and San Marino (seven studies126,220-

225), UK (four studies226-229), or other countries (Spain230, the Netherlands,231,232 Switzerland,233

and Germany234). 

Studies of the prevalence of CD in populations at risk were divided as follows: 18 studies of 

the first-degree relatives of CD patients,129,167,206,235-249 and 34 studies in patients with type 1 

diabetes.234,250-282

Studies of the prevalence of CD in patients with associated clinical presentations were 

divided as follows: 12 studies in anemia and/or iron deficiency,283-294 four studies in metabolic 

bone disease,295-298 and 13 studies of patients with suspected CD on the basis of their clinical 

presentation.206,238,299-309 The clinical manifestations that were included in the “suspected CD 

category” were: chronic diarrhea, weight loss, malabsorption or abdominal pain in adults and 

failure to thrive, short stature, malabsorption, chronic diarrhea, and abdominal pain in children. 

Four studies included groups at multiple-risk levels.206,234,238,272
 67

Incidence of CD in the General Population 

The incidence of CD in North America and Western Europe was derived from studies from 

the following countries: US,128,205 England,201 Italy,202, Sicily,203 Spain,204 Netherlands,200

Sweden,195 Denmark,196,197 and Finland (Evidence Table 3, Appendix I; Table 34).198,199 In the 

report, crude incidence is defined as the number of new cases per 100,000 population-at-risk per 

year and cumulative incidence as the number of new cases per 1,000 live births; cumulative 

incidence is age-specific and its denominator reflects the total number of individuals from the 

same year of birth (i.e., birth cohort). 
 68

Table 34: Included studies of incidence of CD in the general population 

Incidence 

Study 

Country, 

period 

Group 

at risk 

Period related 

to results 

Crude incidence 

(# cases/100,000 

patient year) 

Cumulative 

incidence 

(# cases/1,000 

births) 

1997 (0-2 y) 51 

(95% CI: 36-70) 

1996 (2-5 y) 33 

(95% CI: 24-44) 

Ivarsson, 2003 

Duplicate 

Ivarsson, 

2000193

Sweden, 

1973-97 

Children 

1996 (5-15 y) 10 

(95% CI: 7-13) 

Age 2 (1995): 

1.7 (95% CI: 

1.3-2.1) 

Weile, 1993 

Duplicate 

Weile, 1993196

Denmark, 

1960-88 

Children 1960-88 Age 5 (1988): 

0.118 

Maki, 1990 

Duplicate ref194

Finland, 

1960-84 

Children 1974-83 3.46 

(95% CI: n/r) 

Hawkes, 2000 England, 

1981-95 

Children 1991-95 2.15 

(95% CI: n/r) 

Magazzu, 1994 Sicily 

1975-89 

Children 1989 birth 

cohort 

 Age 5 (1989): 

1.16 

95% CI: 0.92-

1.42 

1981-90 6.87 

(95% CI: 5.26-8.83) 

Children 

0-14 y 

1991-99 16.04 

(95% CI: 12.99-19.59) 

LopezRodriguez, 

2003 

Spain, 

1981-99 

Children 

0-4 y 

1991-99 42.04 

(95% CI: n/r) 

Hoffenberg, 

2003 

US (Denver, 

Colorado), 

1993-99 

Children 1993-99 Age 5 (1999): 9 

(95% CI: 4-20) 

Jansen, 1993 Netherlands 

1990-92 

All ages 1991-92 1.0 

(95% CI: n/r) 

Corrao, 1995 Italy 

1990-91 

All ages 1990-91 2.13 

(95% CI: n/r) 

Age 5 (1991): 

0.81 

1960-90 1.2 

(95% CI: 0.7-1.6) 

Talley, 1994 US 

1960-90 

Olmstead 

County 

All ages 

1980-90 1.7 

(95% CI: n/r) 

Bodé, 1996 Denmark, 

1976-91 

Adults 1976-91 1.27 

(95% CI: n/r) 

Collin, 1997 Finland, 

1975-94 

Adults 1990-94 17.2 

(95% CI: n/r) 

Hawkes, 2000 England, 

1981-95 

Adults 1991-95 3.08 

(95% CI: n/r) 

Incidence in children: The crude incidence of CD in children age 0 to 15 years varied from 2.15 

to 51 cases per 100,000 patient years.193-195,198,201,204 When reported, the relative risk (RR) of CD 

was greatest for the 0- to 2-year age group, as well as for women, and varied from 32.26 to 
 69

42.4193,195,204 and from 1.9 to 3.34,128,193,195 respectively. The cumulative incidence at age 5, 

when reported, varied between 0.089 and 9 cases per 1,000 live births.128,196,202,203 (see Table 34).

The incidence of CD has been most studied in the Scandinavian countries, particularly 

Sweden,193,195,310-313 Denmark,196,197,313,314 and Finland,194,198,199 where important disparities have 

been observed over time and between countries. Reports from these countries have the 

advantage of being derived from comprehensive prospective databases and from populations 

which are genetically fairly stable, shedding light on potential environmental causal 

exposures,195,196 or on variations in practice patterns. 

In Scandinavia, the highest incidences of CD in children were found in Sweden for the 0- to 

2-year age group from 1987 to 1997, where an average of 198 new cases per 100,000 patient 

years (95% CI: 186-210) were observed.193,195 This peak in incidence was followed by a rapid 

decline, observed during 1995-97, where incidences dropped to an average of 51/100,000 patient 

years (95% CI: 36-70). In contrast, the incidence of CD in children aged 2 to 4.9 years and 5 to 

15 years was only slightly increased over the 1973-97 period, with a peak in 1996 of 33 cases 

(95% CI: 24-44) per 100,000 patient years and 10 cases (95% CI: 7-13) per 100,000 patient years 

for these respective age groups. A cohort effect was noted in that the cumulative incidences at 2 

years of age for the children belonging to birth cohorts from 1984 to 1994 were on the gradual 

rise (up to 4.4 cases/1,000 births [95% CI: 3.8-5.0] for the 1993 cohort), while a progressive 

decline was observed for birth cohorts from 1994 to 1996 (down to 1.7 cases [95% CI: 1.3-2.1] 

per 1,000 births for the 1995 cohort). Most of these cases were symptomatic, so that these 

observations are unlikely to be due to changes in screening practices. Interestingly, these 

changes mirrored changes in the composition of infant formulas, with the highest values of a 

wheat/rye/barley exposure index during the years 1982-1994. 

In contrast, the incidence of CD in Denmark, a neighbouring country, has been significantly 

lower and very stable from 1960 to 1988,196 with an average incidence of 0.089/1,000 live births 

for that period.313 A comparison of dietary exposures between Swedish and Danish children 

diagnosed with CD between 1972 and 1989 showed that by the age of 8 months, the Swedish 

diet contained more than 40 times more gliadin than the Danish diet.313 In Finland, incidences 

have also been fairly stable, and have in fact decreased among infants but increased among older 

children.198 However, these observations date back to 1984 and can therefore not be compared 

with the Swedish epidemics. 

Spain has also seen an increased incidence of CD over the past 25 years, from 6.87 (95% CI: 

5.26-8.83) cases/100,000/year in 1981-90 to 16.04 cases/100,000/year (95% CI: 12.99-19.59) in 

1991-99,204 an observation that was correlated with an increased proportion of silent or atypical 

presentations at diagnosis (i.e., inferring a role for changes in clinical practice). The age at 

diagnosis also correlated positively with the age at which gluten was introduced in the diet. 

The role of dietary exposure during infancy is also highlighted in studies from the UK, where 

recommendations on infant feeding, promoting breastfeeding and later introduction of starches, 

were published in 1974. Subsequent to these recommendations, there was a fall in the incidence 

of childhood CD;315,316 however, this data is not presented in detail because we focused on 

reports from the past 15 years. 

As opposed to the incidences derived from reported cases, the incidence observed from a 

prospective screening protocol are not subject to variations related to practice patterns and are 

obviously more comprehensive and accurate. Hoffenberg et al., from the US, conducted the only 

prospective CD screening study available to date.128 Between December 1993 and September 

1999, a total of 22,346 newborns in Denver, Colorado were screened for HLA genotypes 
 70

associated with CD and type 1 diabetes. A representative sample of at risk HLA DRB1*03 

positive infants were prospectively followed (n=987), for as long as the first seven years of life. 

Serological screening was performed at nine, 15 and 24 months of age, then yearly. Small bowel 

biopsies were recommended if the serology (tTG in most cases) was positive on two separate 

occasions, or in the presence of clinical suspicion. Between 1993 and 1999, 19 children were 

found to have evidence of CD, ten children had biopsy-confirmed CD, whereas, nine children 

had a positive tTG result at least twice. The mean age at presentation of evidence of CD was 4.6 

years (range 2.6-6.5). Compared with HLA-DR3-negative children, the RR for evidence of CD 

was 5.6 (1.5-21, p=0.009) and 9.1 (1.7-48, p=0.003), for those expressing one and two HLADR3 alleles, respectively. The RR of CD in females was 3.34 (1-10.9, p=0.048) times that of 

males. Cognisant of the prevalence of HLA-DR mono- and heterozygotes among the same birth 

cohort, the authors calculated that by the age of 5, the estimated cumulative incidence of CD in 

the general population (defined as either biopsy-proven CD or persistently elevated tTG) was 

9/1000 births (95% CI: 4-20), or 1:104 (1:49 to 1:221). This remarkably high cumulative 

incidence (i.e., twice that of the highest value among Swedish children at 4 years of age – 5.0 

[95% CI: 4.4-5.7]193) has to be interpreted in light of the fact that only ten out of the 19 cases had 

been biopsied; the remaining nine cases were diagnosed on the basis of a persistently elevated 

tTG titre, the PPV of which the same authors reported to be only 70% to 83%.317 However, as 

mentioned above, these results are derived from an actual prospective and systematic screening 

intervention for CD, where asymptomatic cases would be detected. In all likelihood, there is 

therefore an important proportion of CD cases who remain undiagnosed during early childhood. 

Incidence in adults: The crude incidence of CD in adults varied from lows of 1.27 in 

Denmark197 and 3.08 in England, 201 to a high of 17.2 cases per 100,000 patient years in 

Finland,199 where specific efforts had been untaken to encourage screening for CD (see Table 

34). 

As has been observed for children, the incidence of CD in adults seems to have increased 

over the past 20 years.199,201 This is largely explained by a change in practice patterns: 

physicians are more aware of the condition, its atypical manifestations and associated condition, 

while at the same time, serological testing has become widely available. There are therefore 

more diagnoses made on the basis of case-finding. This is reflected by the fact that the 

proportion of patients being diagnosed with CD in the absence of symptoms, or as a result of 

serological testing, has also increased.199,201,318-320

In Finland over the period 1975-94, Collin et al.199 have observed a ten-fold rise in the 

incidence of CD. The authors attributed this to the use of serologic screening (physicians were 

actively told to screen patients with type I insulin-dependent diabetes (IDDM), autoimmune 

thyroid disease, connective tissue diseases, women with infertility, patients with neurologic 

symptoms and first-degree relatives of CD patients), the routine performance of intestinal 

biopsies on all patients undergoing gastroscopy, and to the opening of open-access endoscopy 

clinics, creating the ability of all general practitioners to refer patients for gastroscopy. 

In Italy, a gradual increase in the number of annual new CD diagnoses was observed between 

1968 and 1992;318,320 this increase correlated with an increased proportion of patients with 

subclinical presentations being identified.318,320 Interestingly, despite the changing clinical 

presentation, there was no statistical difference between the histological grades at diagnosis.320
 71

The incidence of CD in individuals of all ages varies from 1.0 in the Netherlands200 to 2.13 in 

Italy.202 In Italy, the RR of CD in adults ranged from 0.11 in the >60 year group to 0.33 in the 

16-39 year group, compared with children.202 The RR of CD for females was 1.90 (95% CI: 

1.48-2.45).202

In the US, the 30-year incidence (1960-90) for Olmstead County was 1.2 (95% CI: 0.7-1.6), 

and the incidence for 1980-90 was slightly higher at 1.7 (95% CI: not reported).205 This 

observation contrasts with the cumulative incidence of 9/1000 by age 5 reported by Hoffenberg 

from Denver, Colorado;128 clearly, further knowledge of the epidemiology of CD in the US is 

required. 

The point prevalence of CD can be calculated from registers of CD cases and the size of the 

population at risk; we found reports of such an observation in three of the included incidence 

studies.199,199,205 The point prevalence of CD was 21.8/100,000 in Olmstead County in 1991,205

2.7/100,000 (95% CI: 11.0-14.5) in the Netherlands in 1992,200 and 204/100,000 (95% CI: 181-

231) in Finland in 1994.199 Of note, the later prevalence from Finland was observed in a 

community where intense efforts had been carried to screen the population at risk for CD. 

Prevalence of CD in the General Population—Different Geographic 

and Racial/Ethnic Populations 

Thirty-seven studies reported on the prevalence of CD in a general population (Evidence 

Table 4, Appendix I; Table 35). Three of these were conducted in the US,206-208 16 in the 

Scandinavian countries,184-187,209-219,232) eight in Italy,126,182,183,220,221,223-225 five in the UK,188,226-229

and five in other countries (Spain,230 Republic of San Marino,222 the Netherlands,231

Switzerland233 and Germany234). Several pairs of duplicate publications were identified 

including two triplets,182-188,211,213,218,220,321 which brought the total number of included unique 

articles down to 30. The articles with the most complete data were used for the report.126,206-234 

Only seven studies were conducted in a child population,206,209,215,220,221,223,232,233 but one large 

American study included separate data for both adults and children.206 All the included studies 

were conducted between 1992 and 2003. A summary of the included study characteristics is 

presented in Table 35. A breakdown of the included studies by screening test and age group is 

provided in Table 36. 

The prevalence of CD by serology in the general unselected populations of North America 

and Western Europe, ranged widely from 152 per 100,000 (0.152% or 1:658) to 2,670 per 

100,000 (2.67% or 1:37). The prevalence by biopsy ranged from 152 per 100,000 (0.152% or 

1:658) to 1,870 per 100,000 (1.87% or 1:53). In four of the studies, a large proportion of the 

serology-positive subjects did not undergo biopsy.206,216,224,232

Among the included studies, there was no clear pattern relating prevalence to study age 

group, or in a consistent way to country, with large numbers of studies clustering around a 

prevalence range of 0.0025 to 0.014 by serology and 0.0025 to 0.010 by biopsy (Table 35; Figure 

26, 27). In fact for prevalence by serology, the 50th, 75th, and 80th percentiles occurred at a 

prevalence of 0.00637 (0.64%), 0.0117 (1.2%), and 0.0125 (1.3%), respectively, while by biopsy 

the 80th percentile was at a prevalence of 0.0074 (0.74%) (Table 37; Figure 26, 27). 

Categorizing the studies by screening test and age group reduced the variability somewhat, but 

significant between study variation persisted. There were not enough studies to divide an 

analysis by screening test, age group, and country, simultaneously. 
 72

Among the studies conducted in the US,206-208 the prevalence ranged from 0.00312 (0.312% 

or 1:320—only child population in this group) to 0.00949 (0.949% or 1:105). The largest of 

these, by Fasano et al.,322 found a prevalence of CD in “not at risk” populations to be 0.95% in 

adults, 0.31% in children, and 0.75% overall (0.0075 or 1:133). This study included a 

predominately Caucasian population, although other ethnic groups were included (94% white; 

3% black; 1.5% hispanic; 1% asian; 0.5% other). Not et al.208 found the prevalence by EMA 

confirmation of initial AGA testing to be 0.004 (0.4% or 1:250) in another predominately 

Caucasian population that also included other ethnic backgrounds (Caucasian [87%], AfricanAmerican [11.5%], and Asian [1.5%]). Finally, Green et al.207 found a prevalence of 0.005 

(0.5% or 1:200) in 1,749 patients undergoing upper endoscopy. The reason for the initial 

endoscopy in this study was not clearly described, and only those patients with endoscopic 

features suggestive of CD were biopsied, which may have underestimated the true prevalence of 

CD. The prevalence of CD among the six Italian studies was similar to that seen in the 

American studies, showing a range from 0.2% to 0.86%.126,221,223-225,230 The prevalence of CD in 

other countries is presented in Table 35. 

Only four studies demonstrated a prevalence of CD of greater than 0.015 (1.5%) (UK,323

Sweden,209,219 Germany234), and an additional six showed a prevalence of between 0.010 (1.0%) 

and 0.015 (1.5%) (UK,228 Sweden,216 Netherlands,232 Ireland,229 Finland214,215). These studies 

would suggest a potentially higher prevalence of CD in these countries, though it should be kept 

in mind that other studies from these same countries showed a prevalence of less than 1.0%, 

including four studies from Sweden211,213,216,217 (Figure 28). Only three of the eight studies 

conducted in a child population demonstrated a prevalence of CD of greater than 1.0% 

(Finland,215 Sweden,209 Netherlands232). 

Among the 30 included studies, there was a considerable amount of variation in the point 

estimates for the prevalence of CD both by serology and by biopsy due to differences in 

serological test strategies, biopsy definitions and patient sampling, making pooled estimates 

unreliable. To further explore the potential sources of variability in the observed prevalence of 

CD, we plotted the studies’ prevalence versus its sample size (Figure 29). This scatter diagram 

visually illustrates the distribution of the prevalence of CD among the included studies. The 

study with the highest reported prevalence of CD (2.67%), was also the one with the smallest 

sample size of 150 healthy patients, and also included several other at-risk groups, which were 

the primary focus of that study.234 Overall, studies with the smallest sample sizes tended to 

produce both the highest and lowest prevalence of CD. Using an arbitrary cut-off of 1,600 

patients to divide “small” and “large” sample size studies, the prevalence by serology ranged 

fairly evenly from 0.17% to 2.67% for the 13 small studies, while 12 of the 18 large studies were 

located within a range of 0.5% to 1.26% (one study did not provide prevalence by serology). 
 73

Table 35: Prevalence of CD by country 

Author, 

year Country 

Age 

group Test 

Total 

patients 

Prevalence 

by serology 

Prevalence 

by biopsy Notes 

Fasano, 

2003 

USA Adults EMA - ME; all 

positive EMA 

tested with 

tTG-HU 

2,845 0.00949 116/350 

biopsied 

Green, 

2000 

USA Adults EGD/biopsy 1,749 0.00515 Not all 

sytematically 

biopsied; only 

those with 

suggestive 

endoscopic 

features 

Not, 1998 USA Adults IgG- and IgAAGA - ELISA; 

confirmed 

with IgA-EMA 

ME or HU 

2,000 0.00400 

Fasano, 

2003 

USA Children 1,281 0.00312 

Johnston, 

1998 

UK Adults IgA-AGA, 

IgA-EMA 

1,823 0.00823 

Sanders, 

2003 

UK Adults IgG- and IgA 

- ELISA; 

EMA-ME 

1,200 0.01917 0.01000 22/23 

biopsied 

West, 2003 U.K. Adults IgA EMA-ME, 

IgA-tTGA 

7,527 0.01156 

Rutz, 2002 Switzerland Children IgA-EMA-ME, 

IgA-tTG, IgGAGA and IgAAGA 

1,450 0.00759 0.00690 10/11 

biopsied 

Borch, 2001 Sweden Adults Biopsy, IgAand IgGAGA; IgAEMA-ME 

482 0.01452 0.01867 

Grodzinsky, 

1996 

Sweden Adults IgA-AGA; 

IgA-EMA 

1,866 0.00589 0.00375 Prevalence by 

IgA-EMA not 

reported 

Ivarsson, 

1999 

Sweden Adults IgA- and IgGAGA - ELISA, 

cut-off not 

recorded; 

IgA-EMA -

ME; serum 

IgA level 

1,894 0.00475 0.00475 

Sjoberg, 

1994 

Sweden Adults IgG- and IgAAGA 1,537 0.01431 0.00065 13/22 

biopsied 

Sjoberg, 

1999 

Sweden Adults IgA-AGA, IgA 

confirmed 

with EMA-ME 

1970 0.00152 0.00152 

EGD=esophagogastroduodenoscopy; IF=immunofluorescence; prevalence expressed as proportion 

(multiply by 100 for percent, or 100,000 for per 100,000 value) 
 74

Table 35 (cont’d): Prevalence of CD by country 

Author, 

year Country 

Age 

group Test 

Total 

patients 

Prevalence 

by serology 

Prevalence 

by biopsy Notes 

Carlsson, 

2001 

Sweden Children AGA, EMA, 

biopsy using 

Watson 

capsule 

690 0.01884 0.01594 

Riestra, 

2000 

Spain Adults IgG/IgA-AGA, 

IgA-EMA; the 

study was 

conducted as 

a 1) two-step 

protocol 

(determinatio

n of IgA/IgGAGA, if 

positive 

measuring 

IgA-EMA); 

and a 2) onestep protocol 

(measuring 

IgA-EMA) 

1,170 0.00171 0.00256 1 CD picked 

up when AGA 

and EMA was 

neg. 

Corazza, 

1997 

Republic of 

San Marino 

Adults IgA-EMA; 

biopsy 

559 0.00179 0.00179 

Hovdenak, 

1999 

Norway Adults IgA- and IgGAGA; IgAEMA 

2,069 0.00387 0.00338 

Rostami, 

1999 

Netherland

s 

Adults IgA-EMA 1,000 0.00300 0.00300 

Csizmadia, 

1999 

Netherland

s 

Children IgA-EMA 6,127 0.01224 0.00506 57/75 

biopsied 

Pittschieler, 

1996 

Italy Adults IgA- and IgGAGA; IgAEMA; biopsy 

4,615 0.00195 0.00195 38 of 140 

biopsied 

Trevisiol, 

1999 

Italy Adults IgA-EMA; 

biopsy 

4,000 0.00250 0.00250 

Volta, 2001 Italy Adults 

(mostly) 

IgA-EMA-HU; 

biopsy 

3,483 0.00574 0.00488 Prevalence of 

0.57% 

(20/3483) if 

included 3 

patients with 

normal villous 

but with 

increased 

IELs 

Catassi, 

2000 

Italy Children IgG-AGA (7 

AU); IgAAGA (15 AU); 

IgA-EMA 

indirect IF 

(1:5 dilution); 

biopsy 

2,096 0.00859 

Catassi, 

1996 

Italy Children IgA- or IgGAGA; 

confirmed 

with EMA and 

biopsy 

17,201 0.00645 0.00477 

EGD=esophagogastroduodenoscopy; IF=immunofluorescence; prevalence expressed as proportion 

(multiply by 100 for percent, or 100,000 for per 100,000 value) 
 75

Table 35 (cont’d): Prevalence of CD by country 

Author, 

year Country 

Age 

group Test 

Total 

patients 

Prevalence 

by serology 

Prevalence 

by biopsy Notes 

Di 

Pietralata, 

1992 

Italy Children IgA-AGA; 

biopsy 

3,022 0.00629 0.00596 

Dickey, 

1992 

Ireland Adults IgA AGA 443 0.01129 

Jager, 2001 Germany Mixed - 

mostly 

adults 

IgA-AGA, 

IgG-AGA, 

IgA-tTG - 

150 0.02667 Mixed group 

of at-risk 

populations, 

healthy group 

used 

Kolho, 1998 Finland Adults EMA -HU 1,070 0.01028 0.00748 

Maki, 2004 Finland Children IgA and IgG 

tTG; IgA and 

IgG EMA - IF; 

total serum 

IgA; HLA DR, 

DQ2 and 

DQ8 

3,654 0.01259 0.00739 

Collin, 2002 Finland Mixed - 

mostly 

adults 

Biopsy 2,974 0.00605 

Weile, 2001 Denmark 

and 

Sweden 

Adults Serum IgA: 

IgG-AGA; 

IgA-AGA, cutoff >40 units; 

EMA; in 

cases of IgA 

<0.07g/L, 

IgG-AGA was 

analyzed 

1,573 0.00254 

EGD=esophagogastroduodenoscopy; IF=immunofluorescence; prevalence expressed as proportion 

(multiply by 100 for percent, or 100,000 for per 100,000 value) 
 76

Table 36: Prevalence of CD by serological screening test 

Screening 

test Age group Number of studies Total patients 

Prevalence 

range 

Primary biopsy Adults 2207,210 4,723 0.00515 - 

0.00605 

Overall 2223,229 3,465 0.00629 - 

0.01129 

Adults 1229 443 0.01129 

IgA AGA 

Children 1223 3,022 0.00629 

IgA / IgG AGA Adults 1216 1,537 0.01431 

Overall 6208,209,211,217,219,226 8,831 0.00152 - 

0.01884 

Adults 5208,209,211,217,219 6,999 0.00152 - 

0.01884 

IgA AGA - IGA 

EMA 

Children 1321 1,823 0.00823 

Overall 7212,213,218,220,221,224,227 30,648 0.00195 - 

0.01917 

Adults 5212,213,218,224,227 11,351 0.00195 - 

0.01917 

IgA/IgG AGA – 

IgA EMA 

Children 

(Italy) 

2220,221 19,297 0.00645 - 

0.00859 

IgA/IgG AGA – 

IgA tTG 

Mostly adults 

(Germany) 

1234 150 0.02667 

Overall 7126,214,222,225,230-232 17,409 0.00171 – 

0.01224 

Adults 7126,214,222,225,230,231 0.00171 – 

0.01028 

IgA EMA 

Children 

(Netherlands) 

1232 6,127 0.01224 

Overall 4206,215,228,233 16,757 0.00312 - 

0.01259 

Adults (USA, 

UK) 

2206,228 10,372 0.00949 - 

0.01156 

IgA EMA – 

IgG tTG 

Children 3 (includes Fasano Child Group)206,215,233 6,385 0.00312 - 

0.01259 

Note: Country of study was indicated when possible; prevalence expressed as proportion (multiply by 100 

for percent, or 100,000 for per 100,000 value) 
 77

Table 37: Prevalence of CD by statistical percentiles 

Percentiles Serology Biopsy 

5 .0016255 .0007378 

10 .0018050 .0015761 

25 .0030919 .0025321 

50 .0063702 .0047672 

60 .0084439 .0050768 

75 .0117290 .0071429 

80 .0125193 .0074416 

90 .0184088 .0147536 

95 .0225417 .0183992 

100 .0266667 .0186722 

Minimum .00152 .00065 

Maximum .02667 .01867 

Prevalence expressed as proportion (multiply by 100 for percent, or 100,000 for per 100,000 value)

Figure 26: Frequency distribution of prevalence of CD by serology among included studies 

SEROLOGY Prevalence

.0276

.0253

.0230

.0207

.0184

.0161

.0139

.0116

.0093

.0070

.0047

.0024

SEROLOGY

Frequency

10

8

6

4

2

0

Std. Dev = .01 

Mean = .0082

N = 30.00
 78

Figure 27: Frequency distribution of prevalence of CD by biopsy among included studies 

BIOPSY Prevalence

.0175

.0150

.0125

.0100

.0075

.0050

.0025

0.0000

BIOPSY

Frequency

8

6

4

2

0

Std. Dev = .00 

Mean = .0056

N = 21.00

Figure 28: Prevalence of CD by country 

0

0.005

0.01

0.015

0.02

0.025

0.03

USA

USA

Italy

Italy

Italy

Spain

Finland

Finland

Sweden

Sweden

Sweden

Norway

Netherlands

Germany

UK

Ireland

Prevalence of CD By Country Prevalence by Serology

Prevalence by biopsy
 79

Figure 29: General population prevalence in relation to sample size 

General Population Prevalence in Relation to 

Sample Size

0.00000

0.00500

0.01000

0.01500

0.02000

0.02500

0.03000

0

20004000

6000

8000

10000

12000

14000

16000

18000

Sample Size

Prevalence

Serology

Biopsy

Prevalence of CD in Patients with Suspected CD 

Adults: The prevalence of CD in adults suspected of the diagnosis was reported in four studies 

(Evidence Table 5, Appendix I; Table 38); three from Italy,300,301,303 and one from the US.206 

The following reasons for suspecting a diagnosis of CD were documented: anemia, persistent 

iron deficiency, bowel disturbances, chronic intermittent diarrhea, abdominal pain, constipation, 

dyspepsia, severe malabsorption, tiredness and weight loss, mineral metabolism deficiencies, 

osteoporosis, arthralgias, arthritis, dermatitis, hypertransaminasemia, type I diabetes mellitus, 

infertility, and gluten intolerance in childhood not further investigated.

All three Italian studies were from referral centers, and intestinal biopsies were performed on 

all suspected cases, which cumulated to 347. The prevalence of CD was very high in these 

series, i.e., 43%,300 50%,301, and 12%.303

In a large study of prevalence of CD in at-risk and not-at-risk individuals in the US, a total of 

1,910 adults with CD-associated symptoms or disorders underwent serological testing with 

EMA. Fifteen of the 28 EMA-positive subjects (53.6%) consented to a biopsy, which was 

confirmatory in all cases.206 The source of these patients and their mode of recruitment/referral 

were not reported. Based on the EMA result, the prevalence of CD in these adults with 

suspected CD was 1.5%. 

Children: The prevalence of CD in children suspected of the diagnosis was reported in nine 

studies (Table 38); three from Canada,304,305,307 two from the US,206,324 and one each from 

Denmark,302 England,308 Italy,309 and New Zealand.306 The following reasons for suspecting a 

diagnosis of CD were documented: abdominal pain,238,304,305,307,309 diarrhea,238,304,305,308 failure to 

thrive/short stature,206,238,304-306,309 weight loss,305 vomiting,304,305 abdominal distension,304,305
 80

chronic GI symptoms,306 inflammatory bowel disease,304 family history of CD,238,304,306,309 type I 

diabetes mellitus,206,238,306 iron deficiency anemia (IDA),309 thyroid disease,304 trisomy 

21,206,304,309 as well as enamel hypoplasia, recurrent aphtous stomatitis, autoimmune diseases, 

IgA deficiency, and occult hypertransaminasemia.309

Five of the eight studies came out of referral centers where all suspected cases (cumulating to 

978) were biopsied.302,304-306,308 The prevalence of CD in these children ranged from 4.6%306 to 

17%.305 

In a case-finding study among 26 family pediatricians in Italy, 240 children were screened 

with EMA based on the presence of risk factors, and 18 diagnoses of biopsy-proven CD were 

made, resulting in a prevalence of 7.5%.309

Three studies, two American206,238 and one Canadian,307 reported the prevalence of CD in 

children with related symptoms or conditions based on EMA testing. The cumulative number of 

children was 2,426, and the prevalence ranged from 1.1% in the Canadian study of children with 

chronic abdominal pain,307 to 4.0% in the large American study of CD prevalence in at-risk and 

not-at-risk populations.206

All ages: Hin et al., performed a case-finding study through nine primary care clinics of central 

England that served a total population of 70,000 (Table 38).299 A thousand patients were 

enrolled for serological screening, satisfying the following entry criteria: irritable bowel 

syndrome, anemia, family history of CD, malabsorption symptoms, diarrhea, fatigue, thyroid 

disease, diabetes mellitus, weight loss, short stature, failure to thrive, epilepsy, infertility, 

arthralgia, or eczema. The mean age of the screened subjects was 42.8 years; 5.3% were aged 

under 10, and 3.1% were aged 80 to 90 years. Thirty patients were EMA-positive, all of whom 

were confirmed by biopsy to have some enteropathy (90% had subtotal or total villous atrophy), 

and only one out of 30 patients had only IELs in the absence of villous atrohpy. The mean age 

of the 30 cases with CD was 42.8 years, and there was only one child diagnosed with CD. The 

prevalence of CD was 3.0%. 
 81

Table 38: Included studies for prevalence of CD in patients with suspected CD 

Study, year; 

country 

Clinical 

setting 

Age 

group Dx criteria N tested Prevalence (%) 

Bardella, 

1991; Italy 

Referral 

center Adults Biopsy 60 43.3 

Bardella, 

2001; Italy 

Referral 

center Adults Biopsy 80 50.0 

Carrocio, 

2002; Italy 

Referral 

center Adults Biopsy 207 11.6 

Fasano, 

2003; USA Not reported Adults EMA 1,910 1.5 

Bode, 1993; 

Denmark 

Referral 

center Children Biopsy 191 7.3 

Day, 2000; 

New 

Zealand 

Referral 

center Children Biopsy 153 4.6 

Thomas, 

1992; 

England 

Referral 

center Children Biopsy 381 7.9 

Chan, 2001; 

Canada 

Referral 

center Children Biopsy 77 13.0 

Chartrand, 

1997; 

Canada 

Referral 

center Children Biopsy 176 17.0 

Ventura, 

2001; Italy 

Community 

pediatricians Children Biopsy 240 7.5 

Fitzpatrick, 

2001; 

Canada 

Community 

pediatricians Children EMA 92 1.1 

Fasano, 

2003; USA Not reported Children EMA 1,326 4.0 

Hill, 2000; 

USA 

Referral 

center Children EMA 1,008 2.5 

Hin, 1999; 

England 

Community 

practice All ages Biopsy 1,000 3.0 

Prevalence of CD in with Type I Diabetes 

The literature search identified 36 studies that assessed the prevalence of CD in patients with 

type I diabetes (insulin-dependent diabetes mellitus [IDDM]).191,192,234,250-282 Two sets of 

duplicate publications were identified.191,192,277,282 The publications with the most complete data 

sets were used.277,282 Of the 34 unique studies (Evidence Table 6, Appendix I; Table 39), seven 

were conducted in an adult population,257,263,266,270,273,277,279 21 in a child population,250-252,254-

256,260-262,264,265,267,271,272,274-276,278,280-282 and six were conducted in a mixed population of adults 

and children.234,253,258,259,268,269 

All the included studies initially screened the study population with one or more antibodies. 

Three studies did not confirm positive serology with biopsy,265-267 whereas in nine studies 

confirmatory biopsies were performed in less than 75% of the screened-positive 

patients.253,259,264,269,272,274,277-279 These studies were not included in the pooled estimates of the 

prevalence of CD by biopsy. All the studies that reported biopsy criteria used partial villous 

atrophy or greater to define CD. 
 82

For all the included studies, the minimum prevalence of CD in IDDM by serology was 1% 

and the maximum was 12%. By biopsy, the minimum and maximum prevalence was 1% and 

11%, respectively. Within a given study, the prevalence by serology was almost uniformly 

greater than the prevalence by biopsy, as would be expected. Table 39 (individual studies) and 

Table 40 (pooled summaries) list the study details, the individual study estimates of CD 

prevalence and the pooled estimates of prevalence when appropriate. 

The prevalence of CD in adults was assessed in seven studies.257,263,266,270,273,277,279 Six of 

these studies used IgA EMA as the screening test,257,263,266,270,273,279 whereas the largest study 

used IgA- and IgG-AGA, followed by EMA for confirmation.277 In this last study, EMA 

confirmation was positive in 22 of the initially screened sample of 848 patients (2.6%), but 

biopsy confirmation was only performed in 14 of these patients, making the estimate of 0.83% 

prevalence by biopsy unreliable. The second largest study (n=509) did not confirm the EMApositive patients with biopsy, and demonstrated the lowest prevalence of CD by EMA (1.4%) of 

all of the studies.266 In another study of 185 patients,279 the prevalence of CD by EMA was 

4.9%, but only five of nine screen-positive patients were biopsied, making the prevalence of 

2.2% (4/185) by biopsy a likely underestimation since four of the five biopsied EMA-positive 

patients were diagnosed with CD. A small study of 62 patients used biopsy as the screening test 

and found the prevalence of CD to be 11.3%, which is the highest prevalence of the group.263 

The remaining studies had uniform biopsy confirmation.257,270,273 In these studies the prevalence 

of CD by EMA ranged from 3.1% to 7.9%, and the prevalence of CD by biopsy ranged from 

2.6% to 6.4%. 

Twenty-one studies assessed the prevalence of CD in children with IDDM.250-252,254-256,260-

262,264,265,267,271,272,274-276,278,280-282 Six of these studies used IgA-AGA or -AGA in combination 

with either IgG-AGA or other antibody tests.254,256,267,271,274,276 The largest study tested 776 

children with AGA and ARA (reticulin antibodies), and found a prevalence of CD by serology of 

9.8%.274 However, only 35 of 76 serology-positive patients were biopsied, making the reported 

prevalence by biopsy of 2.5% a likely underestimation. A single study of 459 patients that used 

IgA-AGA as the screening test found the prevalence of CD by serology to be 4.1%, and the 

prevalence of CD by uniform biopsy confirmation to be 4.6%.276 The second largest study 

(n=498) used a combination of IgA- and IgG-AGA, and found a prevalence of CD by serology 

of 6.0% and a prevalence of CD by biopsy of 3.2%.254 Two other studies that used IgA and IgGAGA271 or paired IgA-AGA measurements,256 found a very similar prevalence by serology of 

10.7% and 8.5%, respectively, and a prevalence by biopsy of 3.95% and 2.8%, respectively. The 

last study in this group did not perform biopsy confirmation of the IgA- and IgG-AGA derived 

prevalence of 3.76%.267

Seven studies used IgA-EMA to screen for CD in children with IDDM.251,252,255,260,272,275,281 

One Hungarian study of 205 children demonstrated a relatively high prevalence by serology and 

biopsy of 11.7% and 8.3%, respectively,252 whereas an Austrian study of 403 children 

demonstrated a relatively low prevalence by serology and biopsy of 3.0% and 1.5%, 

respectively.275 A study by Rossi et al.272 from the US demonstrated a prevalence of CD of 

4.7%. The remaining studies demonstrated fairly consistent results, with the prevalence of CD 

by serology ranging from 5.5% to 7.8%, and the prevalence by biopsy ranging from 3.3% to 

6.5%.251,255,260,281

Three studies used IgA-tTG either alone264 or in combination with IgG-tTG.265,278 IgA-tTG 

was used alone in a study of 503 children which demonstrated a prevalence by serology of 4.4%. 

Ten of the 23 serology-positive patients did not undergo biopsy confirmation, making the 
 83

reported prevalence of 1.7% a likely underestimation. Of the two studies that used IgA- and 

IgG-tTG, the first did not perform biopsy confirmation and reported a prevalence of CD by 

serology of 8.4%,265 whereas, the other found a prevalence of CD by serology of 6.3%, and by 

biopsy of 2.9%, although only eight of 13 serology-positive patients underwent biopsy.278

Five studies used a combination of IgA-EMA and one or more other antibodies, to assess the 

prevalence of CD in children with IDDM.250,261,262,280,282 In three studies, EMA was combined 

with AGA,250,261,280 in one it was combined with tTG,262 and in the one it was combined with 

AGA and tTG.282 In one study, only the confirmed biopsy prevalence of 8.3% was reported.280 

Overall, this group reported prevalences by serology ranging from 5.0% to 9.6%, and by biopsy 

ranging from 3.7% to 8.6%. 

The remaining six studies assessed the prevalence of CD in a mixed-age population of 

patients with IDDM.234,253,258,259,268,269 One study of 1,785 patients found the prevalence of CD 

by IgA AGA to be 4.1%. In this study, only 49 of 73 screen-positive patients underwent biopsy 

confirmation, making the reported prevalence by biopsy of 0.73% an underestimation.269 

Another large study of 1,114 patients used IgA and IgG AGA as an initial screen of screenpositive patients, and then performed a second level screen with IgA EMA before moving on to 

biopsy.259 The EMA confirmed prevalence of CD was 4.9%, whereas, the reported biopsy 

confirmed prevalence was a relatively high 5.7%. In this study, 78 of 121 initial AGA-positive 

patients underwent biopsy, suggesting that most of the EMA-positive patients were biopsied. 

Among the two studies that used IgA EMA as the screening test in a mixed-age population, 

the prevalence of CD by serology was 2.3%258 and 5.7%.268 It was unclear in the first study how 

the final confirmed prevalence of CD of 0.75% was arrived at,258 whereas, in the other study the 

uniformly confirmed biopsy prevalence was 5.7%.268 

The final two studies assessed the prevalence of CD in a mixed-age population of diabetics 

using IgA-tTG.234,253 The prevalence of CD by serology was fairly high in both these studies: 

9.6%234 and 11.5%.253 The first study did not perform biopsy confirmation, whereas, in the last 

study only 20 of 98 screen-positive patients were biopsied, making the reported prevalence of 

CD by biopsy of 1.8% a likely underestimation. 

Clinical heterogeneity existed for some subgroups of this analysis making an overall pooled 

estimate of the prevalence of CD in children and adults with IDDM not entirely possible. 

However, a summary table (Table 40) is provided which presents the data grouped by age group 

and screening test, and Figure 30 presents the prevalence of CD in diabetes by study size. For 

similar studies a weighted pooled prevalence is provided, and individual study data with 

annotation is presented for studies that could not be pooled. 
84

Table 39: Included studies of prevalence of CD in type I diabetes 

Author, year; country Total 

patients 

Age 

group 

Screening 

test(s) 

First 

serology 

Confirmatory 

serology 

Biopsy proven 

Biopsy 

criteria & 

description 

Prevalence 

by serology 

Li Voon Chong, 2002; UK 

509 Adults EMA 7 None n/a None done 0.0138 

Talal, 1997; USA 

185 Adults EMA 9 None 4 ESPGAN 0.0486 

Rossi, 1993 211 Children, 

some 

adults 

EMA 10 None 3 ESPGAN 0.0474 

Kaukinen, 1999; Finland 

62 Adults EMA None 7 ESPGAN 0.0000 

Sjoberg, 1998; Germany 

848 Adults AGA - IgG 

or IgA; 

EMA 

258 22 7 Marsh 0.0259 

SategnaGuidetti, 1994; Italy 

383 Adults EMA 12 None 10 RoyChoudhury 0.0313 

Rensch, 1996; USA 

47 Adults EMA 3 None 3 Loss of villous 

architecture, 

crypt 

hyperplasia, 

and increased 

IELs 

0.0638 

FrazerReynolds, 1998; Canada 

263 Children EMA 17 None 12 Carey capsule; 

Marsh criteria; 

0.0646 

Gillett, 2001; Canada 

233 Children EMA or 

AGA 

19 None 14 Not reported 0.0815 

Hansen, 2001; Denmark 

104 Children EMA or 

tTG 

10 None 9 Partial or total 

villous atrophy, 

crypt 

hyperplasia 

and IEL 

infiltration 

0.0962 

Saukkonen, 1996; Finland 

776 Children AGA or 

ARA 

76 None 19 Not reported 0.0979 

Spiekerkoetter, 2002; Germany 

205 Children tTG IgA or 

IgG 

13 None 6 Marsh 0.0634 

Note: Appendixes and Evidence Tables are provided electronically at 

 

http://www.ahrq.gov/clinic/tp/celiactp.htm

 84 
85

Table 39 (cont’d): Included studies of prevalence of CD in type I diabetes 

Author, year; country 

Total 

patients 

Age 

group 

Screening 

test(s) 

First 

serology 

Confirmatory 

serology 

Biopsy proven 

Biopsy criteria 

& description 

Prevalence 

by serology 

Arato, 2003; Hungary 

205 Children EMA 24 None 17 n/r 0.1171 

Barera,1991; Italy 

498 Children AGA IgA then 

if neg IgG 

AGA 

30 None 16 Subtotal villous 

atrophy 

0.0602 

Barera, 2002; Italy 

273 Children EMA, second 

EMA 

15 10 9 Marsh; type II or 

III lesion 

0.0549 

Valerio, 2002; Italy 

383 Children EMA or IgG 

AGA 

n/r None 32 ESPGAN n/r 

Carelo, 1996; Spain 

141 Children IgA AGA if 

positive on 

two occaions 

12 None 4 Subtotal villous 

atrophy 

0.0851 

Roldan, 1998; Spain 

177 Children IgA, IgG 

AGA, (and 

known cases, 

and some 

tested with 

EMA) 

19 None 7 ESPGAN 0.1073 

Juan, 1998; Spain 

93 Children EMA 7 None 6 ESPGAN 0.0753 

Sigurs, 1993; Sweden 

459 Children AGA 19 None 21 Watson Capsule 0.0414 

Agardh, 2001; Sweden 

162 Children AGA, EMA, 

or tTG IgG or 

IgA 

8 8 6 As described by 

Carlsson et al. 

1999, Pediatrics 

103:1248 

0.0494 

Acerini, 1998; UK 

167 Children EMA or AGA 11 None 8 ESPGAN 0.0659 

De Block, 2001; Belgium 

399 Mixed EMA 9 None 3 No biopsy 

performed 

0.0226 

 

 

 85 
86

Table 39 (cont’d): Included studies of prevalence of CD in type I diabetes 

Author, year; country 

Total 

patients 

Age 

group 

Screening 

test(s) 

First 

serology 

Confirmatory 

serology 

Biopsy proven 

Biopsy 

criteria & 

description 

Prevalence 

by serology 

Jager, 2001 197 Mixed tTG 19 None n/r 0.0964 De Vitis, 1996; Italy 

1114 Mixed IgA, IgG 

then IgA 

EMA 

121 55.00 63 Marsh - "villous 

atrophy" 

0.1086 

Not, 2001; Italy 491 Mixed EMA 28 None 28 Intestinal 

biopsy; 

Marsh's 

modified 

classification 

0.0570 

Bao, 1999; USA 847 Mixed tTG 98 None 15 n/r 0.1157 Kordonouri, 2000; Germany 

520 Mixed - 

mostly 

children 

tTG 23 None 9 Marsh criteria 0.0442 

Aktay, 2001; USA 

218 Mixed - 

mostly 

children 

EMA 17 None 10 Partial or total 

villous atrophy, 

inflammation in 

lamina propria 

with increased 

IELs, and 

hyperplasia of 

crypts; 

classified as 

partial or total 

villous atrophy 

0.0780 

Cronin, 1997; Ireland 

101 Mixed - 

mostly 

adults 

EMA 8 None 5 n/r 0.0792 

Schober, 2000; Austria 

403 Mixed - 

mostly 

children 

EMA 12 None 6 Modified 

Marsh and 

Crowe; 

Watson-type 

capsule 

0.0298 

Lampasona, 1999; Italy 

287 Mixed - 

mostly 

children 

tTG IgA or 

IgG 

24 None n/a No biopsy 0.0836 

 

 

 86 
87

Table 39 (cont’d): Included studies of prevalence of CD in type I diabetes 

Author, year; country 

Total 

patients 

Age 

group 

Screening 

test(s) 

First 

serology 

Confirmatory 

serology 

Biopsy proven 

Biopsy 

criteria & 

description 

Prevalence 

by serology 

Lorini, 1996; Italy 133 Mixed - 

mostly 

children 

AGA IgA or 

IgG 

5 None n/a No biopsy 0.0376 

Page, 1994; Mixed 

1785 n/a AGA 73 None 13 n/a 0.0409 

 

 

 87 
 88 

Table 40: Summary of prevalence of CD in type I diabetes by age groups and screening test 

Number of 

studies 

Total 

patients 

Age 

group 

Screening 

test(s) 

Prevalence by 

serology 

Prevalence by 

biopsy 

1277 848 Adults AGA - IgG or 

IgA; then EMA 

0.0259 0.0083* 

1266 509 Adults EMA 0.0138 n/a 

1279 185 Adults EMA 0.0486 0.0216* 

1263 62 Adults EMA n/a 0.1129

3257,270,273 531 Adults EMA 0.0433 0.0339 

1274 776 Children AGA or ARA 0.0979 0.0245* 

1276 459 Children AGA 0.0414 0.0458 

4254,256,267,271 949 Children AGA – various 

combinations 

0.0695 0.0331 

1252 205 Children EMA 0.1171 0.0829 

1275 403 Children EMA 0.0298 0.0149 

5251,255,260,272

,281

1058 Children EMA 0.0624 0.0437 

4251,255,260,281 847 Children EMA 0.0661 0.0437 

5250,261,262,280

,282

1049 Children EMA - 

combinations 

0.0721 0.0658 

1265 287 Children tTG IgA with IgG 0.0836 n/a 

1278 205 Children tTG IgA with IgG 0.0634 0.0293* 

1264 520 Children tTG 0.0442 0.0173* 

1269 1785 Mixed AGA 0.0409 0.0073* 

1259 1114 Mixed IgA, IgG-AGA 

then IgA-EMA 

0.0494 0.0566* 

1268 491 Mixed EMA 0.0570 0.0570 

1258 399 Mixed EMA 0.0226 0.0075† 

1234 197 Mixed tTG 0.0964 n/a 

1253 847 Mixed tTG 0.1157 0.0177* 

*large proportion of serology-positive patients not biopsied,253,259,264,269,272,274,277-279 these were 

not included in the pooled analysis of prevalence by biopsy 

**no description of how diagnosis made – result not pooled 
89

Figure 30: Prevalence of CD in diabetes by study size 

Prevalence of CD in Diabetes by Study size

0

20

40

60

80

100

120

140

0 500 1000 1500 2000

Study Sample Size

CD by serology

5% Prev

10% Prev

20% prev

EMA Adults

EMA Children

EMA+other - Children

tTG Children

EMA & AGA Mixed pop

AGA Children

AGA & EMA Adults

Prevalence of CD in Relatives of Patients with CD 

There were 18 studies on the risk of CD in first-degree relatives of patients with biopsyproven CD,129,167,206,235-249, four of which also provided data on the risk of CD in second-degree 

relatives (Evidence Table 7, Appendix I; Table 41).206,235,238,239

First-degree relatives: First-degree relatives were directly evaluated with small bowel biopsy in 

five studies; three were performed in England in the 1970’s,242,243,245 and two in Finland during 

the 1990’s.129,167 The biopsy criteria for a diagnosis of CD was not reported in one study,243 and 

implied at least some degree of villous atrophy in the other four.129,167,242,325 The percent of all 

at-risk family members that were studied varied from 34%245 to 100%.243 The study size varied 

between 29242 and 182,245 and the cumulative number of patients tested was 494. The prevalence 

of CD among first-degree relatives undergoing intestinal biopsy varied from 5.5%243 to 22.5%;245

the pooled prevalence was 16%. 

Serological screening of the first-degree relatives of patients with biopsy-proven CD was 

performed in 12 studies.206,235-237,239-241,244,246-249 In seven of those studies, intestinal biopsy was 

performed on at least 80% of the subjects who tested positive serologically, i.e., in 84 % of 

subjects in one study,237 and in 100% of subjects in the other six studies.236,239,244,247-249 

Serological screening was performed with AGA alone in one study,236 whereas, the other six 

studies used EMA, either alone239 or in combination.237,244,247-249 Six studies used criteria 

implying some degree of villous atrophy,236,237,239,244,247,248 whereas, one study included cases 

with Marsh I changes.249 The study size varied from 92248 to 943239 subjects, for a cumulative 

number of 2,607 subjects. For the studies that required some degree of villous atrophy for 

diagnosis, the prevalence varied from 4%236 to 12%,248 and the mean prevalence was 7.6%. 
90

However, when Marsh I lesions were also considered diagnostic, the prevalence of CD among 

first-degree relatives was reported at 44.1%.249

In five other studies of first-degree relatives,206,235,240,241,246 confirmatory biopsy was not 

routinely performed (available in 9%246 to 58%241 of the cases), and the reported prevalence of 

CD was based on the serology results. EMA was used for serological screening in all of these 

studies, either alone,206,240 or in combination with AGA 241,246 or tTG.235

Two of these studies were performed in families where at least two index cases prevailed and 

are, therefore, reviewed separately.235,241 Ninety percent of the at-risk populations from these 

two studies were tested, which represents a cumulative number of 629 subjects. The prevalence 

of CD among these first-degree relatives from families where there are at least two index cases 

of known CD or dermatitis herpetiformis (DH) was 9.4%241 and 17.2%.235

The study size of the other three studies varied from 115240 to 4,508,206 and the cumulative 

number of first-degree relatives tested was 5,265. The prevalence of CD among these serologytested first-degree relatives varied between 2.8%246 and 4.5%206 (mean prevalence 4.3%). 

Other relatives: One study from the US238 reported an EMA-based prevalence of 4.7% in 192 

first- and second-degree relatives; the prevalence from each of the groups of relatives was not 

reported separately.

An American study by Book et al.235 studied the prevalence of CD in second-degree relatives 

and first cousins of CD sibling pairs (i.e., families with two affected index cases). Eighty-two 

second-degree relatives and 47 first cousins were tested with EMA and tTG, and the diagnosis 

was biopsy confirmed in 40% of the cases. The serology-based prevalence was 19.5% in 

second-degree relatives and 17.0% in first cousins. 

Two other studies, one large (n=1,275) American study of prevalence of CD in at-risk and 

not-at-risk subjects,206 and one Hungarian study,239 provided data on the prevalence of CD in 

second-degree relatives. The EMA-based prevalence of CD in those groups was 2.6% and 5.5%, 

respectively (mean prevalence 2.7% on a cumulative number of 1,329 second-degree relatives). 
91

Table 41: Prevalence of CD in relatives of CD patients 

Study, year; 

country 

Relative 

Type Index case Screening Dx criteria N tested Prevalence 

(%) 

Polvi, 1996; 

Finland 1st degree CD in family Biopsy ESPGAN 90 20 

Holm, 1993; 

Finland 1st degree CD in family Biopsy Some VA 121 10.7 

Robinson, 1971; 

England 1st degree CD child in 

family Biopsy Some VA 29 10.3 

Rolles, 1974; 

England 1st degree CD child in 

family Biopsy Not reported 72 5.6 

Stokes, 1976; 

England 1st degree CD in family Biopsy Some VA 182 22.5 

Tursi, 2003; Italy 1st degree CD in family Biopsy Marsh I-IV 111 44.1 

Corazza, 1992; 

Italy 1st degree CD adult in 

family AGA Some VA 328 4.0 

Pittschieler, 

2003; Italy 1st degree CD in family EMA, TTG Some VA 92 12.0 

Rostami, 

2000; 

Netherlands 

1st degree CD in family AGA, EMA, 

Hx ESPGAN 338 10.9 

Hogberg, 

2003; Sweden 

1st degree CD in family AGA, EMA, 

TTG Some VA 120 8.3 

KorponaySzabo, 1998; 

Hungary 

1st degree CD in family EMA Some VA 943 9.1 

Farre, 1999; 

Spain 1st degree CD in family AGA, EMA Some VA 675 5.6 

Kotze, 2001; 

Brazil 1st degree CD in family EMA +ve 

serology* 115 3.5 

Fasano, 2003; 

US 1st degree CD in family EMA +ve serology 4,508 4.5 

Vitoria, 1994; 

Spain 1st degree CD in family AGA, EMA +ve serology 642 2.8 

Mustalahti, 

2002; Finland 1st degree >1 DH or CD 

sib AGA, EMA +ve serology 466 9.4 

Book, 2003; US 1st degree CD sib pairs EMA, TTG +ve serology 163 17.2 

Hill, 2000; US 1st & 2nd

degree CD in family EMA +ve serology 192 4.7 

Fasano, 2003; 

US 2nd degree CD in family EMA +ve serology 1,275 2.6 

KorponaySzabo, 1998; 

Hungary 

2nd degree CD in family EMA +ve serology 54 5.6 

Book, 2003; US 2nd degree CD sib pairs EMA, TTG +ve serology 82 19.5 

Book, 2003; US 1st cousins CD sib pairs EMA, TTG +ve serology 47 17.0 

*EMA titre > = 1/5 

VA = villous atrophy; DH = dermatitis herpetiformis
92

Prevalence of CD in Patients with IDA 

Twelve studies were identified that allowed for the extraction of the prevalence of CD among 

patients who were evaluated for anemia (Evidence Table 8, Appendix I; Table 42).283-294 In all 

of these, IDA was the primary focus of the study or made up the cause of anemia in the majority 

of the study patients. Tables 42 and 43 summarize the characteristics of the included studies. 

Three studies assessed the prevalence of CD in IDA patients with GI symptoms.283,288,290 

The prevalence of CD in these studies ranged from 10.3% to 15% of the studied group. One 

small study assessed the prevalence of CD in a group of patients who had IDA but no identified 

GI source.286 In this study, the prevalence of CD by AGA and confirmed by EMA was 30%. 

In another study, the authors assessed the prevalence of CD in pre-menopausal women with 

IDA.293 The overall prevalence of CD in this population was found to be 12.9% by tTG, and 

8.5% after biopsy confirmation. CD was found in 1 of 22 (4.5%) of women with heavy periods, 

and 4 of 18 (22%) of women with normal menstrual flow. 

Four studies assessed the prevalence of CD in asymptomatic IDA patients by 

serology.285,287,291,292 Two of these used EMA screening,291,292 whereas the other two initially 

screened with AGA and then confirmed with EMA.285,287 The prevalence of CD in this group 

ranged from 2.3% to 5.0%. Another three studies assessed the prevalence of CD by biopsy in 

asymptomatic IDA patients, finding it to be between 2.9% and 6%.284,289,294
93 

Table 42: Included studies of CD in adult patients with anemia 

Author, year; country 

No. of 

pts 

Age 

group Population 

Anemia 

type 

Screening 

test 

First 

serology 

Confirmatory 

serology 

Biospsy 

proven 

Biopsy criteria 

Akerman, 1996; Israel 

93 Adult - 

some teens 

Out-patients 

with IDA (50% 

symptomatic) 

IDA EGD/ 

biopsy 

 13 Subtotal or 

greater 

villous 

atrophy 

Annibale, 2001; Italy 

71 Adults Asymptomatic IDA EGD/ 

biopsy 

 4 Marsh 

Corazza, 1995; Italy 

200 Adults Referred to 

hematology 

IDA IgA/IgGAGA then 

EMA then 

biopsy 

16 10 10 Not 

mentioned 

Dickey, 1997; UK 

10 Adults Asymptomatic, 

previously 

investigated 

no gross GI 

cause found 

IDA IgA AGA 

then EMA 

4 3 Endoscopic 

biopsy; 

criteria n/r; 

finding of 

villous 

atrophy and 

IELs in 

duodenal 

biopsy 

Howard, 2002; UK 

258 Adults IDA identified 

through lab 

IDA, 

folate 

IgA/IgGAGA and 

EMA then 

biopsy 

28 12 Not 

applicabe 

Kepczyk, 1995; USA 

39 Adults Mostly 

symptomatic 

out-patients 

with IDA 

IDA EGD/ 

biopsy 

 4 Villous 

atrophy, 

crypt 

hyperplasia, 

inflammatory 

infiltrate 

McIntyre, 1993; UK 

50 Adults Out-patients 

with IDA 

IDA EGD/ 

biopsy 

 3 Not reported 

*

24/28 biopsied 

 93 
94

Table 42 (cont’d): Included studies of CD in adult patients with anemia 

Author, year; country 

No. 

of 

pts 

Age 

group Population 

Anemia 

type 

Screenin

g test 

First 

serology 

Confirmatory 

serology 

Biospsy 

proven 

Biopsy criteria 

Oxentenko, 2002; USA 

113 Adults Undergoing 

EGD for IDA 

IDA EGD/ 

biopsy 

 17 CD was 

defined as 

total or 

partial villous 

atrophy with 

IELs 

Ransford, 2002; UK 

484 Adults Referred to 

hematology 

IDA EMA then 

EGD/ 

biopsy 

17 11 Revised 

ESPGAN; 

duodenal 

histologic 

changes 

were graded 

according to 

Marsh I-III 

Unsworth, 2000; UK 

483 Adults Blood donors Anemia 

unspecified 

IgA-EMA 

then 

biopsy 

32 22 n/r 

Annibale, 2003; Italy 

59 Adult Premenopausal 

women with 

IDA 

IDA IgA tTG 

then 

biopsy 

7 5 Marsh 

Van Mook, 2001; The Netherlands 

35 Adult Asymptomatic IDA EGD / 

biopsy 

 1 Marsh I 

†5 Marsh I identified by CD3 ‡25/32 biopsied **

5/7 biopsied; 30 had heavy periods; CD in 1/22 with heavy periods, and 4/18 with normal periods 

 94 
95 

Table 43: Summary of prevalence of CD in adult patients with anemia by population and screening 

test 

No. of 

studies 

Total 

patients Population 

Screening 

test(s) 

Prevalence 

by serology 

Prevalence 

by biopsy 

3283,288,290 245 Symptomatic IDA Biopsy n/a 0.139 

1286 10 Asymptomatic, 

previously no gross 

GI cause found 

investigated 

IgA-AGA then 

EMA 

0.3 n/a 

1293 59 Pre-menopausal 

women with IDA 

IgA-tTG then 

Biopsy 

0.119 0.085 

4285,287,291,

292

1,425 Asymptomatic 

serology screened 

IgA-EMA, orAGA followed by 

EMA; all biopsy 

confirmed 

0.061 0.039 

3284,289,294 156 Asymptomatic 

biopsy screened 

Biopsy n/a 0.051 

Prevalence of CD in Patients with Low Bone Mineral Density (BMD) 

Four articles were identified that assessed the prevalence of CD in patients with low BMD 

(Evidence Table 9, Appendix I).295-297,326 The study characteristics and definitions used to define 

low BMD, osteopenia, and CD are presented in Table 44. Three of these studies determined 

BMD using dual energy X-ray absorptiometry (DXA), and defined osteoporosis as a BMD less 

than 2.5 standard deviations from the peak bone mass of sex-matched control,295,297,326 whereas, 

the other used single photon absorptiometry (SPA).296 One study included patients with nontraumatic fractures,295 whereas, in the others, idiopathic osteoporosis was sufficient for inclusion. 

All four studies used serology screening with biopsy confirmation of screen-positive patients. 

Three studies relied on AGA testing as the initial screen295,296,326 followed by biopsy,296 or 

further confirmatory serology testing with EMA295 or tTG326 prior to biopsy. The final study 

screened with EMA-ME, with positive screens moving on to biopsy.297 Two studies defined the 

biopsy criteria for CD and used a fairly standard but rigid requirement of subtotal or greater 

villous atrophy.295,297

In the studies that used this test as the initial screen, AGA was positive in 6% to 21% of the 

patients with osteoporosis. However, in these studies CD was confirmed by biopsy in only 0.9% 

to 3% of patients.295,296,326 The study that used EMA-ME as a screening test identified potential 

CD cases in 7.3% of patients, but none of these met the authors’ biopsy criteria for CD.297
96

Table 44: Prevalence of CD in patients with low BMD 

Author, year; 

country Population BMD definition Test Prevalence 

Lindh, 1992, 

Sweden 

92 consecutive patients 

with idiopathic 

osteoporosis screened 

for CD; 91% F (mean 

age 66+-12 Y); and 9 M 

(mean age 50+-12 Y) 

Bone mineral 

content by photon 

absorptiometry 

(SPA) of nondominant forearm; 

criteria n/r 

IgA-AGA ELISA; cutoff was 2 SD above 

the mean of blood 

donors; confirmatory 

biopsy in 6 - criteria 

n/r 

11/92 (12.0%) AGA 

+ve.; 3% (3/92) biopsy 

confirmed 

Mean proximal SPA 

0.97 g/cm2

Mean distal SPA 0.67 

g/cm2

Gonzalez, 

2002; 

Argentina 

127 postmenopausal 

women with 

osteoporosis; age (Y): 

mean 68, range 50-82; 

747 controls; age (Y): 

mean 29, range 16-79 

History of nontraumatic 

fractures and 

lumbar spine 

and/or femoral 

neck BMD below 

T-score -2.5 

DXA 

IgA and IgG-AGA 

ELISA; cut-off levels: 

for IgA - 15 AU/mL; 

for IgG - 20 AU/mL; 

positives confirmed 

with IgA-EMA-ME 

positive at 1:5 dilution; 

positives confirmed 

with biopsy in EMA 

positives; showing 

villous atrophy, crypt 

hyperplasia and IEL 

>30% 

1/127, or 7.9 x 1000 

(95% CI: 0.2-43.1); test 

positivity: AGA found in 

8 of 127 (6.3%) pts on 

level 1; 1 of these 8 pts 

was EMA positive on the 

2nd level and eligible for 

biopsy which 

established a diagnosis 

of CD in 1 (0.9%) 

Mather, 2001; 

Canada 

Idiopathic low BMD; 

mean age 57 Y; range 

18-86 Y; 81.3% (78) F; 

18.7% M (18) 

All osteopenic; 

45/78 F and 13/18 M 

osteoporotic 

DXA 

Osteopenia: 

BMD <1 SD of 

mean sexmatched peak 

BMD 

Osteoporosis: 

BMD <2.5 SD of 

mean sexmatched peak 

BMD 

IgA- EMA-ME titers of 

≥1:10; and biopsy 

confirmation based on 

subtotal or greater 

villous atrophy 

7 (7.3%) of 96 pts were 

EMA +ve; all biopsies 

were negative based on 

subtotal or greater 

villous atrophy 

prevalence of 0% 

Nuti, 2001; Italy 255 females with 

osteoporosis; mean 

age 66.6 Y range 36-65 

Y 

DXA 

BMD below Tscore -2.5 

IgA-AGA ELISA-cutoff level of 10 AU/mL1; IgA-tTg cut-off >22 

AU; confirmatory 

biopsy criteria n/r 

53/255 (20.8%) +ve IgGAGA; 24/53 +ve for tTG 

antibody (9.4%); 

intestinal biopsy in 10/24 

resulted in 6 (2.4%) with 

confirmed CD 

F=female; M-male; DXA=dual X-ray absorptiometry; Y=years; n/r=not recorded 

Quality Assessment 

Using the cross-sectional checklist, the overall quality of reports of the included studies for 

the Celiac 2 objective, was marginal to fair (Appendix J, Table 2). For example, most of the 

studies did not report on whether the patients were consecutively enrolled, which could possibly 

lead to selection bias. 
97

Celiac 3: Risk of Lymphoma in CD

Literature Search 

Out of 379 references resulting from the literature search on CD and lymphoma, 150 were 

initially excluded because they did not directly address this topic (Appendix F). Of the 229 

studies that were screened using full reports of the studies, 211 were excluded for the following 

reasons: review articles (n=73; 19.3% of level 2 articles); did not address the topic (n=33); 

assessed the risk of CD in lymphoma (n=28); were uncontrolled studies, including surveys 

(n=53); or, studied the basic mechanisms and the pathogenesis of lymphoma in CD (n=24). 

The following eight exclusions were made from the 18 publications that reached level 3 (i.e., 

eligibility criteria): duplicate publications (n=7);127,327-332 (for two of these reports,328,332 patients 

originated from the same center [i.e., General Hospital, Birmingham]) and the reports were 

conducted during the same periods as other reports,329,330,333 and we could not rule out that they 

were not similar series); data was not extractable (n=1).334

The nine controlled studies selected for data extraction were grouped as follows: eight cohort 

studies,333,335-341 and one case-control study342 (Evidence Table 10, Appendix I; Table 45). 

Mortality data from one controlled study in refractory CD is presented at the end of this section 

for reference.343
98

Table 45: Included studies for risk of lymphoma in CD 

Study, 

year; 

country, 

period Study type Participants 

Risk of 

lymphoma Mortality 

Other 

observations 

Cottone, 

1999; 

Sicily, 

1980-97 

Retrospective 

cohort 

• 228 CD patients 

• 76% females 

• mean age at Dx 34.7 

• 98% adult Dx 

• 100% on strict GFD 

• Incidence NHL 

3.1% 

• SIR NHL 3.75, p 

<0.01 

SMR all causes 

3.8 (1.9-6.7) 

Holmes, 

1989; 

England, 

1941-85 

Prospective 

cohort 

• 210 CD patients 

• 55% females 

• 51% on strict GFD 

• Incidence NHL 

4.3% 

• SIR NHL 42.7 

(19.6-81.4) 

SMR not 

reported 

SIR NHL vs GFD 

compliance: 

• Strict GFD 44.4 

• Gluten diet 100 

Logan, 

1989; 

Scotland, 

1979-1986 

Prospective 

cohort 

• 653 CD patients 

• 60% females 

 Mortality from 

NHL 2.6% 

SMR from 

lymphoma 31 

p<0.001 

SMR all causes 

1.9 (1.5-2.2) 

SMR childhood Dx 

1.4 (0.4-3.7) 

SMR adult dx 1.9 

(1.5-2.3) 

Askling, 

2002; 

Sweden, 

1964-94 

Retrospective 

cohort 

• 11,019 CD patients 

• 59% females 

• Mean age at Dx 

17.4 (range 0->70) 

• Incidence NHL 

0.34% 

• SIR NHL 6.3 

(4.2-125) 

SMR from NHL 

11.4 (7.8-16) 

SMR all causes 

2 (1.8-2.1) 

SIR NHL childhood 

Dx 1.9 (0.4-5.5) 

SIR NHL adult Dx 

7.0 (5.0-9.5) 

Collin, 

1996; 

Finland, 

1970-93 

Prospective 

cohort 

• 383 CD patients 

• 73% females 

• Mean age at Dx 

41.8 (range 16-78) 

• 75% on strict GFD 

• Incidence NHL 

0.26% 

• SIR NHL 2.66 

(0.07-14.8) 

 

Corrao, 

2001; Italy, 

1962-94 

Prospective 

cohort 

• 1,072 CD patients 

• 76% females 

• mean age at Dx 

35.7 (range 18->50) 

• 59% on strict GFD 

 SMR from NHL: 

69.3 (40.7-

112.6) 

SMR all causes: 

2.0 (1.5-2.7) 

SMR age 18-29 at 

Dx: 2.5 (0.5-7.3) 

SMR age 30-49 at 

Dx: 2.4 (1.3-4.0) 

SMR age >50 at 

Dx: 1.9 (1.3-2.6) 

SMR strict GFD: 

0.5 (0.2-1.1) 

SMR unlikely GFD: 

6.0 (4.0-8.8) 

Green, 

2003; USA, 

1981-2000 

Prospective 

cohort 

• 381 CD patients 

• 64% females 

• mean age at Dx 44 

+/- 18 

• Incidence NHL 

1.3% 

• SIR NHL 6.2 

(2.9-14) 

 

Selby, 

1979; 

Australia, 

1959-78 

Retrospective 

cohort 

• 93 CD patients 

• 67% females 

• mean age at Dx 40 

(range 14-70) 

• Incidence NHL 

4.3% 

• SIR NHL 4.94, 

p<.0005 

 

Delco, 

1999; USA, 

1986-95 

Case-control • 458 CD patients 

• 4% females 

• OR NHL 4.53 

(2.01-10.23) 

 

Dx=diagnosis; SIR=standardized inidence ratio; NHL=non-Hodgkin’s lymphoma; SMR=standardized mortality 
99

Measures of Risk 

Eight out of nine studies were cohort studies, either prospective or retrospective. The 

standardized incidence ratio (SIR) was the most commonly reported measure of association; it 

was calculated as the incidence observed in the patient cohort divided by the expected incidence 

from the control population, along with a measure of precision (i.e., its 95% CI). The results 

were expressed either as SIRs of lymphoma or as the standardized mortality ratio (SMR) from 

lymphoma (SMR-NHL). The all-cause mortality was also reported in some studies. 

It was not possible to pool these measures of risk, since SIRs by definition incorporate 

variables inherent to each population. The attributable risk (AR), was calculated whenever the 

incidence rates of NHL in CD patients and in the age-adjusted general population, were 

available. 

Study Characteristics 

There were eight cohort studies (five prospective 333,336,338-340 and three retrospective 

335,337,341) and one case-control study.342 Two studies were from Italy,335,339 two from the 

UK,333,336 two from Scandinavia,337,338 two from the US,340,344 and one from Australia.341 The 

observation periods varied from 7 years336 to 44 years (1941-85;333), and the mean duration of 

patient follow-up varied from 6 years335,339-341 to 18.6 years.333 Patients were either selected 

from a national patient register,336 from hospital discharge databases,337,342 or represented all 

consecutive cases from a single333,335,338,340,341 or multiple339 institution(s). The cohort sizes 

varied from 93341 to 11019;337 55% to 76% of patients with CD were female, except for the study 

by Delco et al.,342 which used discharge diagnoses databases from the US Veterans Affairs 

hospitals (4% female CD patients). The mean age at diagnosis of CD was reported in six studies: 

in four studies, the diagnosis of CD was made almost exclusively in adulthood.335,338,339,341 The 

mode of presentation was reported in four studies.335,338,339,341 Adherence to a GFD was reported 

in five studies,333,335,338,339,341 and could be used in the analysis in three of them.333,338,339 Control 

data for the cohort studies was derived from local and national mortality data and cancer 

registers. 

Types of Lymphomas 

The total number of lymphomas diagnosed in each study and their histological type was not 

uniformly reported. Of the 84 lymphomas that were mentioned within these nine studies, 64 

were referred to as “non-Hodgkin lymphoma (NHL)” not otherwise specified, one as 

“lymphoma,” nine as “ enteropathy-associated T-cell lymphoma (ETCL),” five as “B cell 

lymphoma”, two as “large cell lymphoma,” one each as a “T-cell other than ETCL,” 

“lymphosarcoma” (currently classified as small cell lymphoma), and “histiocytic medullary 

reticulosis” (currently termed hairy-cell leukemia). Logan et al.336 reported that they found 

“mostly lymphosarcomas (i.e., small-cell lymphomas) or reticulum-cell sarcomas (i.e., large-cell 

lymphomas) as well as two Hodgkin’s lymphomas,” whereas, the remaining authors 

systematically excluded Hodgkin’s lymphomas from their respective analyses. 
100

Incidence of Lymphoma and Related Mortality Data 

The case definition of CD differed between the reports of institutional series and those 

derived from database analysis. The results will therefore be presented differently according to 

each of these two study designs. 

Institutional series: By institutional studies, we mean reports on the evolution of cases 

consecutively diagnosed with CD and followed in one or several selected institution(s) over a 

specific period. Six out of the nine controlled studies were performed in that setting; in five out 

of six studies, the data originated from a single referral center.333,335,338,340,341 The sixth study is 

the product of a collaborative effort between nine Italian centers.339 In these studies, all cases 

were biopsy-proven CD. 

Holmes et al., from Birmingham England, reported on a series of 210 biopsy-proven CD 

patients diagnosed and followed between 1941 and 1985.333 This series was originally reported 

by Harris in 1967,329 and reviewed in 1976330 and in 1989333 by Holmes. By this third 

publication, the authors had excluded all non biopsy-proven cases of CD, as well as the cases of 

cancer that arose either prior to or within 12 months of diagnosis of CD. The length of follow-up 

was of a minimum 13 years, 17.4 patient-years for men and 19.4 patient-years for women. 

Based on the original publication by Harris, we can assume that a large proportion of these 

patients (80% in Harris’ series) were diagnosed with CD in adulthood. There were nine cases of 

NHL, compared with an expected 0.21, resulting in a SIR-NHL of 42.7 (95% CI: 19.6-81.4), 

which was the highest reported degree-of-risk for lymphoma among the controlled studies we 

identified. 

Green et al.340 prospectively followed 381 patients with biopsy-proven CD from New York 

City, most of whom were of European descent, and diagnosed between 1981 and 2000. The 

mean age at CD diagnosis was 44 +/- 18 years, and the duration of CD-related symptoms prior to 

diagnosis was 5 +/- 8 years. The mean follow-up was 6 +/- 11 years, for a total of 1,977 patientyears following the diagnosis of CD. There were a total of nine cases of NHL, occurring any 

time before or after the diagnosis of CD, leading to an attributable risk of NHL from CD of 120.2 

cases per 100,000 patient years. The SIR-NHL, diagnosed at any time, was 9.1 (95% CI: 4.7-

13), and the SIR-NHL for any lymphoma diagnosed at least one month after the diagnosis of CD 

was 6.2 (95% CI: 2.9-14). 

Cottone et al.335 reported on 228 patients with biopsy-proven CD and followed from 1980 to 

1997, from a large referral center in Sicily. Ninety-eight percent of the patients had been 

diagnosed with CD during adulthood and the mean age at diagnosis was 34.7 years. The mean 

duration of follow-up was 6 years (range: 1 month to 17 years). No case of refractory CD was 

mentioned. There were seven cases of NHL, compared with an expected number of 1.824 (SIRNHL of 3.75 (p<0.01)). The cumulative incidence of NHL was 3%, compared with an expected 

of 0.8%, leading to a risk difference or AR of 2.2%. The mean age at diagnosis of lymphoma 

was 59.4 years, and the mean time from the diagnosis of CD was 6.5 years. Lymphomas 

occurring prior to or within 6 months of CD diagnosis were excluded. 

A large Italian multicenter study by Corrao et al.,339 prospectively followed 1,072 patients 

with CD and spanned from 1962 to 1994, totaling 6,444 patient years. The mean follow-up was 

6 years, and all patients were diagnosed with CD during adulthood (mean age at diagnosis of CD 

35.7 years). The outcomes were strictly measured in terms of mortality data, i.e., mortality from 

NHL and from all causes. Events occurring at the time of CD diagnosis were included. There 
101

were 16 instances of death from NHL. The SMR-NHL was 69.3 (95% CI: 40.7-112.6), whereas, 

the SMR of death from all cause (SMR-all cause) was 2.0 (95% CI: 1.5-2.7), showing that the 

risk of death from NHL in CD is disproportionately elevated. 

Selby et al.341 reported on a series of 93 patients with CD that were followed at a single 

institution in Australia between 1959 and 1978, for a mean duration of 6 years. Patients 

presented either during the teenage or adulthood, all were symptomatic at the time of diagnosis, 

and there were no refractory cases. There were four patients with NHL (simultaneous CD and 

lymphoma diagnosis included), compared with an expected of 0.081 (SIR-NHL 4.94, p<0.0005). 

Collin et al.338 reported on a prospective cohort of 383 patients with CD, diagnosed and 

followed at a single institution over the 1970-93 period, for a mean follow-up of 8.1 years (3,107 

patient years in total). The mean age at diagnosis was advanced: 41.8 years, with a range of 16 

to 78 years. Seventy-five percent of the patients adhered to a strict GFD and 82% of patients 

were symptomatic at the time of CD diagnosis. Simultaneous lymphoma and CD diagnoses 

were not excluded. There was a single case of lymphoma, compared with an expected 0.4 (SIRNHL 2.66 [95% CI: 0.07-14.8]). As well, the 10- and 15-year survival of CD patients did not 

differ significantly from those of the general population. 

Large database and register series: Logan et al.336 reviewed the death certificates of CD 

patients belonging to a comprehensive register of CD patients that exists in Scotland since 1979, 

constituting a cohort of 653 CD patients gathered from 1979 to 1986. There were 17 deaths 

attributed to lymphoma, instead of an expected 0.55. Both Hodgkin and NHL were included, 

and so were those lymphomas occurring simultaneously to the diagnosis of CD. The SMRlymphoma was 31 (p<0.001), which was disproportionately increased compared with the SMRall causes, which was 1.9 (95% CI: 1.5-2.2).

Askling et al.337 reported on the largest CD patient cohort (n=11,019), gathered from a 

comprehensive Swedish database of hospital discharge diagnoses over 1964 to 1994. It was not 

possible to ascertain how the diagnosis of CD was made or confirmed. The mean age at 

diagnosis of CD was 17.4 (range 0 to >70), and the mean follow-up was 9.8 years (range 0-32), 

for a total of 97,236 patient years. The ascertainment of outcome was achieved through the 

Swedish cancer register, as well as the register of causes of death. Lymphomas arising prior to 

or within 12 months of CD diagnosis were excluded, as for the incident lymphomas found at 

autopsy. There were 38 cases of NHL, and a SIR-NHL of 6.3 (95% CI: 4.2-125) was calculated. 

The SMR-NHL was 11.4 (95% CI: 7.8-16), which was disproportionately elevated compared 

with the SMR-all causes (2.0 [95% CI: 1.8-2.1]). 

Delco et al.342 used the database of discharge diagnoses from all US Veteran Affair hospitals 

to gather a total of 458 CD patients, hospitalized between 1986 and 1995. The concomitant 

diagnoses received by those patients were compared with those of five controls per CD patient, 

randomly selected from the same year’s discharge database (total 2,692 controls). The mean age 

of the CD group was 63.8 +/- 12.4 years and the mean age of the control group was 59.7 +/- 14.8 

years (p<0.001). Ninety-three percent of the patients with CD were white, compared with 74% 

of the control subjects (p<0.0001). The odds ratio (OR) of NHL (OR-NHL) in CD, was 4.53 

(2.01-10.23). 
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Role of a GFD 

The impact of GFD compliance was analyzed and reported in only two of the nine studies. 

Holmes et al.333 reported a SIR of NHL in patients on a strict GFD (SIR 44.4), versus those who 

did not adhere to a GFD (SIR 100). Corrao et al.339 observed that the mortality from all causes 

was lower in patients on a strict GFD, as opposed to those who were unlikely GFD-compliant 

(SMR 0.5 [95% CI: 0.2-1.1] and 6.0 [95% CI: 4.0-8.8], respectively). Although, in the study by 

Askling337, compliance could not be directly ascertained, the SIR of lymphoma 1 to 4 years after 

diagnosis was 9.7 (95% CI:6.3-14), wheres, it dropped to 3.8 (95% CI: 2.2-6) five or more years 

after diagnosis, suggesting that the risk of lymphoma decreases over time on a GFD. 

Risk of Lymphoma Versus Symptoms 

The mode of presentation leading to the diagnosis of CD was not commonly reported. The 

reports from Italy335,339 were unique in that they both detailed the circumstances by which the 

diagnosis of CD was diagnosed, portraying their cohorts as largely asymptomatic, since 45%335

and 70%339 of their patients had subclinical presentations, i.e., either mild symptoms, anemia, or 

were detected through screening. Conversely, it is reasonable to suggest that the studies that 

used hospital discharge diagnoses of CD as entry criteria would be largely made up of 

symptomatic CD patients. Unfortunately, it is not possible to compare the measured risk of 

lymphoma in the Italian studies to those of our other reports, because of the great disparities in 

populations, data collection and analyses amongst them. 

The presence or absence of symptom at the time of CD diagnosis was not evaluated as a risk 

factor for lymphoma per se. Corrao et al.339 did, however, analyze the impact of the mode of 

presentation on the mortality from all causes in CD. They observed that patients diagnosed with 

mild symptoms or by antibody screening did not show any relevant excess mortality, compared 

with the symptomatic group (SMR 1.2 [95% CI: 0.1-7.0] and 2.5 [95% CI: 1.8-3.4], 

respectively).339

Impact of the Age at Diagnosis of CD 

Several studies analyzed the risk of lymphoma with respect to the age at diagnosis of CD. 

Patients who were diagnosed with CD during adulthood were either 1) asymptomatic during 

childhood or 2) symptomatic but eluded the diagnosis. For the later circumstance, authors have 

referred to “diagnostic delay” as a symptomatic period in the absence of diagnosis or treatment. 

The impact of the diagnostic delay was analyzed in two studies.336,339 Corrao et al.339 compared 

the mortality from all causes in patients who had suffered a diagnostic delay of more than 10 

years, one to 10 years, or less than 1 year (no diagnostic delay), and found that the longer the 

untreated symptomatic period, the greater the mortality from all causes (SMR 3.8 [95% CI: 2.2-

6.4], 2.6 [95% CI: 1.6-4.1], and 1.5 [95% CI: 0.9-2.3], respectively). Logan et al.,336 on the other 

hand, reported opposite results: while the SMR-all causes was significantly greater than 1 for 

their entire cohort (1.9 [95% CI: 1.5-2.2]), for those CD patients diagnosed only in adult-life 

despite an obvious childhood illness typical of CD, all-cause mortality was similar to that of 

other CD patients diagnosed in adult life. A difference in methodology might explain this 

discrepancy, since the ascertainment of outcomes was derived from registers in Logan’s study 
103

and was probably not as accurate and reliable for outcomes such as the presence or absence of 

symptoms during childhood. 

Logan et al.336 also reported that the all-cause mortality was increased in the patients 

diagnosed as adults, but not those who were diagnosed as children (SMR 1.9 [95% CI: 1.5-2.3] 

and 1.4 [95% CI: 0.4-3.7], respectively). 

The patients from Corrao’s cohort were exclusively diagnosed with CD as adults. The SMRall causes for patients diagnosed between 18 and 29 years was slightly less, and not significantly 

different from 1.0, compared with those who were diagnosed later on in life, i.e., 2.5 (95% CI: 

0.5-7.3) for those diagnosed at age 30 years versus 2.4 (95% CI: 1.3-4.0) for those diagnosed at 

age 49 years and 1.9 (95% CI: 1.3-2.6) for those diagnosed at age >50 years. 

Askling et al.345 reported on 11,019 patients with CD, diagnosed at all ages, and found that 

the SIR-NHL was not significantly greater than one in CD patients who were diagnosed during 

childhood, in contrast with those who were diagnosed as adults (SIR-NHL 1.9 [95% CI: 0.4-5.5] 

for diagnoses made at ages 0 to 19 years compared with 7.7 [95% CI: 4.9-12] for those 

diagnosed between 20 and 59 years). Part of the increased risk in adults may be explained by the 

fact that in some of these cases the diagnosis of lymphoma can be made simultaneously or soon 

after that of CD. However, cases of lymphoma diagnosed within 12 months of CD diagnosis 

were excluded from Askling’ study, so that the risk of lymphoma in adult CD diagnosis remains 

elevated independently of cases with simultaneous presentation. 

Risk of Lymphoma in Refractory CD 

We were unable to identify a single source of controlled data on the risk of lymphoma in 

refractory CD. There was one indirect source of controlled evidence on the mortality in CD. 

Nielsen et al.,343 from Denmark, published the mortality data from 98 patients with CD 

diagnosed between 1964 and 1982, 24% of which were treated with prednisone because they did 

not respond to a GFD, i.e., probable refractory CD. The mortality in CD exceeded that of the 

general population (controlled for age and sex) by a factor of 3.4 (p<0.025); in GFD-responders, 

this factor was 2.2 (p<0.025), whereas it was 5.8 (p<0.005) in the non-responders. The causes of 

death were poorly documented, and therefore, will not be described here. 

Quality Assessment 

The overall quality of the included studies was good (Appendix J, Tables 3-5). For example 

the assessment of outcomes was complete in the included studies. 
104

Celiac 4: Consequences of Testing for CD 

Out of 1,199 citations that were identified by the search strategy for the Celiac 4 objective, 

140 met the level 1 screening criteria (excluded 1059) (Appendix E). Of these, 126 met the level 

2 screening criteria (excluded 14). At level 3, 35 articles satisfied the screening criteria 

(Evidence Table 11, Appendix H)346-380 (excluded 72 articles at level 3). Eleven relevant articles 

were identified in other celiac objectives: five from Celiac 2;381-385 four from Celiac 

3;331,335,336,343 and two from Celiac 5.386,387

The search strategy did not identify any studies that would allow us to address the specific 

benefits and harms of testing with different strategies for CD. The consequences such as falsepositive results were dealt with in Celiac 1. We address the response to treatment in the sections 

that follow. 

For the consequence of osteoporosis/fracture, an additional search was conducted with the 

search terms osteoporosis and CD, and five additional relevant studies were identified.388-392

The consequences that were included in this review were: 1) costs, 2) patients complying 

with treatment, 3) response to treatment in terms of symptoms, and 4) clinical outcomes such as 

reduced risk of complications–osteoporosis, mortality, anemia. 

Given the recent recognition that the number of subclinical and silent CD cases may be eight 

times that of classically symptomatic cases, it is important to determine if the clinical outcomes 

vary according to type of clinical presentation. Where possible, results of the analysis according 

to type of clinical presentation are presented. 

Part A 

Most papers included in the consequences of testing for CD dealt with patients (who were 

newly diagnosed) after they initiated a GFD. Most studies evaluating the consequences of 

nutritional status were before/after studies. In total, 15 studies dealing with either nutritional 

status, weight, body mass index (BMI) and body composition, were identified.346-

350,352,357,359,361,363-365,369-371

Seven studies were case control,347-349,352,357,364,369 one a cohort study,346 and in seven studies, 

the patients acted as their own control group.350,359,361,363,365,370,371

Eight studies were based on children with CD,347,349,350,352,357,359,369,370, three studies were 

based on adolescents with CD363-365 and four studies were based on adults with CD346,348,361,371. 

There were five studies that evaluated costs of screening as a consequence.360,366,379,380,382 

Type 1 diabetes and CD. Four studies evaluated diabetes and CD in children.347,357,359,370 Three 

studies were from Europe (UK,347 Hungary,359 and Finland370) and one was from Australia.357 

Two were case control studies347,357 and two studies had patients with CD act as their own 

controls.359,370 All the studies assessed the effect of a GFD diet (range 3-12 months) on the 

diabetic control of type 1 diabetes.

The UK study347 evaluated 230 children with type 1 diabetes who were screened for CD with 

serology. Those children with positive serology were biopsied. Eleven children were diagnosed 

with CD and followed longitudinally. The control subjects were the children diagnosed with 

type 1 diabetes with negative serology. The controls were matched for age, sex and duration of 

diabetes in a 2:1 ratio (22 controls:11 cases). At baseline, the weight (standard deviation score; 
105

SDS), BMI SDS and HbA1c of the cases were statistically lower than the controls. No statistical 

difference was noted for height SDS, C-peptide level and insulin requirements. Also, the cases 

(type I diabetes with positive CD serology) received significantly less intensive insulin regimens 

compared with controls. Six type 1 diabetic children with CD participated in the GFD. After 12 

months of a GFD, the differences seen in the BMI SDS was reversed between the cases and 

controls. HgA1c levels did not improve significantly on a GFD. Insulin dose requirements 

increased for both cases and controls, but still did not significantly differ from each other. 

Insulin regimens were not statistically different between cases and controls after a GFD. 

The Australian study357 included children and adolescents with coexisting type 1 diabetes and 

CD, which were identified from a database of the Diabetes Center at the Royal Alexandra 

Hospital for Children. CD had to be biopsy-proven. Twenty patients (5M:15F) were enrolled 

out of 36 patients identified on the database. Forty control patients from the same database were 

matched for age, sex and duration of IDDM. No immediate criteria on screening from the 

database was given in the study. At baseline, the current height SDS, current weight SDS, BMI 

SDS and HbA1c were not significantly different from controls. Compliance with a GFD was 

based on dietary records classifying patients to: no detectable gluten; trace of gluten; and, gluten 

containing. For compliance, 30% of patients were classified as adhering to a strict GFD, 30% 

consumed trace amounts of gluten, and 40% had a significant amount of gluten in their diet. No 

differences were detected in growth parameters or HbA1c according to compliance to a GFD. 

The Hungarian study359 included 205 children with type 1 diabetes that were randomly 

selected from screening for CD. None of these patients had suspicion for CD. Twenty-four 

children were positive for EMA and 17 (7 boys and 10 girls) had subtotal villous atrophy. The 

height of the children with CD and type 1 diabetes were normal compared with children with 

only type 1 diabetes at baseline. But the BMI of the 17 children was significantly lower (14.2 vs 

16.3 kg/m2

) compared to controls. After three months of a GFD, BMI significantly increased 

(14.2 vs 16.8 kg/m2

). Furthermore, significant increases in insulin requirements (0.64 U/kg vs 

0.48 U/kg) occurred after a GFD. The percentage of HbA1c did not change on a GFD compared 

with baseline (7.82% versus 7.67%). 

The study from Finland by Saukkonen et al.,370 retrospectively screened 776 children with 

type 1 diabetes over a 2.7 year period with serology and, if positive, jejunal biopsy. Eighteen 

children (2.3%) had confirmed CD. HbA1c levels did not change after introduction of a GFD. 

Correlation of height SDS and mean weight for height were not compared post-GFD. 

Body composition and anthropometrics. Six studies specifically detailed body composition 

after a GFD.348-350,352,369,371 Of these studies, four examined children,349,350,352,369 and two 

included adults.348,371

Of the studies conducted in adult patients with CD, one was from Italy348 and the other from 

Argentina.371 In the Italian case-control study, 212 treated patients with histologically-confirmed 

CD were assessed. Of these, 71 (33.4%) (51 women and 20 men) were asymptomatic, had 

maintained a constant body weight during the previous 6 months, and were on a strict GFD. 

Forty-three of the patients were diagnosed as children (28 women and 15 men; average age 5.2 

years) and 28 were diagnosed as adults (23 women and 5 men; average age 28 years). The 

average consumption of a GFD was ≥ 2 years. For each patient, there were two sex- and agematched healthy controls (142 controls). Body composition was calculated by means of DEXA. 

The weight and BMI of female CD patients were lower than the controls (55.5 kg vs 58.7 kg, 
106

p=0.004 and 20.9 kg/m2 vs 22.4 kg/m2, p=0.03). The height and BMD were not significantly 

different, although BMD for those diagnosed as adults was lower than controls. Fat mass (22.9% 

vs 27.5%, p<0.05) and lean mass (38.8% vs 40.5%, p<0.03) were also significantly lower in 

cases versus controls. The weight (69.2 kg vs 73.3 kg, p=0.03), height (175 cm vs 178 cm, 

p=0.05) and BMI (21.9 kg/cm2

 vs 23.5 kg/cm2, p=0.05) of male patients were significantly lower 

than in controls. Fat mass (13.9% versus 16.8%, p<0.05) and lean mass (55.5% versus 56.7%, 

p<0.03) were also significantly lower than in controls. 

The study from Argentina by Smecuol et al.,371 enrolled 47 (41 females, 6 males) unselected, 

consecutive patients with newly diagnosed CD (diagnosed between Sept 1991 and Oct 1993). 

Twenty-five patients were re-evaluated in 1995 (24 females and 1 male). The diagnosis of CD 

was based on clinical features of classic and atypical symptoms, with positive small bowel 

biopsy and positive serology. Three patients were asymptomatic, the rest had classical features 

of CD. After 12 months, all patients on an initial GFD, improved. In the study, the patients 

acted as their own control—15 patients adhered strictly to the GFD, while ten were on a partial 

GFD. Patients on a strict GFD consumed less calories than patients who were poor compliers 

(p<0.05). After treatment, fat mass (18.2 kg, p<0.0001) and bone mass (2 kg/m2

, p<0.002) 

increased significantly. Lean tissue mass did not increase. Body weight (55.7 kg, p<0.0001), 

BMI (22.2 kg/m2, p<0.001) and triceps skinfold thickness (15.8, p<0.0001) were increased 

significantly; mid-arm muscle circumference and muscle mass did not change. Patients who 

more strictly adhered to the GFD tended to demonstrate greater increases, although the trend was 

not significant. 

Of the four studies that evaluated children, two were from Italy349,352, one was from the 

Netherlands,350 and one was from India.369 Both Italian studies were case-control studies, 

whereas, in the Netherlands study, the patients acted as their own control. In one of the Italian 

studies by Barera et al.,349 29 consecutive children (14 boys and 15 girls) with a diagnosis of CD 

were enrolled (mean age 9.54 ± 3.42 yr). Diagnosis was according to ESPGAN criteria. Four 

patients had classic symptoms, while the rest had atypical CD. The patients were studied over 

1.02 ± 0.15 years of GFD. Each patient was age- and sex-matched to a healthy control patient 

(n=29). At baseline, children with CD weighed less than the controls (28.3 ± 11 kg vs 34.5 ± 

14.1 kg, p=0.04), had lower lean mass of limbs (8.4 ± 4.8 kg vs 10.8 ± 4.7 kg, p=0.0013), less fat 

mass (4.6 ± 3.5 kg vs 7.5 ± 4.9 kg, p=0.006), less percentage of fat mass (17.4 ± 8.3% vs 23.7 ± 

8.4%, p=0.002) and lower bone mineral content (1067.2 ± 451.3 g vs 1317 ± 553.8 g, p=0.006). 

Height, BMI, lean mass, and ratio of lean mass to height, did not differ from controls at baseline. 

After an average of 1 year on a GFD in 23 children, no significant differences were found in 

weight, height, BMI, lean mass, lean mass to height, lean mass of limbs, fat mass, percentage of 

fat mass or bone mineral content (BMC), compared with controls. Compliance was good in all 

patients as assessed by EMA (only three subjects were still positive). 

The second Italian study by Rea et al.,352enrolled 23 children (8 boys and 15 girls, mean age 

4.7 ± 0.76 yr) from Jan 1992 to Dec 1994, according to ESPGAN criteria. They were sex- and 

age-matched to healthy controls from the ambulatory clinic. At baseline, the height, BMC, arm 

muscle area (AMA), triceps skinfold (TSF), subscapular skinfold (SSSF), and fat area index 

(FAI), were significantly lower than controls. The BMI and weight for height index (WHI) were 

not different. After GFD, all the parameters improved when compared with patients to before 

GFD. Height, BMC, AMA, BMI, TSF, SSF, FAI and WHI all significantly improved. If 

patients post-GFD were compared with controls, the height was still significantly lower (p=0.01) 

but the rest of the values were not significant. After a GFD, the blood chemistry of these patients 
107

was assessed. The hemoglobin, iron, protein, albumin triglycerides, calcium, and zinc levels 

were significantly different from the baseline value; however, transferrin, cholesterol, 

phosphorus and alkaline phosphatase levels were not different. 

The study from the Netherlands by Boersma et al.,350 enrolled 28 children (9 boys and 19 

girls) with newly diagnosed CD (between Jan 94 to Jan 95). All children had classic symptoms 

and had positive small bowel biopsies. After 3 years of a GFD, the BMI SDS and height SDS 

improved significantly (p<0.0001 for both). The initial improvement of BMI SDS was seen in 

the initial 6 months with subsequent gradual improvement. The height SDS improved 

continuously over the 3 year period, and the improvement was significant. 

In a study from India by Poddar et al.,369 104 children evaluated for CD between Sept 1997 

to Dec 1998 were included. All children had diarrhea, failure to thrive or pallor as a clinical 

presentation. Fifty-seven were diagnosed as having CD (by modified ESPGAN score) and the 

remaining 47 were controls. Seven children who did not respond to a GFD and were excluded, 

were diagnosed with other diseases. The mean follow-up of patients after starting a GFD was 

19.6 ± 8 months (range 4-36 months). The remaining 50 children had a dramatic response to the 

GFD. Symptoms subsided in 16±9.8 days (range 4-30) and all showed significant weight gain 

(66% ± 14% vs 86% ± 11% of expected, p<0.001). Height gain improved, but was not 

significant (88 ± 5% vs 94 ± 5% of expected, p=not significant). Seventeen percent of the 

children had poor compliance to the GFD. No attempt at subdividing patients into poor versus 

good compliance was made. 

Nutritional status. Two studies looked at nutritional status with biochemical markers. 

In the study from Finland by Kemppainen346 nutritional status of newly diagnosed patients 

with CD before and after GFD was reported. Forty patients with CD diagnosed between Nov 

1988 to Dec 1990 were included. All had abdominal symptoms. Diagnosis was made on 

presence of partial villous atrophy (eight patients), subtotal villous atrophy (17 patients) or total 

villous atroph (15 patients). On mean histomorphometric index, there was a statistically 

significant trend (p=0.004) comparing partial villous atrophy (0.018 ± 0.003), subtotal villous 

atrophy (0.0015 ± 0.002) and total villous atrophy (0.013 ± 0.002). When biochemical 

measurements were examined according to grade of villous atrophy, significant differences were 

seen for ferritin (p<0.01) and transferrin (p<0.05). Serum ferritin was still significantly lower in 

total villous atrophy, as was erythrocyte folate levels if sex was standardized in an analysis of 

variance. Severity of villous atrophy also correlated with ferritin, erythrocyte folate, and serum 

vitamin B12. Abnormal values of serum protein, vitamin A, and vitamin B12, were low. There 

were no abnormal vitamin E levels. Villous atrophy improved in all patients within 12 months 

of a GFD. Two patients had subtotal villous atrophy, 29 had partial villous atrophy and three 

had normal villi after a GFD. Six patients withdrew from the study. BMI increased after a GFD, 

as did most of the biochemical measurements. One patient with subtotal villous atrophy still had 

a low hemoglobin value. Of the 29 patients with partial villous atrophy, three had low folate 

levels, seven had low hemoglobin, one had low vitamin B12, one had low protein, five had low 

vitamin A, five were low in ferritin, five had low iron, and ten patients had low zinc levels. Only 

one patient (out of three) who had normal villi also had low hemoglobin levels. 

In the study from Italy, by Bardella et al.,361 26 adults (five male and 21 female, mean age 

42.2, range 22-81) with malabsorption and biopsy-confirmed CD were enrolled. They were 

followed for a mean of 55.4 months (range 13-137 months) on a GFD. Eight patients remained 

in good health with normal blood tests. The remaining 18 patients had abnormalities despite 
108

GFD. No correlation was noted with severity of symptoms of malabsorption and biochemical 

abnormalities. Iron deficiency was found in five patients. Abnormal calcium, phosphorus, 

alkaline phosphatase and/or bone density was found in seven patients. Macrocytic anemia was 

found in four patients. Clinical symptoms were seen in 11 patients. No correlations between 

abnormal values and grade of histology on biopsy were found. 

Compliance. Three studies were identified that looked at compliance, 363-365. All studies were 

conducted in Italy and assessed an adolescent population.

In the first study of adolescents that looked at dietary compliance, Fabiani et al.363 evaluated 

28 biopsy-proven CD patients (17 females and 11 males). These 28 adolescents were selected 

from a group of 6,315 students, age 11 to 14 years, who had previously been screened for CD. 

All were advised to start a GFD. Twenty-three of the 28 patients participated in this study. The 

mean follow-up duration was 23 ± 7 months (range 9-3 months). Fifty-two percent (12/23) were 

on a strict GFD and 47% (11/23) partially adhered to the diet. Improvement in most patients was 

seen after starting a GFD. Weight gain was reported in 12 patients (52%)—11 had increased 

height velocity and appetite, eight had disappearance of symptoms of abdominal pain, six had 

resolution of diarrhea, five had disappearance of anemia and three had disappearance of recurrent 

aphthous stomatitis. Three patients did not demonstrate any change. 

The second study, also by Fabiani,364 was a 5-year case-control study that enrolled two 

groups of patients. The first group (group A) included subjects between the ages of 11 and 14 

years, who were diagnosed as a result of a mass screening program. The second group (group B) 

were patients diagnosed due to typical symptoms of CD between 1985 to 1986. All patients had 

biopsy-proven CD according to ESPGAN criteria. All patients were followed for 5 years and 

advised to start a GFD. Twenty-seven patients were in group A and 22 agreed to participate; 24 

patients were in group B and 22 agreed to participate. There were no differences between the 

patients in group A and group B in terms of BMI and height SDS. No difference was found 

between the two groups in terms of symptoms. Adherence to the treatment was significantly 

lower in patients from group A compared with group B. There were a significantly greater 

proportion of patients in group B that demonstrated strict adherence to a GFD (15/22; 68%) 

compared with patients in group A (5/22; 23%). 

The third study to look at compliance looked at 306 teenage patients with CD (mean age 15.9 

yr; range 10-27 yr) recruited consecutively from a CD clinic.365 Of the patients, 186(60%) were 

female and 120 were male. Diagnosis of CD was biopsy confirmed. Recall questionnaire was 

used to evaluate diet and compliance. Compliance was recorded in three categories: 1) strict 

gluten diet (n=223 [73%]); 2) occasional relapse (n=46) 15%; and, 3) gluten-containing diet 

(n=37) 12%. Eighty percent of the female patients, compared with 64.2% of the male patients, 

adhered to a strict diet (p=0.012). Compliance also varied with age, with older age associated 

with less compliance (p=0.05). Growth status was grouped according to compliance to a GFD—

the mean standardized height, the relative weight for age, and the relative weight for height, did 

not differ significantly between the compliance groups. Symptom scores were relatively good 

among all groups. No statistically significant differences were noted. School performance was 

not significantly different between good versus poor compliers. 
109

Costs. Five studies included an assessment of costs involved in different screening 

strategies.360,366,379,380,382

Harewood et al.366 performed a decision analysis to compare costs of serological testing 

versus small bowel biopsy (AGA vs EMA versus small bowel biopsy) for diagnosis of CD. The 

analytic technique used was a cost minimization and the viewpoint was third-party payer. A 

sensitivity analysis was conducted. The authors demonstrated that initial screening with EMA is 

the least costly strategy for diagnosis in a low to medium risk population. 

Gomez et al.382 evaluated a screening algorithm for CD in 1,000 consecutive subjects who 

were screened while attending a central laboratory. Gomez and colleagues compared two 

screening protocols: (1) three-level screen–IgG/IgA-AGA antibodies at the first level, then IgAEMA, and finally intestinal biopsy versus screening, and (2) tTG-GP and total IgA as first-line 

screen, and EMA for positive patients followed by intestinal biopsy. The analytic framework 

and viewpoint were not stated. In this study, a comparative cost analysis was performed. They 

found that the combination of a highly-sensitive test at the first step with a highly-specific test at 

the second step appears to be a more reliable screening mechanism. 

Zaccari et al.,379 in an Italian model, proposed a four-level screening protocol for children at 

least 15 months of age, including: 1) AGA, 2) EMA, 3) intestinal permeability, and 4) small 

bowel biopsy. In this study, they evaluated only the total costs at each level of screening. 

Atkinson et al.,360 in a Canadian study, evaluated the operating costs of EMA in the diagnosis 

of CD using a cost-minimization model with a decision analytic approach with three strategies. 

The analytic perspective used was the societal viewpoint, and costs were discounted at 5% per 

annum. A one-way sensitivity analysis of all probability and cost estimates was performed. 

Incremental costs of the GFD were estimated from a survey of 25 patients which resulted in a 

lifetime incremental cost of $44,000. If a small bowel biopsy was performed initially, the cost 

was $997; for EMA followed by small bowel biopsy, the cost was $866. The total cost was 

$3,714, which resulted in an incremental cost savings of $2,177 if small bowel biopsy had been 

performed first. In the sensitivity analysis, the specificity of EMA would have to be greater than 

95% to make EMA least expensive. 

Part B 

There were 27 studies that examined the response of various endpoints to a GFD. 

One Italian study,354 used a case-control design to evaluate the effect of a GFD on thyroid 

status. The study by Annibale et al.,358 evaluated the impact of a GFD on anemia and iron 

deficiency in newly diagnosed CD cases identified from screening of adults with IDA in Italy. 

In a case-control study, Ciacci et al.351 investigated the impact of a GFD on pregnancy outcomes, 

and Addolorato et al.374 evaluated the impact of a GFD on anxiety and depression in a population 

of CD patients in Italy. Mortality was evaluated in seven cohort studies.331,335,336,343,362,367,368 

Seventeen studies assessed either change in BMD or fracture as an endpoint in individuals with 

CD. 

Thyroid study. In the Italian study,354 241 consecutive adults with biopsy-confirmed CD were 

enrolled between Jan 1996 and July 1998 (177 women and 64 men). Forty percent of patients 

had classical symptoms, 44% had atypical symptoms and 16% had silent CD. Two hundred and 

twelve patients, matched for age, sex and ethnic origin, were used as controls. All newlydiagnosed CD patients were started on a GFD and patients with hypo- or hyperthyroidism were 
110

started on appropriate medical therapy. Thyroid dysfunction was found in 73 (61 women and 12 

men) of 241 patients with CD, and in 24 (19 women and 5 men) of the 212 patients in the control 

group (p<0.0005). The difference was statistically significant for women when divided by sex 

(p<0.0005). Hypothyroidism was diagnosed in 31 patients (12.9%) and nine controls (4.2%) 

(p<0.003); it was subclinical in 29 CD patients and eight controls and overt in the remainding 

patients. The difference was only significant for women (p=0.0045). Twenty-one patients and 

four controls had non-autoimmune hypothyroidism. Ten patients and five controls had 

autoimmune hypothyroidism. Hyperthyroidism was diagnosed in three patients and seven 

controls; it was subclinical in two patients and five controls. Autoimmune thyroid disease with 

euthyroidism was present in 39 patients and eight controls. The difference was only statistically 

significant in women (p<0.0005). At diagnosis, the BMI, hemoglobin, iron, and albumin levels 

were similar between patients with thyroid disease and those without. After 1 year of a GFD, 

128 patients were reassessed. Ninety-one patients had normal thyroid function, whereas, 37 had 

some impairment. Compliance to diet was not different between the two groups. Subclinical 

hypothothyroidism improved in 10/14 patients with non-autoimmune hypothyroidism. Three of 

five patients with autoimmune hypothyroidism shifted to autoimmune thyroid disease with 

euthyroidism; four out of five patients with no improvement in thyroid function had poor 

compliance with diet. Significant improvement in nutritional indices was also seen with BMI in 

females, HBG in both sexes, and serum albumin and serum iron in both sexes. 

Iron deficiency. In this Italian prospective study,358 190 consecutive patients (160 women and 

30 men) who were referred to the GI department from the hematology for IDA between Jan 1994 

to May 1997, were examined. Twenty-six patients were diagnosed with CD (24 women and 2 

men); average age 31.3 years (range 20 -72). Seventy-seven percent of patients had total villous 

atrophy and 23% had subtotal atrophy; repeat endoscopy with biopsy specimens were taken after 

6 months. After GFD, 20 patients (18 women and 2 men) were followed for 24 months. After 6 

months, 14 of the 18 female patients (77%) recovered from IDA. Only 5/18 reversed from iron 

deficiency as defined by normal ferritin levels. At 12 months, 17/18 recovered from IDA. Nine 

patients reversed from iron deficiency. After 24 months, the same patient still did not reverse 

from IDA. Ten patients (55%) reversed their iron deficiency. Of the two males, at 6 months of a 

GFD, only one recovered from anemia but not from iron deficiency (low ferritin). At 12 months, 

both patients reversed their anemia and iron deficiency. At 24 months, further increases in 

ferritin were observed. In a subgroup of patients that had repeat small bowel biopsies at 6 and 12 

months, there was a significant inverse correlation between increases in Hb concentrations and 

decreases in histological scores of duodenitis. This study demonstrated that recovery from IDA 

occurs within the first 6 to 12 months, but reversal from iron deficiency occurs in 50% of cases 

(predominantly premenopausal women). Long-term follow-up of ferritin results and small bowel 

biopsies in subjects with CD would be helpful to determine if iron deficiency resolves 

completely. 

Pregnancy outcomes. In this case-control study from Italy by Ciacci et al.,351 297 women with 

CD were enrolled. Three types of analyses were used. Analysis A was a case-control study 

between untreated women (n=94; at least one pregnancy when symptoms of CD were present 

and lead to eventual diagnosis) and treated CD women (n=31; at least one pregnancy after 1 year 

of a GFD). At baseline, weight, height and body mass index were the similar between the two 

groups. However, the treated group was significantly younger than the untreated group (37.3 ± 
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12 yrs vs 22.4 ± 1.6 yrs, p<0.01), which may have biased the results. The number of pregnancies 

per woman was also lower for the treated group (2.72 ± 0.16 vs 1.6 ± 0.11, p<0.0001). The 

number of abortions per woman (0.489 ± 0.085 vs 0.032 ± 0.032, p<0.0001), as well as the 

abortion to pregnancy ratio, was much lower for the treated group compared with the untreated 

group(0.153 ± 0.027 vs 0.024 ± 0.024, p<0.005). Subgroup analysis taking into account the age 

at diagnosis, demonstrated that for those women diagnosed at age 30 years or less (n=27), the 

number of abortions per woman was 0.556 ± 0.156 and the abortion to pregnancy ratio was 

0.234 ± 0.066. The prevalence of abortion in pregnancies was 17.8% in untreated CD patients, 

compared with 2.4% in treated patients (p<0.001). The RR of abortion was 8.9. Low-birthweight baby to pregnancy ratio (0.126 ± 0.037 vs 0.024 ± 0.024, p<0.03) was significantly lower 

in the treated group. The duration of breast feeding was significantly longer for the treated group 

(2.77 ± 0.52 vs 7.03 ± 1.17, p<0.0003). The threatened abortion to pregnancy ratio and 

premature delivery to pregnancy ratio was not significantly different from untreated to treated 

CD women. For the subgroup of women <30 years (n=27), birth weight, baby to pregnancy 

ratio, and duration of breast feeding, did not alter the statistical significance. The prevalence of 

low birth weight babies in nonabortive pregnancies was 12.7% for untreated patients and 2.4% 

for treated patients (p<0.05). The RR of low birth weight babies was 5.84 times greater in the 

untreated group compared with the treated group. 

In Analysis B, women with CD were all untreated and then analyzed depending on whether 

diarrhea was present or not. The authors found that the abortion to pregnancy ratio and the 

premature delivery ratio were found to be lower in CD women without diarrhea compared with 

those women with diarrhea, although the difference was not statistically significant. 

In Analysis C, the effect of a GFD on pregnancy outcome was analyzed. The study 

examined 12 women with CD after 1 year of a GFD (own control); there was at least one 

pregnancy without treatment. All outcomes were better in the group of women on the GFD: 

number of pregnancies 2.5 ± 1.24 versus 1.08 ± 0.29 (p<0.003); number of abortions per woman 

1.08 ± 1.16 versus 0.08 ± 0.28 (p<0.02); abortion to pregnancy ratio 0.405 ± 0.140 versus 0.074 

± 0.280, p<0.02); and, low birth weight baby to pregnancy ratio 0.292 ± 0.129 versus 0 (p=0.05). 

The threatened abortion to pregnancy ratio, premature delivery to pregnancy ratio, and duration 

of breast feeding, were not significantly different between the two groups. The prevalence of 

abortion was 43.3% for the untreated group, compared with 7.7% for the treated group of CD 

women (p<0.01). The RR of abortion was 9.18. There were no low birthweight babies born to 

women in the GFD group, whereas, the prevalence of low weight babies was 29.4% in the 

untreated group (RR=11). 

One of the limitations of the Ciacci et al. study was that it did not include an external control 

group or control for confounders. A historical cohort population-based study of the Danish 

Medical Birth Registry by Norgard, 1999393 evaluated birth outcomes in women with CD. This 

study included 211 newborns born to 127 mothers with CD from 1977-1992 and compared them 

with 1,260 control deliveries. Women with CD were identified from hospital discharge 

diagnoses. Discharge records were linked to Medical Birth Registry which contained 

information on relevant outcomes. Outcomes included birthweight, low birthweight (<2500 g) 

pre-term birth (<37 wk), intrauterine growth retardation (birthweight <2500 g and gestational age 

≥37 wk of pregnancy), and perinatal mortality. Potential confounders including maternal age, 

infant’s gender, parity, and gestational age, were adjusted for in the analyses. The investigators 

could not control for other confounders such as smoking. Another potential limitation is that the 

date of diagnosis of CD was the initial time of discharge from hospital with CD. It is possible 
112

that women may have been initially diagnosed in the ambulatory care clinic. Details about the 

clinical presentation of the women with CD and biopsy findings were not available. The mean 

age at time of delivery was 27.5 years for women with CD and 26.3 years for control women. 

Norgard et al.,393 found that before women were hospitalized for CD, they were at an 

increased risk of low birthweight babies (adjusted OR=2.6 [95% CI: 1.3-5.5]), and intrauterine 

growth retardation (12.3% vs 4.8% of controls; adjusted OR=3.4 [95% CI: 1.6-7.2]). After 

women with CD were first hospitalized, there was no increased risk of low birthweight babies 

(6% post diagnosis) or intrauterine growth retardation, when compared with controls. The 

results of this study have implications for women with undiagnosed (atypical or silent) CD. 

Anxiety and depression. The study from Italy by Addolorato et al.,374 enrolled 43 newlydiagnosed adult patients affected with classic CD, selected from 234 adult CD patients from an 

outpatient clinic between June 1995 and Oct 1998. No psychiatric disorders other than anxiety 

and/or depression were allowed. The diagnosis of CD was based on positive serology and 

biopsy. Of the 43 enrolled patients, eight dropped-out leaving 35 (14 males and 21 females, 

mean age 29.8 ± 7.4 yr) patients for analysis. After a period of 12 months of GFD treatment, the 

patients were analyzed. The adherence to a GFD was evaluated based on patient self-report and 

family member interview. A group of 59 healthy asymptomatic controls (27 males and 32 

females, age 31.7 ± 6.9 yr) were matched for gender, age, residence, employment, 

socioeconomic and marital status. The psychological assessment was performed using a selfrating psychometric test for anxiety (State and Trait Anxiety Inventory test) and another for 

depression (SDS Zung self rating depression scale). Both tests were administered before and 

after GFD. Of the 59 controls, 23.7% showed high levels of anxiety, 15.2% showed trait 

anxiety, and 9.5% were positive for depression. Of the 35 untreated CD patients, 71.4% had 

high levels of anxiety, 25.7% showed trait anxiety and 57.1% were positive for depression. 

After 1-year of GFD, 25.7% had high levels of anxiety, 17.1% had trait anxiety, and 45.7% were 

still depressed. The levels of high anxiety (71.4% vs 23.7%, p<0.0001) and levels for depression 

(57.1% vs 9.6%, p<0.0001) were significantly higher in the CD patients than in the controls. 

The proportion of untreated CD patients with trait anxiety did not differ from controls. After a 1-

year GFD, a significant decrease in high-state anxiety (71.4% vs 25.7%, p<0.001) was found 

when treated patients were compared with the untreated group. No significant differences were 

found for trait anxiety or depression. 

Fractures. We identified six controlled studies that addressed the outcome of fractures in a CD 

population385,388-390,394and two reviews.381,391 The study by Cook et al.395 was not included since 

it did not have a comparison or control group. The study characteristics and methods for each 

study are summarized in Evidence Tables 12 (Appendix H).

All six studies were retrospective and there were two cohort studies385,388 . Two studies 

included individuals that had biopsy-confirmed CD. All studies included controls as a 

comparator, and in three studies the controls appeared to be population-based.385,388,394 With 

regards to the ascertainment of the outcome of fracture, data was obtained from self-report data 

from administrative databases,394 patient register,385,388,394 or from interview/case reports.389,390,392 

Only two studies mentioned inclusion of asymptomatic subjects.389,392 Bone histology was 

mentioned as an outcome in a subset of patients in one study.390 
113

The case-control study by Fickling and colleagues,390 compared individuals with CD 

attending a GI outpatient department and/or members of local celiac societies. The authors 

found a higher prevalence of past history of fractures in the CD patients (21%[16/765]) 

compared with a control group (3% [2/75]; RR 7.0). There was no difference in BMD T-score 

results between those with and without a history fracture, although those patients with a fracture 

history were older (p<0.02). Limitations of this study include the fact that they did not identify 

whether CD was biopsy-confirmed, and a potential for selection bias. 

Thomason et al.,373 in a case-control study, used self-report data for 244 patients with biopsyproven CD and found that fractures were not significantly increased in those with CD compared 

with controls (OR 1.05, 95% CI: 0.68-1.02), although there did seem to be a trend to increased 

wrist fractures (OR 1.21, 95% CI: 0.66-2.25). The mean age of these patients was older (60.2) 

and the mean BMI was higher (23.9) than that reported in other studies. However, this study 

may have been limited by potentially not having adequate power to detect fractures. In addition, 

all the fracture data was self-reported. 

Vasquez et al.,389 in a retrospective case-control study, found that 25% (41/165) of CD 

patients had one to four fractures, compared with 8% in age- and sex-matched controls. The 

majority of fractures occurred prior to diagnosis of CD and the most common fracture site was 

the wrist (OR 3.5, 95% CI: 1.8-7.2). Potential sources of bias for this study include the fact that 

the cases were from a malabsorption clinic and may therefore represent patients with more 

severe disease (mean BMI=21.4). The OR for vertebral fractures was 2.8 (95% CI: 0.7-1.15), 

although there was incomplete ascertainment of X-rays, since not all X-rays were of adequate 

quality. This was the only study to include an assessment of the proportion of patients on a strict 

versus a reduced GFD. 

Two studies were population-based.385,388 Vestergaard et al.,388 evaluated all individuals with 

CD in Denmark captured from hospital discharge data, and did not find an increase in fractures 

requiring hospitalization in patients with CD (n=1,021; 7,774 patient years) relative to controls 

(n=23; 316 patient years) with an independent independent relative risk (IRR) at pre-diagnosis of 

0.70 (95% CI: 0.45-1.09) for all fractures. For spine, the IRR pre-diagnosis was 2.14 (95% CI: 

0.70-6.57) and 1.07 (95% CI: 0.39-2.95) for rib and pelvis. There are significant limitations to 

this study since the diagnosis of fractures was hospital-based and therefore, fractures that did not 

require hospitalization would be missed and could lead to under-reporting. In addition, the 

diagnosis of CD was only validated in a sample of nine cases (with a validity of 78%), and all 

cases of CD had to be hospitalized to be included. 

West et al.,385 in the largest analysis of fractures in CD patients identified from the UK 

GPRD primary care database, found an increase in fractures in CD patients relative to controls. 

The mean age at diagnosis was 43.5 years, and the ascertainment of fractures was from an 

administrative database. For any fracture, the hazard ratio was 1.3 (95% CI: 1.16-1.46; 

137.9/10,000 patient years vs 105.9/10,000 patient years in controls]). The hazard ratio for hip 

fracture was 1.9 (95% CI: 1.2-3.02) and the hazard ratio for wrist fracture was 1.77 (95% 1.35-

2.34). The absolute difference in the overall fracture rate was 3.2/1,000 person years and 

0.97/1,000 for hip fractures in those older than age 45. In contrast to earlier studies, the authors 

did not find a difference in the risk of fracture after CD diagnosis compared with before 

diagnosis. 

A recent case-control cross-sectional study by Moreno et al.,392 compared fractures in 148 

CD patients (53% classically symptomatic, 36% subclinical CD, and 11% silent CD-detected by 

screening} to 296 controls (functional GI disorders). The fracture data was self-report obtained 
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by interview/and pre-designed questionnaire. Moreno et al. found an increased number of 

fractures in the peripheral skeleton for classically symptomatic subjects compared with controls, 

but did not find an increased number of fractures in the subjects with subclinical or silent CD. 

BMD. BMD is a surrogate outcome for fracture, and it is easier to evaluate in short-term studies. 

Previous studies of osteoporosis therapies in postmenopausal osteoporosis have shown that there 

may not, however, be a direct correlation between fracture reduction and increases in BMD. 

Osteoporosis/osteopenia may be a sign of subclinical CD and persisting osteopenia/osteoporosis 

in a patient with known CD may be a sign that the mucosa has not normalized. 

BMD is an areal two-dimensional measure of bone mass and does not give a true volumetric 

measure and, therefore, may not be an accurate reflection of bone mass in children. 

We found 11 articles that addressed the outcome of BMD/BMC in newly diagnosed subjects 

with CD.348,352,353,355,356,375-378,386,387 The study characteristics are summarized in the Evidence 

Tables (see Appendix H). 

The majority of these studies assessed BMD at baseline and the percentage change after a 

variable follow-up period (1 to 5 years in duration). Two studies evaluated the BMD of children 

with CD,352,377 one study evaluated a mixed population,348 and the remaining studies evaluated 

adults. All studies included individuals with biopsy-proven CD and in most of the studies BMD 

was compared with a control population. Only two studies had patients with CD act as their own 

controls.353,376 The female to male prevalence ratio in CD is 2:1, and in these studies the 

proportion of females varied from 50% to 80%. 

Five studies included assessments of dietary compliance to a GFD and three studies included 

data on whether subjects were on co-interventions (e.g., vitamin D or calcium), which may have 

impacted the BMD results. Only two studies356,376 looked at the potential relationship between 

the change in histological grade on small bowel biopsy and change in BMD. 

Prevalence of osteoporosis/osteopenia. The studies consistently found that BMD results were 

lower in untreated subjects with CD compared with controls. Regarding the prevalence of 

osteopenia/osteoporosis in newly diagnosed patients with CD, the estimates varied. SatgenaGuidetta et al.353 noted a mean Z-score of -1.5 at lumbar spine, and -1.8 at the femoral neck, with 

34% of subjects having normal BMD, 40% having osteopenia and 26% osteoporosis. 

Valdimarsson et al.355 found the prevalence of severe osteopenia, as defined by a Z-score less 

thatn -2, to be 15% at the spine, 9% at the femoral neck, and 22% at the forearm. The prevalence 

of mild osteopenia (defined as -2 ≤ Z < -1) was 23% at the lumbar spine and 24% at the forearm. 

There was not any difference in lumber spine BMD between those patients who presented with 

malabsorption, compared with those patients without malabsorption. Valdimarsson et al., found 

that 27% of subjects had secondary hyperparathyroidism. After 1 year on a GFD, the prevalence 

of those with severe osteopenia decreased from 23% to 14%. 

In a recent review the authors pooled prevalence results and found that patients with 

untreated CD had a mean Z-score of -1.42, and a hip Z-score of -1.14.381

Valdimarsson et al.,356 in a prospective study of 105 newly-diagnosed CD patients, 

performed follow-up small bowel biopsies. Of the 105 subjects, 28 had secondary 

hyperparathyroidism. They found a greater reduction in BMD in individuals who had secondary 

hyperparathyroidism (PTH>65). In this group, the BMD increased significantly, but did not 

completely normalize after 3 years of a GFD. In contrast, in those with normal PTH at 

diagnosis, the baseline BMD was not as low and there was a 2.5% increase after 1 year with the 
115

BMD normalizing after 2 years of a GFD. Valdimarsson also noted that 22 patients with stage 

III-IV had lower median Z-scores than 76 patients with mucosal changes grade I-II. In this 

study, compliance with the GFD was 100% in those with high PTH, and lower at 87% in those 

with normal PTH levels. 

Kemppainen et al.,376 in a 5-year cohort study of 28 patients in which the cases served as own 

controls, found that BMD increased or remained stable in 69% of patients at the lumbar spine 

and in 67% of patients at the femoral neck. In this study, the authors did not notice an effect of 

the grade of villous atrophy on the mean BMD values or percentage change in BMD. They also 

did not observe any correlation between adherence to the GFD and the change in BMD. 

Bai,375 in a small cohort of 45 (25 completed) newly-diagnosed CD patients, assessed 

compliance with the GFD and found that 84% of patients increased their lumbar spine BMD 

(mean increase of 12%) and total body BMD (mean increase of 7.3%), compared with 151 

control subjects. The greatest increase in BMD was noted within the first year. Bai375

documented prior fractures in two patients, but did not report any fractures during the 4-year 

follow-up period. 

Sategna-Guidetti et al.,353 in a longitudinal study of 86 CD patients, noted a similar 

proportion of patients (83.7%) increased their spine BMD after 1 year, with an increase of 5.3% 

in LS BMD after 1 year (change in Z-score of 0.5 at the spine). 

Ciacci et al.,386 in a retrospective cohort of 41 consecutively diagnosed patients with CD, 

noted a significant increase in BMD (14% lumbar spine, and 10.4% femoral neck), after 1 year 

on a GFD. The authors also found that pretreatment BMD predicted response to treatment. 

Mustalahati et al.,378 noted a significant increase in lumber spine and femoral neck BMD 

with treatment after 1 year compared with controls, and noted that the BMD was lower in 

symptom-free patients (n=15), suggesting patients with silent CD may have mucosal lesions for 

longer periods of time. 

Bardella,348 in a case-control study of 71 CD patients (43 who had started a GFD in 

childhood and 28 who were diagnosed as adults and were on a GFD and in remission), found that 

the BMD of the adult CD patients was significantly lower than the control value (0.9 g/cm2

 vs 

1.1 g/cm2

, p<0.01). 

McFarlane et al.,387in a case control study of 21 biopsy-confirmed subjects with CD, 

documented that the baseline lumbar spine BMD was 85% of that seen in controls, and the 

increase in lumbar spine BMD over the first year was 6.6% (95% CI: 3.1-10.1) and 5.5% in the 

femoral neck. 

Children/adolescents. Mora et al.,377 in a study of 19 patients (211 controls), noted a lower 

BMD in CD patients versus controls at baseline, and an increase in total body BMD (using 

DXA) during the first year when compared with controls (15.2%). 

Rea et al.,352 noted an improvement in forearm Z-score after 1 year on a GFD in 23 newly 

diagnosed children with CD. 

Mortality. There were seven cohort studies that addressed mortality data in CD. Two were 

Italian studies, 335,362 one was from Denmark,343 one from Sweden,331 and three were from the 

UK.336,367,368 All seven were cohort studies. 

Corraro et al.,362 identified 1,072 biopsy-proven CD subjects from the records of 11 GI units 

between Jan 1962 to Dec 1994. The inclusion criteria were complete records and reliable 
116

diagnosis of CD. The ratio of men to women was 1 to 3, the mean age at diagnosis was 35.7 

years, mean follow-up was 6.0 years and median diagnostic delay was 17 months. Forty-five 

percent of the population had mild (39%) or asymptomatic disease, and 50 patients were lost to 

follow-up. Data were collected over accumulated 6,444 patient years of follow-up, with a mean 

follow-up of 6 years. Adherence to a GFD was assessed. Fifty-three CD patients died compared 

with 25.9 expected deaths. An increase in mortality was noted in the entire cohort population 

(SMR 2.0 [95% CI: 1.5-2.7]). The overall SMR did not differ by sex, age of diagnosis, or year 

of presentation. Diagnostic delay by more than 1 year significantly increased the SMR (2.6 

[95% CI: 1.6-4.1]). There was significant mortality among patients presenting with 

malabsorption (SMR 2.5 [95% CI: 1.8-3.4]). No excess mortality was seen with patients with 

mild or asymptomatic CD. Significant mortality was also seen when patients did not adhere to a 

GFD on clinical records (SMR 10.7 [95% CI: 6.0-17.1]) and on patient interview (SMR 6.1 

[95% CI: 4.2-8.6]). The causes of death showed an excess of death from malignancy (24 

observed cases, SMR 2.6 [95% CI: 1.7-3.9]) and diseases of the respiratory (SMR 3.6 [95% CI: 

1.1-8.4]) and digestive tracts (SMR 6.1 [95% CI: 3.0-10.9]). NHL was seen in two-thirds of the 

malignant cases (n=16). The other malignancies included gastric (n=2), small intestinal (n=1), 

liver (n=2), pancreatic (n=1), pleura (n=1), and leukemia (n=1). (Table 45) 

Cottone et al.335 evaluated mortality in a prospective cohort study of 228 biopsy-proven CD 

subjects in Sicily. Mortality was ascertained by reviewing hospital medical records and 

pathology specimens. Records were incomplete for 5% of patients. The mean age at diagnosis 

was 34.7 years and 100% of patients were on a GFD. Seventy-six percent were females. The 

clinical presentation was anemia in 60% of cases, malabsorption in 20% of cases, and 

asymptomatic in another 10% of cases. The mean follow-up was 73 months. Twelve deaths 

were observed, with 3.12 deaths expected and the SMR from all causes was 3.8 (95% CI: 1.9-

6.7). The mortality rate was increased within the initial 4 years from diagnosis, giving an SMR 

of 5.8 (95% CI: 2.5-11.5). 

Nielsen et al.343 from Denmark, conducted a retrospective cohort study of 98 CD patients 

between 1964-1982. Sixty-one percent of patients were females and the median age at diagnosis 

was 41 years (range 2 to 74 yrs). Twenty-four percent of patients had unclassified CD and were 

treated with prednisone, since they did not respond to a GFD and had probable refractory CD. 

Twenty-three deaths occurred during the study (four due to malignancy). Nielsen et al. found 

that the 5-year survival rate was 88%, the 10-year survival rate 68.5%, and that mortality 

exceeded that of age- and sex-matched controls in the general population by a factor of 3.4 

(p<0.025). There was no difference in mortality between males and females (2.7 and 2.3, 

respectively). Subjects who responded to a GFD had an extra mortality factor of 2.2 (p<0.025), 

and those who did not respond to a GFD had an extra mortality factor of 5.8 (p<0.005). Causes 

of death were poorly documented. 

Peters et al.,331 in a retrospective cohort study, compared 10,032 symptomatic subjects with 

CD who had been discharged at least once from hospital, to controls who were age/sex-matched 

for the calendar period cancer incidence rate. Fifty-nine percent were females. Mean follow-up 

was 9.8 years. Mortality was ascertained from a national death register. There were 828 deaths, 

with 419.3 expected, resulting in a SMR of 2 (95% CI: 1.8-2.1). Mortality risk decreased 

slightly with increasing number of years of follow-up (p for trend, 0.004). Mortality risks were 

increased for patients with NHL, cancer of the small intestine, autoimmune diseases (RA), 

allergic disorders, inflammatory bowel disorders, diabetes, and tuberculosis. 
117

The first UK study was conducted in Birmingham, by Holmes et al.367 Series I included 202 

patients with idiopathic steatorrhea or CD, followed from 1965-1975. Ten patients had a 

positive biopsy for CD. Eleven patients could not be traced. In the 10-year period, 20 deaths 

were seen, with ten due to malignancy. Series II (1989) had 210 patients (94 males and 116 

females) with biopsy-proven CD. Seventy patients were on a normal diet and 134 were on a 

GFD for more than 12 months at the end of the survey. Forty-three patients had died from all 

causes (expected was 20.82 deaths, p<0.001); 21 deaths were due to malignancy—13 reticulum 

cell sarcomas, six GI tract cancers and two other malignancies. Of the 21, 13 had a GFD for a 

mean of 41 months. Deaths from all malignancies, irrespective of diet, were statistically 

increased as a whole (expected 5.048 vs observed 21, p<0.001) and divided by sex (men 

expected 2.878 vs observed 12, p<0.001 and women expected 2.170 vs observed 9, p<0.001). 

Patients taking a normal diet were at increased risk of developing a malignant tumor (p<0.05). 

Clinical response did not predict the risk of developing malignancy. 

Johnston et al.368 examined CD in subjects from Northern Ireland using the Belfast MONICA 

project. MONICA I was the first survey, and began in Oct 1983 with 1,204 subjects. Of the 

subjects, 102 (52 males and 50 females, mean age 58.1 years) had positive serology, 72 

consented to follow-up (34 males and 38 females) for 11.6 years (range 11.3-11.9 years), and 20 

of the 72 gave consent to biopsy. Three subjects had villous atrophy. Thirteen subjects in 

MONICA I (seven males and six females) died (mean age at death 67.3 yrs; range 56-75 yr). 

Cause of death was obtained from death certificates from the General Register Office or General 

Practitioner records. Four patients died with malignant disease–pancreas, stomach, bile duct 

lymphoma and metastatic melanoma. None of the patients had CD, but all had positive serology. 

The number of cancer-related deaths and all cause mortality in the MONICA I follow-up study 

did not show an excess number of deaths compared with the general population of Northern 

Ireland. 

Logan et al.336 followed a prospective cohort of 653 patients with CD in Edinburgh between 

1979 and 1981. All patients had biopsy-proven CD and mortality was ascertained from death 

certificates. Sixty percent of the patients were females and the mean follow-up was 13.5 years. 

Six percent of subjects were lost to follow-up. Clinical presentation was not reported. The 

subjects with CD were compared with age/sex-matched controls. There were 115 deaths from 

all causes; the expected number was 61.8 for a SMR of 1.9 (95% CI: 1.5-2.2). The increased 

mortality was greatest during the initial year after diagnosis and declined over time. The 

mortality rate for those diagnosed during childhood was similar to that of the general population. 

Quality Assessment 

The majority of studies included in this objective were single group “before–after” studies, 

although some studies also included a comparative healthy control group. We could not identify 

any quality instruments for this type of study design and in general, this type of study is 

considered weak, particularly in the absence of a control group. Overall, however, the strength 

of the evidence for this objective was fair to good (Appendix J, Tables 6-8). 
118

Celiac 5: Promoting or Monitoring Adherence to a GFD 

Out of 502 citations identified by the search strategy for the Celiac 5 objective, 189 met level 

1 screening criteria (Appendix F). Of these, 86 met level 2 screening criteria and 20 studies met 

level 3 inclusion criteria.396-415

Of the included studies, eight studies offered correlation between serology and mucosal 

histological grade,397,398,403,404,407,409,413,415 and eight reported on serology only.396,399-402,408,410,412 

Four studies focused on histologic changes without serology.405,406,411,414 Nine of the included 

studies were conducted in an adult population, six in a pediatric or adolescent population, and 

five studies in mixed populations consisting of adults and children. 

Included articles were divided by study population (adult/children/mixed), antibody type 

(IgG or IgA), and by antibody methodology (e.g., ME or HU). 

None of the identified studies directly assessed the efficacy of a specific intervention on the 

promotion of adherence to a GFD. Six studies hint at interventions that could potentially be 

effective.416-421 Four of these studies were applicable to a pediatric population and two studies 

were applicable to adults. 

Monitoring Adherence to a GFD 

Biopsy. To evaluate serology in assessing adherence, some information regarding mucosal 

recovery on GFD must first be known. Although mucosal recovery is generally assumed to 

occur within 6 to 12 months after starting GFD, there is evidence that recovery may be slower 

and more incomplete than previously assumed. 

In a mixed population, Wahab et al.405 followed the histologic profiles of 158 patients after 

institution of a GFD. Histological recovery, defined as the absence of villous atrophy (Marsh 0-

II), was seen in only 65% of the patients within 2 years. Within 5 years, 85.3% of patients 

showed recovery, and an incremental improvement to 89.9% occurred after 5 years. Of the 

10.1% of patients not achieving histological recovery during the follow-up period, 11 had 

symptoms of CD and were therefore, considered to have refractory CD (7% of all patients). 

Patients with Marsh IIIb and IIIc histology initially had lower rates of recovery, compared with 

those with Marsh IIIa histology. In a subgroup analysis of 25 children, recovery seemed to occur 

faster—96% showed histological recovery within 2 years (p<0.01 vs adults) and 100% recovered 

in long-term follow-up. It is important to point out that the validity defining a Marsh II lesion as 

histological recovery is uncertain. If these patients were not included, rates of histological 

recovery would be even slower. Nonetheless, clinical improvement was seen despite the slow 

histological improvement. 

An early study by McNicholl et al.,406 is consistent with the finding of more complete 

mucosal recovery in children. Thirty-six children on a GFD for a mean of 5.8 years underwent 

duodenal biopsy. Mucosal morphology was normal in 16 (44%) patients, while the remainder of 

the patients had minimal changes. Villous atrophy was not seen. IEL counts were normal in 30 

(83%) patients. A subsequent gluten-challenge confirmed the diagnosis in all 36 children. 

Lee et al.,411 in a retrospective cohort of 39 adult patients, also found incomplete mucosal 

recovery. After a mean duration of a GFD for 8.5 years (range 1 to 14 years), histology was 

normal in only 21% of patients, and partial and total villous atrophy was seen in 69% and 10% of 

patients, respectively. These patients were felt not to have refractory CD since they had a good 
119

clinical response to the GFD. Also of concern were the results of serologic testing at the time of 

follow-up biopsy in 31 patients. Despite the relatively high number of patients with some degree 

of villous atrophy, IgG-AGA, IgA-AGA and IgA-EMA were negative in the majority of patients. 

In fact, 77% of the 31 patients having serologic tests were negative for all the listed serological 

tests. The exact number of these 31 patients who had some degree of villous atrophy was not 

reported, but would be expected to be similar to the overall numbers listed above. 

Selby et al.414 investigated whether the failure of mucosal recovery was due to 

noncompliance with a GFD. Eighty-nine adult patients with CD on a GFD for a mean in excess 

of 8 years underwent dietary assessment by a dietician, questionnaire and food diary. They were 

then classified as either Codex GFD, which allows up to 0.03% of protein from a gluten source, 

or no-detectable gluten GFD (NDG-GFD). Villous atrophy persisted at high rates in both 

groups, with 46% of those on Codex GFD and 40% of those on NDG-GFD having persistent 

villous atrophy. The patients in this study did not have clinical features of refractory sprue. 

Based on the fact that there were similar histologic profiles in both groups, the authors postulate 

that persisting mucosal abnormalities may be unrelated to gluten non-compliance. Of course, 

gluten intake in the NDG-GFD group undetected by study protocols cannot be ruled out. 

Serology. The studies assessing the utility of serology in monitoring adherence can be divided 

into those with,397,398,403,404,407,409,413,415 and those without396,399-402,408,410,412 biopsy correlation. 

The studies without biopsy correlation are reviewed first. They establish an association between 

serologic positivity and patient compliance.

Bartholomeusz et al.396 demonstrated higher rates of IgA-AGA positivity in non-compliant as 

compared with compliant CD patients in a mixed population. How compliance was ascertained 

is not described. Three of the 17 (17.6 %) patients compliant with a GFD for greater than 6 

months were IgA-AGA positive as compared with 11 of 12 (91.6%) non-compliant patients. The 

PPV for non-compliance was calculated to be 78.5%. 

Burgin-Wolff et al.400 showed that, as expected, serology becomes positive with gluten 

challenge. One hundred and thirty-four children with CD underwent gluten challenge and were 

assessed for IgA-AGA and IgA-EMA-ME. At baseline, the rate of serologic positivity was 23% 

for AGA and 13% for EMA. Within 3 months of gluten challenge, 97% of children were 

positive for AGA and 65% positive for EMA. Between 3 months and 1 year, 85% of children 

were positive for AGA and 84% positive for EMA. 

In a mixed population, Fabiani et al.408 demonstrated significantly higher IgA-tTG-GP values 

in patients deemed to be non-compliant with a GFD as compared with compliant patients. 

Bardella et al.399 demonstrated that the positivity of various serologic markers falls in adults 

with duration on a GFD (Evidence Tables, Appendix I). The five groups in this study were 

untreated CD, poor GFD compliance, GFD less than 2 years, GFD greater than 2 years, and a 

control group. As expected, IgA-AGA, IgA-EMA-ME and IgA-tTG-GP were positive in 

virtually all untreated CD patients. Also, as expected, there was a low rate of positive serology 

in the control group, with a higher percentage being IgA-AGA positive than either IgA-EMAME or IgA-tTG-PG. In the poorly-compliant CD group, all were positive for all three serologic 

tests. In patients on a GFD less than 2 years, the rates of positive AGA, EMA and tTG were 

40.9%, 54.5%, and 63.6%, respectively. In patients on a GFD for more than 2 years, the rates 

were 16.2%, 9.5% and 14.2%, respectively. The overlap of CIs intervals was such that no 

differences between the serologic tests could be determined. 
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Vahedi et al.402 studied IgA-EMA and IgA-tTG in adult CD patients. Based on dietary 

inquiry, patients were divided into those on a strict GFD, those with minor transgressions and 

those with major transgressions. It was not reported whether the EMA was ME or HU, nor was 

it reported whether tTG was GP or HR. The median duration of GFD was 75 months. Among 

those on a strict GFD, 2.5% and 3% were IgA-EMA and IgA-tTG positive, respectively. Among 

those with minor transgressions, positivity was only 37% and 31%, respectively. Among those 

with major transgressions, positivity was 86% and 77%, respectively. The sensitivity of IgAEMA for any dietary transgression was 66%, and for minor transgression it was 37%. For IgAtTG, the sensitivities were 52% and 31%, respectively. No statistically significant differences 

were detected between the two serologic tests. 

In a mixed population, Scalaci et al.401 showed a low reliability for IgA-EMA in picking up 

dietary transgressions reported at interview. It is not reported whether ME or HU was used. In 

patients on a GFD for at least 6 months, only 11.1% those patients reporting one dietary 

transgression per month were positive, and only 19% reporting one dietary transgression per 

week were positive. 

Fabiani et al.410 showed a similarly low rate of serologic detection of non-compliance in 

screen-detected adolescents. Of 6,315 screened students, 28 biopsy-proven CD patients were 

found. Of these, 23 agreed to participate in a follow-up study. The mean duration of GFD was 

23 months. IgG-AGA, IgA-AGA and IgA-EMA were measured. Whether EMA was ME or HU 

was not reported. Of the 11 patients reporting any dietary transgression, only two patients (19%) 

were positive for any of the serologic tests. 

Pacht et al.,412 in a similar study, showed different results. Seventeen children deemed 

compliant with GFD for at least 1 year were all IgA-EMA-ME-negative, whereas, 22 children 

deemed non-compliant were IgA-MA-ME-positive. This study suggests a much higher 

sensitivity for EMA than in other studies. 

A number of further studies include serology and biopsy correlation. These are reviewed 

below. 

Sategna-Guidetti et al.413 looked at 47 adults with CD. All were IgA-EMA-ME positive at 

diagnosis. After 8 to 30 months of GFD, a second biopsy was taken and IgA-EMA-ME was 

remeasured. Total AGA was also measured in 39 patients. No patient in which the mucosa 

recovered to normal had a positive EMA. Only one patient with normal histology had a positive 

AGA (2.6%). EMA was positive in only five of 23 patients with partial villous atrophy, three of 

13 patients with subtotal villous atrophy, and one of two patients with total villous atrophy. 

AGA was positive in only seven of 20 patients with partial villous atrophy, five of ten patients 

with subtotal villous atrophy, and two of two patients with total villous atrophy. The PPV of 

EMA for abnormal histology was 100%, but the NPV was only 23%. The PPV-AGA (total) for 

abnormal histology was 93.8%, whereas the NPV was only 25%. There was a clear inability of 

serology to adequately reflect the mucosal state in this study, and serology was negative in a 

significant number of patients with villous atrophy. 

Valentini et al.407 also found a significant rate of negative serology despite the presence of 

villous atrophy. In an adult population on a GFD for a mean of 9.9 months (range 6-12 months), 

24 patients were IgA-EMA-ME negative on a GFD. Seventeen of these 24 patients (71%) had 

varying degrees of villous atrophy on biopsy (14 had partial villous atrophy and three had 

subtotal villous atrophy). 
121

Dickey et al.409 also showed that disappearance of IgA-EMA-ME did not necessarily indicate 

mucosal recovery. In adults on GFD for 1 year, IgA-EMA-ME was positive in only two of 22 

(9%) with partial villous atrophy, and three of ten (30%) with subtotal/total villous atrophy. 

Mengozzi et al.403 investigated adult CD patients on a GFD for 1 year. Most (95%) had a 

Marsh III histology at diagnosis. In general agreement with the prior studies, only 12% had 

normal histology at follow-up biopsy 1 year later. Fifty percent were Marsh I and 38% were 

Marsh II or III (individual results for Marsh II and III were not reported). IgA-EMA-ME, IgAtTG-HR (four different assays: DRG Diagnostics, Eurospital, Immunodiagnostik, and Celikey), 

and IgA-tTG-GP were measured. Taking complete mucosal recovery as a negative biopsy and 

all other biopsies as positive, the authors looked at concordance of serology to biopsy results. 

Concordance for EMA, tTG1, tTG2, tTG3, tTG4 and tTG5-PG were 48%, 29%, 65%, 14%, 

16%, 19%, respectively. The validity of a Marsh I or perhaps Marsh II histology being classified 

as positive is unclear, and it would have been interesting to know the corresponding concordance 

rates if Marsh 0-I and Marsh 0-II were considered normal. 

Kaukinen et al.398 similarly found a lack of correlation between IgA-EMA-HU, IgA-tTG-GP 

and histologic state. Of 87 adult patients on a GFD for a median of 1 year, 27 still had a Marsh 

III villous atrophy. Among those with Marsh III villous atrophy, EMA was negative in 74% and 

tTG was negative in 59% of patients. Furthermore, of 11 patients admitting regular dietary 

lapses, 55% were EMA and tTG negative. The sensitivity, specificity, PPV, and NPV of EMA 

for Marsh III villous atrophy was 26%, 93%, 63%, and 74%, respectively. The values for tTG 

were 41%, 88%, 61% and 77%, respectively. 

The issue arises as to whether serology might more accurately reflect mucosal state in longterm follow-up. In patients on GFD over 5 years,398 two of four patients with Marsh III villous 

atrophy were EMA and tTG negative, and five of nine patients (56%) admitting dietary 

transgressions were EMA and tTG negative. In this study, there was no clear advantage of tTG 

over EMA. 

One study by Fotoulaki et al.397 did show a good correlation between serology and mucosal 

state. In a mixed population of 30 patients, IgG AGA, IgA AGA and IgA-EMA-ME was 

measured after 12 months of GFD. Contrary to the preceeding studies, all patients had either a 

Marsh I or II biopsy on a GFD, and all were IgA AGA and IgA EMA negative, while 40% were 

still IgG-AGA positive. The age range of patients in this study was much younger (1 to 24 

years). 

Troncone et al.415 demonstrated that serology could miss dietary transgressions in children. 

Twenty-three adolescents were divided into four groups, depending on assessment of gluten 

intake. IgA-EmA-ME was present in seven of seven patients assessed to be taking >2 g/day of 

gluten. All seven also had villous atrophy. Conversely, four patients on a strict GFD, had 

normal histology and negative EMA. For patients with intermediate levels of gluten intake, one 

of six patients with a gluten intake of less than 0.5 g/d had a positive EMA. This patient also had 

partial villous atrophy. Three patients in this group had lesser mucosal abnormalities (increased 

IELs) and negative serology. For patients ingesting 0.5 to 2 g/d of gluten, three had a positive 

EMA; two of these had villous atrophy. Five patients had increased numbers of IELs. 

Interventions to Promote Adherence to a GFD 

Anson et al.416 investigated 43 Jewish Israeli children with CD, and their parents. Thirty-one 

of the children (70%) were judged compliant based on a combination of clinical symptoms, 
122

biopsy and AGA. It is unclear if serology and biopsy was performed in all children to assess 

compliance. Parental knowledge was studied using a structured questionnaire. A significant 

positive correlation between the father being a professional and compliance was found (p<.01). 

Parental level of education was also significantly correlated with compliance. Significant 

differences in parental ability to choose GFD items from a specific menu were found. Ninety 

three percent of parents of compliant children were able to pick all five GFD items out of an 

eight-item menu. This compared with only 67% of parents of non-compliant children (p<.05). 

In another parental questionnaire, Jackson et al.418 found that 30 of 50 (60%) parents reported 

their children to be on a strict GFD. Dietary compliance correlated with membership in the 

Celiac Society (p<0.0001). It also correlated with parental score on an eight-question test related 

to knowledge of CD (p<0.001). 

Ljungman et al.420 found self-reported GFD compliance in children to be positively 

associated with knowledge of CD. In this study of 47 Swedish children, those deemed compliant 

scored 14.03 out of 15 on a knowledge test related to CD. This compared with an average score 

of 12.44 in the non-compliant group. 

Lamontagne et al.419 surveyed 617 past and present members of the Quebec Celiac 

Foundation. A final sample size of 234 was obtained. Self-reported compliance difficulty with a 

GFD was inversely correlated with a high level of confidence in treatment information from 

gastroenterologists and dieticians (p<.005). 

Hogberg et al.421 looked at the effect age of diagnosis might have on compliance. In a study 

population of 29 adults with CD, 15 were deemed compliant with a GFD on the basis of a 

questionnaire and serology (IgA EMA, IgG EMA and IgA tTG). Eighty percent of patients 

diagnosed prior to age 4 were GFD compliant compared with 36% of patients diagnosed after 

age 4 (p<.05). A drawback of this study is that serologic markers were collected about 3 years 

prior to the dietary questionnaire. This risks misclassification of patients if their compliance 

varied over time. 

In an important study with relevance to outcomes of population screening, Fabiani et al.417

showed a lower compliance in 22 adolescents identified by a mass screening program as 

compared with 22 age-matched controls with identified CD on the basis of symptoms. All 

patients had been prescribed a GFD for more than 5 years. Twenty-three percent of screendetected patients reported being on a strict GFD as compared with 68% of those diagnosed with 

CD on the basis of symptoms. Patients in the screen-detected group were diagnosed at a later 

age (mean 14.0 yrs) versus patients identified on the basis of symptoms (mean 4.3 yrs). 

A colouring book intervention has been developed to promote GFD compliance,422 but the 

effectiveness of this intervention has not been assessed in children with CD. 

Quality Assessment 

The majority of studies in this objective were of a “before–after” design. In this setting, this 

design may not pose a major limitation for monitoring studies, since the purpose of the study was 

to assess the change in serology and histology after introduction of a GFD. In this regard, the 

strength of the evidence for monitoring adherence to a GFD was fairly good. However, there is 

almost a complete absence of studies of interventions for the promotion of adherence to a GFD. 
Note: Appendixes and Evidence Tables are provided electronically at 

http://www.ahrq.gov/clinic/tp/celiactp.htm 

123

Chapter 4. Discussion 

Celiac 1: Sensitivity and Specificity of Tests for CD 

Serology 

Systematic reviews of studies of diagnostic accuracy are similar in many ways to reviews of 

other study types, such as randomized controlled trials. However, important differences exist in 

large part because of the weaknesses inherent to the diagnostic-accuracy study design and its 

potential sources of bias.24 In addition to these considerations, the topic of CD introduces further 

difficulties, and bias because of the nature of how the disease itself is defined, and the methods 

of patient selection for inclusion in the study. Ideally, a diagnostic-accuracy study should 

include a consecutive or randomly selected sample of patients from a clinically relevant patient 

population. That is to say, a study population who’s characteristics match those of the 

population in which the test will ultimately be used, and both patients and controls are selected 

from this population. Unfortunately, selection spectrum bias is common in studies of diagnostic 

tests in general, and in practice it is easier for investigators to select cases and controls as 

separate groups in a case-control design. The practice of choosing cases that have previously 

been identified as having the disease, especially if more severe, introduces bias in the estimates 

of sensitivity (artificially raising it), while choosing completely healthy individuals as controls 

introduces bias in the estimates of specificity—artificially raising it as well.24 The importance of 

these biases comes back to the issue of the relevant clinical population. If the test is to be used in 

screening healthy individuals, then the estimate of the reported sensitivity is higher than it 

should, but the specificity estimate is likely valid. On the other hand, if the test is to be applied 

to suspected cases of the disease, then the reported estimate of sensitivity may not be that far off, 

but the specificity estimate would be higher than it should. Other important sources of bias also 

exist in relation to the study population, such as the mix of other diseases present in the 

population with similar features as the disease in question, and ensuring an appropriate mix of 

disease severity in the tested population. This last point regarding disease severity is especially 

important for this report, and is discussed at length below. 

Lijmer et al.423 reviewed 11 meta-analyses of diagnostic tests, and assessed the characteristics 

of the included studies using multivariate regression analysis. The authors identified several 

threats to the validity of a diagnostic study’s results. Case-control designs overestimated 

diagnositic odds ratios (DORs) by three-fold compared with studies using a clinical cohort 

(relevant clinical population). As well, studies that applied different reference tests to those with 

and without disease (in case control) or to those testing positive or negative (in relevant clinical 

populations) overestimated the DOR by 2.2-fold. Interpreting the reference test, with knowledge 

of the results of the test under study, overestimated the DOR by 1.3-fold. DORs from studies 

without adequate descriptions of the test or study population were 70% and 40% higher, 

respectively, than in studies reporting these details. Inadequate descriptions of the reference test 

were also identified as sources of bias. 

With this information at hand we tried to minimize bias in this report, by using what some 

may consider fairly strict inclusion criteria which also eliminated many poor quality studies. We 

included both case-control studies and cohort (relevant clinical population) designs but grouped 
124

them separately. Studies were only included if an adequate description of the test under study 

and the reference test (biopsy, and a statement of the criteria defining CD) were provided, and 

both the cases and controls had to have had the same reference test (i.e., biopsy) applied at the 

same definition or level (i.e., biopsy grade). 

The results of the systematic review demonstrate that in the studied populations IgA-EMA 

and IgA-tTG have sensitivities and specificities each in excess of 90% in both children and 

adults. In fact, the pooled specificity of EMA was 100% in adults using either EMA-ME or 

EMA-HU. In studies of children, the specificity of EMA using these two substrates was 97% 

and 95%, respectively, with overlapping 95% CIs, suggesting no statistical difference between 

these values. In adults, the pooled specificity of tTG-GP and tTG-HR were 95% and 98%, 

respectively, with overlapping CIs. Similarly, in children the specificities were 96% and 99%, 

again with overlapping CIs. Among the three studies in adults,32,45,70 and four studies in 

children35,52,70,79 that assessed both EMA and tTG, the specificities were nearly identical. 

Overall, these results suggest that EMA and tTG antibodies demonstrate extremely high 

specificities in both adults and children. 

We identified a tendency towards greater variability in sensitivity between studies and 

between antibodies, compared with specificity. IgA-EMA-ME demonstrated sensitivities of 

97% and 96% in adults and children, respectively. EMA-HU demonstrated a similar sensitivity 

of 97% in children, although the pooled estimate in adults was somewhat lower at 90%. Among 

two studies that assessed both EMA-ME and EMA-HU in adults, one demonstrated identical 

sensitivities of 95%,81 whereas, the other57 showed a lower sensitivity of HU compared with ME 

(90% vs 100%). This last study only included 20 untreated patients with CD, all of whom were 

ME positive, but two of whom were HU negative. None of the included mixed-age studies 

assessed both of these antibodies. Heterogeneity existed in the analyses of sensitivity of tTG-GP 

in the adult, but it is likely close to 90%. In children, the pooled estimate was 93%. The 

sensitivity of tTG-HR was 98% in adults and 96% in children, although in both cases the CIs 

included a low of 90%. In studies of mixed-age populations the sensitivity was 90%. 

Estimates of the sensitivity of the IgG class antibodies of EMA and tTg suggest that these 

tests have poor sensitivities around 40%, although the specificities were quite high at around 

98%. These finding suggest that this class of antibody would be inappropriate as a single test for 

CD, but may be useful in IgA deficient patients, or in combination with an IgA class antibody. 

One study that assessed the use of IgA-tTG-HR with IgG-tTG-HR found a sensitivity of 99% 

and a specificity of 100% for the combination.72

The analyses of all the AGA subgroups demonstrated significant heterogeneity, making 

pooled estimates impossible. Be that as it may, the sensitivity of IgA-AGA in adults is likely not 

much higher than 80%, but seems somewhat higher in children. The specificity likely lies 

between 80% and 90%, in adults and children, although the studies of serial testing of AGA 

followed by EMA or tTG in the prevalence section of this report suggest that the specificity is 

low as well. Even if one considers an optimistic range, the performance of IgA-AGA in both 

adults and children is inferior to that of the other antibodies discussed above. 

The analyses of IgG-AGA suffered from significant clinical and statistical heterogeneity, 

making even general summary statements difficult. With this in mind, the typical sensitivity of 

this test likely lies below 80% in adults, and between 80% and 90% in children. The specificities 

are likely close to 80% in adults and between 80% and 90% in children with the same warning 

coming from the prevalence studies, suggesting that in the era of EMA and tTG, testing for CD 

with AGA has a limited role. 
125

In assessing the PPV and NPV of these tests it is important to keep in mind the prevalence of 

CD in the tested population. In all the included studies, the prevalence of CD would be 

considered quite high, the minimum study prevalence was 9%, and many studies demonstrated 

prevalences in excess of 40%. In comparison, Fasano et al.15 found the prevalence of CD in atrisk first-degree relatives of CD patients to be 4.55%. In general, based on our report, the 

prevalence of CD in high-risk groups such as suspected CD patients, and first-degree relatives 

was less than 20% (in non-tertiary centers), and the prevalence in patients with anemia and 

diabetes was generally less than 10% (Celiac 2 section). As expected, overall the included 

studies demonstrated the classic relationship between prevalence and the PPV and NPVs. At the 

relatively high prevalence of CD in these studies, the PPV (the chance that a positive test 

represents a true positive test) was quite high (>90%), but started dropping at a prevalence below 

35% to values generally below 80%. Figures 21 and 22 represent the actual unweighted 

individual study data. It is therefore not surprising that the studies maintaining a high PPV at a 

low prevalence were all studies of small sample sizes. In the expected reverse relationship, at a 

prevalence above 45% the included studies showed a drop in the NPVs. However, in contrast to 

the situation with the PPV, the NPV would be expected to be between 95% and 100%, if not 

actually close to 100%, at the expected prevalence of CD in most clinical situations. The same 

relationship was seen when the pooled estimates of the sensitivity and specificity for each 

analysis group was used to calculate the PPV over a range of prevalences (Figure 23). 

Therefore, the potential problem with EMA and tTG serological testing lies in their performance 

in situations of “low” prevalence of CD (i.e., less than 20%, a value that is still higher than the 

prevalence of CD in most at-risk groups). Unfortunately, it was difficult to directly estimate the 

PPV of EMA and tTG based on the prevalence studies, such as the one by Fasano et al., since 

many of the studies only performed serology testing, or there was incomplete biopsy 

confirmation. However, in studies where it could be estimated using the best performing EMA 

or tTG serological test, the PPV ranged from 66.7% to 95.0%,209,211,212,214,215,220,223,323 with all but 

one study having a PPV of less than 88.9%. Most of the studies had PPVs in the range of 70% to 

80%. In this same group of studies that assessed the prevalence of CD in a general population, 

five studies showed 100% PPV, however, in all these studies there was less than ten confirmed 

CD cases,213,217,222,225,231,269 and in three studies there were three or fewer confirmed 

cases.217,222,231 The PPV of IgA/IgG AGA screening alone was considerably worse, and it was 

not uncommon in serial testing studies to see a ten-fold drop in potential cases when moving 

from AGA to subsequent EMA and tTG confirmation. 

From the preceding discussion it is clear that in the diagnostic studies of the serological tests, 

the sensitivities of EMA and tTG antibodies for the detection of CD are quite high. Furthermore 

the specificities and NPVs are nearly perfect, making these antibodies appealing candidates for 

screening, as well as for the diagnosis of suspected CD patients. However, the pressing question 

is whether the reported high sensitivities and PPVs in these studies, and the enthusiasm 

surrounding these antibody tests, will hold true when these tests are applied to different clinically 

relevant populations. Of concern, is the true PPV of these tests when they are applied in 

populations with a relatively “low” prevalence (<10%-20%) of CD. This is an important issue, 

since the proportion of patients who would undergo unnecessary further testing will rise as the 

PPV falls. For example, if the PPV falls to a value of 80% (based on the examination of Figure 

21), then 20% of screen-positive individuals would undergo unnecessary testing and/or 

treatments. From the estimates discussed above derived from the population screening studies, 
126

and from the plots of PPV versus prevalence, it would appear that the PPV of these tests is 

potentially lower than the diagnositic test studies suggest it is. 

The vast majority of studies, as well as our own TEP, required that the small intestinal 

mucosa show at least partial villous atrophy histologically for the diagnosis of CD to be made. In 

fact, most of the studies used patients with subtotal or total villous atrophy. Furthermore, 

inherent to the clinical definitions of classic, atypical, and silent CD described in the methods, is 

the requirement of having a “fully developed” villous atrophy. However, Fasano et al.,15 in a 

large American prevalence study, found that only 34% of biopsied EMA-positive subjects had 

subtotal or total villous atrophy (modified Marsh IIIb or IIIc). In this study, no EMA-positive 

patient had a Marsh I lesion, 26% had a Marsh II lesion and 40% had a Marsh IIIa lesion. It is 

clear from this study, and from the discussion about biopsy later in this section, that true CD 

exists in patients with histologic grades less severe than classic Marsh III lesions, and that 

patients with silent CD do not have to have fully developed villous atrophy. The problem that 

then arises is whether the reported sensitivities of these antibodies holds in the majority of 

patients who have CD, yet with less severe histology. As well, if the sensitivity is not as high as 

reported then, by definition, the nearly perfect NPV of IgA EMA and tTG would also be 

expected to suffer. 

This question has been answered in several studies that have correlated histology with the 

sensitivity of these serological markers, and also mirrors to some extent the antibody response 

that occurs once patients with CD are placed on a GFD. A description of results of these studies 

follows below, while a full narrative with tables is located in the Appendix H. 

Rostami et al.16 evaluated the diagnostic value of IgA EMA and AGA in 101 untreated 

patients with CD. The combination of the two tests showed an overall sensitivity of 76%. But, 

alarmingly, the sensitivity of EMA in these patients dropped precipitously with milder 

histological grades. EMA demonstrated a sensitivity of 100% in Marsh IIIc, 70% in Marsh IIIb 

and only 30% in Marsh IIIa. The authors did not consider patients with Marsh I or II lesions as 

having CD. 

Tursi et al.424 assessed the relationship of the histologic grade to tTG positivity in 119 

consecutive adult CD patients defined by characteristic duodenal biopsy and “permanent gluten 

sensitive enteropathy.” In this study, the frequency of tTG-positivity (sensitivity) and mean tTG 

levels, were greatest with the highest modified Marsh grade, and dropped steadily with milder 

histologic grades reaching a low of only 8% positivity in CD patients with Marsh I lesions. The 

sensitivities of tTG in Marsh IIIc, IIIb, IIIa, and II were 96%, 84%, 56%, and 33%, repectively. 

In another publication, likely using the same population of “permanent gluten-sensitive 

enteropathy,” Tursi et al.425 demonstrated similar results with AGA and EMA in a population of 

atypical CD (defined in methods). The sensitivities of EMA in Marsh IIIc, IIIb, IIIa, II, and I, 

were 97%, 92%, 89%, 40%, and 0%, respectively. The results with AGA showed a similar 

pattern, with the sensitivity dropping from 90% to 30% in March IIIc to Marsh II. 

Furthermore, in likely the same population of “permanent gluten-sensitive enteropathy,” 

Tursi et al.426 found a relationship between clinical manifestation of CD and EMA sensitivity. 

EMA was positive in 77 of 96 (80.8%) patients with atypical CD and in 17 of 27 (63.0%) 

patients with silent CD. EMA was negative in patients with Marsh I lesions. Once again, 

assuming that all these patients with “permanent gluten-sensitive enteropathy” are truly CD 

patients, then EMA would miss 19% of atypical CD, and 37% of silent CD that were picked up 

on the basis of biopsy. 
127

Demir et al.427 studied the presentation and clinical features of 104 newly diagnosed Turkish 

children. EMA and biopsy correlation was available for 72 children. Similar to what was 

described above, EMA was positive in 92% of patients with Marsh III lesions versus 66.6% of 

patients with Marsh I-II lesions. Kotze et al.428 assessed 47 symptomatic subjects with CD with 

intestinal biopsy, tTG and EMA antibodies. The authors found a statistically significant 

correlation between antibody titres of EMA and tTG, and histologic grades. 

Hoffenberg et al.317 studied a group of children at risk of CD who were part of a large 

prospective study of the genetic and environmental factors associated with autoimmune diseases. 

No relationship was found between Marsh grade and the genetic risk factor leading to screening, 

but a significant correlation was found between Marsh grade and tTG (r=0.57, p<0.01). 

In a small case-control study assessing the diagnostic value of EMA, Sategna-Guidetti et al. 

also found that in patients with documented CD, EMA positivity correlated with the severity of 

the histologic grade.429 In this study, EMA was falsely negative in 50% of CD patients without 

villous atrophy. 

The findings of the large prevalence study by Fasano et al.,15 however, require further 

discussion within this context. This study demonstrated a very high prevalence of CD of 0.95% 

(1:105) in asymptomatic not-at-risk adults using IgA-EMA. Additionally, 34% of biopsied EMA 

positive subjects had subtotal or total villous atrophy (modified Marsh IIIb or IIIc), 40% had a 

Marsh IIIa lesion, and 26% had a Marsh II lesion. No CD patient in this study had a Marsh I 

lesion, although this is in part likely due to how they defined CD. In any case, there are at least 

two ways to interpret these results. The first is that EMA testing does pick up the mild Marsh 

grades, given the high prevalence of CD in this study. While the second interpretation is that 

based on the preceding discussion and the serology monitoring data, this study has missed an 

unknown number of CD patients with milder histological grades. Unfortunately, since we do not 

have follow-up data on the screen-negative patients in this study, this question will be difficult to 

answer and arguments can be made on both sides. 

The question that remains, however, is whether subjects with low grade histologic lesions are 

at the same risk of long-term complications as those with more advanced histologic grades. On 

the one hand, it is apparent that symptoms may not correlate with histologic grade but rather with 

the length of affected small bowel. When the distribution of histological grades is compared 

among patients with CD who are clinically asymptomatic versus symptomatic, the same 

distribution of grades is seen. For practical reasons, few of the studies we identified assessed 

length of small bowel involvement with CD. But another question arises: are patients with early 

March lesions who test positive for serology the ones who have more extensive small bowel 

disease?430 These questions add to the uncertainty regarding the true performance of serological 

testing, and whether missing early grade histologic lesions is important. Although we could not 

find direct evidence comparing outcomes in patients based on their histologic grades, it is not 

unreasonable to think that a patient with Marsh I-II lesions would still have an increased risk of 

CD complications (see Celiac 4 and 5 for some data regarding this point). 

In summary, it is clear that from our pooled estimates of the included studies that IgA-EMA 

and IgA-tTG antibodies provide excellent specificity for the diagnosis of CD. However, the high 

reported sensitivities may only apply to the selected group of patients with villous atrophy. 

Furthermore, if the sensitivity is in fact lower when the entire biopsy spectrum of CD is 

considered, then the nearly perfect NPV of these tests, particularly in low prevalence 

populations, would also be expected to suffer. Finally, the PPV of these tests may not be as high 

as suggested when the tests are applied in low-prevalence populations, as demonstrated by our 
128

estimates of PPV from the population screening studies. These potential limitations of 

serological testing can have profound implications for population screening initiatives, and 

verification of the sensitivity of these antibodies in a large population of CD patients showing the 

full histological spectrum is urgently required. 

HLA DQ2/DQ8 

The HLA DQ2 haplotype represents the occurrence of the HLA class II heterodimer alleles 

DQA1*0501 and DQB1*0201. These typically occur in a cis position as HLA DR3-DQ2 or in a 

trans position as HLA DR5/DR7- DQ2. The HLA DQ8 haplotype DQA1*0301/DQB1*302 

typically occurs in association with DR4. HLA DQ2 occurs in about 20% to 40% of the general 

population,9,10,15,100,135,136,138-141,143,146,147,150-157,159,167 48% to 65% of healthy relatives of patients 

with CD,158,161,164,166,167,169,172,177 and in up to 73% of non-CD patients with type I diabetes.97,165 

In one study, 100% of patients with enteropathy associated T-cell lymphoma (EATCL) were 

HLA DQ2 positive.151 Non-CD patients with Down Syndrome appeared to have the same 

frequency of HLA DQ2 as the general population.109,134,160

Populations of non-Western European descent demonstrated very wide variations in the 

frequencies of HLA DQ2 both in CD patients and controls.120,137,142,148,159,163

Overall, it can be seen that HLA DQ2 alone offers a sensitivity in excess of 90%, which can 

be improved to close to 100% if a strategy of testing for both HLA DQ2 and HLA DQ8 is 

utilized (either test being positive). The specificity of both tests together, or either test alone, is 

not as good as the sensitivity, falling in the range of 55% to 80%. The specificity becomes 

considerably worse if a population with a higher expected frequency of HLA DQ2 or HLA DQ8, 

such as first-degree relatives of patients with CD or patients with type 1 diabetes, is tested. The 

PPV, (the probability that a positive test represents a true positive result) of testing for HLA 

DQ2/8 in an average population is generally low. One, however, needs to keep in mind the 

dependence of predictive values on the prevalence of CD in the population to be tested. 

Therefore, in high-risk groups, such as first-degree relatives or patients with type I diabetes, the 

PPV tends to be higher. Conversely, it appears that the value of testing for HLA DQ2/8 is 

highest when a negative test is found. Given the high NPV of this test, average-risk patients can 

have the diagnosis of CD excluded based on a negative test. The situation is more complex in 

high-risk groups, since the NPV decreases with increasing prevalence, and with the recognition 

that there are HLA DQ2/DQ8-negative patients with CD. These findings, along with the cost of 

HLA testing, make routine use of this modality for screening or diagnosis inappropriate. 

However, the use of this test is most useful in cases of diagnositic uncertainty or as part of a 

multi-test gold standard in clinical studies. 
129

Biopsy 

Unfortunately, we could not identify any studies that assessed the sensitivity or specificity of 

biopsy for the diagnosis of CD. This is perhaps not surprising considering that CD has 

historically been, and for the most part continues to be, diagnosed based on characteristic 

histological features. These histologic features have been classified and categorized by Marsh 

and others,1,16 and criteria for the diagnosis of CD have been proposed,2

 and modified4

(Appendix A). A biopsy showing characteristic features that improves with a GFD and recurs 

with gluten challenge is by definition the gold standard for the diagnosis of CD and therefore 

would be expected to be highly specific (some patients such as those with refractory sprue will 

not improve on a GFD but are still considered to have CD, so the specificity of this definition is 

not absolute nor perhaps completely valid). Although we do not have actual numbers, it would 

appear from the qualitative assessment of the identified articles that a biopsy classified as a Mash 

IIIa or higher is likely to have a high specificity for the diagnosis of CD. However, as seen in the 

study by Fasano et al.,15 such criteria would be expected to have a low sensitivity. Alternatively, 

one would expect that biopsy could have a very high sensitivity if a Marsh I lesion was used to 

define CD, though clearly given the wide differential of mild histologic changes (Table 1, 

Appendix A), the specificity would be expected to drop. Therefore, to try to estimate the 

sensitivity and specificity of biopsy, and particularly the lower histology grades, we have 

compiled some articles below that provide “uncontrolled indirect information” on this subject. 

Inter-observer agreement in the histologic assessment of small bowel pathology. As 

previously described, there are several potential criteria for the diagnosis of CD. The original 

and modified ESPGAN criteria2,4 appear direct. Most of these criteria, as well as the assembled 

TEP, felt that some degree of villous abnormality is required for the diagnosis of CD. In 

practical terms, even distinguishing between a Marsh II (no villous abnormality) and a Marsh 

IIIa (minimal villous changes) can be difficult.431. This concern is further confounded by 

potential problems with the biopsy specimens themselves such as size, orientation, quality, and 

proper biopsy sampling. Hence, agreement between different pathologists and between the same 

pathologist at different times becomes important. The biopsy literature search identified a few 

articles that addressed pathologist aggreement. 

Weile et al.432 assessed inter and intra-observer agreement among three experienced Swedish 

and Danish pathologists reading the small bowel histology of patients suspected of having CD. 

Ninety small-bowel biopsies taken by capsule near the ligament of Treitz from 73 children were 

selected at random from a larger sample taken from 1987 to 1994. The final diagnosis was made 

on the basis of evaluation of specimens by dissecting microscopy, formalin-fixed H&E-stained 

slides, intestinal disaccaridases, serology and clinical presentation. The initial biopsy reports 

from patient files were sorted into normal (66; normal or minor nonspecific abnormalities—85% 

were on a gluten-containing diet [GCD]), pathological (17; total and severe villous atrophy, all 

on GCD), and inconclusive (seven; because of poor orientation, small sample, or autolysis). 

Several years later (1997) the same three pathologists who read the initial biopsies, performed a 

second reading of the slides given to them in random order. In comparison with the first reading, 

the number of inconclusive readings rose from seven to 22, there was a corresponding fall in the 

number biopsies read as normal and pathological. Considering the overall biopsy reading and 

diagnosis, the Kappa statistics (a statistical measure of agreement “correcting” for chance433) 
130

were (0.57, 0.63, and 0.75) for the three pair-wise comparisons of the three pathologists. These 

kappa values were reported to be “moderate” (for two out of the three agreement kappa scores) 

to “substantial” in terms of agreement, and suggest that agreement is far from perfect even when 

the same pathologist reads the same slide twice 

Vilela et al.431 also assessed inter-observer agreement among Brazilian pathologists in the 

diagnosis of CD. Three experienced masked pathologists independently read the slides of 34 

patients with CD based on ESPGAN criteria. Agreement differed among the three possible pairwise comparisons, with the best agreement occurring between pathologists A and C. Good to 

excellent agreement (kappa 0.61-0.85) was obtained for the assessment of villous structure. 

Reasonable to good agreement was observed for increased number of crypt mitosis (kappa 0.63), 

and decrease in the overall number of villi (kappa 0.47-0.53). However, agreement about the 

number of IELs using standard staining was weak (kappa 0.39). Interestingly, the agreement 

regarding overall histologic grade was also weak between two pathologist pairs, and reasonable 

to good for the last pair. As with the above study, it is difficult to comment on the 

generalizability of these results. The authors suggest that the number of CD cases seen was 

fewer than expected, and qualitative rather than quantitative measures of such parameters as 

villous height and IELs were used. Still, the findings suggest that agreement regarding the 

histologic grades should not be taken for granted. 

Several authors have suggested that quantitating various histologic features, such as the 

number of IELs per 100 or more enterocytes, results in greater reproducibility of biopsy 

readings.434 Authors that used quantitiative criteria during studies of inter-observer agreement 

likewise showed better agreement than reported above.435-437 These studies suggest that the use 

of quantative methods in the reading and reporting of small bowel histology, by pathologists 

experienced in the reading of CD biopsy specimens, leads to greater agreement among 

pathologists and presumably more uniform and standardized reporting. 

Latent CD. The presence of latent CD is a threat to the diagnostic accuracy of biopsy, since 

these patients truly have normal intestinal histology. 

Stenhammar et al.438 conducted an initial study of 100 first-degree relatives of 32 patients 

with CD. All 100 relatives were biopsied and two cases of CD were identified. In a 20-year 

follow-up study, Hogberg and Stenhammar247 performed serological evaluation (AGA, EMA, 

tTg) on these same 100 relatives and their offspring, with positive results prompting intestinal 

biopsy. All relatives with initial “mild or moderate mucosal” abnormalities remained unchanged 

and were not considered to have CD. Eight new CD cases were identified, two of these were 

relatives of the two cases diagnosed in the first study. One of these, a parent of an affected child, 

had a grade II-III lesion in the first study that normalized on a GFD, and remained normal after 3 

years of a GCD; she was not classified as CD, though in retrospect she likely represents a late 

relapser rather than transient gluten intolerance or a true latent CD. The other patient had a grade 

II lesion, but initially was not regarded as having CD because of the absence of symptoms. She 

was also found to be DQ2 positive. The remaining six newly diagnosed subjects were offspring 

of index CD cases and were not part of the initial cohort. In all, only two subjects of the initial 

biopsied cohort were “missed” in the first study. In retrospect, these subjects should have been 

included. This suggests that biopsy has the potential of high sensitivity and specificity for CD. 

Unfortunately, in the follow-up study, the number and HLA status of those with mild-tomoderate mucosal abnormalities (serology negative) was not reported, and since not all subjects 
131

were rebiopsied it is also unclear if there is a group of serology-negative, initially normal biopsy 

relatives that have developed higher grade histology at follow-up, suggesting latent CD. 

Maki et al.62 likewise after an initial biopsy screen of 113 first-degree relatives of CD 

patients, discovered 13 relatives with villous atrophy and crypt hyperplasia. During a 3-year 

follow-up period another three relatives, with previously “normal biopsies” who were AGA 

positive, were found to have CD. Unfortunately, the authors do not report on the number of 

relatives with low-grade histologic lesions, and whether the new cases were in patients with 

completely normal (Marsh 0) lesions or normal in terms of absence of villous atrophy. 

Troncone et al.439 searched the medical records of 25 centres in Italy over a 10-year period to 

identify children with latent CD defined as either individuals with initial normal biopsies who 

later developed villous atrophy and responded to a GFD (Group 1), or people who were 

previously diagnosed with CD by ESPGAN criteria and who were subsequently found to have 

normal histology on a GCD for 2 years (Group 2). Nineteen such cases were found. All these 

patients had normal morphometric analysis and IEL counts on the initial biopsy. Four of the 14 

GFD responders were considered at risk of CD (first degree, diabetes). The authors suggested 

that the five Group 2 patients could either represent true transient gluten-intolerance, or, in their 

opinion, more likely be late relapsers. These results of apparent post-pubertal recovery from CD 

are similar to those reported by Maki et al.440 and by Schmitz.441 Although the authors do not 

report on the number of charts or children screened, the findings of this study suggest that latent 

CD is very rare and unlikely to impact on the diagnostic accuracy of biopsy. It, however, 

underscores the importance of a time dimension in studies of CD, to accurately assess the true 

false positive and negative rates of diagnostic tests for CD. 

IELs with normal villous structure. CD exists in patients with normal villous structure. The 

biopsy can pick up these patients on the basis of crypt changes and/or changes in the number and 

type of IELs. 

Ferguson et al.442 assessed the relationship of raised levels of IELs to the final diagnosis 

among children with diarrhea. The authors found a lack of correlation between IEL counts and 

morphologic grading of the biopsy. However, among seven children ultimately found to have no 

organic disease, all had normal IEL counts in the range of 14-25/100 epithelial cells (ECs). Two 

of three children with CD on a GFD also had normal IEL counts. In contrast, the values were 

elevated to greater than 38 IEL/100 ECs in untreated CD patients. High counts were also found 

in three children with failure to thrive or diarrhea of unknown etiology, and in three of nine 

children with giardiasis. Though in these cases, the mean values were lower than in the 

untreated CD cases. Interestingly, among 14 children with gastroenteritis, ten had abnormalities 

of the villi, crypts or lamina propria, but all but one had IEL counts within the normal range. 

Although, the differential of mild mucosal changes is large, this study suggests that one of the 

histologic features of CD can distinguish between CD and other mild enteropathies, and could 

potentially allow for a relatively high sensitivity by allowing CD to be defined by a low-grade 

Marsh lesion, while maintaining some of the specificity. This theme will be revisited in studies 

that follow. 

Iltanen et al.136 assessed the γδ+ IELs in patients with and without CD. One hundred and 

seven patients were evaluated for possible CD. Twenty seven were found to have CD (25%) on 

the basis of ESPGAN criteria. As well, 28 biopsy-negative adults who underwent endoscopy for 

dyspepsia were used as controls. Table 46 details the main study findings. 
132

Table 46: Results of study assessing γδ+ IELs in patients with and without CD136

Test Celiac (n=27) 

CD excluded on 

biopsy (n=79) 

Biopsy-negative 

controls (n=28) 

Mean # of γδ+ IELs 40.4 (95%CI: 32.7-48.2) 6.7 (95%CI: 4.8-8.5) 1.6 (95% CI: 1.1-2.1) 

Elevated γδ+ IELs (> 

4.4 cells/mm) 

27 (100%) 39 (49%) n/a 

AGA positive 21/26 (81%) 33/66 (50%) n/a 

Reticulin antibodies 27/27 (100%) 18/78 (23%) n/a 

HLA DQ2 19/21 (90%) 20/67 (30%) 

The mean density of γδ+ IELs was significantly greater in CD patients compared with those 

patients where CD was excluded on biopsy, and compared with biopsy-negative controls. The 

density of these IELs was also significantly higher in patients with CD excluded on biopsy 

compared with controls. Because the authors used the ESPGAN criteria, which requires some 

degree of villous atrophy, the 50% of subjects with CD excluded based on this criteria who were 

AGA positive begs the question of how many of these were actually CD patients. However, 

based on the reported data, elevated γδ+ IELs were calculated to have a sensitivity of 100%, but 

a specificity of only 50.6%, although the true specificity is likely higher. In the biopsy-negative 

suspected CD group, 66 out of the 79 underwent testing for HLA DQ2. Out of these patients, 46 

tested negative for HLA DQ2. Given the high NPV of this test, it is likely that most of those 

patients do not have CD. Recalculating the specificity based on this assumption would raise its 

value, but unfortunately a breakdown of the number of patients with normal and elevated IEL in 

relation to HLA DQ2 was not reported. In any case, a better comparison would have been with 

the biopsy-negative control subjects, but the number of control subjects with raised IELs is not 

reported. Based on the mean density of IELs in this group, the number of patients with elevated 

IELs is likely to be low. During follow-up of the children suspected of having CD, but with 

normal mucosal biopsy and positive serology, four patients developed CD and responded to a 

GFD, further suggesting that this “control” group of patients with CD “excluded” on biopsy 

likely contained true CD patients who did not have villous atrophy. The results also suggest that 

the measurement of γδ+ IELs can be valuable in the diagnosis of CD, and hints at the fact that 

the requirement of villous atrophy on biopsy may miss some subjects with CD, particularly if 

they have raised IEL levels , positive serology and are HLA DQ2 positive. 

Kutlu et al.443 also studied the density of γδ+ IELs in untreated CD, treated CD and control 

patients (Table 47). The study population was made up of five children with classic CD with 

total villous atrophy and improvement on a GFD (Group A), seven patients studied after 1 to 11 

years of a GFD with mucosal recovery (Group B), and 22 patients with CD by ESPGAN criteria 

who were left on a normal diet for 1 month to 10 years (Group C). The control group consisted 

of 15 children with various GI disorders other than CD, and 15 adults undergoing intestinal 

surgery for gastric and pancreatic disorders. The report aggregated data from groups A and C. 
133

Table 47: Results of study assessing density of γδ+ IELs in patients with untreated CD, treated CD 

and control patients443

Sub-total/total 

villous 

atrophy 

(n=18) 

Moderate 

villous 

atrophy 

(n=7) 

Normal 

mucosa 

(n=9) 

Pediatric 

controls 

(n=15) 

Adult 

controls 

(n=15) 

Diet normal GFD n/a 

γδ+ IELs/100 ECs 14.8 17.5 14.5 3.1 3.6 

The density of γδ+ IELs/100 enterocytes was significantly higher in CD patients (15.4, n=34) 

compared with pediatric and adult control patients (3.1 and 3.6, respectively). However, the 

density did not correlate with histologic grade or with a GFD. Unfortunately, this study has 

several methodological flaws, and estimates of the sensitivity and or specificity of IEL in CD 

could not be derived. However, the study does indicate the potential usefulness of measuring 

γδ+ IELs in the overall evaluation of biopsy specimens for possible CD, and again demonstrates 

that CD patients can have a biopsy with normal villous structure which can be distinguished 

from normals by assessing the number of IELs. 

In an interesting comparative study of the correlation of IELs with AGA positivity by 

ELISA, O’Farrelly et al.444 studied 25 patients who had typical histologic features of CD and 

who were subsequently placed on a GFD. Ten of these were AGA positive, whereas 15 were 

negative. The second group consisted of 28 subjects suspected of CD but with “normal” small 

bowel histology. Twelve were AGA positive and 16 were negative. Increased levels of IELs 

were seen in both AGA positive (82.5) and negative (74.3) CD patients (difference not 

significant). On the other hand, among those with “normal” histology, AGA positive subjects 

had a significantly higher density of IELs than those who were AGA negative (42.4 vs 17, 

p<0.001). This data suggests that subjects suspected of CD with normal villous atrophy who 

have raised IEL densities should be further evaluated for CD, especially if serology is positive. 

These are also the types of patients where response to a GFD may be invaluable to firmly 

establish the diagnosis and help clarify the diagnostic value of low-grade histologic lesions. 

Saputo et al.445 compared the density of IELs between patients with confirmed CD, those 

undergoing investigation for CD, and control subjects (Table 48). The normal IEL range was 

determined to be between 4.68 and 17.60 based on the control group mean +/- 2 SD. 

Table 48: Results of study comparing density of γδ+ IELs in patients with confirmed CD, those 

undergoing investigation for CD, and control subjects445

Confirmed CD 

(n=9) 

CD under 

investigation (n=40)

Controls 

(n=143) 

IELs/50 ECs 68.55 51.21 11.14 

# with raised IELs 

(estimated from figure) 

9 40 2 

These results again suggest the usefulness of IELs in the evaluation of histology of patients 

being assessed for CD, and suggest a sensitivity of raised IELs of 100%, and a specificity of 

98.6%. Unfortunately, the authors do not report the number of individuals under investigation 

for CD who actually ended up having CD, so as to estimate the diagnostic parameters in this 

group. 
134

Similarly, Jarvinen436 studied IEL density and villous/crypt ratio in 928 Finnish patients with 

a suspicion of CD, and 59 biopsy-negative controls with dyspepsia (Table 49). CD was 

diagnosed on the basis of a suggestive small intestinal biopsy showing some degree of villous 

atrophy with subsequent later improvement on GFD. The main results excluding DH patients 

are presented below. 

Table 49: Results of study comparing IEL density and villous/crypt ratio in patients with a 

suspicion of CD, and 59 biopsy-negative controls with dyspepsia436

Untreated CD 

(n=138) 

Treated CD 

(n=198) 

Suspicion of CD 

with normal villi 

(n=545) Controls (n=59) 

CD3 + IELs 68* 40* 26 30 

γδ+ IELs 19.8* 12* 3.2 2.3 

Villous/crypt 

ratio 

0.6* 1.9* 2.8 3.0 

*statistically different from control 

The authors noted that using a cut off of 37 cells/mm for CD3+ and 4.3 cells/mm for γδ+ 

IELs, the sensitivities and specificities were 93% and 73% for CD3+, and 93% and 88% for 

raised γδ+ IELs, respectively. The PPVs and NPVs for raised γδ+ IELs were 95% and 85%, 

respectively, in this population. However, these results are based on the well-documented clearcut CD group, and did not take into consideration the CD patients that might be in the suspicious 

but normal villi group. Among the patients with a suspicion of CD but normal villi and high γδ+ 

IELs (>4.3), 28% were EMA positive compared with only 8% with normal γδ+ IELs (<4.3). 

Unfortunately, the outcomes of these patients are not reported, so one cannot comment further 

based on this study about the usefulness of IELs in Marsh I or II patients. 

Mino et al.446 assessed the density of IELs in routinely stained specimens compared with 

specimens stained with the readily available CD3 antibody. Twenty-eight subjects with 

architecturally normal duodenal biopsies, which were well-oriented and demonstrated greater 

than 20 IELs/100 ECs were included in the study. AGA, EMA and tTG antibodies were 

measured. Subjects were divided in the groups listed in Table 50. Controls consisted of seven 

normal individuals, two patients with reflux, and two patients with irritable bowel syndrome. 

Table 50: Results of study assessing IEL density in routinely stained specimens compared with 

specimens stained with the CD3 antibody446

 CD (n=8) 

Treated CD 

(n=4) Non-CD (n=16) Controls (n=11) 

Mean age 33.5 46.3 46.4 39.1 

IELs/100 ECs by H&E 

staining 

42.1 29.2 36.8 Not increased 

IEL/100 ECs in villous 

tip by CD 3 staining 

47.5 29.4 33.2 8.2 

There were no statistically significant differences between any of the groups when IELs were 

measured with H&E staining. However, all pair-wise comparisons were statistically different, 

except between the treated CD group and the non-CD group, when villous-tip IELs were counted 

with CD3 staining. The authors conclude that villous tip IELs are more specific indicators of 

CD, particularly with CD3 staining (which is more readily available than staining for γδ+ IELs), 
135

and suggest that the specificity of low grade Marsh lesions could be improved by these 

techniques. 

In a similar study, Goldstein et al.447 compared IEL density and villous distribution among 

patients suspected of CD. Twelve patients were diagnosed with CD based on histologic features 

and response to a GFD, whereas in 66 patients the diagnosis of CD was excluded based on 

biopsy, and supported by negative serology (and in some cases a lack of response to a GFD). 

Control cases consisted of patients with dyspepsia who underwent endoscopy and biopsy. The 

main results are summarized in Table 51. 

Table 51: Results of study comparing IEL density and villous distribution among patients 

suspected of CD447

CD (n=12) Non-CD (n=66) Controls (n=24) 

Mean age 35.2 36.1 34.5 

Iga EMA 8 3 (no response to GFD) n/a 

IgA AGA 5 13 (all EMA neg.) n/a 

Villous tip IELs 11.6 4.3 2.2 

IELs distributed 

evenly along the 

villi 

9/12 (75%) 3/68 (4%) 0 

n/a = not applicable 

The authors found that the mean villous tip IEL density was significantly greater in the CD 

group than in the non-CD and control group. A more even distribution of IEL along the villi was 

also found to be significantly more common in the CD group compared with the other groups. 

However, this last point is controversial. Unfortunately, given that this is a small study, the 

authors did not look at differences in these characteristics among CD patients with different 

histologic grades. 

Kuitumen et al.448 compared the histologic features of children with untreated CD, treated 

CD, other GI disorders (cow’s milk allergy, DH, congenital lactase deficiency, acrodermatitis 

enteropathica, and giardiasis) and a group of control subjects without GI pathology. Of the 52 

children with CD in this group, all had severe villous atrophy. CD patients had the lowest 

enterocyte height, and the most intense IEL infiltration of the studied groups. The authors found 

no overlap between CD patients and controls for the density of IELs, villous height, crypt depth, 

and villous height to crypt depth; all these parameters were statistically different between the CD 

patients and controls. 

Kaukinen et al.449 studied 96 consecutive adults found to be ARA or AGA positive and 

compared them with 27 ARA- and AGA-negative patients with dyspepsia. All patients 

underwent duodenal biopsy and CD was diagnosed on the basis of a villous height to crypt depth 

of less than two and crypt hyperplasia. Twenty-nine patients met their biospsy criteria of CD (18 

ARA- and AGA-positive patient, nine ARA-positive patients, and two AGA-positive patients). 

The 29 CD patients were placed on a GFD and of the 21 who were rebiopsied at 6 to 12 months, 

all showed unequivocal histologic improvement. The mean density of IELs in CD, serology 

positive, biopsy negative, and control patients were 87, 38, and 25 cells/mm, respectively. These 

numbers were statistically different. The mean density of γδ+ IELs among the CD patients was 

16.6. Eleven serology-positive patients with normal villous structure (presumably Marsh I and 

II) expressed HLA DR and had higher levels of γδ+ IELs (mean of 13.4 cells/mm) than the nonCD controls. A repeat biopsy (time unspecified) was performed in 12 serology-positive patients 
136

with normal villous structure at the time of the first biopsy. Ten of these had raised γδ+ IELs 

density on biopsy (Marsh I or greater). Five of these 12 were found to have villous atrophy 

(Marsh IIIa or greater). This study further illustrates the later development of CD in subjects 

with mild histologic changes, and suggests that although the specificity of villous atrophy may 

be high (all patients responded to a GFD), the sensitivity of villous atrophy (Marsh IIIa or 

higher) is lower than that of the serological test used in this study. This suggests that using a 

lower biopsy cut-off grade could improve sensitivity, albeit at the cost of specificity. 

Using another approach, Wahab450,451 identified 38 patients with symptoms of malabsorption 

who only demonstrated raised epithelial lymphocytes on duodenal biopsy (Marsh I). These 

patients were given a gluten challenge of 30g/day for 2 months, while maintaining their normal 

GFC. Twelve of 38 patients developed worsening mucosal lesions of crypt hyperplasia and 

partial or subtotal villous atrophy. After institution of a GFD all 12 patients showed 

improvement of their malabsorption, and improvement of their histology, suggesting that they 

truly had CD. 

The same authors,451 similarly studied 27 patients referred for malabsorption who were found 

to have a Marsh II lesion. HLA DQ2 or DQ8 was found in 21 of 27 patients (78%). The authors 

motivated 25 patients to follow a GFD, and all showed symptomatic improvement. The two 

patients who refused the GFD progressed to a Marsh IIIa lesion at follow-up. Although these 

data provide evidence of the true existence of CD in patients with Marsh II lesions, the frequency 

is unlikely to be as high as reported here. The high NPV of HLA DQ2/DQ8 suggests that at least 

some of the six testing negative likely don’t have CD. In any case, this study adds further 

evidence to the notion that a Marsh III cut-off will miss some patients with CD. 

In a very interesting study, Mahadeva et al.452 identified all duodenal biopsies performed 

over a 1-year period with increased levels of IELs, yet normal villous structure. Biopsies were 

formalin fixed and stained with H&E. Other biopsies showing at least subtotal villous atrophy 

and increased IELs were considered as “suggestive of CD.” Two normal control duodenal 

biopsies for every case of increased IELs with normal villous structure were also obtained. The 

upper limit of normal for IEL levels in this study was 22 IELs/100 ECs. Out of 626 biopsies 

assessed, 14 (2.2%) were found to have increased IEL and normal villous structure, whereas 15 

(2.4%) cases of CD were identified. Normal histology was found in 502 (80.2%) of the biopsies. 

The biopsies with raised IELs had a mean of 38 IELs/100 ECs (range of 27-46). Control 

biopsies on the other hand had a mean of 12.4 IELs/100 ECs (range of 2-20). The presence of 

GI symptoms did not differentiate those with raised IELs from controls or CD patients in this 

cohort. Six of the 14 patients with raised IELs had positive EMA and/or unexplained anemia 

and were suggested as having “latent” CD by the authors. Unfortunately, follow-up in this group 

was incomplete with only three of these patients undergoing repeat biopsy. As with the 

previously described studies, the presence of patients evaluated for possible CD who have 

isolated increased IELs may contain a subset of true CD patients. In fact, if one assumes that the 

six EMA positive subjects with raised IELs do in fact have CD, then one can estimate that using 

a lower histologic grade to define CD in this population would have resulted in a sensitivity of 

biopsy of 100%, and a specificity of 98%—since only eight patients out of the studied sample of 

531 would have been misclassified as having CD when in fact they did not. Of course, the 

expected specificity would not be as high as the one produced in this exercise since the authors 

do not tell us the histologic features or the diagnoses of the remaining 95 patients (626 biopsied, 

minus 502 normal, minus 15 CD, minus 14 raised IEL and normal villous structure = 95). 

However, taking this exercise further, if we assume that all of the other 95 patients were 
137

misclassified as having CD, then the specificity would drop to a still respectable 83%. Clearly, 

this type of study is the starting point in assessing the diagnostic parameters of the biopsy itself 

as a test. However, what is needed to fully assess biopsy as a test is a clearer measure of the 

false positive and negative rates. This can only be accomplished by using a battery of tests 

(biopsy, serology, HLA) to act as a gold standard to initially identify all potential cases, and then 

a follow-up period (response to GFD or gluten challenge) to assess the permanence of the 

diagnosis and the utility of biopsy at various cut-offs when used alone. 

Kaukinen et al.453 performed a study partially fulfilling the above requirements. Ten patients 

with suspected CD but only Marsh I or II lesions were compared with 27 biopsy-normal controls. 

The suspected cases were assessed before and after a GFD. The main results are presented in 

Table 52. 

Table 52: Results of study assessing patients with suspected CD and Marsh I or II, before and 

after a GFD453

 Histology EMA+ TTG+ HLA DQ2 γδ+ IELs 

Initially Marsh III – 2 

(patchy) 

Marsh II – 7 

Marsh I – 1 

8/10 9/10 9/9 Marsh III – 25 

cells/mm 

Marsh I-II – 13 

Controls – 1.4 

After GFD All Marsh II rebiopsied 

Marsh I – 2 

Marsh 0 – 5 

0/10 1/10 

(Slightly 

elevated) 

Same Reported as 

decreased values 

not reported. 

Although this is a small study with possible selection bias, the authors demonstrate that in a 

subset of patients suspected of having CD but without villous abnormalities, CD was diagnosed 

in all on the basis of a response to a GFD. Raised levels γδ+ IELs, positive serology, and HLA 

DQ2 positivity, supported the diagnosis of CD. Patients with CD and Marsh I-II lesions had 

significantly higher levels of IELs than controls. Unfortunately, this study did not include a 

larger sample of patients with Marsh I-II histology that included serology-negative subjects. 

Although it is clear based on this study that CD can exist in patients with Marsh I-II lesions with 

raised γδ+ IELs, it is difficult to generalize these results to an unselected sample of suspected CD 

patients. 

In a somewhat complicated but important study, Kuakinen et al.98 assessed 271 patients with 

suspected CD by biopsy. Forty-five patients were classified as having definite CD on the basis 

of a Marsh III lesion. While in 136 patients, CD was excluded on the basis of a Marsh 0 lesion 

and normal levels of γδ+ IELs. The remaining 76 patients had an uncertain diagnosis of CD 

based on biopsy (absence of villous atrophy) and underwent HLA DQ2 and DQ8 testing. In 59 

of these patients, there were minor mucosal lesions or positive serological markers, while 17 

were already on a GFD prior to biopsy. CD was excluded in 11 of these 17 patients on a GFD. 

Of the remaining 59 patients, CD was excluded in 22 because of a negative HLA DQ2/8 given 

the high NPV of this test, whereas 37 were DQ2/8 positive and remained with the suspicion of 

CD. Overall, CD was excluded in 33 of 76 patients. Among patients suspected of CD, but 

without villous atrophy, Marsh I-II lesions were found in 20 DQ2/8-positive patients versus in 

five DQ2/8-negative patients. Elevated levels of γδ+ IELs were found in 20 patients who were 

DQ2/8 positive compared with seven patients who were DQ2/8 negative, and IgA-EMA was 

found in 16 patients who were DQ2/8 positive compared with 0 patients who were DQ2/8 

negative. Although data is not provided for some patients, one can estimate the sensitivity of 
138

using a Marsh III cut-off. We know that CD was diagnosed outright in 45 out of 271 patients, 

but with subsequent testing a further 37 patients were found to be positive for HLA DQ2 or 

DQ8. At least 16 (EMA positive) and likely 20 (increased IEL counts) of these patients likely 

have CD. Based on these assumptions, the sensitivity of a Marsh III cut-off is between 69% (20 

DQ2/8 patients with increased IELs have CD) and 74% (16 EMA and DQ2/8-positive patients 

have CD). The sensitivity would be lower if more of the DQ2/8 positive patients turned out to 

have CD. The specificity of that cuff-off would appear to be 100%, although we are not told if 

the Marsh III patients all improved on a GFD. Clearly using a biopsy cut-off lower than Marsh 

III would have increased the sensitivity, but unfortunately we are not given enough information 

to estimate this reliably. 

This study with its battery of tests comes closer to the ideal design to estimate the diagnostic 

characteristics of biopsy, but unfortunately, it has significant short comings. To be fair the intent 

of the study was not to determine the sensitivity of a Marsh III cut-off. However, for the sake of 

future studies in this area, several design changes could have allowed this estimation. This study 

had two important positive aspects: it used a relevant clinically important population of patients 

suspected of having CD, and all the subjects underwent biopsy. However, it would have been 

ideal, if all the subjects also underwent HLA testing and serology. Furthermore, a follow-up of 

positive and negative patients, and or the assessment of the response to a GFD or the use a 

gluten-challenge in difficult to diagnose patients, would have allowed for the estimation of false 

positive and negative cases. 

Relationship of serology to histology. As the data from the previous discussion suggests, CD 

clearly exists in patients with histological grades milder than Marsh IIIa. The fact that the 

sensitivity of biopsy is improved by using a lower grade as a cut-off brings up an important 

question. If the preceding statement is true, then what test is most sensitive for detecting CD 

with mild histologic changes—biopsy or serology? The issues surrounding this discussion have 

been addressed in the later portion of the serology discussion section, and a detailed narrative 

summary of the studies of the relationship of serology to histology can be found in Appendix H. 

However, to summarize, data from these studies as well as some data from Celiac 5 suggest that 

the sensitivity of serology drops with milder histologic grades, and suggests that serology alone 

would miss CD patients with mild histology grades.

In summary, CD exists in patients with histology grades less than Marsh IIIa. The sensitivity 

of biopsy at a Marsh IIIa or higher cut-off is likely less than that of serology with EMA or tTG. 

If lower Marsh grades are used, the sensitivity of biopsy increases, and it is possible that if 

morphometeric techniques including assessing IEL densities are used, the specificity may not 

suffer greatly. Ultimately, the question of the true sensitivity of biopsy can only be answered 

with a well-conducted study that attempts to identify all possible CD patients in a given 

clinically relevant population using multiple simultaneous tests (e.g., serology, HLA) in addition 

to biopsy. All patients, those who clearly have CD, those in whom CD seems excluded, as well 

as equivocal cases, need to be followed for the assessment of the permanence of their 

“diagnoses.” Equivocal cases could also be considered for further testing, either with assessing 

response to a GFD or gluten challenge, to help in the clarification of their diagnosis. Although 

there are other potential variables to consider, with these measures, assessment of the false 

positive and false negative rates of biopsy, and hence a clearer estimate of the sensitivity and 

specificity, can be determined. 
139

Celiac 2: Incidence and Prevalence of CD 

Incidence in the General Population—Different Geographic and 

Racial/Ethnic Populations 

The crude incidence of CD among western European and North American countries over the 

past 25 years has varied between 1 and 51 per 100,000, and the cumulative incidence by age 5 

between 0.118 and 9 per 1,000 livebirths. Notable variations in CD incidence have not only 

been striking between neighbouring countries, such as is the case for Sweden and Denmark, but 

also between time periods for the same region, such was noted in the UK between the 70’s and 

80’s as well as in Sweden over the 90’s. 

It is important to note that there were important methodological differences among the 

studies, from using patient registers200 to actively screening at-risk patients.128 Clinical practice 

also varied between time periods and regions. The advent of serological testing in the early 90’s 

changed attitudes towards screening and identifying populations at risk with resulting higher 

detected incidences of CD. In some studies, active efforts were made to detect CD among 

asymptomatic subjects, such as the case in Finland where all subjects referred for endoscopy 

underwent small intestinal biopsy, independent of the cause for referral.199 The incidence of CD 

is also expected to vary according to the genetic make-up of the studied population, although the 

prevalence of at-risk HLA haplotypes was only noted in one study.128 These observations also 

highlighted the importance of dietary factors in triggering so-called CD epidemics among 

genetically predisposed populations. It would appear that breastfeeding bears a protective role, 

while early introduction of gluten, as well as the amount of gluten content in the diet may 

promote the early serological and pathological manifestations of CD. It is unknown whether 

these factors trigger an earlier expression of a disease which would become manifest anyway, or 

whether they trigger the appearance of a disease which may not otherwise occur, even later on in 

life. 

In conclusion, caution should be exercised when extrapolating the noted incidence for one 

given region to a whole country, in particular in countries such as the US where there are 

differing population ethnicities among regions, between rural and urban areas, as well as 

between small and large cities. However, it remains that the true incidence and prevalence of 

CD are if anything greater than reported in clinical settings, since observations derived from 

screening and case-finding efforts were consistently greater than those relying on the diagnosis 

of clinically suspected cases. Lastly, it is important to bear in mind that, considering the large 

proportion of subjects with silent CD (the so-called celiac iceberg), observed incidences will 

depend upon the efforts spent screening cases, as is well illustrated by the difference in the 

relatively low incidence observed over 30 years in Olmstead county, where the majority of cases 

had clinically overt disease, as opposed to the very high incidence noted in Denver Colorado that 

resulted from a systematic and prospective screening of newborns and children at risk. 
140

Prevalence in the General Population—Different Geographic and 

Racial/Ethnic Populations 

The included prevalence studies demonstrated important differences in execution, tests for 

prevalence assessment, and in patient sampling, making pooled estimates of prevalence 

unreliable. Furthermore, the discussions regarding the operational characteristics of the 

serological tests themselves, the influence of disease prevalence on the PPVs and NPVs of these 

tests, and the criteria by which clinical and histological CD is defined, have to be kept in mind 

when considering the results of this section. The last point regarding the histologic definition of 

CD is particularly important in this setting, since one-third of the included studies did not seek 

histologic confirmation of serology diagnosed CD, and in another four studies, a large proportion 

of the serology-diagnosed patients did not undergo histologic confirmation. Finally, because of 

the previously discussed concerns regarding the sensitivity of serological tests in lower grade 

histological lesions, and the potential for missing true CD patients based on histologic criteria 

that require villous atrophy, the true prevalence of CD in the general population may still have 

been underestimated in these studies. 

With these points in mind, the results of this report suggest that the prevalence of CD in the 

general unselected populations of North America and Western Europe is quite high and likely 

falls within the range of 0.5% to 1.26% (1:200 to 1:79). Smaller sample-size studies tended to 

give wider estimates ranging from 0.17% to 2.67%. Among the studies from the US, the range 

of prevalence was 0.4% to 0.95% in adults, and 0.31% in children. In Italy, the range of 

prevalence was between 0.2% and 0.8%, whereas the Scandinavian countries, Ireland and the 

UK, tended to show a higher prevalence of CD of approximately 1.0% to 1.5%, although there 

were also studies from those same countries that showed a lower prevalence. 

In summary, the prevalence of CD in Western populations is likely close to 1% (1:100) and 

may be higher in Northern European countries. A firm estimate of the prevalence is impeded by 

between-study differences, and uncertainties regarding the performance of serological tests at 

these relatively “low” prevalences, compared with the 40% to 60% prevalences in the studies of 

the diagnostic characteristics of these same tests (Celiac 1). 

Prevalence of CD in Patients with Suspected CD 

The prevalence of CD is greatly affected by the study population. In populations where the 

diagnosis of CD is clinically suspected, either because of the presenting symptoms or the 

presence of associated conditions, its prevalence varied between 1.1%307 and 50%.301 This 

illustrates well how the patient selection process will influence the prevalence of the condition—

studies reporting very high prevalence had populations that originated from tertiary, referral 

centers, while studies reporting low prevalence had populations that tended to originate from 

general practice. Although the report of the large American study of CD prevalence in at-risk 

and not-at-risk individuals did not specify how their subjects had been gathered,206 we can 

assume that these were derived from community practices, considering their large number. 

Altogether the variations between the study populations, the diagnostic criteria and the study 

design were such that it was inappropriate to statistically combine the observed prevalence to 

obtain a summary measure. Nonetheless, considering studies with subjects who were not 

originating from a specialized referral centre, the observed prevalence of CD in subjects with 

symptoms or conditions associated with CD ranged between 1% and 4%. 
141

Prevalence of CD in Patients with Type I Diabetes 

The findings of this report suggest that the prevalence of CD in patients with type I diabetes 

is higher than the prevalence in the general not-at-risk population. These findings appear to be 

consistent across the studied age groups, and by the screening method. Although the magnitude 

of the risk of CD among patients with diabetes varied to some degree from study to study, many 

of these differences can be explained by issues of study design. An overall pooled estimate of 

the prevalence of CD in diabetes could was not calculated due to these study differences. 

Almost uniformly, the prevalence of CD by biopsy was to some degree lower than the 

prevalence by serology. This may reflect the fact that there were some false-positive serology 

results in the prevalence of CD seen in these studies. Additionally, all these studies used some 

degree of villous atrophy to make a diagnosis of CD, which may underestimate the true biopsy 

prevalence of CD, since CD patients with Marsh I or II lesions were not considered. The 

prevalence by biopsy seemed to be lower still in studies that require subtotal or greater villous 

atrophy to make a diagnosis of CD. Furthermore, the prevalence by biopsy was uniformly low, 

as would be expected, in studies in which a large proportion of the screen-positive patients did 

not undergo biopsy. In these studies, the prevalence by biopsy was typically less than two 

percent, which likely represents an underestimation of the true prevalence of CD in this 

population. 

The prevalence of CD by serology varied greatly with lows near 1% and highs close to 12%. 

However, the majority of studies, and particularly those using EMA or tTG, demonstrated 

prevalences in the range of 4% to 6%. Although the prevalence by biopsy also varied, the 

typical study with complete biopsy confirmation of serology-positive patients demonstrated 

prevalences in the range of 3% to 6%. 

This evidence report has gathered the reported studies examining the relationship between 

diabetes and CD. Baring in mind the limitations noted above, we believe there is sufficient 

evidence to show individuals with type I diabetes are at higher risk of CD. The prevalence of 

CD in this population is likely between 3% and 6%. 

Prevalence of CD in Relatives of Patients with CD 

The prevalence is CD in relatives of patients with CD is elevated, both in first-degree and 

second-degree relatives. That prevalence varied between 2.8%246 and 17.2%235 in first-degree 

relatives and between 2.6%206 and 19.5%235 in second-degree relatives. The prevalence remains 

elevated among first cousins, and was 17% in the only study of these subjects.235

We have identified several factors that can be responsible for the variation in the observed 

prevalence. In particular, the selection of the families, of the relation to the index case, the 

diagnostic criteria, and the choice of study design. 

The prevalence of CD appears to be generally higher in families with multiple known cases, 

such as reported by Book et al.235 and Mustalahti et al.241 Most other studies referred to their 

subjects as originating from a “CD family,” without systematically documenting the proportion 

of families with multiple known cases of either CD or DH. 

As expected, in studies that looked at various degrees of relation, the risk was greatest in the 

first-degree relatives.206,235,239 However, Book et al.235 found no difference in prevalence 
142

between second-degree relatives and first cousins, i.e., 19.5% (95% CI: 15.1-23.9) and 17.0% 

(95% CI: 6.4-27.7), respectively. 

Also, the age of the screened population might be a factor even beyond infancy, since it has 

been observed by prospective serological248 and histological237 follow-up studies that the 

serological and histological markers of CD can develop after an initial negative screen in a 

genetically predisposed individual. Therefore, a one-time assessment or screen in these 

individuals may be insufficient. 

The serological diagnosis of CD will be affected by the diagnostic accuracy of the test. 

Fortunately, 11 out of 12 studies that used serological screening were EMA-based, a test with 

good diagnostic accuracy in populations with relatively high prevalence, such as relatives of CD 

patients. The single non-EMA study236 used AGA, a test with a lower sensitivity and specificity 

than EMA, but all seropositive subjects underwent a confirmatory intestinal biopsy. 

The histologic diagnostic criteria also affect the reported prevalence, as was well illustrated 

by the study by Tursi et al.,249 where Marsh grades of I and II were also considered diagnostic, 

resulting in a prevalence of 44.1%. 

The study design, especially whether all at-risk individuals are biopsied as opposed to solely 

those that satisfy a non-invasive criteria, is also to be considered. The EMA-based serological 

tests can miss milder forms of enteropathy as has been discussed, and this may explain why the 

prevalence of CD was generally higher in studies where all identified relatives were biopsied. 

Prevalence of CD in Patients with Anemia 

The results of this report demonstrate an increased prevalence of CD in patients with IDA. 

The prevalence is highest (between 10% and 30%) in studies of patients with GI symptoms, or in 

patients who have no gross lesions seen at initial investigation. CD appears to also be common 

in premenopausal women, both with (4.5%) and without (33%) heavy periods. Overall, in 

asymptomatic IDA patients assessed by serology or biopsy, the prevalence of CD was between 

2.3% and 6%. Therefore, patients with IDA, particularly those without a clearly identifiable 

cause, should be evaluated for CD as part of their investigation. 

Prevalence of CD in Patients with Low BMD 

The studies of the prevalence of CD in patients with low BMD suggest that between 0.9% 

and 3% of patients with osteoporosis have CD. As a comparison, Fasano et al.15 found that in 

the United States 0.75% of the general not-at-risk population, and 4.55% of first degree relatives 

of CD patients were found to have CD. 

The results from these studies should be interpreted within the context of some 

methodological limitations. Three of them used AGA as the initial screening test to prompt 

further investigation, and we have shown that the sensitivity of this test is not high. Furthermore, 

the biopsy criteria used to define CD was either not reported, or required the presence of 

subtotal, or greater villous atrophy (Marsh IIIb or greater). We have also shown that CD exists 

in patients with lower grade histological lesions. Furthermore, the study results are 

contradictory. Two showed a risk of CD higher than the general population,296,298 while the 

other two did not. In particular, the study by Mather et al.297 found that seven out of the 96 

screened patients were positive for EMA-ME, but none of these were positive on biopsy. From 

what we have seen regarding the specificity of this test being close to 100% (and therefore the 
143

PPV would be expected to be high as well), it is unlikely that there are so many false positives 

even if the prevalence of CD was low, and raises the question of whether early grade CD patients 

remained undiagnosed. As such, it is difficult to draw any firm conclusions about the true 

prevalence of CD in this population, given the contradictory results, the fact that lower grade 

lesions were not considered, and that no follow-up data was provided on the patients who 

screened positive for serology but did not meet the biopsy criteria. Taking into account these 

limitations, it is likely that the prevalence of CD in patients with osteoporosis is higher than that 

in the general population. 

Celiac 3: Risk of Lymphoma in CD 

The association between malabsorption and lymphoma is a concept that has evolved over the 

past century. The observation that a significant proportion of patients with intestinal lymphoma 

also had villous atrophy at a distance from the malignancy, or had previously been diagnosed 

with CD, led to the publication of several series on the topic. 

Although the objective of the task order was not to determine the risk of CD in lymphoma 

per se, the broad coverage of our search strategy also allowed us to systematically appraise the 

literature on this question, and were able to identify only two controlled studies on this 

association, which we describe here.454,455

Johnson et al.455 performed a retrospective search of the five main pathology laboratories 

serving Northern Ireland to identify all the incident cases of small bowel lymphomas (SBL) and 

small bowel adenocarcinoma from 1987 to 1996. The clinical presentation of the cases, as well 

as the presence or absence of villous atrophy at a distance, were noted. The prevalence of CD in 

this group of SBLs was compared with that of the general population in Northern Ireland, as 

observed from serological screening of the population at large.188 There were 13 cases of CD 

(gender not reported) out of 69 cases of SBL, all of which were ETCLs. Only one out the 13 CD 

cases was known to have CD prior to the diagnosis of SBL. The OR of CD in SBL was 27.98 

(95% CI: 11.88-65.81) compared with the general population. The OR of unrecognized CD in 

SBL was 15.72 (95% CI: 9.71-25.45) compared with the general population. 

In a prospective multicenter Italian study conducted between 1996 and 1999, Catassi et al.454

screened newly diagnosed adult patients with NHL for CD using EMA and AGA testing; EMApositive or IgA-deficient patients underwent small bowel biopsy. There were six cases of CD 

out of 653 patients with NHL (prevalence 0.92%). Three had B-cell and three had T-cell 

lymphomas. Four out of six cases had lymphoma primarily located in the gut. Two patients 

were known to have CD for more than 1 year, one of whom was poorly adhering to a GFD. Two 

cases had been diagnosed with CD within 1 year of the diagnosis of NHL, whereas two other 

cases had no prior CD diagnosis. The prevalence of CD among these NHL patients was 

compared with that observed in two Italian studies which performed large scale screening for 

CD.126,222 The OR of CD in NHL was 3.1 (95% CI: 1.3-7.6) compared with an age-and sexmatched population. 

These observations point to a clear association between CD and lymphoma. To determine 

the degree of association, or to quantify the risk of lymphoma in CD, we searched the literature 

for controlled studies of the incidence of lymphoma in CD. Unfortunately, the majority of 

publications on lymphoma in CD were uncontrolled. Typically, patients diagnosed with CD in a 

single institution were followed over time and the incident cases of lymphoma were described, 
144

along with characteristics of the affected patients, the course of their CD and the histological 

type of lymphoma. Unfortunately, such studies provide little confidence to estimate the true risk 

of lymphoma in CD, since lymphoma per se will occur in the general population. The incidence 

of lymphoma has to be compared with “controls,” matched on various characteristics such as 

age, sex, period and population. Any study that did not adjust the observed incidence to the 

expected incidence for age- and sex-matched individuals of the same population was deemed 

uncontrolled and excluded. 

Cohort studies, either prospective or retrospective, constituted the majority of controlled 

studies. The incidence of lymphoma in a cohort of biopsy-proven CD patients, calculated as the 

number of lymphomas divided by the number of patient-years of follow up, was compared with 

that of an age- and sex-matched population from the same geographic area and time-period. 

The SIR therefore represents the likelihood of lymphoma in CD patients relative to those 

who do not have CD in the same population. The value of the denominator reflects the incidence 

of lymphoma in a given population, so that it is not possible to pool SIR’s from different 

populations. 

The AR, however, is a measure of association that provides information about the absolute 

excess risk of disease in CD patients compared with “non-afflicted” individuals. This measure is 

defined as the difference between the incidence rates in the CD patients and normal population 

and, in a cohort study, can be calculated as the difference of cumulative incidence (risk 

difference) or incidence densities (rate difference) depending on the study design. The AR is a 

measure of risk which can be pooled; however, since incidence rates were reported in only two 

studies, we had insufficient data to generate a representative summary statistic. 

Furthermore, studies varied greatly at several levels, in particular with respect to the 

definition of an incident case of lymphoma, the reported outcome measure, and the CD 

population selection. 

Studies differed in their definition of observed cases of lymphoma, in the following manners: 

1. Inclusion of malignancies that antedated the diagnosis of CD. In one American study, the 

number of at-risk years was calculated both from the time of CD diagnosis and from the 

time of onset of symptoms that could be attributed to CD.340 In a prior national survey to 

patients with CD,456 these authors had collected evidence to support that there is usually a 

long duration of symptoms before a diagnosis of CD is made in the United States, so that 

they considered this account justifiable. However, authors from other countries would 

specifically exclude the malignancies that were diagnosed prior to CD, assuming that it 

was unknown whether these were truly “at-risk” periods and that this account could 

falsely inflate the incidence of lymphoma in CD.333 Considering that publications 

uniformly calculated and reported the incidence ratio based on the time period from the 

CD diagnosis, this is the measure of risk that we selected. 

2. Inclusion of malignancies that were recognized simultaneously to the diagnosis of CD 

(i.e., within 1 to 12 months of diagnosis). In some cases, the diagnosis of CD can be 

unknown until the presentation of lymphoma. This fact highlights the possibility that 

lymphoma can occur in asymptomatic patients with CD. Although the importance of 

such cases is undeniable, the account of such cases can introduce bias and inflate the 

incidence of lymphoma in CD. In other words, the simultaneous diagnosis of CD and 

lymphoma is similar to an incident case in a patient with a “zero” duration of follow-up, 

i.e., is closer to a measure of prevalence than incidence. The inclusion of cases of 
145

lymphoma occurring in patients with previously undiagnosed CD should theoretically be 

related to all cases of CD, diagnosed and undiagnosed, in order to give an accurate 

estimate of incidence, which is obviously impossible. However, some studies chose to 

include such cases, while others excluded them from the incidence calculation. This 

distinction was noted in the results presentation. 

3. Exclusion of malignancies that were diagnosed incidentally at autopsy. In their large 

Swedish cohort of individuals hospitalized with CD, Askling et al.337 also excluded 

unsuspected autopsy diagnoses of lymphoma, assuming that such entities would have 

been silent during life, and that they therefore could not be controlled for in the 

comparator group. 

4. Case definition of lymphoma. Lymphomas are broadly categorized as Hodgkin’s 

lymphomas and NHLs. The lymphomas that have been associated with CD have 

typically been of the NHL type, and so the majority of studies sought cases of NHL, with 

the exception of the Scottish study from Logan,336 where both Hodgkin’s and NHLs were 

reported. 

The reported outcome measures also varied and impaired our ability to combine 

observations. Some studies reported the incidence of lymphoma, while others, relying on death 

certificates for ascertainment of outcomes, reported on the mortality from lymphoma. 

Finally, the patient selection also varied, along with the reporting of the circumstances that 

led to the diagnosis of CD. These factors limited our ability to draw conclusions on the risk of 

lymphoma in symptomatic versus asymptomatic patienst with CD. 

We were also unable to find controlled data on the risk of lymphoma in refractory CD, an 

objective which had been suggested by the TEP. We did find, however, two prospective studies 

and one retrospective study that could lend support to the notion that the risk of lymphoma in 

refractory CD is greater than that of responsive CD.457-459

In the Netherlands, Wahab et al.457 prospectively followed 158 biopsy-proven CD patients to 

assess the recovery of histological changes with a GFD over time. There were 11 incident cases 

of refractory CD with more than 5-years of follow-up, five of whom developed ETCL, in 

contrast to none of the remaining GFD-responding CD patients. 

Goerres458 reported on 18 patients diagnosed with refractory CD between 1998 and 2000, 

gathered from all over the Netherlands, whom they treated with azathioprine and prednisone. 

There were three men and 15 women, with a mean age of 58 years (range 39-82). Subtypes of 

IEL populations were analyzed by flow cytometry, allowing for the classification of refractory 

CD patients into two types: type I refractory CD (n=10), in which a normal IEL population is 

seen, and type II refractory CD (n=8), in which an aberrant IEL population is present. All of the 

patients with type I refractory CD responded to combined azathioprine-prednisone therapy, 

whereas none of the patients with type II refractory CD showed a response. In fact, six of the 

eight patients with type II refractory CD developed EATL within a 3-year period, and a seventh 

patient died with blastic T-cell-like cells in the small bowel and the liver, and myeloproloferative 

changes in the bone marrow. The authors concluded that type II refractory CD is a premalignant 

condition with a very poor prognosis. 

In a French national cooperative study, the clinical information and tissue specimen 

necessary for IEL subpopulation analysis were gathered from 21 patients diagnosed with 

refractory CD between 1974 and 1998.459 There were five men and 16 women, with a mean age 

of 51 years (range 29-73 years). Nine of the 21 patients (43%) died from severe malnutrition 
146

and/or lymphoma (three patients) after a mean of 6.7 (range 1-14) years after the onset of 

symptoms of refractory CD. A phenotypically abnormal IEL population associated with 

evidence of clonality was found in eight of the nine patients that could be tested. The authors 

suggested that refractory CD may be the missing link between CD and ETCL. 

This systematic review identified nine controlled studies that met inclusion criteria. The 

major observation of our review is that the risk of lymphoma in CD was significantly increased 

compared to an age-matched population from the same region and period in 8 out of 9 studies. 

The SIR (NHL) varied from 2.66338 to 42.7,333 whereas, the SMR from NHL or lymphoma in CD 

varied from 11.4337 to 69.3.339 This increased risk persists even when the cases that are 

diagnosed with lymphoma simultaneously or within 1 year of the diagnosis of CD are excluded 

from the calculation. 

Some observational studies suggest that the risk of lymphoma, relative to patients of the 

same age without CD, may be highest in individuals who were diagnosed during adulthood,336,337

and appears to decrease with adherence to a GFD, as shown by several authors.333,336-339 It is 

also interesting to note that the only study that did not report a significant increased risk of 

lymphoma was one where 75% of patients were on a strict GFD.338

The differential risk of lymphoma among patients diagnosed with CD in adulthood versus 

childhood may indicate that early diagnosis and treatment with a GFD is protective. The 

possibility that a GFD may be protective is also supported by Askling et al.337 who found that the 

risk of lymphoma dropped to unity after 15 years of follow up. Limitations in the designs of 

these studies, however, prevents firm conclusions. These studies have followed relatively few 

patients diagnosed as children through middle age when the risk of lymphoma rises, and they 

may not have accounted for other factors (severity of symptoms, or other marker of disease 

activity) which might affect risk. The distinction between childhood and adult diagnosis of CD 

in the published cohorts relies on the presence or absence of CD-related symptoms during 

childhood, which has historically been a key factor in CD diagnosis. Based on the observations 

from these groups of patients, it would seem that continuous gluten exposure and ongoing 

mucosal damage sets the stage for malignancy later on in life. It remains unclear, however, why 

some individuals would have persistent mucosal damage in the absence of symptoms. Would 

these individuals also carry other characteristics that modulate their risk of malignancy? As we 

tap into the base of the “celiac iceberg” through systematic screening, we will hopefully in the 

future be able to observe the incidence of lymphoma in child and adult CD populations who were 

identified through population screening, and placed on a GFD despite them being asymptomatic 

during that period of their lives. The notion that lymphoma arises from prolonged antigenic 

stimulation should be confirmed if the risk of lymphoma is, as expected, lower than historical 

CD cohorts in those individuals. 

Celiac 4: Consequences of Testing for CD 

The search strategy did not identify any studies that would allow us to address the specific 

benefits and harms of testing with different strategies for CD. At present, there is inadequate 

information from the published literature on the benefits and harms of screening and the potential 

risks of undetected CD. Prospective trials of screening would be helpful to provide the data 

necessary to construct the tables that depict the consequences of screening specific populations. 
147

Information on the consequences of screening will come from the currently ongoing large 

population based prevalence studies. 

The consequences of such issues as false-positive results were dealt with in the Celiac 1 

Discussion. As discussed in that section, the definition of CD used and the prevalence of CD in 

the test populations, have a great impact on the diagnostic parameters of the available tests. We 

have presented data that show that the sensitivity of the available tests declines considerably 

when applied to patients with low-grade histological lesions. Unfortunately, there is insufficient 

data to address the question of what is the consequence of missing patients with low-grade 

histological lesions if serological screening alone is used. As described in Celiac 1, all the 

diagnositic test studies of the various serological markers were undertaken in study populations 

in which the prevalence of CD exceeded the that observed in most clinical situations. We have 

shown that the positive predictive value, which is predominately influenced by the test 

specificity and the prevalence of CD in the test population, drops from the reported values to 

much lower values when the test is applied in typical clinical populations. To illustrate this 

point, Figure 31 highlights the expected PPV when applied to different test populations. 

Figure 31: PPV based on pooled estimates of sensitivity and specificity 

As can be seen from Figure 31, the PPV—the probability that a positive test result actually 

represents true CD—drops with the prevelance of the population in which the test is applied. 

This relationship holds true for all the summary curves, but differ in degree. It is important to 

note that the PPV is predominantly influenced by the specificity of the test and prevalence. 

Since we have identified that the specificity of EMA and tTG is quite high, the major influence 

on the PPV in these analyses is the prevelance of CD in the population being tested. The 

practical importance of this discussion, is that despite having very high specificity, the use of 

these serological markers in low-prevalence populations would be expected to result in high 

false-positive rates. Below a prevalence of 5%, the false-positive rates may be as high as 30% to 

PPV Based on the Pooled Estimates of Sensitivity 

and Specificity

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

1

0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1

Prevalence

PPV

IgA-EMA-HU-ADULT

IgA-tTG-GP-ADULT

IgA-tTG-HR-ADULT

IgA-EMA-ME-CHILD

IgA-tTG-GP-CHILD

IgA-tTG-HR-CHILD

IgA-EMA-HU-MIXED

IgA-tTG-HR-MIXED

IDDM & Fe Deficiency anemia 

Average population 

1st degree relatives 
148

50% based on our estimates. This may seem counterintuitive, given that the specificity is greater 

than 95% and close to 100% in some cases. One must keep in mind that unless the specifity 

actually equals 100%, the prevalence of CD will influence the PPV. As the specificity 

approaches 100%, the influence of the prevalence decreases. The same interplay occurs between 

the negative predictive value (the probability that a person with a negative test does not have 

CD), and the sensitivity of the test. However, in this case, the NPV rises as the prevalence of the 

disease falls (see Celiac 1 Figures). Given that we have identified that EMA and tTG have a 

sensitivity in the range of 95%, the NPV would be expected to be very high (>96%), particularly 

in low-prevalence populations. This would mean that the false-negative rates with these tests are 

less than 1% to 4%. These data would then suggest that a negative test result would have a high 

probability of being a true negative result, but that a positive test would have to be considered in 

light of the expected prevalence of CD in the tested population. If the expected prevalence is in 

the range of 10% or lower, then the possibility that the result represents a false-positive should 

be considered. Lastly, one must not forget the discussion regarding the true sensitivity of these 

serological markers when lower grade CD lesions are considered. The studies by Rostami et 

al.16 and others, suggest that the sensitivity can be lower than 80%. In fact, both Rostami et al.16

and Tursi et al.424 suggest that the sensitivity for grades less than Marsh IIIa, is in the range of 

30% to 40%. If this is the case, then the nearly perfect NPV discussed above would be expected 

to fall, particularly in groups with a higher prevalence of CD. For example, if the sensitivity was 

really 75%, then the NPV would drop to 88% (12% false negatives) if a population of patients 

with suspected CD was tested. However, because of the strong influence of a low prevalence 

(<15%) on the NPV, the NPV will remain higher than 90%, as long as the sensitivity of the test 

is greater than 50%. 

Expected Outcomes of Treatment of CD 

The four studies of diabetes and CD in children/adolescents that evaluated the impact of a 

GFD found that body composition parameters improved on the GFD, but HbA1c levels did not 

improve. Some studies observed an increase in the insulin requirements after introduction of a 

GFD, which could be explained by improved absorption of nutrients. 

The results of studies on anthropometrics and body composition in CD patients are variable 

due to differences in populations, and methods used to evaluate body composition. Overall, 

weight and BMI improves after starting a GFD. Individuals with CD may have a lower BMI 

when compared with controls because of lower daily energy intakes, particularly in those who 

strictly follow a GFD. 

A few small studies have evaluated the impact of the diet on nutritional parameters in newly 

diagnosed symptomatic CD patients. These studies found that nutritional status does improve in 

the majority of subjects with CD on a GFD. Certain biochemical parameters such as ferritin may 

take longer to normalize. There is evidence that the recovery of nutritional status is linked to 

improvement of villous atrophy. Larger studies of nutritional status in those with classical and 

silent CD patients and the relationship of biochemical values to changes in histological grade on 

small bowel biopsy and compliance with the GFD would be helpful. 

Compliance with the GFD was assessed in adolescent populations in three studies and the 

results varied. Compliance with a strict GFD was greater in those who were symptomatic, 

compared with those who were diagnosed via a screening program. Another study in adults by 

Ciacci et al.460 looked at the correlation between intestinal biopsy and compliance (assessed by 
149

dietary interview) and found that that intestinal damage was significantly associated with dietary 

compliance. Low or very low compliance with a GFD had a PPV of 92.8%, and good 

compliance had a negative PPV of 96.8%. This study also suggested that those with more severe 

symptoms at diagnosis were more likely to have better compliance. Given the poorer 

compliance in those without symptoms, different strategies to promote adherence with the GFD 

may need to be developed if screening for CD is promoted. 

The justification for screening the general population for CD would be strengthened by wellconducted comprehensive cost-effective analyses. Only one study360 appeared to include the 

majority of the components that have been recommended for the reporting of cost-effectiveness 

analyses (CCOHTA, Guidelines for Economic Evaluation of Pharmaceuticals: Canada, 1997). 

None of the analyses incorporated the use of health related quality of life or utility assessments. 

Fractures/BMD/Osteoporosis/Osteopenia 

There were a number of methodological limitations in the studies that examined bone-related 

consequences of CD. Limitations included: selection of representative cases and controls, 

ascertainment of the outcome and failure to identify and control for relevant co-interventions 

such as calcium and vitamin D. 

The issue of whether fractures are increased with individuals with CD appears to be 

somewhat controversial based on results of the included studies. Both Thomason et al.394 and 

Vestergaard et al.388 did not find increased fracture rates for CD subjects, whereas, the recent 

population-based study by West et al.385 did find an increased rate of fractures. This is an 

important issue to clarify since osteoporotic fractures are one of the key reasons for promoting 

strict adherence to the GFD and for making decisions about screening. In some studies, the 

sample sizes were small and may not have been large enough to detect an increased risk in 

fractures in subjects with CD relative to controls. In addition, methodologies and study 

populations varied, and not all studies controlled for duration of CD. Moreno et al.392 found that 

the risk of fracture in subclinical and silent cases of CD was not significantly different from that 

of controls. Overall, the risk of fracture seemed to increase with age as one would anticipate and 

may be greater in those patients who were clinically symptomatic. Based on results of current 

studies, the risk of fracture appears to be highest prior to diagnosis of CD and diminishes once 

individuals are on GFD. This latter finding would be consistent with the increase in BMD that is 

seen after 1 year on a GFD. Additional population based fracture studies would be useful to 

clarify the relative and absolute risk of fracture in CD and to determine if it differs in 

asymptomatic cases. 

Overall, the studies consistently documented an increased prevalence of 

osteoporosis/osteopenia in newly diagnosed patients relative to controls. There was a significant 

increase in BMD, especially within the first year of being on a GFD. Some of the variability in 

the results could be attributed to proportion that were compliant with the diet and use of cointerventions such as calcium and vitamin D. Moreno et al.392 found that the lumbar spine BMD 

did not differ in groups according to clinical presentation, but they did find a significantly lower 

T score of the femoral neck BMD in classically symptomatic cases versus subclinical or silent 

cases. Mustalahti et al.,378 however, found that BMD in the spine was lower in asymptomatic 

cases. 

Based on the two studies in children,352,377 BMD appears to normalize in children after 

treatment with a GFD. The normalization of BMD in children would support the need for early 
150

diagnosis of CD and treatment. However, in children skeletal growth may affect BMD, with 

some of the change relating to changes in growth. Most studies of BMD in adults on a GFD 

have found that the BMD is still reduced at all sites when compared to normal controls. One 

study suggested that those without secondary hyperparathyroidism at time of diagnosis may 

normalize their BMD, but this finding was not replicated. A large BMD study with baseline and 

follow-up small bowel biopsy data, and documentation of clinical presentation, percent 

compliance with the GFD and adjustment of co-interventions is recommended to give us 

accurate information on bone-related consequences of CD. 

Mortality 

The majority of observational studies have demonstrated an increase in overall mortality rate 

(SMR of 2 or greater) in subjects with CD when compared with the general population. The 

increase in mortality can be attributed to deaths from malignant diseases, respiratory, and 

digestive diseases. The increase in mortality appears to be greatest within the first 3 years after 

diagnosis and declines over time. The mortality rate seems to increase with longer delays in 

diagnosis and poor adherence to the GFD. Perhaps one of the most important points from the 

Corraro study,362 is that the mortality rate was not increased compared to the general population 

for those individuals who had mild symptoms or were asymptomatic. This latter result has 

potential implications for population screening for CD. 

Celiac 5: Promoting or Monitoring Adherence to a GFD 

Monitoring Adherence to a GFD 

Some of the same concerns expressed in the other celiac objectives, regarding clinical 

definitions, histological criteria, and the performance of the serological tests, are repeated when 

the results of the studies on monitoring adherence to a GFD are considered. Foremost in 

facilitating the interpretation of these studies is the question of what to consider as the 

histological criteria to define recovery on a GFD. Certainly normalization to Marsh 0 would 

constitute recovery, but what about improvement to Marsh I or II, or even accepting Marsh IIIa? 

The distinction has important implications for assessing the strength of the correlation between 

histological and serological improvement, and in this regard, different studies have adopted 

different cut-offs. 

It is clear from the presented studies that improvement of symptoms does not offer an 

accurate assessment of adherence to a GFD as judged by interview or by biopsy. This point is 

illustrated in the study by Kluge et al.461. In follow-up of 18 adult patients with CD, all patients 

felt well and appeared to be clinically in remission. Nonetheless, only 17% of the patients 

reported being on a strict GFD. Biopsy assessment of eight patients showed six with total villous 

atrophy including one patient who reported strict adherence to GFD. The remaining two patients 

did not have villous atrophy but the mucosa was not normal, including an excess of IELs. Thus, 

small amounts of gluten may provoke a histologic change without clinical symptoms which may 

be an important reason why adherence to GFD may be less than perfect. In other words, noncompliance does not necessarily translate into noticeable consequences for the patient. 
151

Furthermore, it is increasingly recognized that most CD patients don’t have symptoms, so 

reliance on symptomatic improvement is clearly not adequate. 

There is good evidence that mucosal recovery following institution of GFD is slower and 

more incomplete than previously assumed, especially in adults.405,411,414 Whether this slow 

recovery is due to dietary transgression, inadvertent gluten intake or whether this is simply the 

natural history of the disease is less clear. This has definite implications for the interpretation of 

both biopsy and serology results in monitoring adherence to GFD, particularly in the short run. 

With the advent of the newer and more sensitive serologic tests for CD (EMA, tTG), the 

possibility of a reduction in the need for follow-up biopsies and a move towards non-invasive 

serological monitoring has been proposed. The question arises as to whether serology can detect 

dietary transgressions and reasonably mirror histological improvement on a GFD. 

A number of studies show that values of serologic markers will fall with increasing duration 

of GFD, whether one looks at IgA-AGA, IgA-EMA, or IgA-tTG. As well, several studies 

suggest that in both adults and children, increasing degrees of non-compliance with a GFD, are 

more likely to be associated with positive serologic tests.396,402,408. The question, however, is not

whether serology can pick-up major transgressions such as with a gluten challenge which it is 

clearly capable of assessing,400,404 but rather if serology can pick-up milder degrees of dietary 

non-compliance and reasonably reflect histological status. A high rate of falsely-negative 

serology with lesser degrees of dietary transgression would diminish serology as a means of 

accurately monitoring adherence. 

In both adults and children, the sensitivity of serology for picking-up dietary transgressions 

based on interview or self-reporting is disappointing.401,402,410,415 One conflicting study412

showed a good correlation between serology and adherence. This likely reflects the way patients 

were categorized, and it is likely that in this study, patients with lesser degrees of dietary 

transgression were categorized as compliant. In general, there is a significant rate of normal 

serology in patients identified as not adhering to a GFD. Furthermore, evidence from several 

studies suggests that serology, regardless of the actual test used, does not adequately reflect the 

mucosal state in adults.398,403,407,409,409,413 Surprisingly, it seems that serology may be normal, not 

only in Marsh I or II lesions, but also when there is villous atrophy present.398,407,409,413 Although 

the specificity of various serologic markers for villous atrophy seems better than sensitivity,398

the NPV of serology would suggest that a negative test does not offer high assurance of the 

absence of villous atrophy. 

As discussed earlier, mucosal recovery can be a slow process. It may be that serologic 

markers may better reflect histology in long-term follow-up. Certainly, in the range of follow-up 

of these studies (6-30 months), serology may be negative despite villous atrophy. There is 

evidence that even in longer follow-up, serology does not accurately reflect adherence.398,402,410

In younger patients, IgA-AGA and IgA-EMA-ME may better represent the mucosal 

state.397,415 These studies are in keeping with the impression that in children and adolescents, 

mucosal recovery is faster and more complete. In children, serology seems to be a better marker 

of the absence of villous atrophy. Still, serology may be negative in the face of lesser degrees of 

histologic abnormality without villous atrophy.397 The significance of such lower-grade biopsy 

abnormalities, although, is unclear. 

It is possible that IgA-AGA may rise faster with non-compliance to GFD than other 

markers.396,400 However, there is little direct evidence to show superiority of one serologic test 

over another in monitoring adherence. 
152

Perhaps an important question that arises from this discussion, with particular relevance to 

symptomatic CD patients, is: “is it good enough for CD patients to show symptomatic 

improvement and a corresponding fall in, or normalization of, a sensitive serological marker 

without need for ‘normalization’ of the intestinal mucosa?” Unfortunately, this question is not 

an easy one to answer since many of the outcome studies in CD, particularly for lymphoma and 

mortality, did not specifically address differences in histologic grade. Furthermore, we identified 

no clear evidence suggesting that refractory sprue was the result of dietary indiscretion as 

opposed to a different spectrum of CD. Nonetheless, histological improvement appears to be 

important. For example, one study356 demonstrated that osteoporotic patients with CD on a GFD 

who had Marsh III lesions had lower median Z-scores than those with grades less than Marsh III, 

while another study demonstrated a significant correlation of nutritional status measured by 

histomorphometric index, with the severity of the histological biopsy grade.346 In the former 

study as well as one other study,358 histologic grade correlated with degree of IDA, all suggesting 

that the goal of monitoring should be to assess degree of histological improvement. 

It can be concluded that the return of serologic markers to normal is associated with duration 

of GFD and degree of patient compliance. Unfortunately, the correlation remains imperfect, 

especially in adults, and seems to reflect gross rather than minor degrees of dietary 

transgressions. Serological tests seem to have a higher specificity than sensitivity for dietary 

transgressions. It is recognized that this area is controvercial and that clinicians are moving 

away from routine follow-up biopsy as a means to assess dietary compliance. It seems 

reasonable to suggest that improvement in clinical parameters, and disappearance of serological 

markers would be an adequate measure of response to a gluten free diet. In children, because of 

their faster and more complete mucosal recovery, this strategy of using serology may be an 

appropriate means to monitor adherence. In adults, however, the situation is somewhat more 

complex. Therefore, while serology certainly can be an adjunct means to monitor adherence to a 

GFD, consideration should be given to assessing histological improvement since some evidence 

exists to suggest that mucosal improvement to at least below a Marsh III appears to be important 

from an outcomes perspective. If biopsy is to be utilized as a means of assessing adherence to a 

GFD in adults, the timing of the biopsy needs to take into consideration the slower mucosal 

healing in adults, and should therefore be performed after 1 year to 1.5 years of a GFD. 

Interventions to Promote Adherence to a GFD 

Changes in dietary habits are difficult to attain and maintain. The barriers to compliance are 

many. No interventions to promote compliance with GFD have been studied and found to be 

effective. Adding to the difficulty of assessing any proposed intervention is the lack of certainty 

as to how best to measure GFD compliance. 

The existing evidence suggests a positive correlation between parental socioeconomic status, 

education, knowledge of CD, and the compliance of their children.416,418 Compliant children 

may also have a better knowledge of CD420 than those children who are non-compliant. 

Improved knowledge in adults also appears to correlate with compliance.419 It is, therefore, not 

unreasonable to suggest that interventions designed to improve knowledge about CD in general, 

and about GFD, and specifically how to identify gluten-containing products, would likely 

improve compliance with a GFD. Improving knowledge regarding gluten-containing food 

products and additives would also likely improve self-confidence in choosing gluten-free foods 

as suggested by Lamontagne et al.419 Improved knowledge of outcomes of untreated CD may 
153

also improve compliance. Such information interventions, however, would need to be 

prospectively evaluated to ensure that they perform as expected. 

Membership in a local celiac society appears to be an effective means of promoting 

compliance with a GFD. This is not surprising since such organizations provide CD patients 

with not only improved knowledge regarding their disease, and the intricacies of the GFD, but 

also provide emotional and social support. 

It is interesting that one study417 has demonstrated lower rates of compliance in children 

detected by screen as compared with those diagnosed on the basis of symptoms. It seems logical 

that if there are no obvious detrimental symptoms from a gluten-containing diet, that children 

and likely adults will be less likely to be compliant. The authors speculate that since screendetected patients had a higher mean age of diagnosis, compliance might be promoted by earlier 

identification. They speculate that earlier detection would avoid the difficulty of changing 

formed eating habits. 

Is early detection of CD an effective intervention to promote compliance? It appears rational 

that it would be easier to follow a GFD if it were introduced at an earlier age. There are some 

interesting observations 417that suggest that diagnosis in early childhood is associated with 

improved compliance.421 Unfortunately, the issue of compliance in asymptomatic screenpositive individuals casts doubt on the positive downstream effects of screening asymptomatic 

populations for CD, particularly if the low-compliance rates in asymptomatic individuals can be 

reproduced in other studies. 

In summary, it is suggested by the results of this report that a multidisciplinary approach to 

patient and parent education and support by physicians, dieticians, and celiac societies, possibly 

employing formal knowledge and decision support interventions that involve the patient (and 

parent) directly, are likely to improve compliance in individuals diagnosed with CD. Formal 

testing of interventions and programs would be valuable. 

Strength of the Body of Evidence 

Celiac 1 

Overall, the quality of the diagnostic studies assessed in the Celiac 1 objective was quite 

good, due largely to our stringent inclusion criteria. However, 59% of the included studies 

reported using a selected patient population that may not be representative of a clinicallyrelevant population. This is likely related to study design. In addition, only 11% of the studies 

reported on whether the reference test was reported without knowledge of the index test. 

However, we felt that this was not a major threat to the validity of the studies. 

Two other factors that affect the interpretation of these results, yet were not captured in the 

quality assessments, are the threshold effects for determining the positivity of a serological test, 

and the high prevalence of CD in these studies (see above). With these considerations in mind, 

the overall strength of the evidence is quite good. 
154

Celiac 2 

The overall quality of reports of the included studies in the Celiac 2 objective was found to 

be marginal to fair. For example, most of the studies did not report on whether the patients were 

consecutively enrolled, a factor that could contribute to selection bias. However, setting aside 

the quality of individual studies, from a policy perspective, the strength of the evidence is fairly 

good in that the study populations were selected to reflect that of a North American/Western 

European descent, that should reflect the demographics of the US population. 

Celiac 3 

The studies included in the Celiac 3 objective were found overall, to be of good quality. 

Again, the overall strength of the evidence is due largely to the stringent inclusion criteria, such 

as the requirement for the reporting of standardised rates for the outcomes based on rates from 

the local general population, and the overall good quality of the included studies. 

Celiac 4 

The majority of studies included in this objective were single group “before–after” studies, 

although some had in addition a comparative healthy control group. We could not identify any 

quality instruments for this type of study design and in general, this type of study is considered 

weak, particularly in the absence of a control group. Overall, however, the strength of the 

evidence for this objective is fair to good and suggests that the results can be used for policy 

decisions with the understanding that this area of CD research is still relatively new and requires 

further high quality studies. 

Celiac 5 

The majority of studies in this objective were also of a “before–after” design. However, in 

this setting, this design may not pose a major limitation, since the purpose of the study is to 

assess the change in serology and histology after introduction of a GFD. In this regard, the 

strength of the evidence for monitoring adherence to a GFD is fairly good. However, there is 

almost a complete absence of studies of interventions for the promotion of adherence to a GFD. 
155

Future Research 

This review has allowed us to identify several areas in need of future research. Perhaps the 

most important of these is a need for the development of a consensus on the definition of CD in 

the era of advanced serological testing. As discussed in the report, this distinction of what one 

calls CD has profound implications for each of the requested task order objectives. Do screenpositive patients without villous atrophy have CD. Certainly the preliminary evidence suggests 

that this is the situation in many cases. However, what is required is a new definition of a gold 

standard for the diagnosis of CD. This new gold standard may include a combination of 

serology, biopsy and HLA testing. Such a gold standard, when used in studies with a time 

dimension (e.g., response to a GFD or gluten challenge; extended follow-up), would help answer 

some of the uncertainties identified in this report including: the real performance of the 

serological tests when low-grade lesions are considered CD; the diagnostic performance of 

biopsy alone; the outcomes of patients with these low-grade lesions; and, those that would be 

“missed” using current screening strategies. Even in the absence of a new gold standard, we 

could not identify a well-conducted study of the diagnostic performance of the various 

serological markers when applied to an average population (i.e., one with a prevalence of CD in 

keeping with the range identified for average risk), with the entire cohort being investigated 

equally (i.e., all are biopsied). Such a study would at least be able to shed light on the 

performance of these tests in average-risk patients, and since all patients are biopsied, the 

relationship of histology to serology could be further assessed. 

On a similar theme, we have identified multiple studies that suggest the importance of 

histological improvement on a GFD. This is a controversial area since in common clinical 

practice, clinicians are moving away from routine follow-up biopsy. It seems reasonable to 

believe that improvement in clinical parameters with loss of serological markers is adequate 

evidence of response to a GFD. In children, this issue may be less important since histological 

improvement is much more rapid and complete than in adults, and correlation with serology 

seems better. However, we have identified multiple studies in adults that suggest poor 

correlation between serology and improvement of histology on a GFD, and other studies that 

suggest that serology is useful for detecting gross dietary indiscretion, but not minor occurrences. 

Therefore, the question that arises is what constitutes adequate improvement on a GFD, and what 

are the criteria to define this improvement. Based on the lymphoma literature that suggests that 

this malignancy may arise from chronic antigenic stimulation and immune activation, what are 

the outcomes of adults with clinical improvement, yet persistent histological abnormalities? Are 

some histological features, such as reduction of mucosal lymphocytes, more important markers 

of improvement and possibly prognosis than other features such as villous height? 

We feel that clarification of these fundamental questions is necessary for the conduct of 

future studies in all areas of CD, and in particular studies of the diagnostic tests and the outcomes 

in CD, since these are so dependent on the definitions discussed above. 
156

Conclusion 

This report has provided a systematic review on five broad areas of CD, with each of these 

areas including important sub-components. Perhaps one of the most important findings of this 

report is the understanding of the importance of how one chooses to define CD in the era of 

serological testing, and how this apparently clear-cut task has profound implications on all the 

results presented in this report. Specifically, can CD be diagnosed solely on the basis of 

serology? Is some degree of villous atrophy necessary for the diagnosis of CD? These questions 

have important implications downstream of the diagnosis as well. Do CD patients without 

symptoms or villous atrophy have the same risk of complications as those with villous atrophy? 

Is serological improvement on a GFD sufficient to reduce CD complications or must there be 

documented histological improvement, and what degree of histological improvement is 

necessary? 

The results of the Celiac 1 objective suggest that in the era of EMA and tTG antibody testing, 

AGA testing in both children and adults has a limited role. The sensitivity and specificity of 

EMA and tTG are quite high (over 95% for sensitivity, and close to 100% for specificity), as are 

their PPVs and NPVs, but as previously discussed, one has to be aware that the reported 

diagnostic parameters are taken from studies in which the prevalence of CD was, for the most 

part, much higher than that seen in usual clinical practice and certainly the PPV of these tests 

may not be as high as reported when these tests are applied in general population screening. The 

bulk of the evidence on the diagnostic characteristics of these tests was derived from studies that 

defined CD as having at least some degree of villous atrophy. We have identified studies that 

suggest that the sensitivity of these tests drops, at times significantly, when applied to 

populations with CD with lower-grade histological lesions. This not only has implications 

regarding those patients with “mild” CD who were missed during screening efforts, but also puts 

into question the nearly perfect NPV of these tests. 

HLA DQ2/DQ8 testing appears to be a useful adjunct in the diagnosis of CD. The test has 

high sensitivity, in excess of 90% to 95%, but because around 30% of the general population and 

an even higher proportion of “high-risk” subjects including diabetics and family members also 

carry these markers, the specificity of this test is not ideal. The greatest diagnostic utility of this 

test appears to be its NPV. 

Biopsy itself, when used with a strict cut-off requiring villous atrophy, appears to have high 

specificity, but poor sensitivity. Using lower grade cut-offs clearly improves sensitivity, but 

because of the wide differential of causes of histological lesions similar to Marsh I to IIIa, the 

specificity suffers. The use of histomorphometric measures, such as quantification of γδ+ IELs, 

are likely to allow for the use of lower-grade cut-offs while maintaining reasonable specificity. 

Ultimately, a trial utilizing multiple diagnostic tests in an attempt to capture as many CD patients 

in a clinically-relevant population as possible, with a time dimension including a response to a 

GFD or gluten challenge, is required to fully assess the diagnostic characteristics of biopsy alone. 

This type of study would be able to characterize the false-positive and false-negative rates if all 

studied patients are followed forward in time. 

The included prevalence studies demonstrated important differences in execution, tests for 

prevalence assessment, and in patient sampling, and their results also have to be interpreted in 

the light of some of the limitations that have been identified regarding the diagnostic 

performance of the tests for CD. Nonetheless, the results of this report suggest that CD is a very 

common disorder with a prevalence in the general population that is likely close to 1:100 (1%). 
157

Several high-risk groups with a prevalence of CD greater than that of the general population 

have been identified including those suspected of having CD, family members of CD patients, 

type I diabetics, and those with IDA or low BMD. Additionally, the review identified multiple 

other high-risk groups such as those with Down Syndrome, short stature, and infertility, to name 

a few, though their inclusion was beyond the scope of this report. These results would suggest 

that at the very least, high-risk groups should be screened for CD. If the performance of the 

noninvasive serological tests can be verified in the relatively “low prevalence” situations in 

general unselected populations, then population screening may also be advisable, particularly if a 

greater understanding of the consequences of missing early low-grade CD can be obtained, and 

the issues of low-compliance with a GFD of asymptomatic screen identified patients can be 

addressed. 

CD is known to be associated with GI lymphoma. The results of this report confirm this 

strong association, with the limitations indicated in the text. Nonetheless, the report identified 

SIR for lymphoma that ranged from 4 to 40, and SMR that ranged from 11 to 70. GI lymphoma 

is believed to arise as a result of chronic antigenic stimulation, which leads to the development of 

a clonal T-cell population with usually a refractory intermediate stage. We have identified 

epidemiologic data that supports this notion, and suggests that a diagnostic delay, and in 

particular diagnosis of CD in adulthood, as apposed to in childhood, is associated with poorer 

outcomes. Fortunately, several studies suggest that adherence to a GFD reduces the risk of 

lymphoma in CD patients. These findings underscore the importance of early diagnosis and 

treatment of CD. 

The consequences of testing for, and identifying CD patients, is expected to have a positive 

impact on patient outcomes be it either from a reduced risk of lymphoma with early diagnosis 

and treatment of CD or from improvements in nutritional status, BMI, and BMD. The 

consequences of testing in at-risk and symptomatic patients appears to be more straightforward 

since these patients appear to be more compliant with a GFD and would be expected to benefit 

from this intervention. The data is less clear for asymptomatic screen-identified patients, 

particularly those who are truly silent and/or don’t have fully developed villous atrophy since, on 

the one hand the outcome of such patients has not been extensively studied, and on the other 

hand, compliance with a GFD appears problematic, particularly for those diagnosed in 

adulthood. 

Finally, no specific interventions have been identified that promote adherence to a GFD, but 

education of patients and family members about CD and about the intricacies of the GFD 

through multidisciplinary teams, and participation in local CD societies, has been show to 

improve compliance. Therefore, the development and evaluation of formal educational 

interventions in collaboration between healthcare professionals and CD societies would appear to 

be a means to build on the methods that appear to already improve patient compliance. 

Monitoring of adherence to a GFD appears to be important, since improvement in histologic 

grade has been associated with improved BMD, IDA, and nutritional status. The serological 

markers appear to be adequate for detecting gross dietary indiscretion, and responding to gluten 

challenge, but unfortunately, they have poor sensitivity for detecting lesser degrees of dietary 

indiscretion, and have inadequate correlation with histological improvement at least in the shortterm. It is true that histological improvement tends to lag behind clinical and serological 

improvement, especially in adults in whom improvement may never be complete, but even 

considering this, a negative serological test has been shown to miss patients with persistent 

villous atrophy. The recognition of persistent villous atrophy appears to be important since 
158

improvement beyond this level is associated with the improved outcomes listed above. It should 

be noted, however, that we could not identify a controlled study that objectively determined the 

level of histological improvement that would be associated with improved outcomes, and this is 

an area for future study. Although somewhat controversial, nonetheless, based on this report it 

would appear that follow-up biopsy, at least 1 year after GFD in adults to document 

improvement of the histological grade, would be valuable. 
Note: Appendixes and Evidence Tables are provided electronically at 

http://www.ahrq.gov/clinic/tp/celiactp.htm 

159

References and Included Studies 

 1. Marsh MN. Gluten, major histocompatibility 

complex, and the small intestine: A molecular 

and immunobiologic approach to the spectrum of 

gluten sensitivity ('celiac sprue'). 

Gastroenterology 1992;102(1):330-54. 

 2. McNeish AS, Harms HK, Rey J, Shmerling DH, 

Visakorpi JK, Walker-Smith JA. The diagnosis of 

coeliac disease. A commentary on the current 

practices of members of the European Society for 

Paediatric Gastroenterology and Nutrition 

(ESPGAN). Archives of Disease in Childhood 

1979;54(10):783-6. 

 3. Oberhuber G, Granditsch G, Vogelsang H. The 

histopathology of coeliac disease: time for a 

standardized report scheme for pathologists. 

European Journal of Gastroenterology & 

Hepatology 1999;11(10):1185-94. 

 4. Walker-Smith JA, Guandalini S, Schmitz J, 

Shmerling DH, Visakorpi JK. Revised criteria for 

diagnosis of coeliac disease. Arch Dis Child 

1990;65(8):909-11. 

 5. van de WY, Kooy Y, van Veelen P, Vader W, 

Koning F, Pena S. Coeliac disease: it takes three 

to tango! Gut 2000;46(5):734-7. 

 6. Papadopoulos GK, Wijmenga C, Koning F. 

Interplay between genetics and the environment 

in the development of celiac disease: perspectives 

for a healthy life. Journal of Clinical 

Investigation 2001;108(9):1261-6. 

 7. Sollid LM, McAdam SN, Molberg O, Quarsten 

H, Arentz-Hansen H, Louka AS, et al. Genes and 

environment in celiac disease. Acta Odontologica 

Scandinavica 2001;59(3):183-6. 

 8. Sollid LM, Markussen G, Ek J, Gjerde H, Vartdal 

F, Thorsby E. Evidence for a primary association 

of celiac disease to a particular HLA-DQ 

alpha/beta heterodimer. Journal of Experimental 

Medicine 1989;169(1):345-50. 

 9. Ploski R, Ek J, Thorsby E, Sollid LM. On the 

HLA-DQ(alpha 1*0501, beta 1*0201)-associated 

susceptibility in celiac disease: a possible gene 

dosage effect of DQB1*0201. Tissue Antigens 

1993;41(4):173-7. 

 10. Ploski R, Ascher H, Sollid LM. HLA genotypes 

and the increased incidence of coeliac disease in 

Sweden. Scand J Gastroenterol 

1996;31(11):1092-7. 

 11. Holopainen P, Mustalahti K, Uimari P, Collin P, 

Maki M, Partanen J. Candidate gene regions and 

genetic heterogeneity in gluten sensitivity. Gut 

2001;48(5):696-701. 

 12. Kagnoff MF. Celiac disease pathogenesis: the 

plot thickens. Gastroenterology 2002;123(3):939-

43. 

 13. Feldman M, Friedman LS, Sleisenger MH. 

Sleisenger and Fordtran's Gastrointestinal and 

Liver Disease. 7th edition W.B. Saunders; 2003. 

 14. Fasano A, Catassi C. Current approaches to 

diagnosis and treatment of celiac disease: an 

evolving spectrum. Gastroenterology 

2001;120(3):636-51. 

 15. Fasano A, Berti I, Gerarduzzi T, Not T, Colletti 

RB, Drago S, et al. Prevalence of celiac disease 

in at-risk and not-at-risk groups in the United 

States: a large multicenter study. Archives of 

Internal Medicine 2003;163(3):286-92. 

 16. Rostami K, Kerckhaert J, Tiemessen R, von 

Blomberg BM, Meijer JW, Mulder CJ. 

Sensitivity of antiendomysium and antigliadin 

antibodies in untreated celiac disease: 

disappointing in clinical practice. American 

Journal of Gastroenterology 1999;94(4):888-94. 

 17. Rosenthal DS, Roop DR, Huff CA, Weiss JS, 

Ellis CN, Hamilton T, et al. Changes in photoaged human skin following topical application of 

all-trans retinoic acid. Journal of Investigative 

Dermatology 1990;95(5):510-5. 

 18. Wahab PJ, Meijer JWR, Goerres MS, Mulder 

CJJ. Coeliac disease: changing views on glutensensitive enteropathy. Scandinavian Journal of 

Gastroenterology Supplement 2002;(236):60-5. 

 19. Whiting P, Rutjes AW, Reitsma JB, Bossuyt PM, 

Kleijnen J. The development of QUADAS: a tool 

for the quality assessment of studies of diagnostic 

accuracy included in systematic reviews. BMC 

Med Res Methodol 2003;3(1):25. Available: 

PM:14606960. 
160 

 20. Wells GA, Shea B, O'Connell D, Peterson 

J,Welch V, Tugwell P. The Newcastle-Ottawa 

Scale (NOS) for assessing the quality of 

nonrandomised studies in meta-analyses. 3rd 

Symposium on Systematic Reviews: Beyond the 

Basics, July 2000 in Oxford.2000. 

 21. Ophthalmology Study Design Worksheet #3 

Noncomparative (nonrandomized, noncontrolled) 

Interventional Case Series. 2004. 

Ref Type: Internet Communication 

 22. Moses LE, Shapiro D, Littenberg B. Combining 

independent studies of a diagnostic test into a 

summary ROC curve: data-analytic approaches 

and some additional considerations. Stat Med 

1993;12(14):1293-316. Available: PM:8210827. 

 23. Littenberg B, Moses LE. Estimating diagnostic 

accuracy from multiple conflicting reports: a new 

meta-analytic method. Med Decis Making 

1993;13(4):313-21. Available: PM:8246704. 

 24. Deeks J. Systematics reviews of evaluations of 

diagnostic and screening test. Systematic 

Reviews in Health Care: Meta-analysis in 

Context. London: BMJ Books, 2001. 

 25. Deeks J, Altman D, Bradburn J. Statistical 

methods for examining heterogeneity and 

combining results from several studies in metaanalysis. Systematic Review in Health Care. 

Meta-Analysis in Context London: BMJ Books; 

2001. 

 26. Altuntas B, Kansu A, Ensari A, Girgin N. Celiac 

disease in Turkish short-statured children and the 

value of antigliadin antibody in diagnosis. Acta 

Paediatr Jpn 1998;40(5):457-60. 

 27. Ascher H, Hahn-Zoric M, Hanson LA, Kilander 

AF, Nilsson LA, Tlaskalova H. Value of 

serologic markers for clinical diagnosis and 

population studies of coeliac disease. 

Scandinavian Journal of Gastroenterology 

1996;31(1):61-7. 

 28. Ascher H, Lanner A, Kristiansson B. A new 

laboratory kit for anti-gliadin IgA at diagnosis 

and follow-up of childhood celiac disease. 

Journal of Pediatric Gastroenterology and 

Nutrition 1990;10(4):443-50. 

 29. Bahia M, Rabello A, Brasileiro FG, Penna FJ. 

Serum antigliadin antibody levels as a screening 

criterion before jejunal biopsy indication for 

celiac disease in a developing country. Brazilian 

Journal of Medical and Biological Research = 

Revista Brasileira De Pesquisas Medicas E 

Biologicas / Sociedade Brasileira De Biofisica Et 

Al 2001;34(11):1415-20. 

 30. Bardella MT, Trovato C, Cesana BM, Pagliari C, 

Gebbia C, Peracchi M. Serological markers for 

coeliac disease: is it time to change? Digestive 

and Liver Disease - Official Journal of the Italian 

Society of Gastroenterology and the Italian 

Association for the Study of the Liver 

2001;33(5):426-31. 

 31. Berger R, Schmidt G. Evaluation of six antigliadin antibody assays. Journal of 

Immunological Methods 1996;191(1):77-86. 

 32. Biagi F, Pezzimenti D, Campanella J, Vadacca 

GB, Corazza GR. Endomysial and tissue 

transglutaminase antibodies in coeliac sera: a 

comparison not influenced by previous 

serological testing. Scandinavian Journal of 

Gastroenterology 2001;36(9):955-8. 

 33. Bode S, Gudmand-Hoyer E. Evaluation of the 

gliadin antibody test for diagnosing coeliac 

disease. Scandinavian Journal of 

Gastroenterology 1994;29(2):148-52. 

 34. Bode S, Weile B, Krasilnikoff PA, GudmandHoyer E. The diagnostic value of the gliadin 

antibody test in celiac disease in children: a 

prospective study. Journal of Pediatric 

Gastroenterology and Nutrition 1993;17(3):260-

4. 

 35. Bonamico M, Tiberti C, Picarelli A, Mariani P, 

Rossi D, Cipolletta E, et al. Radioimmunoassay 

to detect antitransglutaminase autoantibodies is 

the most sensitive and specific screening method 

for celiac disease. American Journal of 

Gastroenterology 2001;96(5):1536-40. 

 36. Bottaro G, Volta U, Spina M, Rotolo N, Sciacca 

A, Musumeci S. Antibody pattern in childhood 

celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 1997;24(5):559-

62. 

 37. Carroccio A, Iacono G, D'Amico D, Cavataio F, 

Teresi S, Caruso C, et al. Production of antiendomysial antibodies in cultured duodenal 

mucosa: usefulness in coeliac disease diagnosis. 

Scandinavian Journal of Gastroenterology 

2002;37(1):32-8. 

 38. Carroccio A, Iacono G, Montalto G, Cavataio F, 

Soresi M, Kazmierska I, et al. Immunologic and 

absorptive tests in celiac disease: can they replace 

intestinal biopsies? Scandinavian Journal of 

Gastroenterology 1993;28(8):673-6. 

 39. Carroccio A, Vitale G, Di Prima L, Chifari N, 

Napoli S, La Russa C, et al. Comparison of antitransglutaminase ELISAs and an anti-endomysial 

antibody assay in the diagnosis of celiac disease: 
161 

a prospective study. Clinical Chemistry 

2002;48(9):1546-50. 

 40. Cataldo F, Lio D, Marino V, Picarelli A, Ventura 

A, Corazza GR. IgG(1) antiendomysium and IgG 

antitissue transglutaminase (anti-tTG) antibodies 

in coeliac patients with selective IgA deficiency. 

Working Groups on Celiac Disease of SIGEP and 

Club del Tenue. Gut 2000;47(3):366-9. 

 41. Chan AW, Butzner JD, McKenna R, Fritzler MJ. 

Tissue transglutaminase enzyme-linked 

immunosorbent assay as a screening test for 

celiac disease in pediatric patients. Pediatrics 

2001;107(1):E8. 

 42. Chartrand LJ, Agulnik J, Vanounou T, Russo PA, 

Baehler P, Seidman EG. Effectiveness of 

antigliadin antibodies as a screening test for 

celiac disease in children. Cmaj - Canadian 

Medical Association Journal = Journal De 

L'association Medicale Canadienne 

1997;157(5):527-33. 

 43. Chirdo FG, Rumbo M, Carabajal P, Castagnino 

N, Mavromatopulos E, Cirincione V, et al. 

Analysis of anti-gliadin antibodies by 

immunoblot analysis and enzyme-linked 

immunosorbent assay using gliadin fractions as 

antigens. Journal of Pediatric Gastroenterology 

and Nutrition 1999;29(2):171-7. 

 44. Chirdo FG, Rumbo M, Carabajal P, 

Mavromatopulos E, Castagnino N, Anon MC, et 

al. Determination of anti-omega-gliadin 

antibodies in serologic tests for coeliac disease. 

Scandinavian Journal of Gastroenterology 

2000;35(5):508-16. 

 45. Dahele A, Aldhous MC, Humphreys K, Ghosh S. 

Serum IgA tissue transglutaminase antibodies in 

coeliac disease and other gastrointestinal 

diseases. Q J Med 2001;94(4):195-205. 

 46. Di Leo M, Weisz G, Ansaldi BN. Serum and 

salivary antiendomysium antibodies in the 

screening of coeliac disease. Panminerva Medica 

1999;41(1):68-71. 

 47. Dickey W, McMillan SA, Hughes DF. Sensitivity 

of serum tissue transglutaminase antibodies for 

endomysial antibody positive and negative 

coeliac disease. Scandinavian Journal of 

Gastroenterology 2001;36(5):511-4. 

 48. Falth-Magnusson K, Jansson G, Stenhammar L, 

Magnusson KE. Serum food antibodies analyzed 

by enzyme-linked immunosorbent assay (ELISA) 

and diffusion-in-gel (DIG)-ELISA methods in 

children with and without celiac disease. Journal 

of Pediatric Gastroenterology and Nutrition 

1994;18(1):56-62. 

 49. Gillett HR, Freeman HJ. Comparison of IgA 

endomysium antibody and IgA tissue 

transglutaminase antibody in celiac disease. 

Canadian Journal of Gastroenterology = Journal 

Canadien De Gastroenterologie 2000;14(8):668-

71. 

 50. Gonczi J, Skerritt JH, Mitchell JD. A reliable 

screening test for coeliac disease: enzyme-linked 

immunosorbent assay to detect anti-gliadin 

antibodies in serum. Australian and New Zealand 

Journal of Medicine 1991;21(5):723-31. 

 51. Hallstrom O. Comparison of IgA-class reticulin 

and endomysium antibodies in coeliac disease 

and dermatitis herpetiformis. Gut 

1989;30(9):1225-32. 

 52. Hansson T, Dahlbom I, Hall J, Holtz A, Elfman 

L, Dannaeus A, et al. Antibody reactivity against 

human and guinea pig tissue transglutaminase in 

children with celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 2000;30(4):379-

84. 

 53. Iltanen S, Rantala I, Laippala P, Holm K, 

Partanen J, Maki M. Expression of HSP-65 in 

jejunal epithelial cells in patients clinically 

suspected of coeliac disease. Autoimmunity 

1999;31(2):125-32. 

 54. Kaukinen K, Turjanmaa K, Maki M, Partanen J, 

Venalainen R, Reunala T, et al. Intolerance to 

cereals is not specific for coeliac disease. 

Scandinavian Journal of Gastroenterology 

2000;35(9):942-6. 

 55. Kolho KL, Savilahti E. IgA endomysium 

antibodies on human umbilical cord: an excellent 

diagnostic tool for celiac disease in childhood. 

Journal of Pediatric Gastroenterology and 

Nutrition 1997;24(5):563-7. 

 56. Kumar V, Lerner A, Valeski JE, Beutner EH, 

Chorzelski TP, Rossi T. Endomysial antibodies 

in the diagnosis of celiac disease and the effect of 

gluten on antibody titers. Immunological 

Investigations 1989;18(1-4):533-44. 

 57. Ladinser B, Rossipal E, Pittschieler K. 

Endomysium antibodies in coeliac disease: an 

improved method. Gut 1994;35(6):776-8. 

 58. Lerner A, Kumar V, Iancu TC. Immunological 

diagnosis of childhood coeliac disease: 

comparison between antigliadin, antireticulin and 

antiendomysial antibodies. Clinical and 

Experimental Immunology 1994;95(1):78-82. 
162 

 59. Lindberg T, Nilsson LA, Borulf S, Cavell B, 

Fallstrom SP, Jansson U, et al. Serum IgA and 

IgG gliadin antibodies and small intestinal 

mucosal damage in children. Journal of Pediatric 

Gastroenterology and Nutrition 1985;4(6):917-

22. 

 60. Lindquist BL, Rogozinski T, Moi H, Danielsson 

D, Olcen P. Endomysium and gliadin IgA 

antibodies in children with coeliac disease. 

Scandinavian Journal of Gastroenterology 

1994;29(5):452-6. 

 61. Lock RJ, Pitcher MC, Unsworth DJ. IgA antitissue transglutaminase as a diagnostic marker of 

gluten sensitive enteropathy. Journal of Clinical 

Pathology 1999;52(4):274-7. 

 62. Maki M, Holm K, Lipsanen V, Hallstrom O, 

Viander M, Collin P, et al. Serological markers 

and HLA genes among healthy first-degree 

relatives of patients with coeliac disease. Lancet 

1991;338(8779):1350-3. 

 63. McMillan SA, Haughton DJ, Biggart JD, Edgar 

JD, Porter KG, McNeill TA. Predictive value for 

coeliac disease of antibodies to gliadin, 

endomysium, and jejunum in patients attending 

for jejunal biopsy. Bmj (Clinical Research Ed ) 

1991;303(6811):1163-5. 

 64. Meini A, Pillan NM, Villanacci V, Monafo V, 

Ugazio AG, Plebani A. Prevalence and diagnosis 

of celiac disease in IgA-deficient children. 

Annals of Allergy, Asthma & Immunology - 

Official Publication of the American College of 

Allergy, Asthma, & Immunology 

1996;77(4):333-6. 

 65. Pacht A, Sinai N, Hornstein L, Kumar V, IshShalom N, Lerner A. The diagnostic reliability of 

anti-endomysial antibody in celiac disease: the 

north Israel experience. Israel Journal of Medical 

Sciences 1995;31(4):218-20. 

 66. Picarelli A, Sabbatella L, Di Tola M, Gabrielli F, 

Greco R, Di Cello T, et al. Celiac disease 

diagnosis in misdiagnosed children. Pediatric 

Research 2000;48(5):590-2. 

 67. Poddar U, Thapa BR, Nain CK, Prasad A, Singh 

K. Celiac disease in India: are they true cases of 

celiac disease? Journal of Pediatric 

Gastroenterology and Nutrition 2002;35(4):508-

12. 

 68. Rich EJ, Christie DL. Anti-gliadin antibody panel 

and xylose absorption test in screening for celiac 

disease. Journal of Pediatric Gastroenterology 

and Nutrition 1990;10(2):174-8. 

 69. Russo PA, Chartrand LJ, Seidman E. 

Comparative analysis of serologic screening tests 

for the initial diagnosis of celiac disease. 

Pediatrics 1999;104(1 Pt 1):75-8. 

 70. Salmaso C, Ocmant A, Pesce G, Altrinetti V, 

Montagna P, Descalzi D, et al. Comparison of 

ELISA for tissue transglutaminase autoantibodies 

with antiendomysium antibodies in pediatric and 

adult patients with celiac disease. Allergy 

2001;56(6):544-7. 

 71. Sategna-Guidetti C, Grosso S, Bruno M, Grosso 

SB. Comparison of serum anti-gliadin, antiendomysium, and anti-jejunum antibodies in 

adult celiac sprue. Journal of Clinical 

Gastroenterology 1995;20(1):17-21. 

 72. Sblattero D, Berti I, Trevisiol C, Marzari R, 

Tommasini A, Bradbury A, et al. Human 

recombinant tissue transglutaminase ELISA: an 

innovative diagnostic assay for celiac disease. 

American Journal of Gastroenterology 

2000;95(5):1253-7. 

 73. Sulkanen S, Collin P, Laurila K, Maki M. IgAand IgG-class antihuman umbilical cord antibody 

tests in adult coeliac disease. Scandinavian 

Journal of Gastroenterology 1998;33(3):251-4. 

 74. Sulkanen S, Halttunen T, Laurila K, Kolho KL, 

Korponay-Szabo IR, Sarnesto A, et al. Tissue 

transglutaminase autoantibody enzyme-linked 

immunosorbent assay in detecting celiac disease. 

Gastroenterology 1998;115(6):1322-8. 

 75. Tesei N, Sugai E, Vazquez H, Smecuol E, 

Niveloni S, Mazure R, et al. Antibodies to human 

recombinant tissue transglutaminase may detect 

coeliac disease patients undiagnosed by 

endomysial antibodies. Alimentary 

Pharmacology & Therapeutics 

2003;17(11):1415-23. 

 76. Troncone R, Maurano F, Rossi M, Micillo M, 

Greco L, Auricchio R, et al. IgA antibodies to 

tissue transglutaminase: An effective diagnostic 

test for celiac disease. Journal of Pediatrics 

1999;134(2):166-71. 

 77. Valdimarsson T, Franzen L, Grodzinsky E, 

Skogh T, Strom M. Is small bowel biopsy 

necessary in adults with suspected celiac disease 

and IgA anti-endomysium antibodies? 100% 

positive predictive value for celiac disease in 

adults. Digestive Diseases and Sciences 

1996;41(1):83-7. 

 78. Valentini RA, Andreani ML, Corazza GR, 

Gasbarrini G. IgA endomysium antibody: a 

valuable tool in the screening of coeliac disease 
163 

but not its follow-up. Italian Journal of 

Gastroenterology 1994;26(6):279-82. 

 79. Vitoria JC, Arrieta A, Ortiz L, Ayesta A. 

Antibodies to human tissue transglutaminase for 

the diagnosis of celiac disease. Journal of 

Pediatric Gastroenterology and Nutrition 

2001;33(3):349-50. 

 80. Vogelsang H, Genser D, Wyatt J, Lochs H, 

Ferenci P, Granditsch G, et al. Screening for 

celiac disease: a prospective study on the value of 

noninvasive tests. American Journal of 

Gastroenterology 1995;90(3):394-8. 

 81. Volta U, Molinaro N, De Franceschi L, 

Fratangelo D, Bianchi FB. IgA anti-endomysial 

antibodies on human umbilical cord tissue for 

celiac disease screening. Save both money and 

monkeys. Digestive Diseases and Sciences 

1995;40(9):1902-5. 

 82. Whelan A, Willoughby R, Weir D. Human 

umbilical vein endothelial cells: a new easily 

available source of endomysial antigens. 

European Journal of Gastroenterology & 

Hepatology 1996;8(10):961-6. 

 83. Wolters V, Vooijs-Moulaert A, Burger H, 

Brooimans R, De Schryver J, Rijkers G, et al. 

Human tissue transglutaminase enzyme linked 

immunosorbent assay outperforms both the 

guinea pig based tissue transglutaminase assay 

and anti-endomysium antibodies when screening 

for coeliac disease. European Journal of 

Pediatrics 2002;161(5):284-7. 

 84. Di Leo M, Weisz G, Ansaldi BN. Serum and 

salivary antiendomysium antibodies in the 

screening of coeliac disease. Panminerva Medica 

1999;41(1):68-71. 

 85. Artan R. Antigliadin antibody measurement as a 

screening test for childhood coeliac disease. Int 

Med J 1998;5(3):209-12. 

 86. Dahele A, Kingstone K, Bode J, Anderson D, 

Ghosh S. Anti-endomysial antibody negative 

celiac disease: does additional serological testing 

help? Digestive Diseases and Sciences 

2001;46(1):214-21. 

 87. Brandborg LL, Goldberg SB, Breidenbach WC. 

Human coccidiosis--a possible cause of 

malabsorption. New England Journal of Medicine 

1970;283(24):1306-13. 

 88. Hazama H, Omagari K, Masuda J, Ohba K, 

Kinoshita H, Matsuo I, et al. Automated 

enzymatic mitochondrial antibody assay for the 

diagnosis of primary biliary cirrhosis: 

applications of a routine diagnostic tool for the 

detection of antimitochondrial antibodies. Journal 

of Gastroenterology and Hepatology 

2002;17(3):316-23. 

 89. Cheli R, Giacosa A. Inflammatory cell count and 

identification in specific duodenitis. (Celiac 

disease, Whipple's disease and Crohn's disease). 

Comparison with jejunal findings. Endoscopy 

1977;9(3):147-51. 

 90. Talbot HS. A report on sexual function in 

paraplegics. J Urol 1949;61:265-70. 

 91. Fernandez-Arquero M, Polanco I, Escobar H, 

Figueredo MA, de la Concha EG, ClericiLarradet N, et al. HLA-DQ alleles and 

susceptibility to celiac disease in Spanish 

children. Tissue Antigens 1995;45(2):145-7. 

 92. Palavecino EA, Mota AH, Awad J, DeRosa S, 

Herrera M, Chertkoff L, et al. HLA and celiac 

disease in Argentina: involvement of the DQ 

subregion. Disease Markers 1990;8(1):5-10. 

 93. Spurkland A, Ingvarsson G, Falk ES, Knutsen I, 

Sollid LM, Thorsby E. Dermatitis herpetiformis 

and celiac disease are both primarily associated 

with the HLA-DQ (alpha 1*0501, beta 1*02) or 

the HLA-DQ (alpha 1*03, beta 1*0302) 

heterodimers. Tissue Antigens 1997;49(1):29-34. 

 94. Hall MA, Lanchbury JS, Lee JS, Welsh K, I, 

Ciclitira PJ. HLA-DQ2 second-domain 

polymorphisms may explain increased transassociated risk in celiac disease and dermatitis 

herpetiformis. Human Immunology 

1993;38(4):284-92. 

 95. Spurkland A, Sollid LM, Ronningen KS, Bosnes 

V, Ek J, Vartdal F, et al. Susceptibility to develop 

celiac disease is primarily associated with HLADQ alleles. Human Immunology 1990;29(3):157-

65. 

 96. Bao F, Yu L, Babu S, Wang T, Hoffenberg EJ, 

Rewers M, et al. One third of HLA DQ2 

homozygous patients with type 1 diabetes express 

celiac disease-associated transglutaminase 

autoantibodies. Journal of Autoimmunity 

1999;13(1):143-8. 

 97. Martin-Villa JM, Lopez-Suarez JC, Perez-Blas 

M, Martinez-Laso J, Ferre-Lopez S, Garcia-Torre 

C, et al. Coeliac- and enteropathy-associated 

autoantibodies in Spanish insulin-dependent 

diabetes mellitus patients and their relation to 

HLA antigens. Journal of Diabetes and Its 

Complications 2001;15(1):38-43. 
164 

 98. Kaukinen K, Partanen J, Maki M, Collin P. HLADQ typing in the diagnosis of celiac disease. 

American Journal of Gastroenterology 

2002;97(3):695-9. 

 99. Saukkonen T, Ilonen J, Akerblom HK, Savilahti 

E. Prevalence of coeliac disease in siblings of 

patients with Type I diabetes is related to the 

prevalence of DQB1*02 allele. Diabetologia 

2001;44(8):1051-3. 

 100. Congia M, Frau F, Lampis R, Frau R, Mele R, 

Cucca F, et al. A high frequency of the A30, B18, 

DR3, DRw52, DQw2 extended haplotype in 

Sardinian celiac disease patients: further evidence 

that disease susceptibility is conferred by DQ 

A1*0501, B1*0201. Tissue Antigens 

1992;39(2):78-83. 

 101. Herrera M, Theiler G, Augustovski F, Chertkoff 

L, Fainboim L, DeRosa S, et al. Molecular 

characterization of HLA class II genes in celiac 

disease patients of Latin American Caucasian 

origin. Tissue Antigens 1994;43(2):83-7. 

 102. Petronzelli F, Ferrante P, Triglione P, Bonamico 

M, Mazzilli MC. Oligotyping of celiac multiplex 

families with the 11th International 

Histocompatibility Workshop reagents. Tissue 

Antigens 1991;38(5):238-9. 

 103. Mantovani V, Corazza GR, Angelini G, Delfino 

L, Frisoni M, Mirri P, et al. Molecular analysis of 

HLA-DQ A alleles in coeliac disease lack of a 

unique disease-associated sequence. Clinical and 

Experimental Immunology 1991;83(1):74-8. 

 104. Agardh D, Nilsson A, Carlsson A, Kockum I, 

Lernmark A, Ivarsson SA. Tissue 

transglutaminase autoantibodies and human 

leucocyte antigen in Down Syndrome patients 

with coeliac disease. Acta Paediatrica (Oslo, 

Norway - 1992) 2002;91(1):34-8. 

 105. Bonamico M, Mazzilli MC, Morellini M, Vania 

A, Carpino F, Nicotra MR, et al. Expression of 

class II MHC antigens in the intestinal epithelium 

of pediatric celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 1989;9(3):269-

75. 

 106. Bonamico M, Morellini M, Mariani P, Triglione 

P, Trabace S, Lulli P, et al. HLA antigens and 

antigliadin antibodies in coeliac disease. Dis 

Markers 1991;9(6):313-7. 

 107. Brett PM, Yiannakou JY, Morris MA, Vaughan 

R, Curtis D, Ciclitira PJ. Common HLA alleles, 

rather than rare mutants, confer susceptibility to 

coeliac disease. Annals of Human Genetics 

1999;63(Pt 3):217-25. 

 108. Collin P, Syrjanen J, Partanen J, Pasternack A, 

Kaukinen K, Mustonen J. Celiac disease and 

HLA DQ in patients with IgA nephropathy. 

American Journal of Gastroenterology 

2002;97(10):2572-6. 

 109. Csizmadia CG, Mearin ML, Oren A, Kromhout 

A, Crusius JB, von Blomberg BM, et al. 

Accuracy and cost-effectiveness of a new 

strategy to screen for celiac disease in children 

with Down syndrome. Journal of Pediatrics 

2000;137(6):756-61. 

 110. Falchuk ZM, Katz AJ, Shwachman H, Rogentine 

GN, Strober W. Gluten-sensitive enteropathy: 

genetic analysis and organ culture study in 35 

families. Scandinavian Journal of 

Gastroenterology 1978;13(7):839-43. 

 111. Fedrick JA, Pandey JP, Verkasalo M, Teppo AM, 

Fudenberg HH. Immunoglobulin allotypes and 

the immune response to wheat gliadin in a 

Finnish population with celiac disease. 

Experimental and Clinical Immunogenetics 

1985;2(4):185-90. 

 112. Hansson T, Anneren G, Sjoberg O, Klareskog L, 

Dannaeus A. Celiac disease in relation to 

immunologic serum markers, trace elements, and 

HLA-DR and DQ antigens in Swedish children 

with Down syndrome. J Pediatr Gastroenterol 

Nutr 1999;29(3):286-92. 

 113. Lampasona V, Bonfanti R, Bazzigaluppi E, 

Venerando A, Chiumello G, Bosi E, et al. 

Antibodies to tissue transglutaminase C in type I 

diabetes. Diabetologia 1999;42(10):1195-8. 

 114. Lorini R, Scotta MS, Cortona L, Avanzini MA, 

Vitali L, De Giacomo C, et al. Celiac disease and 

type I (insulin-dependent) diabetes mellitus in 

childhood: follow-up study. Journal of Diabetes 

and Its Complications 1996;10(3):154-9. 

 115. Lundin KE, Sollid LM, Anthonsen D, Noren O, 

Molberg O, Thorsby E, et al. Heterogeneous 

reactivity patterns of HLA-DQ-restricted, small 

intestinal T-cell clones from patients with celiac 

disease. Gastroenterology 1997;112(3):752-9. 

 116. Mearin ML, Koninckx CR, Biemond I, Polanco I, 

Pena AS. Influence of genetic factors on the 

serum levels of antigliadin antibodies in celiac 

disease. Journal of Pediatric Gastroenterology 

and Nutrition 1984;3(3):373-7. 

 117. Silva EM, Fernandes M, I, Galvao LC, 

Sawamura R, Donadi EA. Human leukocyte 

antigen class II alleles in white Brazilian patients 

with celiac disease. Journal of Pediatric 
165 

Gastroenterology and Nutrition 2000;31(4):391-

4. 

 118. Stern M. Comparative evaluation of serologic 

tests for celiac disease: a European initiative 

toward standardization. Journal of Pediatric 

Gastroenterology and Nutrition 2000;31(5):513-

9. 

 119. Bevan S, Popat S, Braegger CP, Busch A, 

O'Donoghue D, Falth-Magnusson K, et al. 

Contribution of the MHC region to the familial 

risk of coeliac disease. Journal of Medical 

Genetics 1999;36(9):687-90. 

 120. Catassi C, Doloretta MM, Ratsch IM, De 

Virgiliis S, Cucca F. The distribution of DQ 

genes in the Saharawi population provides only a 

partial explanation for the high celiac disease 

prevalence. Tissue Antigens 2001;58(6):402-6. 

 121. Clot F, Gianfrani C, Babron MC, Bouguerra F, 

Southwood S, Kagnoff MF, et al. HLA-DR53 

molecules are associated with susceptibility to 

celiac disease and selectively bind gliadinderived peptides. Immunogenetics 

1999;49(9):800-7. 

 122. Holm K, Savilahti E, Koskimies S, Lipsanen V, 

Maki M. Immunohistochemical changes in the 

jejunum in first degree relatives of patients with 

coeliac disease and the coeliac disease marker 

DQ genes. HLA class II antigen expression, 

interleukin-2 receptor positive cells and dividing 

crypt cells. Gut 1994;35(1):55-60. 

 123. Karell K, Holopainen P, Mustalahti K, Collin P, 

Maki M, Partanen J. Not all HLA DR3 DQ2 

haplotypes confer equal susceptibility to coeliac 

disease: transmission analysis in families. Scand 

J Gastroenterol 2002;37(1):56-61. 

 124. Meddeb-Garnaoui A, Zeliszewski D, Mougenot 

JF, Djilali-Saiah I, Caillat-Zucman S, Dormoy A, 

et al. Reevaluation of the relative risk for 

susceptibility to celiac disease of HLA-DRB1, -

DQA1, -DQB1, -DPB1, and -TAP2 alleles in a 

French population. Human Immunology 

1995;43(3):190-9. 

 125. Ruiz MY, Olivares JL. Three-loci HLA 

haplotypes in Spanish celiac children and healthy 

subjects: estimation of linkage disequilibrium and 

haplotype frequencies. Am J Gastroenterol 

2001;96(5):1455-9. 

 126. Volta U, Bellentani S, Bianchi FB, Brandi G, De 

Franceschi L, Miglioli L, et al. High prevalence 

of celiac disease in Italian general population. 

Dig Dis Sci 2001;46(7):1500-5. 

 127. O'Driscoll BR, Stevens FM, O'Gorman TA, 

Finnegan P, McWeeney JJ, Little MP, et al. HLA 

type of patients with coeliac disease and 

malignancy in the west of Ireland. Gut 

1982;23(8):662-5. 

 128. Hoffenberg EJ, MacKenzie T, Barriga KJ, 

Eisenbarth GS, Bao F, Haas JE, et al. A 

prospective study of the incidence of childhood 

celiac disease. J Pediatr 2003;143(3):308-14. 

 129. Holm KH. Correlation of HLA-DR alleles to 

jejunal mucosal morphology in healthy firstdegree relatives of coeliac disease patients. Eur J 

Gastroenterol Hepatol 1993;5(1):35-9. 

 130. Louka AS, Moodie SJ, Karell K, Bolognesi E, 

Ascher H, Greco L, et al. A collaborative 

European search for non-DQA1 *05-DQB1 *02 

Celiac disease loci on HLA-Dr3 haplotypes: 

Analysis of transmission from homozygous 

parents. Hum Immunol 2003;64(3):350-8. 

 131. Agrawal S, Gupta A, Yachha SK, MullerMyhsok B, Mehrotra P, Agarwal SS. Association 

of human leucocyte-DR and DQ antigens in 

coeliac disease: a family study. Journal of 

Gastroenterology and Hepatology 

2000;15(7):771-4. 

 132. Louka AS, Lie BA, Talseth B, Ascher H, Ek J, 

Gudjonsdottir AH, et al. Coeliac disease patients 

carry conserved HLA-DR3-DQ2 haplotypes 

revealed by association of TNF alleles. 

Immunogenetics 2003;55(5):339-43. 

 133. Van Belzen MJ, Meijer Jos WR, Sandkuijl LA, 

Bardoel Alfons FJ, Mulder Chris JJ, Pearson PL, 

et al. A major non-HLA locus in celiac disease 

maps to chromosome 19. Gastroenterology 

2003;125(4):1032-41. 

 134. Castro M, Crino A, Papadatou B, Purpura M, 

Giannotti A, Ferretti F, et al. Down Syndrome 

and celiac disease: the prevalence of high IgAantigliadin antibodies and HLA-DR and DQ 

antigens in trisomy 21. Journal of Pediatric 

Gastroenterology and Nutrition 1993;16(3):265-

8. 

 135. Fine KD, Do K, Schulte K, Ogunji F, Guerra R, 

Osowski L, et al. High prevalence of celiac 

sprue-like HLA-DQ genes and enteropathy in 

patients with the microscopic colitis syndrome. 

American Journal of Gastroenterology 

2000;95(8):1974-82. 

 136. Iltanen S, Holm K, Partanen J, Laippala P, Maki 

M. Increased density of jejunal gammadelta+ T 

cells in patients having normal mucosa--marker 
166 

of operative autoimmune mechanisms? 

Autoimmunity 1999;29(3):179-87. 

 137. Perez-Bravo F, Araya M, Mondragon A, Rios G, 

Alarcon T, Roessler JL, et al. Genetic differences 

in HLA-DQA1* and DQB1* allelic distributions 

between celiac and control children in Santiago, 

Chile. Human Immunology 1999;60(3):262-7. 

 138. Arranz E, Telleria JJ, Sanz A, Martin JF, Alonso 

M, Calvo C, et al. HLA-DQA1*0501 and 

DQB1*02 homozygosity and disease 

susceptibility in Spanish coeliac patients. 

Experimental and Clinical Immunogenetics 

1997;14(4):286-90. 

 139. Boy MF, La Nasa G, Balestrieri A, Cherchi M, 

V, Usai P. Distribution of HLA-DPB1, -DQB1 -

DQA1 alleles among Sardinian celiac patients. 

Disease Markers 1995;12(3):199-204. 

 140. Djilali-Saiah I, Caillat-Zucman S, Schmitz J, 

Chaves-Vieira ML, Bach JF. Polymorphism of 

antigen processing (TAP, LMP) and HLA class II 

genes in celiac disease. Human Immunology 

1994;40(1):8-16. 

 141. Djilali-Saiah I, Schmitz J, Harfouch-Hammoud 

E, Mougenot JF, Bach JF, Caillat-Zucman S. 

CTLA-4 gene polymorphism is associated with 

predisposition to coeliac disease. Gut 

1998;43(2):187-9. 

 142. Erkan T, Kutlu T, Yilmaz E, Cullu F, Tumay GT. 

Human leukocyte antigens in Turkish pediatric 

celiac patients. Turkish Journal of Pediatrics 

1999;41(2):181-8. 

 143. Fernandez-Arquero M, Figueredo MA, Maluenda 

C, de la Concha EG. HLA-linked genes acting as 

additive susceptibility factors in celiac disease. 

Human Immunology 1995;42(4):295-300. 

 144. Ferrante P, Petronzelli F, Mariani P, Bonamico 

M, Mazzilli MC. Oligotyping of Italian celiac 

patients with the 11th International 

Histocompatibility Workshop reagents. Tissue 

Antigens 1992;39(1):38-9. 

 145. Mazzilli MC, Ferrante P, Mariani P, Martone E, 

Petronzelli F, Triglione P, et al. A study of Italian 

pediatric celiac disease patients confirms that the 

primary HLA association is to the DQ(alpha 

1*0501, beta 1*0201) heterodimer. Human 

Immunology 1992;33(2):133-9. 

 146. Michalski JP, McCombs CC, Arai T, Elston RC, 

Cao T, McCarthy CF, et al. HLA-DR, DQ 

genotypes of celiac disease patients and healthy 

subjects from the West of Ireland. Tissue 

Antigens 1996;47(2):127-33. 

 147. Ruiz del Prado MY, Olivares Lopez JL, Lazaro 

AA, Lasierra Diaz MP. HLA system. Phenotypic 

and gene frequencies in celiac and healthy 

subjects from the same geographical area. 

Revista Espanola De Enfermedades Digestivas - 

Organo Oficial De La Sociedad Espanola De 

Patologia Digestiva 2001;93(2):106-13. 

 148. Tighe MR, Hall MA, Ashkenazi A, Siegler E, 

Lanchbury JS, Ciclitira PJ. Celiac disease among 

Ashkenazi Jews from Israel. A study of the HLA 

class II alleles and their associations with disease 

susceptibility. Human Immunology 

1993;38(4):270-6. 

 149. Tighe MR, Hall MA, Barbado M, Cardi E, Welsh 

K, I, Ciclitira PJ. HLA class II alleles associated 

with celiac disease susceptibility in a southern 

European population. Tissue Antigens 

1992;40(2):90-7. 

 150. Tuysuz B, Dursun A, Kutlu T, Sokucu S, Cine N, 

Suoglu O, et al. HLA-DQ alleles in patients with 

celiac disease in Turkey. Tissue Antigens 

2001;57(6):540-2. 

 151. Howell WM, Leung ST, Jones DB, Nakshabendi 

I, Hall MA, Lanchbury JS, et al. HLA-DRB, -

DQA, and -DQB polymorphism in celiac disease 

and enteropathy-associated T-cell lymphoma. 

Common features and additional risk factors for 

malignancy. Hum Immunol 1995;43(1):29-37. 

 152. Sacchetti L, Calcagno G, Ferrajolo A, 

Sarrantonio C, Troncone R, Micillo M, et al. 

Discrimination between celiac and other 

gastrointestinal disorders in childhood by rapid 

human lymphocyte antigen typing. Clinical 

Chemistry 1998;44(8 Pt 1):1755-7. 

 153. Pettersson A, Sjoberg K, Lernmark A, Eriksson 

S. HLA genotypes in coeliac disease and healthy 

individuals carrying gliadin antibodies. Eur J 

Gastroenterol Hepatol 1993;5(6):445-50. 

 154. Arnason A, Skaftadottir I, Sigmundsson J, 

Mooney E, Bjornsson J, Cariglia N, et al. The 

association between coeliac disease, dermatitis 

herpetiformis and certain HLA-antigens in 

Icelanders. European Journal of Immunogenetics 

- Official Journal of the British Society for 

Histocompatibility and Immunogenetics 

1994;21(6):457-60. 

 155. Balas A, Vicario JL, Zambrano A, Acuna D, 

Garcia-Novo D. Absolute linkage of celiac 

disease and dermatitis herpetiformis to HLA-DQ. 

Tissue Antigens 1997;50(1):52-6. 

 156. Colonna M, Mantovani W, Corazza GR, Barboni 

P, Gasbarrini G, Ferrara GB, et al. Reassessment 
167 

of HLA association with celiac disease in special 

reference to the DP association. Human 

Immunology 1990;29(4):263-74. 

 157. Congia M, Cucca F, Frau F, Lampis R, Melis L, 

Clemente MG, et al. A gene dosage effect of the 

DQA1*0501/DQB1*0201 allelic combination 

influences the clinical heterogeneity of celiac 

disease. Human Immunology 1994;40(2):138-42. 

 158. Lio D, Bonanno CT, D'Anna C, De Luca S, 

Gervasi F, Cavataio F, et al. Gluten stimulation 

induces an in vitro expansion of peripheral blood 

T gamma delta cells from HLA-DQ2-positive 

subjects of families of patients with celiac 

disease. Experimental and Clinical 

Immunogenetics 1998;15(1):46-55. 

 159. Tumer L, Altuntas B, Hasanoglu A, 

Soylemezoglu O, Arinsoy T. Pattern of human 

leukocyte antigens in Turkish children with celiac 

disease. Pediatrics International - Official Journal 

of the Japan Pediatric Society 2000;42(6):678-81. 

 160. Book L, Hart A, Black J, Feolo M, Zone JJ, 

Neuhausen SL. Prevalence and clinical 

characteristics of celiac disease in Downs 

syndrome in a US study. American Journal of 

Medical Genetics 2001;98(1):70-4. 

 161. Farre C, Humbert P, Vilar P, Varea V, Aldeguer 

X, Carnicer J, et al. Serological markers and 

HLA-DQ2 haplotype among first-degree relatives 

of celiac patients. Catalonian Coeliac Disease 

Study Group. Digestive Diseases and Sciences 

1999;44(11):2344-9. 

 162. Iltanen S, Collin P, Korpela M, Holm K, Partanen 

J, Polvi A, et al. Celiac disease and markers of 

celiac disease latency in patients with primary 

Sjogren's syndrome. American Journal of 

Gastroenterology 1999;94(4):1042-6. 

 163. Kaur G, Sarkar N, Bhatnagar S, Kumar S, 

Rapthap CC, Bhan MK, et al. Pediatric celiac 

disease in India is associated with multiple DR3-

DQ2 haplotypes. Human Immunology 

2002;63(8):677-82. 

 164. Neuhausen SL, Weizman Z, Camp NJ, Elbedour 

K, Sheffield VC, Zone JJ, et al. HLA DQA1-

DQB1 genotypes in Bedouin families with celiac 

disease. Human Immunology 2002;63(6):502-7. 

 165. Sumnik Z, Kolouskova S, Cinek O, Kotalova R, 

Vavrinec J, Snajderova M. HLA-DQA1*05-

DQB1*0201 positivity predisposes to coeliac 

disease in Czech diabetic children. Acta 

Paediatrica (Oslo, Norway - 1992) 

2000;89(12):1426-30. 

 166. Liu J, Juo S, Holopainen P, Terwilliger J, Tong 

X, Grunn A, et al. Genomewide linkage analysis 

of celiac disease in Finnish families. American 

Journal of Human Genetics 2002;70(1):51-9. 

 167. Polvi A, Eland C, Koskimies S, Maki M, 

Partanen J. HLA DQ and DP in Finnish families 

with celiac disease. Eur J Immunogenet 

1996;23(3):221-34. 

 168. Larizza D, Calcaterra V, Luinetti O, Villani L, De 

Silvestri A, Autelli M, et al. Evidence for 

immunogenetic predisposition in children with 

celiac disease and autoimmune thyroid disease. 

Int J Med Biol Environ 2001;29(2):143-8. 

 169. Book L, Zone JJ, Neuhausen SL. Prevalence of 

celiac disease among relatives of sib pairs with 

celiac disease in U.S. families. American Journal 

of Gastroenterology 2003;98(2):377-81. 

 170. Failla P, Ruberto C, Pagano MC, Lombardo M, 

Bottaro G, Perichon B, et al. Celiac disease in 

Down Syndrome with HLA serological and 

molecular studies. J Pediatr Gastroenterol Nutr 

1996;23(3):303-6. 

 171. Maki M, Mustalahti K, Kokkonen J, Kulmala P, 

Haapalahti M, Karttunen T, et al. Prevalence of 

Celiac disease among children in Finland. New 

England Journal of Medicine 2003;348(25):2517-

24. 

 172. Mustalahti K, Sulkanen S, Holopainen P, Laurila 

K, Collin P, Partanen J, et al. Coeliac disease 

among healthy members of multiple case coeliac 

disease families. Scandinavian Journal of 

Gastroenterology 2002;37(2):161-5. 

 173. Zubillaga P, Vidales MC, Zubillaga I, Ormaechea 

V, Garcia-Urkia N, Vitoria JC. HLA-DQA1 and 

HLA-DQB1 genetic markers and clinical 

presentation in celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 2002;34(5):548-

54. 

 174. Bouguerra F, Babron MC, Eliaou JF, Debbabi A, 

Clot J, Khaldi F, et al. Synergistic effect of two 

HLA heterodimers in the susceptibility to celiac 

disease in Tunisia. Genetic Epidemiology 

1997;14(4):413-22. 

 175. Popat S, Hearle N, Wixey J, Hogberg L, Bevan S, 

Lim W, et al. Analysis of the CTLA4 gene in 

Swedish coeliac disease patients. Scand J 

Gastroenterol 2002;37(1):28-31. 

 176. Karell K, Louka AS, Moodie SJ, Ascher H, Clot 

F, Greco L, et al. HLA types in celiac disease 

patients not carrying the DQA1 *05-DQB1 *02 

(DQ2) heterodimer: Results from the European 
168 

genetics cluster on celiac disease. Hum Immunol 

2003;64(4):469-77. 

 177. Lewis C, Book L, Black J, Sawitzke A, CannonAlbright L, Zone J, et al. Celiac disease and 

human leukocyte antigen genotype: accuracy of 

diagnosis in self-diagnosed individuals, dosage 

effect, and sibling risk. J Pediatr Gastroenterol 

Nutr 2000;31(1):22-7. 

 178. Howard FM, Carter CO, Candy DC, Harries JT. 

A family study of protracted diarrhoea in infancy. 

Journal of Medical Genetics 1981;18(2):81-6. 

 179. Volta U, Molinaro N, De Franceschi L, Bianchi 

FB. Human umbilical cord as substrate for IgA 

antiendomysial antibodies allows large scale 

screening for celiac sprue. J Clin Gastroenterol 

1996;23(1):18-20. 

 180. Trevisiol C, Ventura A, Baldas V, Tommasini A, 

Santon D, Martelossi S, et al. A reliable 

screening procedure for coeliac disease in clinical 

practice. Scand J Gastroenterol 2002;37(6):679-

84. 

 181. Bonamico M, Mariani P, Mazzilli MC, Triglione 

P, Lionetti P, Ferrante P, et al. Frequency and 

clinical pattern of celiac disease among siblings 

of celiac children. J Pediatr Gastroenterol Nutr 

1996;23(2):159-63. 

 182. Catassi C, Ratsch IM, Fabiani E, Ricci S, 

Bordicchia F, Pierdomenico R, et al. High 

prevalence of undiagnosed coeliac disease in 

5280 Italian students screened by antigliadin 

antibodies. Acta Paediatr 1995;84(6):672-6. 

 183. Catassi C, Ratsch IM, Fabiani E, Rossini M, 

Bordicchia F, Candela F, et al. Coeliac disease in 

the year 2000: exploring the iceberg. Lancet 

1994;343(8891):200-3. 

 184. Grodzinsky E, Hed J, Lieden G, Sjogren F, Strom 

M. Presence of IgA and IgG antigliadin 

antibodies in healthy adults as measured by 

micro-ELISA. Effect of various cutoff levels on 

specificity and sensitivity when diagnosing 

coeliac disease. Int Arch Allergy Appl Immunol 

1990;92(2):119-23. 

 185. Grodzinsky E, Franzen L, Hed J, Strom M. High 

prevalence of celiac disease in healthy adults 

revealed by antigliadin antibodies. Ann Allergy 

1992;69(1):66-70. 

 186. Lagerqvist C, Ivarsson A, Juto P, Persson LA, 

Hernell O. Screening for adult coeliac disease - 

which serological marker(s) to use? J Intern Med 

2001;250(3):241-8. 

 187. Weile B, Grodzinsky E, Skogh T, Jordal R, 

Cavell B, Krasilnikoff PA. Screening Danish 

blood donors for antigliadin and antiendomysium 

antibodies. Acta Paediatr 1996;412(Suppl):46. 

 188. McMillan SA, Watson RP, McCrum EE, Evans 

AE. Factors associated with serum antibodies to 

reticulin, endomysium, and gliadin in an adult 

population. Gut 1996;39(1):43-7. 

 189. Stenhammar L, Brandt A, Wagermark J. A 

family study of coeliac disease. Acta Paediatr 

Scand 1982;71(4):625-8. 

 190. Maki M, Holm K, Lipsanen V, Hallstrom O, 

Viander M, Collin P, et al. Serological markers 

and HLA genes among healthy first-degree 

relatives of patients with coeliac disease. Lancet 

1991;338(8779):1350-3. 

 191. Sjoberg K, Wassmuth R, Reichstetter S, Eriksson 

KF, Ericsson UB, Eriksson S. Gliadin antibodies 

in adult insulin-dependent diabetes--autoimmune 

and immunogenetic correlates. Autoimmunity 

2000;32(4):217-28. 

 192. Carlsson AK, Axelsson IE, Borulf SK, Bredberg 

AC, Lindberg BA, Sjoberg KG, et al. Prevalence 

of IgA-antiendomysium and IgA-antigliadin 

autoantibodies at diagnosis of insulin-dependent 

diabetes mellitus in Swedish children and 

adolescents. Pediatrics 1999;103(6 Pt 1):1248-52. 

 193. Ivarsson A, Persson LA, Nystrom L, Ascher H, 

Cavell B, Danielsson L, et al. Epidemic of 

coeliac disease in Swedish children. Acta 

Paediatr 2000;89(2):165-71. 

 194. Maki M, Holm K. Incidence and prevalence of 

coeliac disease in Tampere. Coeliac disease is not 

disappearing. Acta Paediatrica Scandinavica 

1990;79(10):980-2. 

 195. Ivarsson A, Persson LA, Nystrom L, Hernell O. 

The Swedish coeliac disease epidemic with a 

prevailing twofold higher risk in girls compared 

to boys may reflect gender specific risk factors. 

Eur J Epidemiol 2003;18(7):677-84. 

 196. Weile B, Krasilnikoff PA. Extremely low 

incidence rates of celiac disease in the Danish 

population of children. J Clin Epidemiol 

1993;46(7):661-4. 

 197. Bode S, Gudmand-Hoyer E. Incidence and 

prevalence of adult coeliac disease within a 

defined geographic area in Denmark. Scand J 

Gastroenterol 1996;31(7):694-9. 
169 

 198. Maki M, Kallonen K, Lahdeaho ML, Visakorpi 

JK. Changing pattern of childhood coeliac 

disease in Finland. Acta Paediatrica Scandinavica 

1988;77(3):408-12. 

 199. Collin P, Reunala T, Rasmussen M, Kyronpalo S, 

Pehkonen E, Laippala P, et al. High incidence 

and prevalence of adult coeliac disease. 

Augmented diagnostic approach. Scand J 

Gastroenterol 1997;32(11):1129-33. 

 200. Jansen Th TLA, Mulder CJJ, Karssen PHZ, 

Wagenaar CGJ. Epidemiological survey of the 

Dutch Coeliac Disease Society: An update 1992. 

Eur J Gastroenterol Hepatol 1993;5(2):73-8. 

 201. Hawkes ND, Swift GL, Smith PM, Jenkins HR. 

Incidence and presentation of coeliac disease in 

South Glamorgan. Eur J Gastroenterol Hepatol 

2000;12(3):345-9. 

 202. Corrao G, Usai P, Galatola G, Ansaldi N, Meini 

A, Pelli MA, et al. Estimating the incidence of 

coeliac disease with capture-recapture methods 

within four geographic areas in Italy. J Epidemiol 

Community Health 1996;50(3):299-305. 

 203. Magazzu G, Bottaro G, Cataldo F, Iacono G, Di 

Donato F, Patane R, et al. Increasing incidence of 

childhood celiac disease in Sicily: results of a 

multicenter study. Acta Paediatr 

1994;83(10):1065-9. 

 204. Lopez-Rodriguez MJ, Canal Macias ML, Lavado 

Garcia JM, Sanchez BM, Robledo AP, Pedrera 

Zamorano JD. Epidemiological changes in 

diagnosed coeliac disease in a population of 

Spanish children. Acta Paediatr 2003;92(2):165-

9. 

 205. Talley NJ, Valdovinos M, Petterson TM, 

Carpenter HA, Melton LJ. Epidemiology of 

celiac sprue: a community-based study. Am J 

Gastroenterol 1994;89(6):843-6. 

 206. Fasano A, Berti I, Gerarduzzi T, Not T, Colletti 

RB, Drago S, et al. Prevalence of celiac disease 

in at-risk and not-at-risk groups in the United 

States: a large multicenter study. Arch Intern 

Med 2003;163(3):286-92. 

 207. Green PH, Shane E, Rotterdam H, Forde KA, 

Grossbard L. Significance of unsuspected celiac 

disease detected at endoscopy. Gastroenterol Int 

2000;51(1):60-5. 

 208. Not T, Horvath K, Hill ID, Partanen J, Hammed 

A, Magazzu G, et al. Celiac disease risk in the 

USA: high prevalence of antiendomysium 

antibodies in healthy blood donors. Scand J 

Gastroenterol 1998;33(5):494-8. 

 209. Carlsson AK, Axelsson IE, Borulf SK, Bredberg 

AC, Ivarsson SA. Serological screening for celiac 

disease in healthy 2.5-year-old children in 

Sweden. Pediatrics 2001;107(1):42-5. 

 210. Collin P, Rasmussen M, Kyronpalo S, Laippala 

P, Kaukinen K. The hunt for coeliac disease in 

primary care. Q J Med 2002;95(2):75-7. 

 211. Grodzinsky E. Screening for coeliac disease in 

apparently healthy blood donors. Acta Paediatr 

1996;412(Suppl):36-8. 

 212. Hovdenak N, Hovlid E, Aksnes L, Fluge G, 

Erichsen MM, Eide J. High prevalence of 

asymptomatic coeliac disease in Norway: a study 

of blood donors. Eur J Gastroenterol Hepatol 

1999;11(2):185-7. 

 213. Ivarsson A, Persson LA, Juto P, Peltonen M, 

Suhr O, Hernell O. High prevalence of 

undiagnosed coeliac disease in adults: a Swedish 

population-based study. J Intern Med 

1999;245(1):63-8. 

 214. Kolho KL, Farkkila MA, Savilahti E. 

Undiagnosed coeliac disease is common in 

Finnish adults. Scand J Gastroenterol 

1998;33(12):1280-3. 

 215. Maki M, Mustalahti K, Kokkonen J, Kulmala P, 

Haapalahti M, Karttunen T, et al. Prevalence of 

Celiac disease among children in Finland. New 

Engl J Med 2003;348(25):2517-24. 

 216. Sjoberg K, Alm R, Ivarsson SA, Lindstrom C, 

Eriksson S. Prevalence and clinical significance 

of gliadin antibodies in healthy children and 

adults. Scand J Gastroenterol 1994;29(3):248-54. 

 217. Sjoberg K, Eriksson S. Regional differences in 

coeliac disease prevalence in Scandinavia? Scand 

J Gastroenterol 1999;34(1):41-5. 

 218. Weile I, Grodzinsky E, Skogh T, Jordal R, Cavell 

B, Krasilnikoff PA. High prevalence rates of 

adult silent coeliac disease, as seen in Sweden, 

must be expected in Denmark. APMIS 

2001;109(11):745-50. 

 219. Borch K, Grodzinsky E, Petersson F, Jonsson KA, Mardh S, Valdimarsson T. Prevalence of 

coeliac disease and relations to Helicobacter 

pylori infection and duodenitis in a Swedish adult 

population sample: A histomorphological and 

serological survey. Inflammopharmacology 

2000;8(4):341-50. 

 220. Catassi C, Fabiani E, Ratsch IM, Coppa G, V, 

Giorgi PL, Pierdomenico R, et al. The coeliac 
170 

iceberg in Italy. A multicentre antigliadin 

antibodies screening for coeliac disease in 

school-age subjects. Acta Paediatr 

1996;412(Suppl):29-35. 

 221. Catassi C, Fanciulli G, D'Appello AR, El Asmar 

R, Rondina C, Fabiani E, et al. Antiendomysium 

versus antigliadin antibodies in screening the 

general population for coeliac disease. Scand J 

Gastroenterol 2000;35(7):732-6. 

 222. Corazza GR, Andreani ML, Biagi F, Corrao G, 

Pretolani S, Giulianelli G, et al. The smaller size 

of the 'coeliac iceberg' in adults. Scand J 

Gastroenterol 1997;32(9):917-9. 

 223. Mazzetti dP, Giorgetti GM, Gregori M, De 

Simone M, Leonardi C, Barletta PA, et al. 

Subclinical coeliac disease. Ital J Gastroenterol 

1992;24(6):352-4. 

 224. Pittschieler K, Ladinser B. Coeliac disease: 

screened by a new strategy. Acta Paediatr 

1996;412(Suppl):42-5. 

 225. Trevisiol C, Not T, Berti I, Buratti E, Citta A, 

Neri E, et al. Screening for coeliac disease in 

healthy blood donors at two immuno-transfusion 

centres in north-east Italy. Ital J Gastroenterol 

Hepatol 1999;31(7):584-6. 

 226. Johnston SD, Watson RG, McMillan SA, Sloan J, 

Love AH. Coeliac disease detected by screening 

is not silent--simply unrecognized. Q J Med 

1998;91(12):853-60. 

 227. Sanders DS, Patel D, Stephenson TJ, Ward AM, 

McCloskey EV, Hadjivassiliou M, et al. A 

primary care cross-sectional study of 

undiagnosed adult coeliac disease. Eur J 

Gastroenterol Hepatol 2003;15(4):407-13. 

 228. West J, Logan RFA, Hill PG, Lloyd A, Lewis S, 

Hubbard R, et al. Seroprevalence, correlates, and 

characteristics of undetected coeliac disease in 

England. Gut 2003;52(7):960-5. 

 229. Dickey W, McMillan SA, Bharucha C, Porter 

KG. Antigliadin antibodies in blood donors in 

Northern Ireland. Eur J Gastroenterol Hepatol 

1992;4(9):739-41. 

 230. Riestra S, Fernandez E, Rodrigo L, Garcia S, 

Ocio G. Prevalence of Coeliac disease in the 

general population of northern Spain. Strategies 

of serologic screening. Scand J Gastroenterol 

2000;35(4):398-402. 

 231. Rostami K, Mulder CJ, Werre JM, van Beukelen 

FR, Kerchhaert J, Crusius JB, et al. High 

prevalence of celiac disease in apparently healthy 

blood donors suggests a high prevalence of 

undiagnosed celiac disease in the Dutch 

population. Scand J Gastroenterol 

1999;34(3):276-9. 

 232. Csizmadia CGDS, Mearin ML, Von Blomberg 

BME, Brand R, Verloove-Vanhorick SP. An 

iceberg of childhood coeliac disease in the 

Netherlands. Lancet 1999;353(9155):813-4. 

 233. Rutz R, Ritzler E, Fierz W, Herzog D. Prevalence 

of asymptomatic celiac disease in adolescents of 

eastern Switzerland. Swiss Med Wkly 

2002;132(3-4):43-7. 

 234. Jaeger C, Hatziagelaki E, Petzoldt R, Bretzel RG. 

Comparative analysis of organ-specific 

autoantibodies and celiac disease--associated 

antibodies in type 1 diabetic patients, their firstdegree relatives, and healthy control subjects. 

Diabetes Care 2001;24(1):27-32. 

 235. Book L, Zone JJ, Neuhausen SL. Prevalence of 

celiac disease among relatives of sib pairs with 

celiac disease in U.S. families. Am J 

Gastroenterol 2003;98(2):377-81. 

 236. Corazza G, Valentini RA, Frisoni M, Volta U, 

Corrao G, Bianchi FB, et al. Gliadin immune 

reactivity is associated with overt and latent 

enteropathy in relatives of celiac patients. 

Gastroenterology 1992;103(5):1517-22. 

 237. Farre C, Humbert P, Vilar P, Varea V, Aldeguer 

X, Carnicer J, et al. Serological markers and 

HLA-DQ2 haplotype among first-degree relatives 

of celiac patients. Catalonian Coeliac Disease 

Study Group. Dig Dis Sci 1999;44(11):2344-9. 

 238. Hill I, Fasano A, Schwartz R, Counts D, Glock 

M, Horvath K. The prevalence of celiac disease 

in at-risk groups of children in the United States. 

J Pediatr 2000;136(1):86-90. 

 239. Korponay-Szabo I, Kovacs J, Lorincz M, Torok 

E, Goracz G. Families with multiple cases of 

gluten-sensitive enteropathy. Z Gastroenterol 

1998;36(7):553-8. 

 240. Kotze LM, Utiyama SR, Nisihara RM, Zeni MP, 

de Sena MG, Amarante HM. Antiendomysium 

antibodies in Brazilian patients with celiac 

disease and their first-degree relatives. Arq 

Gastroenterol 2001;38(2):94-103. 

 241. Mustalahti K, Sulkanen S, Holopainen P, Laurila 

K, Collin P, Partanen J, et al. Coeliac disease 

among healthy members of multiple case coeliac 

disease families. Scand J Gastroenterol 

2002;37(2):161-5. 
171 

 242. Robinson DC, Watson AJ, Wyatt EH, Marks JM, 

Roberts DF. Incidence of small-intestinal 

mucosal abnormalities and of clinical coeliac 

disease in the relatives of children with coeliac 

disease. Gut 1971;12(10):789-93. 

 243. Rolles CJ, Myint TO, Sin WK, Anderson M. 

Proceedings: Family study of coeliac disease. Gut 

1974;15(10):827. 

 244. Rostami K, Mulder CJ, van Overbeek FM, 

Kerckhaert J, Meijer JW, von Blomberg MB, et 

al. Should relatives of coeliacs with mild clinical 

complaints undergo a small-bowel biopsy despite 

negative serology? Eur J Gastroenterol Hepatol 

2000;12(1):51-5. 

 245. Stokes PL, Ferguson R, Holmes GK, Cooke WT. 

Familial aspects of coeliac disease. Quarterly 

Journal of Medicine 1976;45(180):567-82. 

 246. Vitoria JC, Arrieta A, Astigarraga I, GarciaMasdevall D, Rodriguez-Soriano J. Use of 

serological markers as a screening test in family 

members of patients with celiac disease. J Pediatr 

Gastroenterol Nutr 1994;19(3):304-9. 

 247. Hogberg L, Falth-Magnusson K, Grodzinsky E, 

Stenhammar L. Familial prevalence of coeliac 

disease: A twenty-year follow-up study. Scand J 

Gastroenterol 2003;38(1):61-5. 

 248. Pittschieler K, Gentili L, Niederhofer H. Onset of 

coeliac disease: A prospective longitudinal study. 

Acta Paediatr Int J Paediatr 2003;92(10):1149-52. 

 249. Tursi A, Brandimarte G, Giorgetti GM, 

Inchingolo CD. Effectiveness of the sorbitol 

HSUB2 breath test in detecting histological 

damage among relatives of coeliacs. Scand J 

Gastroenterol 2003;38(7):727-31. 

 250. Acerini CL, Ahmed ML, Ross KM, Sullivan PB, 

Bird G, Dunger DB. Coeliac disease in children 

and adolescents with IDDM: clinical 

characteristics and response to gluten-free diet. 

Diabet Med 1998;15(1):38-44. 

 251. Aktay AN, Lee PC, Kumar V, Parton E, Wyatt 

DT, Werlin SL. The prevalence and clinical 

characteristics of celiac disease in juvenile 

diabetes in Wisconsin. J Pediatr Gastroenterol 

Nutr 2001;33(4):462-5. 

 252. Arato A, Korner A, Veres G, Dezsofi A, Ujpal I, 

Madacsy L. Frequency of coeliac disease in 

Hungarian children with type 1 diabetes mellitus. 

Eur J Pediatr 2002;162(1):1-5. 

 253. Bao F, Yu L, Babu S, Wang T, Hoffenberg EJ, 

Rewers M, et al. One third of HLA DQ2 

homozygous patients with type 1 diabetes express 

celiac disease-associated transglutaminase 

autoantibodies. J Autoimmun 1999;13(1):143-8. 

 254. Barera G, Bianchi C, Calisti L, Cerutti F, 

Dammacco F, Frezza E, et al. Screening of 

diabetic children for coeliac disease with 

antigliadin antibodies and HLA typing. Arch Dis 

Child 1991;66(4):491-4. 

 255. Barera G, Bonfanti R, Viscardi M, Bazzigaluppi 

E, Calori G, Meschi F, et al. Occurrence of celiac 

disease after onset of type 1 diabetes: a 6-year 

prospective longitudinal study. Pediatrics 

2002;109(5):833-8. 

 256. Calero P, Ribes-Koninckx C, Albiach V, Carles 

C, Ferrer J. IgA antigliadin antibodies as a 

screening method for nonovert celiac disease in 

children with insulin-dependent diabetes mellitus. 

J Pediatr Gastroenterol Nutr 1996;23(1):29-33. 

 257. Cronin CC, Feighery A, Ferriss JB, Liddy C, 

Shanahan F, Feighery C. High prevalence of 

celiac disease among patients with insulindependent (type I) diabetes mellitus. Am J 

Gastroenterol 1997;92(12):2210-2. 

 258. De Block CE, De L, I, Vertommen JJ, Rooman 

RP, Du CM, V, Van Campenhout CM, et al. 

Beta-cell, thyroid, gastric, adrenal and coeliac 

autoimmunity and HLA-DQ types in type 1 

diabetes. Clin Exp Immunol 2001;126(2):236-41. 

 259. De V, I, Ghirlanda G, Gasbarrini G. Prevalence 

of coeliac disease in type I diabetes: a multicentre 

study. Acta Paediatr 1996;412(Suppl):56-7. 

 260. Fraser-Reynolds KA, Butzner JD, Stephure DK, 

Trussell RA, Scott RB. Use of immunoglobulin 

A-antiendomysial antibody to screen for celiac 

disease in North American children with type 1 

diabetes. Diabetes Care 1998;21(11):1985-9. 

 261. Gillett PM, Gillett HR, Israel DM, Metzger DL, 

Stewart L, Chanoine JP, et al. High prevalence of 

celiac disease in patients with type 1 diabetes 

detected by antibodies to endomysium and tissue 

transglutaminase. Can J Gastroenterol 

2001;15(5):297-301. 

 262. Hansen D, Bennedbaek FN, Hansen LK, HoierMadsen M, Hegedu LS, Jacobsen BB, et al. High 

prevalence of coeliac disease in Danish children 

with type I diabetes mellitus. Acta Paediatr 

2001;90(11):1238-43. 

 263. Kaukinen K, Collin P, Mykkanen AH, Partanen 

J, Maki M, Salmi J. Celiac disease and 
172 

autoimmune endocrinologic disorders. Dig Dis 

Sci 1999;44(7):1428-33. 

 264. Kordonouri O, Dieterich W, Schuppan D, Webert 

G, Muller C, Sarioglu N, et al. Autoantibodies to 

tissue transglutaminase are sensitive serological 

parameters for detecting silent coeliac disease in 

patients with Type 1 diabetes mellitus. Diabet 

Med 2000;17(6):441-4. 

 265. Lampasona V, Bonfanti R, Bazzigaluppi E, 

Venerando A, Chiumello G, Bosi E, et al. 

Antibodies to tissue transglutaminase C in type I 

diabetes. Diabetologia 1999;42(10):1195-8. 

 266. Li Voon Chong JSW, Leong KS, Wallymahmed 

M, Sturgess R, MacFarlane IA. Is coeliac disease 

more prevalent in young adults with coexisting 

Type 1 diabetes mellitus and autoimmune thyroid 

disease compared with those with Type 1 

diabetes mellitus alone? Diabet Med 

2002;19(4):334-7. 

 267. Lorini R, Scotta MS, Cortona L, Avanzini MA, 

Vitali L, De Giacomo C, et al. Celiac disease and 

type I (insulin-dependent) diabetes mellitus in 

childhood: follow-up study. J Diabetes 

Complications 1996;10(3):154-9. 

 268. Not T, Tommasini A, Tonini G, Buratti E, 

Pocecco M, Tortul C, et al. Undiagnosed coeliac 

disease and risk of autoimmune disorders in 

subjects with Type I diabetes mellitus. 

Diabetologia 2001;44(2):151-5. 

 269. Page SR, Lloyd CA, Hill PG, Peacock I, Holmes 

GK. The prevalence of coeliac disease in adult 

diabetes mellitus. Q J Med 1994;87(10):631-7. 

 270. Rensch MJ, Merenich JA, Lieberman M, Long 

BD, Davis DR, McNally PR. Gluten-sensitive 

enteropathy in patients with insulin-dependent 

diabetes mellitus. Ann Intern Med 

1996;124(6):564-7. 

 271. Roldan MB, Barrio R, Roy G, Parra C, Alonso 

M, Yturriaga R, et al. Diagnostic value of 

serological markers for celiac disease in diabetic 

children and adolescents. J Pediatr Endocrinol 

Metab 1998;11(6):751-6. 

 272. Rossi TM, Albini CH, Kumar V. Incidence of 

celiac disease identified by the presence of serum 

endomysial antibodies in children with chronic 

diarrhea, short stature, or insulin-dependent 

diabetes mellitus. J Pediatr 1993;123(2):262-4. 

 273. Sategna-Guidetti C, Grosso S, Pulitano R, 

Benaduce E, Dani F, Carta Q. Celiac disease and 

insulin-dependent diabetes mellitus. Screening in 

an adult population. Dig Dis Sci 

1994;39(8):1633-7. 

 274. Saukkonen T, Savilahti E, Reijonen H, Ilonen J, 

Tuomilehto-Wolf E, Akerblom HK. Coeliac 

disease: frequent occurrence after clinical onset 

of insulin-dependent diabetes mellitus. Childhood 

Diabetes in Finland Study Group. Diabet Med 

1996;13(5):464-70. 

 275. Schober E, Bittmann B, Granditsch G, Huber 

WD, Huppe A, Jager A, et al. Screening by antiendomysium antibody for celiac disease in 

diabetic children and adolescents in Austria. J 

Pediatr Gastroenterol Nutr 2000;30(4):391-6. 

 276. Sigurs N, Johansson C, Elfstrand PO, Viander M, 

Lanner A. Prevalence of coeliac disease in 

diabetic children and adolescents in Sweden. 

Acta Paediatr 1993;82(9):748-51. 

 277. Sjoberg K, Eriksson KF, Bredberg A, Wassmuth 

R, Eriksson S. Screening for coeliac disease in 

adult insulin-dependent diabetes mellitus. J Intern 

Med 1998;243(2):133-40. 

 278. Spiekerkoetter U, Seissler J, Wendel U. General 

screening for celiac disease is advisable in 

children with type 1 diabetes. Horm Metab Res 

2002;34(4):192-5. 

 279. Talal AH, Murray JA, Goeken JA, Sivitz W, I. 

Celiac disease in an adult population with 

insulin-dependent diabetes mellitus: use of 

endomysial antibody testing. Am J Gastroenterol 

1997;92(8):1280-4. 

 280. Valerio G, Maiuri L, Troncone R, Buono P, 

Lombardi F, Palmieri R, et al. Severe clinical 

onset of diabetes and increased prevalence of 

other autoimmune diseases in children with 

coeliac disease diagnosed before diabetes 

mellitus. Diabetologia 2002;45(12):1719-22. 

 281. Vitoria JC, Castano L, Rica I, Bilbao JR, Arrieta 

A, Garcia-Masdevall MD. Association of insulindependent diabetes mellitus and celiac disease: a 

study based on serologic markers. J Pediatr 

Gastroenterol Nutr 1998;27(1):47-52. 

 282. Agardh D, Nilsson A, Tuomi T, Lindberg B, 

Carlsson AK, Lernmark A, et al. Prediction of 

silent celiac disease at diagnosis of childhood 

type 1 diabetes by tissue transglutaminase 

autoantibodies and HLA. Pediatr Diabetes 

2001;2(2):58-65. 

 283. Ackerman Z, Eliakim R, Stalnikowicz R, 

Rachmilewitz D. Role of small bowel biopsy in 

the endoscopic evaluation of adults with iron 
173 

deficiency anemia. Am J Gastroenterol 

1996;91(10):2099-102. 

 284. Annibale B, Capurso G, Chistolini A, D'Ambra 

G, DiGiulio E, Monarca B, et al. Gastrointestinal 

causes of refractory iron deficiency anemia in 

patients without gastrointestinal symptoms. Am J 

Med 2001;111(6):439-45. 

 285. Corazza GR, Valentini RA, Andreani ML, 

D'Anchino M, Leva MT, Ginaldi L, et al. 

Subclinical coeliac disease is a frequent cause of 

iron-deficiency anaemia. Scand J Gastroenterol 

1995;30(2):153-6. 

 286. Dickey W, Kenny BD, McMillan SA, Porter KG, 

McConnell JB. Gastric as well as duodenal 

biopsies may be useful in the investigation of iron 

deficiency anaemia. Scand J Gastroenterol 

1997;32(5):469-72. 

 287. Howard MR, Turnbull AJ, Morley P, Hollier P, 

Webb R, Clarke A. A prospective study of the 

prevalence of undiagnosed coeliac disease in 

laboratory defined iron and folate deficiency. J 

Clinl Path 2002;55(10):754-7. 

 288. Kepczyk T, Kadakia SC. Prospective evaluation 

of gastrointestinal tract in patients with irondeficiency anemia. Dig Dis Sci 1995;40(6):1283-

9. 

 289. McIntyre AS, Long RG. Prospective survey of 

investigations in outpatients referred with iron 

deficiency anaemia. Gut 1993;34(8):1102-7. 

 290. Oxentenko AS, Grisolano SW, Murray JA, 

Burgart LJ, Dierkhising RA, Alexander JA. The 

insensitivity of endoscopic markers in celiac 

disease. Am J Gastroenterol 2002;97(4):933-8. 

 291. Ransford Rupert AJ, Hayes M, Palmer M, Hall 

MJ. A controlled, prospective screening study of 

celiac disease presenting as iron deficiency 

anemia. J Clin Gastroenterol 2002;35(3):228-33. 

 292. Unsworth DJ, Lock RJ, Harvey RF. Improving 

the diagnosis of coeliac disease in anaemic 

women. Br J Haematol 2000;111(3):898-901. 

 293. Annibale B, Lahner E, Chistolini A, Gallucci C, 

Di Giulio E, Capurso G, et al. Endoscopic 

evaluation of the upper gastrointestinal tract is 

worthwhile in premenopausal women with irondeficiency anaemia irrespective of menstrual 

flow. Scand J Gastroenterol 2003;38(3):239-45. 

 294. Van Mook WNKA, Bourass-Bremer IHDN, Bos 

LP, Verhoeven HMJM, Engels LGJB. The 

outcome of esophagogastroduodenoscopy (EGD) 

in asymptomatic outpatients with iron deficiency 

anemia after a negative colonoscopy. Eur J Intern 

Med 2001;12(2):122-6. 

 295. Gonzalez D, Sugai E, Gomez JC, Oliveri MB, 

Gomez AC, Vega E, et al. Is it necessary to 

screen for celiac disease in postmenopausal 

osteoporotic women? Calcif Tissue Int 

2002;71(2):141-4. 

 296. Lindh E, Ljunghall S, Larsson K, Lavo B. 

Screening for antibodies against gliadin in 

patients with osteoporosis. J Intern Med 

1992;231(4):403-6. 

 297. Mather KJ, Meddings JB, Beck PL, Scott RB, 

Hanley DA. Prevalence of IgA-antiendomysial 

antibody in asymptomatic low bone mineral 

density. Am J Gastroenterol 2001;96(1):120-5. 

 298. Nuti R, Martini G, Valenti R, Giovani S, 

Salvadori S, Avanzati A. Prevalence of 

undiagnosed coeliac syndrome in osteoporotic 

women. J Intern Med 2001;250(4):361-6. 

 299. Hin H, Bird G, Fisher P, Mahy N, Jewell D. 

Coeliac disease in primary care: case finding 

study. BMJ 1999;318(7177):164-7. 

 300. Bardella MT, Molteni N, Cesana B, Baldassarri 

AR, Binanchi PA. IgA antigliadin antibodies, 

cellobiose/mannitol sugar test, and carotenemia 

in the diagnosis of and screening for celiac 

disease. Am J Gastroenterol 1991;86(3):309-11. 

 301. Bardella MT, Trovato C, Cesana BM, Pagliari C, 

Gebbia C, Peracchi M. Serological markers for 

coeliac disease: is it time to change? Dig Liver 

Dis 2001;33(5):426-31. 

 302. Bode S, Weile B, Krasilnikoff PA, GudmandHoyer E. The diagnostic value of the gliadin 

antibody test in celiac disease in children: a 

prospective study. J Pediatr Gastroenterol Nutr 

1993;17(3):260-4. 

 303. Carroccio A, Vitale G, Di Prima L, Chifari N, 

Napoli S, La Russa C, et al. Comparison of antitransglutaminase ELISAs and an anti-endomysial 

antibody assay in the diagnosis of celiac disease: 

a prospective study. Clin Chem 2002;48(9):1546-

50. 

 304. Chan AW, Butzner JD, McKenna R, Fritzler MJ. 

Tissue transglutaminase enzyme-linked 

immunosorbent assay as a screening test for 

celiac disease in pediatric patients. Pediatrics 

2001;107(1):E8. 
174 

 305. Chartrand LJ, Agulnik J, Vanounou T, Russo PA, 

Baehler P, Seidman EG. Effectiveness of 

antigliadin antibodies as a screening test for 

celiac disease in children. CMAJ 

1997;157(5):527-33. 

 306. Day AS, Cook HB, Whitehead M, Abbott GD. 

Anti-endomysial and anti-gliadin antibodies in 

screening for coeliac disease in children at 

greater risk of developing coeliac disease. N Z 

Med J 2000;113(1119):412-3. 

 307. Fitzpatrick KP, Sherman PM, Ipp M, Saunders N, 

Macarthur C. Screening for celiac disease in 

children with recurrent abdominal pain. J Pediatr 

Gastroenterol Nutr 2001;33(3):250-2. 

 308. Thomas AG, Phillips AD, Walker-Smith JA. The 

value of proximal small intestinal biopsy in the 

differential diagnosis of chronic diarrhoea. Arch 

Dis Child 1992;67(6):741-3. 

 309. Ventura A, Facchini S, Amantidu C, Andreotti 

MF, Andrighetto A, Baggiani A, et al. Searching 

for celiac disease in pediatric general practice. 

Clin Pediatr 2001;40(10):575-7. 

 310. Ascher H, Krantz I, Kristiansson B. Increasing 

incidence of coeliac disease in Sweden. Arch Dis 

Child 1991;66(5):608-11. 

 311. Cavell B, Stenhammar L, Ascher H, Danielsson 

L, Dannaeus A, Lindberg T, et al. Increasing 

incidence of childhood coeliac disease in 

Sweden. Results of a national study. Acta 

Paediatr 1992;81(8):589-92. 

 312. Stenhammar L, Johansson CG. The incidence of 

coeliac disease in children in south-east Sweden. 

Acta Paediatrica Scandinavica 1981;70(3):379-

81. 

 313. Weile B, Cavell B, Nivenius K, Krasilnikoff PA. 

Striking differences in the incidence of childhood 

celiac disease between Denmark and Sweden: a 

plausible explanation. J Pediatr Gastroenterol 

Nutr 1995;21(1):64-8. 

 314. Weile B, Krasilnikoff PA. Low incidence rates 

by birth of symptomatic coeliac disease in a 

Danish population of children. Acta Paediatr 

1992;81(5):394-8. 

 315. Stevens FM, Egan-Mitchell B, Cryan E, 

McCarthy CF, McNicholl B. Decreasing 

incidence of coeliac disease. Arch Dis Child 

1987;62(5):465-8. 

 316. Logan RF, Rifkind EA, Busuttil A, Gilmour HM, 

Ferguson A. Prevalence and "incidence" of celiac 

disease in Edinburgh and the Lothian region of 

Scotland. Gastroenterology 1986;90(2):334-42. 

 317. Hoffenberg EJ, Bao F, Eisenbarth GS, Uhlhorn 

C, Haas JE, Sokol RJ, et al. Transglutaminase 

antibodies in children with a genetic risk for 

celiac disease. Journal of Pediatrics 

2000;137(3):356-60. 

 318. Corazza GR, Frisoni M, Treggiari EA, Valentini 

RA, Filipponi C, Volta U, et al. Subclinical celiac 

sprue. Increasing occurrence and clues to its 

diagnosis. J Clin Gastroenterol 1993;16(1):16-21. 

 319. Sanders DS, Hurlstone DP, Stokes RO, Rashid F, 

Milford-Ward A, Hadjivassiliou M, et al. 

Changing face of adult coeliac disease: 

experience of a single university hospital in 

South Yorkshire. Postgraduate Medical Journal 

2002;78(915):31-3. 

 320. Sategna-Guidetti C, Grosso S. Changing pattern 

in adult coeliac disease: A 24-year survey. Eur J 

Gastroenterol Hepatol 1994;6(1):15-9. 

 321. Holmes GK. Non-malignant complications of 

coeliac disease. Acta Paediatrica Supplement 

1996;412:68-75. 

 322. Suharjono. Intestinal biopsy and coeliac disease. 

Paediatrica Indonesiana 1971;11(3):116-34. 

 323. Mannell A, van Heerden JA, Weiland LH, Ilstrup 

DM. Factors influencing survival after resection 

for ductal adenocarcinoma of the pancreas. 

Annals of Surgery 1986;203(4):403-7. 

 324. Atherton DJ. Diagnosis and management of skin 

disorders caused by food allergy. Annals of 

Allergy 1984;53(6 Pt 2):623-8. 

 325. Di Stefano M, Jorizzo RA, Veneto G, Cecchetti 

L, Gasbarrini G, Corazza GR. Bone mass and 

metabolism in dermatitis herpetiformis. Dig Dis 

Sci 1999;44(10):2139-43. 

 326. Ots M, Uibo O, Metskula K, Uibo R, Salupere V. 

IgA-antigliadin antibodies in patients with IgA 

nephropathy: the secondary phenomenon? 

American Journal of Nephrology 

1999;19(4):453-8. 

 327. Collin P, Reunala T, Pukkala E, Laippala P, 

Keyrilainen O, Pasternack A. Coeliac disease--

associated disorders and survival. Gut 

1994;35(9):1215-8. 

 328. Cooper BT, Holmes GK, Cooke WT. Lymphoma 

risk in coeliac disease of later life. Digestion 

1982;23(2):89-92. 
175 

 329. Harris OD, Cooke WT, Thompson H, 

Waterhouse JA. Malignancy in adult coeliac 

disease and idiopathic steatorrhoea. Am J Med 

1967;42(6):899-912. 

 330. Holmes GK, Stokes PL, Sorahan TM, Prior P, 

Waterhouse JA, Cooke WT. Coeliac disease, 

gluten-free diet, and malignancy. Gut 

1976;17(8):612-9. 

 331. Peters U, Askling J, Gridley G, Ekbom A, Linet 

M. Causes of death in patients with celiac disease 

in a population-based Swedish cohort. Archives 

of Internal Medicine 2003;163(13):1566-72. 

 332. Cooper BT, Holmes GKT, Ferguson R. Celiac 

disease and malignancy. Medicine 

1980;59(4):249-61. 

 333. Holmes GK, Prior P, Lane MR, Pope D, Allan 

RN. Malignancy in coeliac disease--effect of a 

gluten free diet. Gut 1989;30(3):333-8. 

 334. Sorensen HT, Fonager K. Risk estimation of 

disorders associated with coeliac disease. A 16-

year Danish nationwide follow-up study based on 

hospital discharge data. Implications for 

screening. Int J Risk Saf Med 1996;8(2):137-40. 

 335. Cottone M, Termini A, Oliva L, Magliocco A, 

Marrone C, Orlando A, et al. Mortality and 

causes of death in celiac disease in a 

Mediterranean area. Dig Dis Sci 

1999;44(12):2538-41. 

 336. Logan RF, Rifkind EA, Turner ID, Ferguson A. 

Mortality in celiac disease. Gastroenterology 

1989;97(2):265-71. 

 337. Askling J, Linet M, Gridley G, Halstensen TS, 

Ekstrom K, Ekbom A. Cancer incidence in a 

population-based cohort of individuals 

hospitalized with celiac disease or dermatitis 

herpetiformis. Gastroenterology 

2002;123(5):1428-35. 

 338. Collin P, Pukkala E, Reunala T. Malignancy and 

survival in dermatitis herpetiformis: a 

comparison with coeliac disease. Gut 

1996;38(4):528-30. 

 339. Corrao G, Corazza GR, Bagnardi V, Brusco G, 

Ciacci C, Cottone M, et al. Mortality in patients 

with coeliac disease and their relatives: a cohort 

study. Lancet 2001;358(9279):356-61. 

 340. Green PHR, Fleischauer AT, Bhagat G, Goyal R, 

Jabri B, Neugut AI. Risk of malignancy in 

patients with celiac disease. Am J Med 

2003;115(3):191-5. 

 341. Selby WS, Gallagher ND. Malignancy in a 19-

year experience of adult celiac disease. Dig Dis 

Sci 1979;24(9):684-8. 

 342. Delco F, El Serag HB, Sonnenberg A. Celiac 

sprue among US military veterans: associated 

disorders and clinical manifestations. Dig Dis Sci 

1999;44(5):966-72. 

 343. Nielsen OH, Jacobsen O, Pedersen ER, 

Rasmussen SN, Petri M, Laulund S, et al. Nontropical sprue. Malignant diseases and mortality 

rate. Scand J Gastroenterol 1985;20(1):13-8. 

 344. Shainoff JR, Valenzuela R, Urbanic DA, DiBello 

PM, Lucas F, V, Graor R. Fibrinogen A alpha 

and gamma-chain dimers as potential differential 

indicators of atherosclerotic and thrombotic 

vascular disease. Blood Coagulation & 

Fibrinolysis - an International Journal in 

Haemostasis and Thrombosis 1990;1(4-5):499-

503. 

 345. Ribes-Koninckx C, Alfonso P, Ortigosa L, 

Escobar H, Suarez L, Arranz E, et al. A beta-turn 

rich oats peptide as an antigen in an ELISA 

method for the screening of coeliac disease in a 

paediatric population. European Journal of 

Clinical Investigation 2000;30(8):702-8. 

 346. Kemppainen TA, Kosma VM, Janatuinen EK, 

Julkunen RJ, Pikkarainen PH, Uusitupa M, I. 

Nutritional status of newly diagnosed celiac 

disease patients before and after the institution of 

a celiac disease diet--association with the grade 

of mucosal villous atrophy. Am J Clin Nutr 

1998;67(3):482-7. 

 347. Amin R, Murphy N, Edge J, Ahmed ML, Acerini 

CL, Dunger DB. A longitudinal study of the 

effects of a gluten-free diet on glycemic control 

and weight gain in subjects with type 1 diabetes 

and celiac disease. Diabetes Care 

2002;25(7):1117-22. 

 348. Bardella MT, Fredella C, Prampolini L, Molteni 

N, Giunta AM, Bianchi PA. Body composition 

and dietary intakes in adult celiac disease patients 

consuming a strict gluten-free diet. Am J Clin 

Nutr 2000;72(4):937-9. 

 349. Barera G, Mora S, Brambilla P, Ricotti A, Menni 

L, Beccio S, et al. Body composition in children 

with celiac disease and the effects of a gluten-free 

diet: a prospective case-control study. Am J Clin 

Nutr 2000;72(1):71-5. 

 350. Boersma B, Houwen RHJ, Blum WF, van Doorn 

J, Wit JM. Catch-up growth and endocrine 

changes in childhood celiac disease. Endocrine 
176 

changes during catch-up growth. Horm Res 

2002;58(Suppl 1):57-65. 

 351. Ciacci C, Cirillo M, Auriemma G, Di Dato G, 

Sabbatini F, Mazzacca G. Celiac disease and 

pregnancy outcome. Am J Gastroenterol 

1996;91(4):718-22. 

 352. Rea F, Polito C, Marotta A, Di Toro A, Iovene A, 

Collini R, et al. Restoration of body composition 

in celiac children after one year of gluten-free 

diet. J Pediatr Gastroenterol Nutr 

1996;23(4):408-12. 

 353. Sategna-Guidetti C, Grosso SB, Grosso S, 

Mengozzi G, Aimo G, Zaccaria T, et al. The 

effects of 1-year gluten withdrawal on bone mass, 

bone metabolism and nutritional status in newlydiagnosed adult coeliac disease patients. Aliment 

Pharmacol Ther 2000;14(1):35-43. 

 354. Sategna-Guidetti C, Volta U, Ciacci C, Usai P, 

Carlino A, De Franceschi L, et al. Prevalence of 

thyroid disorders in untreated adult celiac disease 

patients and effect of gluten withdrawal: an 

Italian multicenter study. Am J Gastroenterol 

2001;96(3):751-7. 

 355. Valdimarsson T, Lofman O, Toss G, Strom M. 

Reversal of osteopenia with diet in adult coeliac 

disease. Gut 1996;38(3):322-7. 

 356. Valdimarsson T, Toss G, Lofman O, Strom M. 

Three years' follow-up of bone density in adult 

coeliac disease: significance of secondary 

hyperparathyroidism. Scand J Gastroenterol 

2000;35(3):274-80. 

 357. Westman E, Ambler GR, Royle M, Peat J, Chan 

A. Children with coeliac disease and insulin 

dependent diabetes mellitus--growth, diabetes 

control and dietary intake. J Pediatr Endocrinol 

Metab 1999;12(3):433-42. 

 358. Annibale B, Severi C, Chistolini A, Antonelli G, 

Lahner E, Marcheggiano A, et al. Efficacy of 

gluten-free diet alone on recovery from iron 

deficiency anemia in adult celiac patients. Am J 

Gastroenterol 2001;96(1):132-7. 

 359. Arato A, Korner A, Veres G, Dezsofi A, Ujpal I, 

Madacsy L. Frequency of coeliac disease in 

Hungarian children with type 1 diabetes mellitus. 

Eur J Pediatr 2002;162(1):1-5. 

 360. Atkinson K, Tokmakajian S, Watson W, Gregor 

J. Evaluation of the endomysial antibody for 

celiac disease: operating properties and 

associated cost implications in clinical practice. 

Can J Gastroenterol 1997;11(8):673-7. 

 361. Bardella MT, Molteni N, Quatrini M, Velio P, 

Ranzi T, Bianchi PA. Clinical, biochemical and 

histological abnormalities in adult celiac patients 

on gluten-free diet. Gastroenterol Clin Biol 

1985;9(11):787-9. 

 362. Corrao G, Corazza GR, Bagnardi V, Brusco G, 

Ciacci C, Cottone M, et al. Mortality in patients 

with coeliac disease and their relatives: a cohort 

study. Lancet 2001;358(9279):356-61. 

 363. Fabiani E, Catassi C, Villari A, Gismondi P, 

Pierdomenico R, Ratsch IM, et al. Dietary 

compliance in screening-detected coeliac disease 

adolescents. Acta Paediatr 1996;412(Suppl):65-7. 

 364. Fabiani E, Taccari LM, Ratsch IM, Di Giuseppe 

S, Coppa G, V, Catassi C. Compliance with 

gluten-free diet in adolescents with screeningdetected celiac disease: a 5-year follow-up study. 

J Pediatr 2000;136(6):841-3. 

 365. Greco L, Mayer M, Ciccarelli G, Troncone R, 

Auricchio S. Compliance to a gluten-free diet in 

adolescents, or "what do 300 coeliac adolescents 

eat every day?". Ital J Gastroenterol Hepatol 

1997;29(4):305-10. 

 366. Harewood GC, Murray JA. Diagnostic approach 

to a patient with suspected celiac disease: a cost 

analysis. Dig Dis Sci 2001;46(11):2510-4. 

 367. Holmes GK, Stokes PL, Sorahan TM, Prior P, 

Waterhouse JA, Cooke WT. Coeliac disease, 

gluten-free diet, and malignancy. Gut 

1976;17(8):612-9. 

 368. Johnston SD, Watson RG, McMillan SA, Sloan J, 

Love AH. Coeliac disease detected by screening 

is not silent--simply unrecognized. Qjm 

1998;91(12):853-60. 

 369. Poddar U, Thapa BR, Nain CK, rasad A, ingh K. 

Celiac disease in India: are they true cases of 

celiac disease? J Pediatr Gastroenterol Nutr 

2002;35(4):508-12. 

 370. Saukkonen T, Vaisanen S, Akerblom HK, 

Savilahti E. Coeliac disease in children and 

adolescents with type 1 diabetes: a study of 

growth, glycaemic control, and experiences of 

families. Acta Paediatr 2002;91(3):297-302. 

 371. Smecuol E, Gonzalez D, Mautalen C, Siccardi A, 

Cataldi M, Niveloni S, et al. Longitudinal study 

on the effect of treatment on body composition 

and anthropometry of celiac disease patients. Am 

J Gastroenterol 1997;92(4):639-43. 
177 

 372. Bowron A, Moorghen M, Morgan JE, Osborne 

JR, Stansbie D, Stone JE. Cost-effective strategy 

for the serological investigation of coeliac 

disease. Ann Clin Biochem 2000;37(4):467-70. 

 373. Thomason K, West J, Logan RFA, Coupland C, 

Holmes GKT. Fracture experience of patients 

with coeliac disease: a population based survey. 

Gut 2003;52(4):518-22. 

 374. Addolorato G, Capristo E, Ghittoni G, Valeri C, 

Masciana R, Ancona C, et al. Anxiety but not 

depression decreases in coeliac patients after oneyear gluten-free diet: a longitudinal study. Scand 

J Gastroenterol 2001;36(5):502-6. 

 375. Bai JC, Gonzalez D, Mautalen C, Mazure R, 

Pedreira S, Vazquez H, et al. Long-term effect of 

gluten restriction on bone mineral density of 

patients with coeliac disease. Aliment Pharmacol 

Ther 1997;11(1):157-64. 

 376. Kemppainen T, Kroger H, Janatuinen E, Arnala I, 

Lamberg-Allardt C, Karkkainen M, et al. Bone 

recovery after a gluten-free diet: a 5-year followup study. Bone 1999;25(3):355-60. 

 377. Mora S, Barera G, Beccio S, Menni L, Proverbio 

MC, Bianchi C, et al. A prospective, longitudinal 

study of the long-term effect of treatment on bone 

density in children with celiac disease. J Pediatr 

2001;139(4):516-21. 

 378. Mustalahti K, Collin P, Sievanen H, Salmi J, 

Maki M. Osteopenia in patients with clinically 

silent coeliac disease warrants screening. Lancet 

1999;354(9180):744-5. 

 379. Zaccari G, Mazzetti dP, Paone FM, 

Guidiceandrea P. A proposal for coeliac disease 

screening of all infants at the age of fifteen 

months. Gastroenterol Int 1996;9(1):11-5. 

 380. Bowron A, Moorghen M, Morgan JE, Osborne 

JR, Stansbie D, Stone JE. Cost-effective strategy 

for the serological investigation of coeliac 

disease. Ann Clin Biochem 2000;37(4):467-70. 

 381. Bernstein CN, Leslie WD, Leboff MS. AGA 

technical review on osteoporosis in 

gastrointestinal diseases. Gastroenterology 

2003;124(3):795-841. 

 382. Gomez JC, Selvaggio G, Pizarro B, Viola MJ, La 

Motta G, Smecuol E, et al. Value of a screening 

algorithm for celiac disease using tissue 

transglutaminase antibodies as first level in a 

population-based study. American Journal of 

Gastroenterology 2002;97(11):2785-90. 

 383. Kemppainen T, Kroger H, Janatuinen E, Arnala I, 

Kosma VM, Pikkarainen P, et al. Osteoporosis in 

adult patients with celiac disease. Bone 

1999;24(3):249-55. 

 384. Mora S, Barera G, Beccio S, Proverbio MC, 

Weber G, Bianchi C, et al. Bone density and bone 

metabolism are normal after long-term glutenfree diet in young celiac patients. Am J 

Gastroenterol 1999;94(2):398-403. 

 385. West J, Logan Richard FA, Card TR, Smith C, 

Hubbard R. Fracture risk in people with celiac 

disease: a population-based cohort study. 

Gastroenterology 2003;125(2):429-36. 

 386. Ciacci C, Maurelli L, Klain M, Savino G, 

Salvatore M, Mazzacca G, et al. Effects of 

dietary treatment on bone mineral density in 

adults with celiac disease: factors predicting 

response. Am J Gastroenterol 1997;92(6):992-6. 

 387. McFarlane XA, Bhalla AK, Robertson DA. 

Effect of a gluten free diet on osteopenia in adults 

with newly diagnosed coeliac disease. Gut 

1996;39(2):180-4. 

 388. Vestergaard P, Mosekilde L. Fracture risk in 

patients with celiac Disease, Crohn's disease, and 

ulcerative colitis: a nationwide follow-up study of 

16,416 patients in Denmark. Am J Epidemiol 

2002;156(1):1-10. Available: PM:12076883. 

 389. Vasquez H, Mazure R, Gonzalez D, Flores D, 

Pedreira S, Niveloni S, et al. Risk of fractures in 

celiac disease patients: a cross-sectional, casecontrol study. Am J Gastroenterol 

2000;95(1):183-9. Available: PM:10638580. 

 390. Fickling WE, McFarlane XA, Bhalla AK, 

Robertson DA. The clinical impact of metabolic 

bone disease in coeliac disease. Postgrad Med J 

2001;77(903):33-6. Available: PM:11123392. 

 391. Bianchi ML, Bardella MT. Bone and celiac 

disease. Calcif Tissue Int 2002;71(6):465-71. 

Available: PM:12232681. 

 392. Moreno ML, Vazquez H, Mazure R, Smecuol E, 

Niveloni S, Pedreira S, et al. Stratification of 

bone fracture risk in patients with celiac disease. 

Clin Gastroenterol Hepatol 2004;2(2):127-34. 

Available: PM:15017617. 

 393. Norgard B, Fonager K, Sorensen HT, Olsen J. 

Birth outcomes of women with celiac disease: A 

nationwide historical cohort study. Am J 

Gastroenterol 1999;94(9):2435-40. 
178 

 394. Thomason K, West J, Logan RFA, Coupland C, 

Holmes GKT. Fracture experience of patients 

with coeliac disease: a population based survey. 

Gut 2003;52(4):518-22. 

 395. Cook HB, Burt MJ, Collett JA, Whitehead MR, 

Frampton CM, Chapman BA. Adult coeliac 

disease: prevalence and clinical significance. J 

Gastroenterol Hepatol 2000;15(9):1032-6. 

 396. Bartholomeusz RC, Labrooy JT, Davidson GP, 

Hetzel P, Johnson RB, Shearman DJ. Polymeric 

IgA antibody to gliadin in the serum of patients 

with coeliac disease. J Gastroenterol Hepatol 

1990;5(6):675-81. 

 397. Fotoulaki M, Nousia-Arvanitakis S, 

Augoustidou-Savvopoulou P, KanakoudiTsakalides F, Zaramboukas T, Vlachonikolis J. 

Clinical application of immunological markers as 

monitoring tests in celiac disease. Dig Dis Sci 

1999;44(10):2133-8. 

 398. Kaukinen K, Sulkanen S, Maki M, Collin P. IgAclass transglutaminase antibodies in evaluating 

the efficacy of gluten-free diet in coeliac disease. 

Eur J Gastroenterol Hepatol 2002;14(3):311-5. 

 399. Bardella MT, Trovato C, Cesana BM, Pagliari C, 

Gebbia C, Peracchi M. Serological markers for 

coeliac disease: Is it time to change? Dig Liver 

Dis 2001;33(5):426-31. 

 400. Burgin-Wolff A, Gaze H, Hadziselimovic F, 

Huber H, Lentze MJ, Nussle D, et al. Antigliadin 

and antiendomysium antibody determination for 

coeliac disease. Arch Dis Child 1991;66(8):941-

7. 

 401. Scalici C, Manzoni D, Licastro G, Varia F, Di 

Prima L, Vitali R. Reliability of EMA assay in 

the evaluation of gluten-free diet compliance in 

celiac patients during follow-up. Acta Med 

Mediterr 2003;19(1):67-9. 

 402. Vahedi K, Mascart-Lemone F, Mary JY, 

Laberenne JE, Bouhnik Y, Morin MC, et al. Are 

Anti-Endomysial (AEM) and AntiTransglutaminase (TTG) Antibodies Reliable 

Markers of Strict Diet Compliance in Adult 

Celiacs on a Gluten Free Diet (GFD)? 

Gastroenterology 2000;118(4 Suppl. 2 Part 

1):AGA. 

 403. Martini S, Mengozzi G, Aimo G, Giorda L, Pagni 

R, Guidetti CS. Comparative evaluation of 

serologic tests for celiac disease diagnosis and 

follow-up. Clin Chem 2002;48(6 Pt 1):960-3. 

 404. Valletta EA, Trevisiol D, Mastella G. IgA antigliadin antibodies in the monitoring of gluten 

challenge in celiac disease. J Pediatr 

Gastroenterol Nutr 1990;10(2):169-73. 

 405. Wahab PJ, Meijer Jos WR, Mulder Chris JJ. 

Histologic follow-up of people with celiac 

disease on a gluten-free diet: slow and 

incomplete recovery. American Journal of 

Clinical Pathology 2002;118(3):459-63. 

 406. McNicholl B, Egan-Mitchell B, Stevens F, Keane 

R, Baker S, McCarthy CF, et al. Mucosal 

recovery in treated childhood celiac disease 

(gluten-sensitive enteropathy). J Pediatr 

1976;89(3):418-24. 

 407. Valentini RA, Andreani ML, Corazza GR, 

Gasbarrini G. IgA endomysium antibody: a 

valuable tool in the screening of coeliac disease 

but not its follow-up. Ital J Gastroenterol 

1994;26(6):279-82. 

 408. Fabiani E, Catassi C. The serum IgA class antitissue transglutaminase antibodies in the 

diagnosis and follow up of coeliac disease. 

Results of an international multi-centre study. 

International Working Group on Eu-tTG. Eur J 

Gastroenterol Hepatol 2001;13(6):659-65. 

 409. Dickey W, Hughes DF, McMillan SA. 

Disappearance of endomysial antibodies in 

treated celiac disease does not indicate 

histological recovery. Am J Gastroenterol 

2000;95(3):712-4. 

 410. Fabiani E, Catassi C, Villari A, Gismondi P, 

Pierdomenico R, Ratsch IM, et al. Dietary 

compliance in screening-detected coeliac disease 

adolescents. Acta Paediatr 1996;412:65-7. 

 411. Lee SK, Lo W, Memeo L, Rotterdam H, Green 

Peter HR. Duodenal histology in patients with 

celiac disease after treatment with a gluten-free 

diet. Gastrointest Endosc 2003;57(2):187-91. 

 412. Pacht A, Sinai N, Hornstein L, Kumar V, IshShalom N, Lerner A. The diagnostic reliability of 

anti-endomysial antibody in celiac disease: the 

north Israel experience. Isr J Med Sci 

1995;31(4):218-20. 

 413. Sategna-Guidetti C, Grosso S, Bruno M, Grosso 

SB. Reliability of immunologic markers of celiac 

sprue in the assessment of mucosal recovery after 

gluten withdrawal. J Clin Gastroenterol 

1996;23(2):101-4. 

 414. Selby WS, Painter D, Collins A, Faulkner-Hogg 

KB, Loblay RH. Persistent mucosal 

abnormalities in coeliac disease are not related to 

the ingestion of trace amounts of gluten. Scand J 

Gastroenterol 1999;34(9):909-14. 
179 

 415. Troncone R, Mayer M, Spagnuolo F, Maiuri L, 

Greco L. Endomysial antibodies as unreliable 

markers for slight dietary transgressions in 

adolescents with celiac disease. J Pediatr 

Gastroenterol Nutr 1995;21(1):69-72. 

 416. Anson O, Weizman Z, Zeevi N. Celiac disease: 

parental knowledge and attitudes of dietary 

compliance. Pediatrics 1990;85(1):98-103. 

 417. Fabiani E, Taccari LM, Ratsch IM, Di Giuseppe 

S, Coppa G, V, Catassi C. Compliance with 

gluten-free diet in adolescents with screeningdetected celiac disease: a 5-year follow-up study. 

J Pediatr 2000;136(6):841-3. 

 418. Jackson PT, Glasgow JF, Thom R. Parents' 

understanding of coeliac disease and diet. Arch 

Dis Child 1985;60(7):672-4. 

 419. Lamontagne P, West GE, Galibois I. Quebecers 

with celiac disease: analysis of dietary problems. 

Canadian Journal of Dietetic Practice and 

Research - a Publication of Dietitians of Canada 

= Revue Canadienne De La Pratique Et De La 

Recherche En Dietetique - Une Publication Des 

Dietetistes Du C 2001;62(4):175-81. 

 420. Ljungman G, Myrdal U. Compliance in teenagers 

with coeliac disease--a Swedish follow-up study. 

Acta Paediatr 1993;82(3):235-8. 

 421. Hogberg L, Grodzinsky E, Stenhammar L. Better 

dietary compliance in patients with coeliac 

disease diagnosed in early childhood. Scand J 

Gastroenterol 2003;38(7):751-4. 

 422. Patin NM, Johnson F, Kirks BA. Promoting 

dietary compliance in gluten-intolerant children. J 

Nutr Educ 1989;21(2):100D. 

 423. Lijmer JG, Mol BW, Heisterkamp S, Bonsel GJ, 

Prins MH, van der Meulen JH, et al. Empirical 

evidence of design-related bias in studies of 

diagnostic tests. JAMA 1999;282(11):1061-6. 

Available: PM:10493205. 

 424. Tursi A, Brandimarte G, Giorgetti GM. 

Prevalence of antitissue transglutaminase 

antibodies in different degrees of intestinal 

damage in celiac disease. Journal of Clinical 

Gastroenterology 2003;36(3):219-21. 

 425. Tursi A, Brandimarte G, Giorgetti G, 

Gigliobianco A, Lombardi D, Gasbarrini G. Low 

prevalence of antigliadin and anti-endomysium 

antibodies in subclinical/silent celiac disease. 

American Journal of Gastroenterology 

2001;96(5):1507-10. 

 426. Tursi A, Brandimarte G, Giorgetti GM. Sorbitol 

H2-breath test versus anti-endomysium 

antibodies for the diagnosis of subclinical/silent 

coeliac disease. Scand J Gastroenterol 

2001;36(11):1170-2. 

 427. Demir H, Yuce A, Kocak N, Ozen H, Gurakan F. 

Celiac disease in Turkish children: presentation 

of 104 cases. Pediatrics International - Official 

Journal of the Japan Pediatric Society 

2000;42(5):483-7. 

 428. Kotze Lorete Maria da Silva, Utiyama Shirley 

Ramos da Rosa, Nisihara RM, de C, V, Ioshii 

SO. IgA class anti-endomysial and anti-tissue 

transglutaminase antibodies in relation to 

duodenal mucosa changes in coeliac disease. 

Pathology 2003;35(1):56-60. 

 429. Sategna-Guidetti C, Bruno M, Pulitano R, 

Ferfoglia G. Disease specificity of IgA class antiendomysium antibodies (IgA-EmA) in adult 

coeliac disease. Eur J Gastroenterol Hepatol 

1991;3(3):251-4. 

 430. Ciacci C, Cavallaro R, Della VN, D'argenio G. 

The Use of Serum Ttg-Ab Assay in Patients on 

Gluten-Free Diet as a Measure of Dietetic 

Compliance. Gastroenterology 2002;122(2):588. 

 431. Garcia VE, De Lourdes de Abreu Ferrari, Alves 

BE, Affonso Barbosa AJ, Brasileiro FG, Hartung 

TN, et al. Agreement between pathologists 

concerning assessment of intestinal biopsies from 

adult celiac disease patients. Gastroenterol Int 

2002;15(1-2):1-8. 

 432. Weile B, Hansen BF, Hagerstrand I, Hansen JP, 

Krasilnikoff PA. Interobserver variation in 

diagnosing coeliac disease. A joint study by 

Danish and Swedish pathologists. Apmis - Acta 

Pathologica, Microbiologica, Et Immunologica 

Scandinavica 2000;108(5):380-4. 

 433. Landis JR, Koch GG. The measurement of 

observer agreement for categorical data. 

Biometrics 1977;33(1):159-74. Available: 

PM:843571. 

 434. Risdon RA, Keeling JW. Quantitation of the 

histological changes found in small intestinal 

biopsy specimens from children with suspected 

coeliac disease. Gut 1974;15(1):9-18. 

 435. Glasgow JF, Corkey CW, Molla A. Critical 

assessment of small bowel biopsy in children. 

Archives of Disease in Childhood 

1979;54(8):604-8. 

 436. Jarvinen TT, Kaukinen K, Laurila K, Kyronpalo 

S, Rasmussen M, Maki M, et al. Intraepithelial 
180 

lymphocytes in celiac disease. American Journal 

of Gastroenterology 2003;98(6):1332-7. 

 437. Corazza GR, Bonvicini F, Frazzoni M, Gatto M, 

Gasbarrini G. Observer variation in assessment of 

jejunal biopsy specimens. A comparison between 

subjective criteria and morphometric 

measurement. Gastroenterology 

1982;83(6):1217-22. Available: PM:7129029. 

 438. Stenhammar L, Brandt A, Wagermark J. A 

family study of coeliac disease. Acta Paediatr 

Scand 1982;71(4):625-8. Available: 

PM:7136679. 

 439. Troncone R, Catassi C, Lambertini A, Zaniboni 

MG, Lazzari R, Bottaro G, et al. Latent coeliac 

disease in Italy. Acta Paediatr Int J Paediatr 

1995;84(11):1252-7. 

 440. Maki M, Lahdeaho ML, Hallstrom O, Viander 

M, Visakorpi JK. Postpubertal gluten challenge 

in coeliac disease. Arch Dis Child 

1989;64(11):1604-7. Available: PM:2604420. 

 441. Schmitz J, Arnaud-Battandier F JJ, Rey J. Long 

term follow-up of childhood coeliac disease 

(CD): Is there a "natural recovery"? Pediatr Res 

1984;18;1052. 

 442. Ferguson A, McClure JP, Townley RR. 

Intraepithelial lymphocyte counts in small 

intestinal biopsies from children with diarrhoea. 

Acta Paediatrica Scandinavica 1976;65(5):541-6. 

 443. Kutlu T, Brousse N, Rambaud C, Le Deist F, 

Schmitz J, Cerf-Bensussan N. Numbers of T cell 

receptor (TCR) alpha beta+ but not of TcR 

gamma delta+ intraepithelial lymphocytes 

correlate with the grade of villous atrophy in 

coeliac patients on a long term normal diet. Gut 

1993;34(2):208-14. 

 444. O'Farrelly C, Graeme-Cook F, Hourihane DO, 

Feighery C, Weir DG. Histological changes 

associated with wheat protein antibodies in the 

absence of villous atrophy. Journal of Clinical 

Pathology 1987;40(10):1228-30. 

 445. Saputo V, Losi S, Mancosu M, Della Morte MA, 

Moschettini GF. Intraepithelial lymphocytes in 

jejunal mucosa: diagnostic significance of 

changes in their number during chronic intestinal 

disease, with particular reference to coeliac 

disease. Schweizerische Rundschau Fur Medizin 

Praxis = Revue Suisse De Medecine Praxis 

1981;70(30):1342-8. 

 446. Mino M, Lauwers GY. Role of lymphocytic 

immunophenotyping in the diagnosis of glutensensitive enteropathy with preserved villous 

architecture. Am J Surg Pathol 2003;27(9):1237-

42. 

 447. Goldstein NS, Underhill J. Morphologic features 

suggestive of gluten sensitivity in architecturally 

normal duodenal biopsy specimens. American 

Journal of Clinical Pathology 2001;116(1):63-71. 

 448. Kuitunen P, Kosnai I, Savilahti E. Morphometric 

study of the jejunal mucosa in various childhood 

enteropathies with special reference to 

intraepithelial lymphocytes. Journal of Pediatric 

Gastroenterology and Nutrition 1982;1(4):525-

31. 

 449. Kaukinen K, Collin P, Holm K, Karvonen AL, 

Pikkarainen P, Maki M. Small-bowel mucosal 

inflammation in reticulin or gliadin antibodypositive patients without villous atrophy. 

Scandinavian Journal of Gastroenterology 

1998;33(9):944-9. 

 450. Wahab PJ, Crusius JB, Meijer JW, Mulder CJ. 

Gluten challenge in borderline gluten-sensitive 

enteropathy. American Journal of 

Gastroenterology 2001;96(5):1464-9. 

 451. Wahab PJ, Meijer Jos WR, Dumitra D, Goerres 

MS, Mulder Chris JJ. Coeliac disease: more than 

villous atrophy. Romanian Journal of 

Gastroenterology 2002;11(2):121-7. 

 452. Mahadeva S, Wyatt J, I, Howdle PD. Is a raised 

intraepithelial lymphocyte count with normal 

duodenal villous architecture clinically relevant? 

Journal of Clinical Pathology 2002;55(6):424-8. 

 453. Kaukinen K, Maki M, Partanen J, Sievanen H, 

Collin P. Celiac disease without villous atrophy: 

revision of criteria called for. Dig Dis Sci 

2001;46(4):879-87. 

 454. Catassi C, Fabiani E, Corrao G, Barbato M, De 

Renzo A, Carella AM, et al. Risk of non-Hodgkin 

lymphoma in celiac disease. JAMA 

2002;287(11):1413-9. 

 455. Johnston SD, Watson RGP. Small bowel 

lymphoma in unrecognized coeliac disease: A 

cause for concern? Eur J Gastroenterol Hepatol 

2000;12(6):645-8. 

 456. Green PHR, Stavropoulos SN, Panagi SG, 

Goldstein SL, Mcmahon DJ, Absan H, et al. 

Characteristics of adult celiac disease in the 

USA: results of a national survey. Am J 

Gastroenterol 2001;96(1):126-31. 

 457. Wahab PJ, Meijer Jos WR, Mulder CJJ. 

Histologic follow-up of people with celiac 
181 

disease on a gluten-free diet: slow and 

incomplete recovery. Am J Clin Pathol 

2002;118(3):459-63. 

 458. Goerres MS, Meijer JWR, Wahab PJ, Kerckhaert 

JAM, Groenen PJTA, Van Krieken JHJM, et al. 

Azathioprine and prednisone combination 

therapy in refractory coeliac disease. Aliment 

Pharmacol Ther 2003;18(5):487-94. 

 459. Cellier C, Delabesse E, Helmer C, Patey N, 

Matuchansky C, Jabri B, et al. Refractory sprue, 

coeliac disease, and enteropathy-associated T-cell 

lymphoma. French Coeliac Disease Study Group. 

Lancet 2000;356(9225):203-8. 

 460. Ciacci C, Cirillo M, Cavallaro R, Mazzacca G. 

Long-term follow-up of celiac adults on glutenfree diet: prevalence and correlates of intestinal 

damage. Digestion 2002;66(3):178-85. 

 461. Kluge F, Koch HK, Grosse-Wilde H, Lesch R, 

Gerok W. Follow-up of treated adult celiac 

disease: clinical and morphological studies. 

Hepatogastroenterology 1982;29(1):17-23. 
182 
Abbreviations and Acronyms 

95% CI- Ninety-five percent confidence interval 

AGA- Antigliadin antibody 

AR- Attributable risk 

BMD- Bone mineral density 

CD – Celiac disease 

DXA- Dual energy X-ray absorptiometry 

EGD- Esophagogastroduodenoscopy 

ELISA- Enzyme-linked immunosorbent assay 

EMA- Endomysial antibody 

ESPGAN- European Society of Pediatric Gastroenterology and Nutrition 

ETCL- Enteropathy-associated T-cell lymphoma 

GFD- Gluten-free diet 

GP- Guinea pig 

HLA- Human leukocyte antigen 

HR- Human recombinant 

HU- Human umbilical cord 

IDA- Iron deficiency anemia 

IDDM- Type I diabetes (insulin dependent) 

IEL- Intraepithelial lymphocytes 

IF- Immunofluorescence 

IgA- Immunoglobulin A 

IgG- Immunoglobulin G 

ME- Monkey esophagus 

NHL- Non-Hodgkin’s lymphoma 

NPV- Negative predictive value 

OR- Odds ratio 

PPV- Positive predictive value 

Prev- Prevalence 

PVA- Partial villous atrophy 

RR- Relative risk 

SD- Standard deviation 

Sens- Sensitivity 

SIR- Standardized incidence ratio 

SMR- Standardized mortality ratio 

SPA- Single photon absorptiometry 

Spec- Specificity 

SVA- Subtotal villous atrophy 

tTG- Tissue transglutaminase 

VA- Villous atrophy 

 183 

 A-1

Appendix A. 

Table 1: Various causes of villous atrophy (VA; Farrell and Kelly, Am J Gastro 

2001;96:3237) 

Celiac disease 

Dermatitis herpetiformis 

Cow’s milk protein intolerance (children) 

Post-gastroenteritis 

Giardiasis 

Peptic duodenitis 

Crohn’s disease 

Small intestinal bacterial overgrowth 

Eosinophilic gastroenteritis 

Radiation or chemotherapy 

Tropical sprue 

Severe malnutrition 

Diffuse small intestinal lymphoma 

Graft versus host disease 

Hypogammaglobulinemia 

Alpha chain disease 
 A-2

Table 2: Marsh (Gastroenterology 1992;102:330) and Rostami (Am J Gastroenterol 

1999;94:888) modified histological criteria for CD 

Criteria Rostami modification (1999) Original Marsh (1992) 

Marsh 0 Same as original Pre-infiltrative: 

• Normal mucosal and villous 

architecture 

Marsh I Same as original Infiltrative: 

• Normal mucosal and villous 

architecture 

• Increased numbers of IELs 

Marsh II Same as original Hyperplastic: 

• Similar to above but with enlarged 

crypts, with increased crypt cell 

division 

a Partial VA: 

• Shortened blunt villi 

• Mild lymphocyte infiltration 

• Enlarged hyperplastic crypts 

b Sub-total VA: 

• Clearly atrophic villi – but still 

recognizable 

• Enlarged crypts whose 

immature epithelial cells are 

generated at an increased rate 

• Influx of inflammatory cells 

Marsh III 

c Total VA: 

• Nearly total VA 

• Severe Marsh atrophic, 

hyperplastic and infiltrative 

lesions 

Destructive lesion: 

• Flat mucosa – complete loss of villi 

• Lymphocyte infiltration 

• Enlarged hyperplastic crypts 

Marsh IV Same as original Hypoplastic: 

• Total VA 

• Normal crypt height but hypoplasia 

• Normal IEL count 

• Many feel this doesn’t exist and 

represents severe malnutrition 

VA=villous atrophy 

IEL=intraepithelial lymphocytes
 A-3

Table 3: Revised ESPGAN criteria 

Criteria ESPGAN*- 1979 ESPGAN†- Revised 199Initial histology 

- Absent or nearly absent villi - Recognized existence of less severe lesion - No consensus on verification of less severe lesions but 

recommended if possible continuing gluten diet and assess histology, or re-challenge after GFD, given the large differential of milder histologic lesions 

- Biopsy must remain the initial step in the diagno- Recommend capsule over endoscopic biopsy - Large well oriented biopsy - Histology: hyperplastic VA with hyperplasia of th

surface epithelium. The IEL count is raised 

- Morphometery and histochemistry are importan- Monoclonal antibodies to IEL may be a future a

Antibody studies 

- n/a - Recognize that IgA AGA, and EMA have a high 

specificity for the diagnosis of CD 

- When such antibodies are present at the time o

typical small intestinal mucosa, and when they dclinical response to a GFD, weight is added to tmay now be said to have been finally establishe

- When biopsy is unavailable in communities wer

enteropathy are rare, the presence of abnormal antibodies strongly suggests that CD is a diagno

- Antibodies can be a marker of response to a GF

compliance 

Improvement on GFD 

- Recognized as central to the definition - Recognized that improvement need not be complete 

- Second mandatory requirement remains a reas

than many months) clinical remission on a strict 

- Control biopsy is always a suitable way of verify

is required in asymptomatic pts 

Gluten Challenge 

- Importance of gluten challenge and re-biopsy emphasized to 

document “permanence” of gluten intolerance 

- However, the panel recognized that challenge was not being 

performed in routine practice (only 652 were performed among several thousand children with gluten intolerance) 

- No longer a requirement - Should be used in equivocal cases such as whe

done, biopsy was inadequate or atypical, in comother enteropathies, or in situations when pts plan uncontrolled way 

- Challenge should be performed after obtaining a - Re-biopsy is performed 3-6 months later with th

can take 5-7 years or more to occur. 

2-year rule - To address the issue of transient gluten intolerance, the 

panel emphasized the usefulness of the 2-year rule after stopping a GFD 

- 619 of 652 gluten challenges redeveloped histology 

compatible with CD by 2 years 

- The 2-year rule is practical in most cases, but se

occurring 5-7 years after gluten rechallenge 

*McNeish et al., Arch Dis Child 1979;54:783 †Walker-Smith et al., Arch Dis Child 1990:65:99 

CD=celiac disease; n/a=not applicable; GFD=gluten-free diet 
 A-4

Appendix B. Search Strategies 

Search Strategy 1 

Celiac 1 – Diagnostic Tests 

Test 1. EMA 

MEDLINE on DIALOG 

1. s anti(w)endomysial(w)antibod? OR antiendomysial(w)antibod? 

2. s anti(w)endomysium(w)antibod? OR antiendomysium(w)antibod? 

3. s endomysial(w)antibod? OR endomysium(w)antibod? OR endomysial(w)autoantibod? OR 

endomysium(w)autoantibod? 

4. s endomysial(n3)iga OR antiendomysial(n3)iga OR iga(n)ema 

5. s endomysium(n3)iga OR antiendomysium(n3)iga OR igg(n)ema 

6. s immunoglobulin?(n3)endomysial OR immunoglobulin?(n3)antiendomysial 

7. s immunoglobulin?(n3)endomysium OR immunoglobulin?(n3)antiendomysium 

8. s ema(n3)antibod? OR ema(n3)autoantibod? OR anti(w)ema OR ema(n3)positiv? 

9. s aea AND (endomysial OR endomysium OR antiendomys?) OR aea(n3)positiv? OR aea(n2)igg OR 

aea(n2)iga 

10. c 1 OR 2 OR 3 OR 4 OR 5 OR 6 OR 7 OR 8 OR 9 

11. s (celiac OR celiacs OR coeliac OR coeliacs OR gluten OR glutens OR glutenin OR glutenins OR 

gliadin OR gliadins OR celiac disease/de) AND (ema OR aea) 

12. s (celiac OR celiacs OR coeliac OR coeliacs OR gluten OR glutens OR glutenin OR glutenins OR 

gliadin OR gliadins OR celiac disease/de) AND autoantibod?(n2) positiv? 

13. c 10 OR 11 OR 12 

14. s epithelial(w)membrane(w)antigen 

15. c 13 NOT 14 

16. s s15/human 

17. s s16/eng 

EMBASE on DIALOG 

1. s anti(w)endomysial(w)antibod? OR antiendomysial(w)antibod? 

2. s anti(w)endomysium(w)antibod? OR antiendomysium(w)antibod? 

3. s endomysial(w)antibod? OR endomysium(w)antibod? OR endomysial(w)autoantibod? OR 

endomysium(w)autoantibod? OR endomysium antibody/de 

4. s endomysial(n3)iga OR antiendomysial(n3)iga OR iga(n)ema 

5. s endomysium(n3)iga OR antiendomysium(n3)iga OR igg(n)ema 6. s immunoglobulin?(n3)endomysial 

OR immunoglobulin?(n3)antiendomysial 

7. s immunoglobulin?(n3)endomysium OR immunoglobulin?(n3)antiendomysium 

8. s ema(n3)antibod? OR ema(n3)autoantibod? OR anti(w)ema OR ema(n3)positiv? 

9. s aea AND (endomysial OR endomysium OR antiendomys?) OR aea(n3)positiv? OR aea(n2)igg OR 

aea(n2)iga 

10. c 1 OR 2 OR 3 OR 4 OR 5 OR 6 OR 7 OR 8 OR 9 

11. s (celiac OR celiacs OR coeliac OR coeliacs OR gluten OR glutens OR glutenin OR glutenins OR 

gliadin OR gliadins OR celiac disease/de) AND (ema OR aea) 

12. s (celiac OR celiacs OR coeliac OR coeliacs OR gluten OR glutens OR glutenin OR glutenins OR 

gliadin OR gliadins OR celiac disease/de) AND autoantibod?(n2)positiv? 

13. c 10 OR 11 OR 12 
 A-5

14. s epithelial(w)membrane(w)antigen 

15. c 13 not 14 

16. s s15/human 

17. s s16/eng 
 A-6

Test 2. tTG 

MEDLINE on DIALOG 

1. s tissue(w)transglutaminase?? OR tissue(w)trans(w)glutaminase?? 

2. s antitissue(w)transglutaminase?? OR anti(w)transglutaminase?? 

3. s human(w)transglutaminase?? OR antitransglutaminase??(n3)antibod? 

4. s (immunoglobulin? OR immunoglobulin a/de OR immunoglobulin g/de) AND (transglutaminase OR 

transglutaminases) 

5. s ttg(n3)antibod? OR ttg(n3)autoantibod? OR ttg(w)(kit OR kits) OR ttga OR httg OR anti(w2)ttg OR 

human(w)ttg OR elisa(n)ttg OR attga 

6. s (transglutaminase?? AND antibod?) OR (transglutaminase?? AND autoantibod?) 

7. s transglutaminase??(n3)iga OR transglutaminase??(n3)igg OR tg2(n5)transglutaminase?? OR 

human(w) recombinant(w)tg2 

8. s anti(w)gamma(w)glutamyltransferase AND (antibod? OR autoantibod?) 

9. c 1 OR 2 OR 3 OR 4 OR 5 OR 6 OR 7 OR 8 

10. s (celiac OR celiacs OR coeliac OR coeliacs OR gluten OR glutens OR glutenin OR glutenins OR 

gliadin OR gliadins OR celiac disease/de) AND (transglutaminase OR transglutaminases OR ttg OR 

tg2) 

11. c 9 OR 10 

12. s s11/human 

13. s s12/eng 

EMBASE on DIALOG 

1. s tissue(w)transglutaminase?? OR tissue(w)trans(w)glutaminase?? 

2. s antitissue(w)transglutaminase?? OR anti(w)transglutaminase?? 

3. s human(w)transglutaminase?? OR antitransglutaminase??(n3)antibod? 

4. s immunoglobulin OR immunoglobulin a/de OR immunoglobulin a1/de OR immunoglobulin a2/de 

5. s immunoglobulin g/de OR immunoglobulin g1/de OR immunoglobulin g2/de OR immunoglobulin 

g2a/de OR immunoglobulin g2b/de OR immunoglobulin g3/de OR immunoglobulin g4/de 

6. s transglutaminase OR transglutaminases 

7. c 4 OR 5 

8. c 7 AND 6 

9. s ttg(n3)antibod? OR ttg(n3)autoantibod? OR ttg(w)(kit OR kits OR assay) OR ttga OR httg OR 

anti(w2)ttg OR human(w)ttg OR elisa(n)ttg OR attga 

10. s (transglutaminase?? AND antibod?) OR (transglutaminase?? AND autoantibod?) 

11. s transglutaminase??(n3)iga OR transglutaminase??(n3)igg OR tg2(n5)transglutaminase?? OR 

human(w) recombinant(w)tg2 

12. s anti(w)gamma(w)glutamyltransferase AND (antibod? OR autoantibod?) 

13. c 1 OR 2 OR 3 OR 8 OR 9 OR 10 OR 11 OR 12 

14. s (celiac OR celiacs OR coeliac OR coeliacs OR gluten OR glutens OR glutenin OR glutenins OR 

gliadin OR gliadins OR celiac disease/de) AND (transglutaminase OR transglutaminases OR ttg OR 

tg2) 

15. c 13 OR 14 

16. s s15/human 

17. s s16/eng 
 A-7

Test 3. AGA 

MEDLINE on DIALOG 

1. s gliadin(w)antibod? OR antigliadin(w)antibod? OR iga(n3)antigliadin OR igg(n3)antigliadin 

2. s antigliadin AND (serology OR serological) 

3. s iga(n2)aga OR igg(n2)aga OR aga(n3)positive? OR anti(w)aga 

4. s (celiac OR celiacs OR coeliac OR coeliacs OR gluten OR glutens OR glutenin OR glutenins OR 

gliadin OR gliadins OR celiac disease/de) AND (aga OR antigliadin?) 

5. c 1 OR 2 OR 3 

6. c 5 OR 4 

7. s s6/human 

8. s s7/eng 

EMBASE on DIALOG 

1. s gliadin(w)antibod? OR antigliadin(w)antibod? OR iga(n3)antigliadin OR igg(n3)antigliadin 

2. s antigliadin AND (serology OR serological) 

3. s iga(n2)aga OR igg(n2)aga OR aga(n3)positive? OR anti(w)aga 

4. s (celiac OR celiacs OR coeliac OR coeliacs OR gluten OR glutens OR glutenin OR glutenins OR 

gliadin OR gliadins OR celiac disease/de) AND (aga OR antigliadin? OR anti(w)gliadin?) 

5. c 1 OR 2 OR 3 

6. c 5 OR 4 

7. s s6/human 

8. s s7/eng 
 A-8

Test 4. HLA DQ2/DQ8 

MEDLINE on DIALOG 

1. s (leukocyte OR leukocytes OR leucocyte OR leucocytes) AND (antigen OR antigens) 

2. s hla OR hla-dq antigens/de OR hla antigens/de OR hladq OR histocompatibility antigens/de OR 

histocompatibility testing/de OR histocompatibility 

3. c 1 OR 2 

4. s dq2? OR dq8? OR hladq2? OR hladq8? OR d2? OR d8? 

5. c 3 AND 4 

6. s celiac OR celiacs OR coeliac OR coeliacs OR gluten OR glutens OR glutenin OR glutenins OR 

gliadin OR gliadins OR celiac disease/de 

7. s hla(w)antigen?? OR hla antigens/de OR hla-dq antigens/de 

8. c 6 AND 7 

9. c 5 OR 8 

10. s s8/human 

11. s s9/eng 

EMBASE on DIALOG 

1. s (leukocyte OR leukocytes OR leucocyte OR leucocytes) AND antigen 

2. s (leukocyte OR leukocytes OR leucocyte OR leucocytes) AND antigens 

3. s hla OR hla dq antigen/de OR hla antigen/de OR hladq OR histocompatibility antigen/de OR 

histocompatibility test/de OR histocompatibility/ti,ab,de 

4. c 1 OR 2 OR 3 

5. s dq2? OR dq8? OR hladq2? OR hladq8? OR d2? OR d8? 

6. c 4 AND 5 

7. s celiac OR celiacs OR coeliac OR coeliacs OR gluten OR glutens OR glutenin OR glutenins OR 

gliadin OR gliadins 

8. s hla(w)antigens?? OR hla antigen/de OR hla dq antigen/de 

9. c 7 AND 8 

10. c 6 OR 9 

11. s s10/human 

12. s s11/eng 
 A-9

Test 5. Small bowel biopsy 

MEDLINE on DIALOG 

1. s celiac???(w)disease OR coeliac???(w)disease OR celiac(w)sprue OR coeliac(w)sprue OR 

celiac(w)syndrome OR coeliac(w)syndrome 

2. s celiacs OR coeliacs OR celiac disease/de 

3. s silent(w)celiac OR silent(w)coeliac OR asymptomatic(w)celiac OR asymptomatic(w)coeliac OR 

undetected(n3)(celiac OR coeliac) 

4. s subclinical(w)celiac OR subclinical(w)coeliac OR sub(w)clinical(w)celiac OR sub(w)clinical(w)coeliac 

OR undiagnosed(n3)celiac OR undiagnosed(n3)coeliac 

5. s nontropical(w)sprue OR non(w)tropical(w)sprue OR endemic(w)sprue 

6. s gluten(n3)enteropath? OR gluten(n3)sensitiv? OR gluten(n3)hypersensitive? OR gluten(n3)intoleran? 

OR glutenin??(n3)hypersensitiv? OR glutenin??(n3) sensitiv? OR glutenin??(n3)intoleran? 

7. s gliadin(n3)hypersentitiv? OR gliadin(n3)intoleran? 

8. s wheat(n3)hypersensitiv? OR wheat(n3)intoleran? OR wheat hypersensitivity/de 

9. s (wheat OR triticum OR gluten) AND food hypersensitivity/de 

10. c 1 or 2 or 3 or 4 or 5 or 6 or 7 or 8 or 9 

11. s celiac disease(l)pathology OR celiac disease(l)diagnosis OR wheat hypersensivitity(l)diagnosis OR 

wheat hypersensitivity(l)pathology 

12. s (wheat OR triticum OR gluten) AND food hypersensitivity(l)diagnosis 

13. s (wheat OR triticum OR gluten) AND food hypersensitivity(l)pathology 

14. c 11 or 12 or 13 

15. s intestine, small(l)pathology OR duodenum(l)pathology OR jejunum(l)pathology OR ileum(l)pathology 

OR small(n2)bowel/ti,ab OR small(n2)intestine?/ti,ab 

16. s biopsy! OR biopsy/ti,ab OR biopsies/ti,ab 

17. c 14 AND 15 AND 16 

18. s small(w)(bowel OR intestine OR intestines) OR intestinal(w)mucosa 

19. c 10 AND 16 AND 18 

20. s (villi OR villus OR villous OR microvilli)(n3)atroph? 

21. c (10 AND 20) OR (14 AND 20) 

22. c 17 OR 19 OR 21 

23. s s22/human 

24. s s23/eng 

EMBASE on DIALOG 

1. s celiac???(w)disease OR coeliac???(w)disease OR celiac(w)sprue OR coeliac(w)sprue OR 

celiac(w)syndrome OR coeliac(w)syndrome 

2. s celiacs OR coeliacs OR celiac disease/de 

3. s silent(w)celiac OR silent(w)coeliac OR asymptomatic(w)celiac OR asymptomatic(w)coeliac OR 

undetected(n3)(celiac OR coeliac) 

4. s subclinical(w)celiac OR subclinical(w)coeliac OR sub(w)clinical(w)celiac OR sub(w)clinical(w)coeliac 

OR undiagnosed(n3)celiac OR undiagnosed(n3)coeliac 

5. s nontropical(w)sprue OR non(w)tropical(w)sprue OR endemic(w)sprue 

6. s gluten(n3)enteropath? OR gluten(n3)sensitiv? OR gluten(n3)hypersensitive? OR gluten(n3)intoleran? 

OR glutenin??(n3)hypersensitiv? OR glutenin??(n3) sensitiv? OR glutenin??(n3)intoleran? 

7. s gliadin(n3)hypersentitiv? OR gliadin(n3)intoleran? 

8. s wheat(n3)hypersensitiv? OR wheat(n3)intoleran? OR wheat allergy/de 

9. s (wheat OR triticum OR gluten OR glutens) AND food allergy/de 

10. c 1 or 2 or 3 or 4 or 5 or 6 or 7 or 8 or 9 

11. s small intestine/de OR duodenum/ti,ab,de OR jejunum/ti,ab,de OR ileum/ti,ab,de OR 

small(n2)bowel/ti,ab OR small(n2)intestine?/ti,ab OR duodenal/ti,ab OR jejunal/ti,ab OR ileal/ti,ab 

12. s dc=a3.60.70? [small intestine] 
 A-10

13. s small(w)(bowel OR intestine OR intestines) OR intestinal(w)mucosa 

14. s intestine mucosa/de or duodenum mucosa/de OR jejunum mucosa/de OR ileum mucosa/de 

15. c 11 OR 12 OR 13 OR 14 

16. s biopsy/ti,ab,de OR biopsies/ti,ab 

17. c 15 AND 16 

18. s intestine biopsy/de OR duodenum biopsy/de OR jejunum biopsy/de OR ileum biopsy/de 

19. c 17 OR 18 

20. c 10 AND 19 

21. s (villi OR villus OR villous OR microvilli)(n3)atroph? 

22. c 10 AND 21 

23. c 20 OR 22 

24. s s23/human 

25. s s24/eng 
 A-11

Celiac 2 – Epidemiology 

MEDLINE on DIALOG 

1. s celiac???(w)disease OR coeliac???(w)disease OR celiac(w)sprue OR coeliac(w)sprue OR 

celiac(w)syndrome OR coeliac(w)syndrome 

2. s celiacs OR coeliacs OR celiac disease/de 

3. s silent(w)celiac OR silent(w)coeliac OR asymptomatic(w)celiac OR asymptomatic(w)coeliac OR 

undetected(n3)(celiac OR coeliac) 

4. s subclinical(w)celiac OR subclinical(w)coeliac OR sub(w)clinical(w)celiac OR sub(w)clinical(w)coeliac 

OR undiagnosed(n3)celiac OR undiagnosed(n3)coeliac 

5. s nontropical(w)sprue OR non(w)tropical(w)sprue OR endemic(w)sprue 

6. s gluten(n3)enteropath? OR gluten(n3)sensitiv? OR gluten(n3)hypersensitive? OR gluten(n3)intoleran? 

OR glutenin??(n3)hypersensitiv? OR glutenin??(n3) sensitiv? OR glutenin??(n3)intoleran? 

7. s gliadin(n3)hypersentitiv? OR gliadin(n3)intoleran? 

8. s wheat(n3)hypersensitive? OR wheat(n3)intoleran? OR wheat hypersensitivity/de 

9. s (wheat OR triticum OR gluten) AND food hypersensitivity/de 

10. c 1 or 2 or 3 or 4 or 5 or 6 or 7 or 8 or 9 

11. s celiac disease(l)epidemiology OR celiac disease(l)ethnology OR wheat 

hypersensitivity(l)epidemiology OR wheat hypersensitivity(l)ethnology 

12. s (wheat OR triticum OR gluten) AND food hypersensitivity(l)epidemiology 

13. s (wheat OR triticum OR gluten) AND food hypersensitivity(l)ethnology 

14. s epidemiolog?/ti,de OR occurrence/ti,de OR prevalence/ti,de OR incidence/ti,de OR pedigree/de OR 

seroprevalence OR seroepidemiol? OR epidemiologic studies! OR epidemiologic measurements/de 

[check!!] 

15. s population characteristics! OR population! OR demography! OR demographic?/ti,ab OR 

population?/ti,de 

16. s minority groups/de OR ethnic groups! OR racial stocks! 

17. s anemia(w2)iron(w)deficiency/de OR anemia(w)hypochromic/de OR iron(w)deficiency(w)anemia OR 

osteoporosis/ti,ab,de OR diabetes mellitus, insulin-dependent! OR juvenile(w)diabetes 

18. s diabetes AND type(w)(1 OR I OR one) 

19. s celiac disease(l)genetics OR gluten(l)genetics OR wheat hypersensitivity(l)genetics 

20. s (wheat OR triticum OR gluten) AND food hypersensitivity(l)genetics 

21. s family! OR genetic predisposition to disease! OR genetic(w)predisposition OR family(n3)(member 

OR members) OR familial 

22. s family/ti,ab OR families/ti,ab OR familial/ti,ab OR brother/ti,ab OR brothers/ti,ab OR sister/ti,ab OR 

sisters/ti,ab OR aunt/ti,ab OR aunts/ti,ab OR uncle/ti,ab OR uncles/ti,ab OR cousin/ti,ab OR 

cousins/ti,ab 

23. s parent/ti,ab OR parents/ti,ab OR mother/ti,ab OR mothers/ti,ab OR father/ti,ab OR fathers/ti,ab OR 

wife/ti,ab OR wives/ti,ab OR husband/ti,ab OR husbands/ti,ab 

24. s son/ti,ab OR sons/ti,ab OR daughter/ti,ab OR daughters/ti,ab OR children/ti,ab OR relatives/ti,ab 

OR sibling/ti,ab OR siblings/ti,ab OR offspring/ti,ab 

25. c 21 OR 22 OR 23 OR 24 

26. c 19 OR 20 

27. c 25 AND 26 

28. c 14 OR 15 OR 16 OR 17 OR 18 

29. c 10 AND 28 

30. c 27 OR 29 OR 11 OR 12 OR 13 

31. s s30/human 

32. s s31/eng 

33. s animal/de 

34. c 32 NOT 33 

EMBASE on DIALOG 
 A-12

1. s celiac???(w)disease OR coeliac???(w)disease OR celiac(w)sprue OR coeliac(w)sprue OR 

celiac(w)syndrome OR coeliac(w)syndrome 

2. s celiacs OR coeliacs OR celiac disease/de 

3. s silent(w)celiac OR silent(w)coeliac OR asymptomatic(w)celiac OR asymptomatic(w)coeliac OR 

undetected(n3)(celiac OR coeliac) 

4. s subclinical(w)celiac OR subclinical(w)coeliac OR sub(w)clinical(w)celiac OR sub(w)clinical(w)coeliac 

OR undiagnosed(n3)celiac OR undiagnosed(n3)coeliac 

5. s nontropical(w)sprue OR non(w)tropical(w)sprue OR endemic(w)sprue OR refractory(w)sprue 

6. s gluten(n3)enteropath? OR gluten(n3)sensitiv? OR gluten(n3)hypersensitive? OR gluten(n3)intoleran? 

OR glutenin??(n3)hypersensitiv? OR glutenin??(n3) sensitiv? OR glutenin??(n3)intoleran? 

7. s gliadin(n3)hypersentitiv? OR gliadin(n3)intoleran? 

8. s wheat(n3)hypersensitive? OR wheat(n3)intoleran? OR wheat allergy/de OR cereal(w)allergy 9. s 

(wheat OR triticum OR gluten?? OR glutinin??) AND (food allergy/de OR allergy/de OR 

hypersensitivity/de OR food allergen/de) 

10. c 1 OR 2 OR 3 OR 4 OR 5 OR 6 OR 7 OR 8 OR 9 

11. s epidemiology/de,id OR dc=c1.270? OR epidemiolog?/ti,ab OR seroepidemiol? OR epidemiological 

data/de 12. s occurrence/ti,de OR prevalence/ti,de OR incidence/ti,de OR pedigree/ti,de OR pedigree 

analysis/de OR dc=g1.385.170? OR seroprevalence 

13. s dc= g1.250.710.715? OR dc= i1.700? OR demography/ti,ab,de OR demographic?/ti,ab OR 

population?/ti,de OR population research/de OR population risk/de 

14. s minority(w)group?? OR ethnic(w)group?? OR minorities/ti,ab OR dc=g1.750? OR dc=i1.275? OR 

dc=m2? OR ethnology/ti,ab,de OR ethnic difference/de OR ethnicity/ti,ab 

15. s iron(w)deficiency(w)anemia OR iron deficiency anemia/de OR anemia(n3)hypochromic/ti,ab 

16. s osteoporosis/ti,ab,de OR dc= c2.275.540.110.650? 

17. s insulin dependent diabetes mellitus/de OR juvenile(w)diabetes OR insulin(w)dependent(w)diabetes 

18. s diabetes AND type(w)(1 OR i OR one) 

19. s familial disease/de OR family study/de OR familial incidence/de 

20. c 11 OR 12 OR 13 OR 14 OR 15 OR 16 OR 17 OR 18 OR 19 

21. s celiac disease/de OR gluten??/ti,ab OR wheat allergy/de OR cereal(w)allergy 

22. s (wheat OR triticum OR gluten?? OR glutinin??) AND (food allergy/de OR allergy/de OR 

hypersensitivity/de OR food allergen/de) 

23. c 21 OR 22 

24. s genetics/de OR q1.340? 

25. c 23 AND 24 

26. s genetic(w)predisposition OR family(n3)(member OR members) 

27. s family/ti,ab OR families/ti,ab OR familial/ti,ab OR brother/ti,ab OR brothers/ti,ab OR sister/ti,ab OR 

sisters/ti,ab OR aunt/ti,ab OR aunts/ti,ab OR uncle/ti,ab OR uncles/ti,ab OR cousin/ti,ab OR 

cousins/ti,ab 

28. s parent/ti,ab OR parents/ti,ab OR mother/ti,ab OR mothers/ti,ab OR father/ti,ab OR fathers/ti,ab OR 

wife/ti,ab OR wives/ti,ab OR husband/ti,ab OR husbands/ti,ab 

29. s son/ti,ab OR sons/ti,ab OR daughter/ti,ab OR daughters/ti,ab OR children/ti,ab OR relatives/ti,ab 

OR sibling/ti,ab OR siblings/ti,ab OR offspring/ti,ab 

30. c 26 OR 27 OR 28 OR 29 

31. c 25 AND 30 

32. c 10 AND 20 

33. c 31 OR 32 

34. s celiac disease(l)epidemiology 

35. s (celiac disease/de OR wheat allergy/de OR cereal(w)allergy) AND epidemiology/de 

36. s (wheat OR triticum OR gluten?? OR glutinin??) AND (food allergy/de OR allergy/de OR 

hypersensitivity/de OR food allergen/de) AND epidemiology/de 

37. c 34 OR 35 OR 36 

38. c 33 OR 37 

39. s s38/human 

40. s s39/eng 
 A-13

Celiac 3 – Lymphomas 

MEDLINE on DIALOG 

1. s celiac???(w)disease OR coeliac???(w)disease OR celiac(w)sprue OR coeliac(w)sprue OR 

celiac(w)syndrome OR coeliac(w)syndrome 

2. s celiacs OR coeliacs OR celiac disease/de 

3. s silent(w)celiac OR silent(w)coeliac OR asymptomatic(w)celiac OR asymptomatic(w)coeliac OR 

undetected(n3)(celiac OR coeliac) 

4. s subclinical(w)celiac OR subclinical(w)coeliac OR sub(w)clinical(w)celiac OR sub(w)clinical(w)coeliac 

OR undiagnosed(n3)celiac OR undiagnosed(n3)coeliac 

5. s nontropical(w)sprue OR non(w)tropical(w)sprue OR endemic(w)sprue 

6. s gluten(n3)enteropath? OR gluten(n3)sensitiv? OR gluten(n3)hypersensitive? OR gluten(n3)intoleran? 

OR glutenin??(n3)hypersensitiv? OR glutenin??(n3) sensitiv? OR glutenin??(n3)intoleran? 

7. s gliadin(n3)hypersentitiv? OR gliadin(n3)intoleran? 

8. s wheat(n3)hypersensitive? OR wheat(n3)intoleran? OR wheat hypersensitivity/de 

9. s (wheat OR triticum OR gluten) AND food hypersensitivity/de 

10. c 1 or 2 or 3 or 4 or 5 or 6 or 7 or 8 or 9 

11. s (villi OR villus OR villous OR microvilli)(n3)atroph? 

12. c 10 OR 11 

13. s lymphoma/ti,ab,de OR lymphomas/ti,ab,de OR lymphoma! OR hodgkin?/ti,ab,de 

14. s intestine/ti,ab,de OR intestinal/ti,ab,de OR duodenum/ti,ab,de OR duodenal/ti,ab.de OR 

jejunum/ti,ab,de OR jejunal/ti,ab,de OR ileum/ti,ab,de OR ileal/ti,ab,de 

15. s small(n2)bowel/ti,ab OR small(n2)intestine?/ti,ab OR large(n2)intestine?/ti,ab OR 

large(n2)bowel/ti,ab OR intestines! 

16. s gastric/ti,ab,de OR gastro?/ti,ab,de OR gi/ti,ab OR stomach/ti,ab,de OR pylorus/ti,ab,de OR 

pyloric/ti,ab,de OR esophagogastr? 

17. c 14 or 15 or 16 

18. c 12 AND 13 AND 17 

19. s s18/human 

20. s s19/eng 

EMBASE on DIALOG 

1. s celiac???(w)disease OR coeliac???(w)disease OR celiac(w)sprue OR coeliac(w)sprue OR 

celiac(w)syndrome OR coeliac(w)syndrome 

2. s celiacs OR coeliacs OR celiac disease/de 

3. s silent(w)celiac OR silent(w)coeliac OR asymptomatic(w)celiac OR asymptomatic(w)coeliac OR 

undetected(n3)(celiac OR coeliac) 

4. s subclinical(w)celiac OR subclinical(w)coeliac OR sub(w)clinical(w)celiac OR sub(w)clinical(w)coeliac 

OR undiagnosed(n3)celiac OR undiagnosed(n3)celiac 

5. s nontropical(w)sprue OR non(w)tropical(w)sprue OR endemic(w)sprue 

6. s gluten(n3)enteropath? OR gluten(n3)sensitiv? OR gluten(n3)hypersensitive? OR gluten(n3)intoleran? 

OR glutenin??(n3)hypersensitiv? OR glutenin??(n3) sensitiv? OR glutenin??(n3)intoleran? 

7. s gliadin(n3)hypersentitiv? OR gliadin(n3)intoleran? Or gluten free diet/de OR gluten(w)free 

8. s wheat(n3)hypersensitive? OR wheat(n3)intoleran? OR wheat allergy/de OR cereal(w)allergy 

9. s (wheat OR triticum OR gluten?? OR glutinin??) AND (food allergy/de OR allergy/de OR 

hypersensitivity/de) 

10. c 1 or 2 or 3 or 4 or 5 or 6 or 7 or 8 or 9 

11. s (villi OR villus OR villous OR microvilli)(n3)atroph? 

12. s refractory/ti,ab OR non(w)respond?/ti,ab OR nonrespond?/ti,ab OR non(w)responsiv?/ti,ab OR 

nonresponsiv?/ti,ab 

13. s sprue OR celiac OR coeliac OR celiac disease/de 

14. c 12 AND 13 

15. c 10 OR 11 OR 14 
 A-14

16. s lymphoma/ti,ab,de OR lymphomas/ti,ab,de OR hodgkin?/ti,ab,de 

17. s dc = c2.385.520.500.510? OR dc = c2.385.520.510.500? OR dc = c6.610.50.50? OR dc = 

c6.610.75.520.510? [var. lymphoma] 

18. c 16 OR 17 

19. s small intestine/de OR small(n2)bowel/ti,ab OR small(n2)intestine?/ti,ab OR duodenum/ti,ab,de OR 

duodenal/ti,ab OR jejunum/ti,ab,de OR jejunal/ti,ab OR ileum/ti,ab,de OR ileal/ti,ab 

20. s large(n2)intestine?/ti,ab OR large(n2)bowel/ti,ab OR cecum/ti,ab,de OR colon/ti,ab,de OR 

colonic/ti,ab,de OR rectum/ti,ab,de OR rectal/ti,ab,de OR anus/ti,ab,de 

21. s intestine/ti,ab,de OR intestinal/ti,ab,de OR dc = a3? [digestive system] 

22. s intestine mucosa/de OR duodenum mucosa/de OR jejunum mucosa/de OR ileum mucosa/de OR 

intestinal(w)mucosa OR colon mucosa/de OR rectum mucosa/de OR small intestine mucosa/de 

23. s gastric/ti,ab,de OR gastro?/ti,ab,de OR gi/ti,ab OR stomach/ti,ab,de OR cardia/ti,ab,de OR 

pylorus/ti,ab,de OR pyloric/ti,ab,de OR esophagogastr? 

24. s digestive system cancer/de OR dc = c2.220.230.210? OR dc = c2.220.230.210? [digestive system 

cancer] 

25. c 19 OR 20 OR 21 OR 22 OR 23 OR 24 

26. c 15 AND 18 AND 25 

27. s stomach lymphoma/de OR intestine lymphoma/de 

28. c 15 AND 27 

29. c 26 OR 28 

30. s s29/human 

31. s s30/eng 
 A-15

Celiac 4 – Screening 

MEDLINE on DIALOG 

1. s celiac???(w)disease OR coeliac???(w)disease OR celiac(w)sprue OR coeliac(w)sprue OR 

celiac(w)syndrome OR coeliac(w)syndrome 

2. s celiacs OR coeliacs OR celiac disease/de 

3. s silent(w)celiac OR silent(w)coeliac OR asymptomatic(w)celiac OR asymptomatic(w)coeliac OR 

undetected(n3)(celiac OR coeliac) 

4. s subclinical(w)celiac OR subclinical(w)coeliac OR sub(w)clinical(w)celiac OR sub(w)clinical(w)coeliac 

OR undiagnosed(n3)celiac OR undiagnosed(n3)coeliac 

5. s nontropical(w)sprue OR non(w)tropical(w)sprue OR endemic(w)sprue 

6. s gluten(n3)enteropath? OR gluten(n3)sensitiv? OR gluten(n3)hypersensitive? OR gluten(n3)intoleran? 

OR glutenin??(n3)hypersensitiv? OR glutenin??(n3) sensitiv? OR glutenin??(n3)intoleran? 

7. s gliadin(n3)hypersentitiv? OR gliadin(n3)intoleran? 

8. s wheat(n3)hypersensitive? OR wheat(n3)intoleran? OR wheat hypersensitivity/de 

9. s (wheat OR triticum OR gluten) AND food hypersensitivity/de 

10. c 1 or 2 or 3 or 4 or 5 or 6 or 7 or 8 or 9 

11. s screen/ti,ab OR screens/ti,ab OR screening/ti,ab OR screened/ti,ab OR mass screening! 

12. c 10 AND 11 

13. s celiac disease(l)diagnosis OR celiac disease(l)pathology 

14. s “sensitivity and specificity”/de 

15. s physician’s practice patterns/de 

16. s reference standards/de OR quality control/de OR evaluation studies/de OR predictive value of 

tests/de OR incidental findings/de 

17. s reproducibility of results/de OR physical examination(l)standards OR diagnosis, differential/de OR 

diagnostic errors! OR follow-up studies/de 

18. s public health/de OR public health practice/de OR population surveillance/de OR clinical protocols/de 

OR critical pathways/de 

19. s quality assurance, health care! OR guideline adherence/de OR social control, formal/de OR 

“outcome assessment (health care)”/de 

20. c 14 or 15 or 16 or 17 or 18 or 19 

21. c 13 AND 20 

22. c 12 OR 21 

23. s s22/human 

24. s s23/eng 

EMBASE on DIALOG 

1. s celiac???(w)disease OR coeliac???(w)disease OR celiac(w)sprue OR coeliac(w)sprue OR 

celiac(w)syndrome OR coeliac(w)syndrome 

2. s celiacs OR coeliacs OR celiac disease/de 

3. s silent(w)celiac OR silent(w)coeliac OR asymptomatic(w)celiac OR asymptomatic(w)coeliac OR 

undetected(n3)(celiac OR coeliac) 

4. s subclinical(w)celiac OR subclinical(w)coeliac OR sub(w)clinical(w)celiac OR sub(w)clinical(w)coeliac 

OR undiagnosed(n3)celiac OR undiagnosed(n3)coeliac 

5. s nontropical(w)sprue OR non(w)tropical(w)sprue OR endemic(w)sprue 

6. s gluten(n3)enteropath? OR gluten(n3)sensitiv? OR gluten(n3)hypersensitiv? OR gluten(n3)intoleran? 

OR glutenin??(n3)hypersensitiv? OR glutenin??(n3) sensitiv? OR glutenin??(n3)intoleran? 

7. s gliadin(n3)hypersentitiv? OR gliadin(n3)intoleran? 

8. s wheat(n3)hypersensitiv? OR wheat(n3)intoleran? 

9. s (wheat OR triticum OR gluten) AND (food allergy/de OR hypersensitivity/de) 

10. c 1 or 2 or 3 or 4 or 5 or 6 or 7 or 8 or 9 

11. s mass screening/de OR mass(w)screen? OR genetic screening/de OR genetic(w)screen? OR 

newborn screening/de OR newborn??(n3)screen? 
 A-16

12. 10 AND 11 

13. s screen/ti,ab OR screens/ti,ab OR screening/ti,ab OR screened/ti,ab 

14. s dc=J2.10? [controlled study] 

15. s dc=J2.40.10? [clinical study] 

16. s dc=J2.50? [methodology] 

17. s evaluation(w)study OR evaluation(w)studies OR physical examination/de OR follow-up studies/de 

18. s dc=E1.215? [diagnosis] 

19. s dc=N7.700? [practice guideline] 

20. s dc=Q1.550.75? [social medicine] 

21. c 14 or 15 or 16 or 17 or 18 or 19 or 20 

22. c 10 AND 13 AND 21 

23. c 12 OR 22 

24. s s23/human 

25. s s24/eng 

CAB and AGRICOLA on DIALOG 

1. s celiac???(w)disease OR coeliac???(w)disease OR celiac(w)sprue OR coeliac(w)sprue OR 

celiac(w)syndrome OR coeliac(w)syndrome 

2. s celiacs OR coeliacs OR celiac syndrome/de 

3. s silent(w)celiac OR silent(w)coeliac OR asymptomatic(w)celiac OR asymptomatic(w)coeliac OR 

undetected(n3)(celiac OR coeliac) 

4. s subclinical(w)celiac OR subclinical(w)coeliac OR sub(w)clinical(w)celiac OR sub(w)clinical(w)coeliac 

OR undiagnosed(n3)celiac OR undiagnosed(n3)coeliac 

5. s nontropical(w)sprue OR non(w)tropical(w)sprue OR endemic(w)sprue 

6. s gluten(n3)enteropath? OR gluten(n3)sensitiv? OR gluten(n3)hypersensitiv? OR gluten(n3)intoleran? 

OR glutenin??(n3)hypersensitiv? OR glutenin??(n3) sensitiv? OR glutenin??(n3)intoleran? 

7. s gliadin(n3)hypersentitiv? OR gliadin(n3)intoleran? 

8. s wheat(n3)hypersensitiv? OR wheat(n3)intoleran? 

9. s (wheat OR triticum OR gluten) AND (food allergies/de OR hypersensitivity/de) 

10. c 1 or 2 or 3 or 4 or 5 or 6 or 7 or 8 or 9 

11. s mass(w)screen? OR genetic(w)screen? OR newborn??(n3)screen? 

12. c 10 AND 11 

13. s screen/ti,ab OR screens/ti,ab OR screening/ti,ab OR screened/ti,ab 

14. s evaluation(w)study OR evaluation(w)studies 

15. c 10 AND 13 AND 14 

16. c 12 OR 15 

17. s s16/human 

18. s s17/eng 

PsycInfo on DIALOG 

1. s celiac???(w)disease OR coeliac???(w)disease OR celiac(w)sprue OR coeliac(w)sprue OR 

celiac(w)syndrome OR coeliac(w)syndrome 

2. s celiacs OR coeliacs 

3. s silent(w)celiac OR silent(w)coeliac OR asymptomatic(w)celiac OR asymptomatic(w)coeliac OR 

undetected(n3)(celiac OR coeliac) 

4. s subclinical(w)celiac OR subclinical(w)coeliac OR sub(w)clinical(w)celiac OR sub(w)clinical(w)coeliac 

OR undiagnosed(n3)celiac OR undiagnosed(n3)coeliac 

5. s nontropical(w)sprue OR non(w)tropical(w)sprue OR endemic(w)sprue 

6. s gluten(n3)enteropath? OR gluten(n3)sensitiv? OR gluten(n3)hypersensitiv? OR gluten(n3)intoleran? 

OR glutenin??(n3)hypersensitiv? OR glutenin??(n3) sensitiv? OR glutenin??(n3)intoleran? 

7. s gliadin(n3)hypersentitiv? OR gliadin(n3)intoleran? 

8. s wheat(n3)hypersensitiv? OR wheat(n3)intoleran? 

9. s (wheat OR triticum OR gluten) AND food allergies/de 

10. c 1 or 2 or 3 or 4 or 5 or 6 or 7 or 8 or 9 
 A-17

11. s mass(w)screen? OR genetic(w)screen? OR newborn??(n3)screen? OR screening/de OR screening 

tests/de OR health screening/de 

12. c 10 AND 11 

13. s screen/ti,ab OR screens/ti,ab OR screening/ti,ab OR screened/ti,ab 

14. s evaluation(w)study OR evaluation(w)studies OR physical examination/de OR followup studies/de 

OR evaluation/de 

15. c 10 AND 13 AND 14 

16. c 12 OR 15 

17. s s16/human 

18. s s17/eng 

Sociological Abstracts at CAB 

Limits set to English 

1. celiac (KW) OR celiacs (KW) OR coeliac (KW) OR coeliacs (KW) 

2. wheat (KW) OR gluten* (KW) OR gliadin* OR food (DE) OR foods (KW) 

3. allergy (KW) OR allergies (KW) OR hypersensitivit* (KW) OR sensitive* (KW) OR intolerance* (KW) 

4. mass public (DE) OR screen (KW OR screens (KW) OR screening (KW) OR screened (KW) 

5. 1 AND 4 

6. 2 and 3 AND 4 

7. 5 OR 6 
 A-18

Celiac 5 – Dietary Compliance 

MEDLINE on DIALOG: 

Part 1

1. s celiac disease(l)psychology OR diet therapy(l)education OR diet therapy(l)methods OR diet 

therapy(l)standards OR diet therapy(l)trends OR diet therapy(l)utilization OR diet therapy(l)psychology 

2. s diet(l)methods OR diet(l)trends OR diet(l)psychology OR diet(l)standards OR diet(l)utilization 

3. s psychological tests/de OR health behavior/de OR patient acceptance of health care! OR health 

education/de OR patient education/de OR nutrition(l)education OR teaching! 

4. s quality of life/de OR menu planning/de OR food habits/de OR feeding behavior/de OR quality of 

health care/de OR compliance/ti,ab OR adherence/ti,ab OR motivation/ti,ab,de 

5. s achievement/de OR motivation/de OR directive counseling/de OR counseling/de OR psychology, 

applied/de OR psychology, educational/de OR learning/de OR child guidance/de 

6. s adaptation, psychological/de OR attitude/de OR attitude of health personnel/de OR professionalpatient relations! OR attitude to health! 

7. s health promotion/de OR decision making! OR risk reduction behavior/de OR early(w)intervention/de 

OR intervention/ti,ab OR interventions/ti,ab OR data collection/de 

8. s diet, protein-restricted(l)methods OR diet, protein-restricted(l)trends OR diet, proteinrestricted(l)psychology OR diet, protein-restricted(l)standards OR diet, protein-restricted(l)utilization 

9. s health surveys/de OR nutrition assessment! OR Behavioral Risk Factor Surveillance System/de OR 

interviews! OR questionnaire?/ti,ab,de 

10. s guideline adherence/de OR evaluation studies/de OR “outcome assessment (health care)” OR 

“process assessment (health care)” OR food labeling/de 

11. c 1 OR 2 OR 3 OR 4 OR 5 OR 6 OR 7 OR 8 OR 9 OR 10 

12. s celiac disease(l)diet therapy 

13. c 11 AND 12 

14. s triticum(l)adverse effects OR wheat hypersensitivity/de OR gluten(n2)withdraw? OR 

gluten(l)adverse effects OR gliadin(l)adverse effects OR gluten(w)free 

15. s diet OR dietary OR diets OR nutrition OR nutritional 

16. c 14 AND 15 

17. c 13 OR 16 

18. s s17/human 

19. s s18/eng 

Part 2

1. s food labeling/de 

2. s celiac OR coeliac OR triticum OR wheat hypersensitivity/de OR gluten OR gliadin OR celiac 

disease/de 

3. c 1 and 2 

4. s s3/human 

5. s s4/eng 

EMBASE on DIALOG 

1. s celiac???(w)disease OR coeliac???(w)disease OR celiac(w)sprue OR coeliac(w)sprue OR 

celiac(w)syndrome OR coeliac(w)syndrome OR celiac(w)syndrome 

2. s celiacs OR coeliacs OR celiac disease/de 

3. s silent(w)celiac OR silent(w)coeliac OR asymptomatic(w)celiac OR asymptomatic(w)coeliac OR 

undetected(n3)(celiac OR coeliac) 

4. s subclinical(w)celiac OR subclinical(w)coeliac OR sub(w)clinical(w)celiac OR sub(w)clinical(w)coeliac 

OR undiagnosed(n3)celiac OR undiagnosed(n3)coeliac 

5. s nontropical(w)sprue OR non(w)tropical(w)sprue OR endemic(w)sprue 
 A-19

6. s gluten(n3)enteropath? OR gluten(n3)sensitiv? OR gluten(n3)hypersensitive? OR gluten(n3)intoleran? 

OR glutenin??(n3)hypersensitiv? OR glutenin??(n3) sensitiv? OR glutenin??(n3)intoleran? 

7. s gliadin(n3)hypersentitiv? OR gliadin(n3)intoleran? 

8. s wheat(n3)hypersensitive? OR wheat(n3)intoleran? OR wheat allergy/de 

9. s (wheat OR triticum OR gluten) AND (hypersensitivity/de OR food allergy/de) 

10. c 1 or 2 or 3 or 4 or 5 or 6 or 7 or 8 or 9 

11. s diet restriction/de OR gluten(w)free(w)diet?? OR diet therapy/de OR diet?(w)intervention OR 

therapeutic(w)diet?? OR diet OR dietary OR diets OR nutrition OR nutritional OR dietary(w) 

restriction?? OR dietary(n3)guideline?? 

12. s intervention??/ti,ab,de OR feeding behavior/de OR gluten(w)free(w)food?/ti,ab OR nutritional 

intolerance/de 

13. c 11 OR 12 

14. c 10 AND 13 

15. s health behavior/de OR illness behavior/de OR adaptive behavior/de OR behavior modification/de 

OR patient attitude/de OR patient compliance/de OR patient education/de OR patient guidance/de 

OR patient counseling/de 

16. s quality of life/de OR coping(w)behavior/ti,ab OR adjustment??/ti,ab,de OR decision making/de OR 

early(w)intervention/ti,ab,de OR compliance/ti,ab OR adherence/ti,ab OR motivation/ti,ab,de OR 

coping behavior/de OR coping/ti,ab,de 

17. s psychosocial(n3)aspect?? OR habit??/ti,ab,de OR attitude??/ ti,ab,de OR psychologic test /de OR 

counsel?/ti,ab,de OR psychological factor/de OR psycholog?/ti,ab,de 

18. c 15 OR 16 OR 17 

19. c 14 AND 18 

20. s s19/human, eng 

CAB and AGRICOLA on DIALOG 

1. s celiac???(w)disease OR coeliac???(w)disease OR celiac(w)sprue OR coeliac(w)sprue OR 

celiac(w)syndrome OR coeliac(w)syndrome OR celiac(w)syndrome 

2. s celiacs OR coeliacs OR celiac syndrome/de 

3. s silent(w)celiac OR silent(w)coeliac OR asymptomatic(w)celiac OR asymptomatic(w)coeliac OR 

undetected(n3)(celiac OR coeliac) 

4. s subclinical(w)celiac OR subclinical(w)coeliac OR sub(w)clinical(w)celiac OR sub(w)clinical(w)coeliac 

OR undiagnosed(n3)celiac OR undiagnosed(n3)coeliac 

5. s nontropical(w)sprue OR non(w)tropical(w)sprue OR endemic(w)sprue 

6. s gluten(n3)enteropath? OR gluten(n3)sensitiv? OR gluten(n3)hypersensitive? OR gluten(n3)intoleran? 

OR glutenin??(n3)hypersensitiv? OR glutenin??(n3) sensitiv? OR glutenin??(n3)intoleran? 

7. s gliadin(n3)hypersentitiv? OR gliadin(n3)intoleran? 

8. s wheat(n3)hypersensitive? OR wheat(n3)intoleran? 

9. s (wheat OR triticum OR gluten) AND (hypersensitivity/de OR food allergies/de) 

10. c 1 or 2 or 3 or 4 or 5 or 6 or 7 or 8 or 9 

11. s gluten(w)free(w)diet?? OR diet treatment/de OR diet?(w)intervention OR therapeutic diets/de OR 

diet OR dietary OR diets OR nutrition OR nutritional 

12. s dietary(w)restriction?? OR dietary(n3)guideline?? OR intervention??/ti,ab,de OR feeding 

behavior/de OR gluten(w)free(w)food?/ti,ab OR 

13. c 11 OR 12 

14. c 10 AND 13 

15. s behavior modification/de OR patient compliance/de OR patient education/de 

16. s quality of life/de OR coping(w)behavior/ti,ab OR adjustment??/ti,ab,de OR decision making/de OR 

early(w)intervention/ti,ab,de OR compliance/ti,ab OR adherence/ti,ab OR motivation/ti,ab,de OR 

coping/ti,ab 

17. s psychosocial(n3)aspect?? OR habit??/ti,ab,de OR attitude??/ ti,ab,de OR counsel?/ti,ab,de OR 

psychological factors/de OR psycholog?/ti,ab,de 

18. c 15 OR 16 OR 17 

19. c 14 AND 18 

20. s s19/human 
 A-20

21. s s20/eng 

PsycInfo on DIALOG 

1. s celiac???(w)disease OR coeliac???(w)disease OR celiac(w)sprue OR coeliac(w)sprue OR 

celiac(w)syndrome OR coeliac(w)syndrome OR celiac(w)syndrome 

2. s celiacs OR coeliacs 

3. s silent(w)celiac OR silent(w)coeliac OR asymptomatic(w)celiac OR asymptomatic(w)coeliac OR 

undetected(n3)(celiac OR coeliac) 

4. s subclinical(w)celiac OR subclinical(w)coeliac OR sub(w)clinical(w)celiac OR sub(w)clinical(w)coeliac 

OR undiagnosed(n3)celiac OR undiagnosed(n3)coeliac 

5. s nontropical(w)sprue OR non(w)tropical(w)sprue OR endemic(w)sprue 

6. s gluten(n3)enteropath? OR gluten(n3)sensitiv? OR gluten(n3)hypersensitive? OR gluten(n3)intoleran? 

OR glutenin??(n3)hypersensitiv? OR glutenin??(n3) sensitiv? OR glutenin??(n3)intoleran? 

7. s gliadin(n3)hypersentitiv? OR gliadin(n3)intoleran? 

8. s wheat(n3)hypersensitive? OR wheat(n3)intoleran? OR wheat(n3)(allergy OR allergies) 

9. s (wheat OR triticum OR gluten) AND food allergies/de 

10. c 1 or 2 or 3 or 4 or 5 or 6 or 7 or 8 or 9 

11. s gluten(w)free(w)diet?? OR diet?(w)intervention OR therapeutic(w)diet?? OR diet OR dietary OR 

diets OR nutrition OR nutritional OR dietary(w)restriction?? OR dietary(n3)guideline?? 

12. s intervention??/ti,ab OR gluten(w)free(w)food?/ti,ab 

13. c 11 OR 12 

14. c 10 AND 13 

15. s health behavior/de OR illness behavior/de OR adaptive behavior/de OR behavior modification/de 

16. s quality of life/de OR coping(w)behavior/ti,ab OR adjustment??/ti,ab,de OR decision making/de OR 

early(w)intervention/ti,ab,de OR compliance/ti,ab OR adherence/ti,ab OR motivation/ti,ab,de OR 

coping behavior/de OR coping/ti,ab 

17. s psychosocial(n3)aspect?? OR habit??/ti,ab,de OR attitude??/ti,ab,de OR counsel?/ti,ab,de OR 

psycholog?/ti,ab,de 

18. c 15 OR 16 OR 17 

19. c 14 AND 18 

20. s s19/human 

21. s s20/eng 

Sociological Abstracts at CAB 

Limits set to English 

1. celiac (KW) OR celiacs (KW) OR coeliac (KW) OR coeliacs (KW) 

2. wheat (KW) OR food (DE) OR foods (kw) OR gluten* (KW) OR gliadin* 

3. allergy (KW) OR allergies (KW) OR hypersensitive* (KW) OR intoleran* (KW) OR sensitive* (KW) 

4. feeding practices (DE) OR feeding (DE) 

5. diet (DE) OR nutrition (DE) 

6. diet (KW) OR diets(KW) OR nutrition (KW)OR nutritional (KW) 

7. 2 AND 3 

8. 4 OR 5 OR 6 

9. 1 AND 8 

10. 7 AND 8 

11. 9 OR 10 
 A-21

Appendix C. Data Assessment and Data Abstraction 

Forms 

Data Assessment Forms 

Level 1 Screening 

Objective 1: 

1. Does this refer to determining the sensitivity or specificity of one of the following 

tests for celiac disease? (biopsy, anti-htTG, anti-endomysial, anti-gliadin 

antibody, anti-gliadin antibody, HLA DQ2/DQ8). 

a. This citation refers to another objective and should be moved or copied 

b. No (move on to next citation) 

c. Yes 

d. Can’t tell 

Objective 2: 

1. Does this refer to the prevalence or incidence of celiac disease? 

a. This citation refers to another objective and should be moved or copied 

b. No (move on to next citation) 

c. Yes 

d. Can’t tell 

Objective 3: 

1. Does this refer to an association between celiac and GI lymphoma? 

a. This citation refers to another objective and should be moved or copied 

b. No (move on to next citation) 

c. Yes 

d. Can’t tell 

Objective 4: 

1. Does this refer to expected consequences of testing for celiac disease 

a. This citation refers to another objective and should be moved or copied 

b. No (move on to next citation) 

c. Yes 

d. Can’t tell 
 A-22

Objective 5:

1. Does this refer to identifying or assessing interventions for promoting or 

monitoring adherence to a gluten free diet? 

a. This citation refers to another objective and should be moved or copied 

b. No (move on to next citation) 

c. Yes 

d. Can’t tell 

Level 2 Screening 

Objective 1: 

1. Does this refer specifically to determining the sensitivity or specificity of one of 

the identified tests for celiac disease? Note: for biopsy and HLA, we may not 

see sensitivity or specificity – keep if you can get data on use as diagnostic test 

or accuracy as a test or if it distinguishes celiac from other diseases etc. 

a. Yes. If this citation also refers to another objective(s), please state 

objective number(s): 

b. No. If this citation refers to another objective(s), please state objective 

number(s): (move on to next citation) 

2. Is this a review article? 

a. Yes (keep for references) 

b. No 

3. What is the test(s) being studied? (Note: we are not interested in any other type 

of test!) 

a. Biopsy 

b. Anti-htTG 

c. Anti-endomysial antibody (EMA) 

d. Anti-gliadin antibody (AGA) 

e. HLA DQ2/DQ8 (note: we are not interested in pathophysiology does the 

article give data using HLA to distinguish celiac from non celiac) 

f. If none of above then – reject citation 

4. What is the “gold standard” the test(s) is compared to? 

a. Biopsy 

b. Anti-htTG 

c. Anti-endomysial antibody (EMA) 

d. Anti-gliadin antibody (AGA) 

e. HLA DQ2/DQ8 

f. Other (list in box) 

5. What is the patient population? 

a. Adults 
 A-23

b. Paediatric 

c. General unselected 

d. Specific ethnic groups (fill in box) 

e. Patients with suspected celiac (symptomatic) 

f. Patients at risk of celiac disease (asymptomatic - relatives of celiac, 

diabetes, Fe Diff, infertility, osteoporosis, short stature) 

g. Other (fill in box) 

Objective 2: 

1. Does this refer specifically to the prevalence or incidence of celiac disease? 

Please remember we are only really interested in the incidence / prevalence of 

celiac in population X or disease X NOT vice verse. 

a. Yes. 

b. No. Exclude

c. No. But this referrers to an association between celiac and another 

disease to state in background /discussion 

2. Is this a review article? 

a. Yes (keep for references) 

b. No 

3. Does the prevalence or incidence refer to: 

a. Classical celiac 

b. Atypical celiac (i.e., Fe diff, infertility, short stature, osteoporosis) 

c. Asymptomatic celiac 

d. Other or (fill in box) 

4. What is the patient population that was tested? 

a. Unselected – general population (e.g., blood donors, routine physical etc) 

b. Patients with suspected celiac 

c. Relatives of celiac patients 

d. Iron deficiency 

e. Osteoporosis 

f. Short stature 

g. Infertility 

h. Other (fill in box) 

5. What was the screening test(s) used? 

a. Biopsy 

b. Anti-htTG 

c. Anti-endomysial antibody (EMA) 

d. Anti-gliadin antibody (AGA) 

e. HLA DQ2/DQ8 

f. Other (fill in box) 
 A-24

6. What is the country/region of origin of the study (fill in box)? 

Objective 3:

1. Does this refer specifically to an association between celiac and GI 

lymphoma? 

a. Yes. 

b. No. Exclude

2. Is this a review article? 

a. Yes (keep for references) 

b. No 

3. Does this give data on the risk of developing GI lymphoma in celiac? 

a. Yes 

b. No 

4. What is the country/region of origin of the study? (fill in box) 

5. What celiac population was evaluated? 

a. Classical celiac 

b. Atypical celiac (i.e., fe dif, infertility, short stature, osteoporosis) 

c. Asymptomatic celiac 

d. Other (fill in box) 

Objective 4: 

1. Does this refer specifically to expected consequences of testing for celiac 

disease?

a. Yes. 

b. No. Exclude

2. Is this a review article? 

a. Yes (keep for references) 

b. No 

3. What consequences were assessed: 

a. False-positive results 

b. Follow-up testing 

c. Invasive procedures (biopsy) 

d. Costs 

e. Cases diagnosed 

f. Patients complying with treatment 

g. Response to treatment 

h. Clinical outcome (reduced risk of complication etc) 

i. Other (fill in box) 
 A-25

4. What is the country/region of origin of the study? (fill in box) 

5. What is the patient population that was tested? 

a. Unselected – general population (e.g., blood donors, routine physical, etc.) 

b. Patients with symptoms suggestive of celiac. 

c. Asymptomatic at risk populations (relatives of celiac patients, iron 

deficiency, osteoporosis, infertility short, stature) 

d. Other (fill in box). 

Objective 5: 

1. Does this specifically refer to identifying or assessing an intervention(s) for 

promoting or monitoring adherence to a gluten free diet? 

a. Yes. 

b. No. Exclude

2. Is this a review article? 

a. Yes (keep for references) 

b. No 

3. Does this refer to: 

a. Promoting adherence 

b. Monitoring adherence 

c. Both 

4. What intervention was assessed? (If monitoring adherence) 

a. Biopsy 

b. Antibody testing 

5. What intervention was used? (If promoting adherence) – fill in box 

Level 3 Screening 

Celiac 1: Sensitivity and specificity of screening tests: 

Inclusion criteria: (a No answer to any of the below excludes the article) 

1. For serology - the study publication date is 1990 or more recent (biopsy studies 

can be earlier) 

a. Yes (include) 

b. No (exclude) 

2. For AGA - the studies uses a standardized commercial ELISA kit (or this study is 

testing such a kit or technique) 

a. Yes (include) 

b. No (exclude) 
 A-26

3. For EMA – the substrate is monkey esophagus or human umbilical cord 

a. Yes (include) 

b. No (exclude) 

4. For tTG – study uses ELISA with the substrate for tTG being guinea pig or 

human recombinant tTG. 

a. Yes (include) 

b. No (exclude) 

5. For any serology and HLA studies – the control group(s) are appropriate and 

controls evaluated with the reference test (i.e., biopsy)? 

a. Yes (include) 

b. No (exclude) 

6. The paper allows for the extraction of the sensitivity or specificity of the test in 

question (AGA, EMA, tTG, HLA DQ2/8, biopsy)? 

a. Yes (include) 

b. No (exclude) 

7. Was the diagnosis of celiac disease appropriate in the celiac disease group 

a. Yes (include) 

b. No (exclude) 
 A-27

Celiac 2: Prevalence and incidence of celiac disease: 

Inclusion Criteria: (a No answer to any of the below excludes the article) 

1. The country of origin must be Western Europe, North America, Australia, New 

Zealand. 

a. Yes (include) 

b. No (exclude) 

2. The publication date was >= 1990 if serology was used to screen (but can be earlier 

for biopsy) 

a. Yes (include) 

b. No (exclude) 

3. The screening test was biopsy, standardized ELISA AGA, EMA (monkey esophagus 

or human umbilical cord), tTG (guinea pig, or human recombinant) 

a. Yes (include) 

b. No (exclude) 

4. The screened population must belong to one of these groups: 

a. Unselected – General population (e.g. Blood donors, routine physical etc) 

b. Patients with suspected celiac 

c. Relatives of celiac patients 

d. Iron deficiency 

e. Osteoporosis 

f. Diabetes 

a. Yes (include) 

b. No (exclude) 
 A-28

Celiac 3: Prevalence/incidence of lymphoma in celiac disease 

1. Does this study specifically give the incidence, prevalence or a measure of risk of 

GI lymphoma (Includes malignant histiocytosis) in a population of celiac patients? 

(Note: we are not interested in other cancers, and we are not interested in how many 

lymphoma patients have celiac disease) 

OR 

Does this study discuss ulcerative jejuno-ileitis or refractory sprue as a precursor or 

marker for GI lymphoma in patients with celiac disease? 

a. Yes (include lymphoma) 

b. Yes (include jejuno-ileitis/refractory sprue) 

c. No (exclude) 

Celiac 4: Consequences of testing for celiac disease 

1. Does this paper report a consequence of testing for celiac listed below: (note: 

false positive, and negative results, follow-up testing and need for invasive 

testing is obtained from Celiac 1 objective) 

a. Costs

b. Patients complying with treatment 

c. Response to treatment – i.e., clinical outcome (reduced risk of 

complication – osteoporosis, lymphoma, anemia, symptoms) 

i. Yes (include) 

ii. No (exclude) 

2. Did the population include one of the following (note: nothing more than listed): 

a. Patients with symptoms suggestive of celiac disease 

b. Asymptomatic, at-risk populations (affected family members, patients with 

type 1 diabetes, osteoporosis, Fe Diff) 

c. General population 

i. Yes (include) 

ii. No (exclude) 

Note: a No to either question excludes the study 
 A-29

Celiac 5: Monitoring or promoting adherence to a GFD 

If a monitoring question: 

Does this paper report monitoring adherence based on serology (standardized 

ELISA AGA publication date >= 1990, EMA (monkey esophagus or human 

umbilical cord), tTG (guinea pig, or human recombinant) or biopsy? 

Note: If this is a study of sensitivity or specificity – it must include actual 

extractable follow-up data (like drop in titre or improvement in biopsy) 

OR 

If a promoting adherence question: 

Does this paper report on an intervention that was used to promote adherence to 

Gluten free diet? 

a. Yes (include promoting) 

b. Yes (include Monitoring) 

c. No (exclude) 
 A-30

Data Abstraction Forms 

Celiac 1: Serology 

1. Paper #: 

2. Title: 

3. Author/year: 

4. Reference: 

5. Reviewer: 

6. Publication type: 

a. Journal 

b. Conference abstract 

c. Other: 

7. Is this a duplicate publication (state refid of duplicate): 

8. Study type: 

a. Relevant clinical population: (cases and controls defined from the 

population based on the results of the test under study) 

b. Case Control: (groups are predefined and may come from different 

populations): 

c. Other: (list) 

9. Country: 

10. Racial Groups and % if different from country: list in box

11. Group demographics 

 Celiac Control 

 Group 1 Group 2 group1 group 2 group 3 group 4 

Group name 

Age groups 

Mean age 

Age range 

% female 

Gluten intake 

12. Type of population (applies to 8 a): (from level 2 database)

a. Unselected – general population (e.g., blood donors, routine physical, etc.) 

b. Patients with suspected celiac 

c. Relatives of celiac patients 

d. Diabetes 

e. Iron deficiency 

f. Osteoporosis 

g. Other (fill in box): not part of extraction – background / discussion only 
 A-31

13. Case and control group types (applies to 8 b): 

a. Celiac group 1 

i. Untreated 

1. Classic 

2. Silent celiac 

3. Atypical celiac 

4. Other 

ii. Treated On GFD 

iii. Refractory (implies on GFD) / ulcerative jejuno-ileitis 

iv. Other/can’t tell: text box 

b. Celiac group 2 – if applicable 

i. Untreated 

1. Classic 

2. Silent celiac 

3. Atypical celiac 

4. Other 

ii. Treated on GFD 

iii. Refractory (implies on GFD) / ulcerative jejuno-ileitis 

iv. Other/can’t tell: text box 

Note: Control groups must have had a negative biopsy otherwise should have been 

excluded at level 3 

c. Control group 1: 

i. Unselected – general population (e.g., blood donors, routine 

physical, etc.) 

ii. Patients with suspected celiac 

iii. Relatives of celiac patients 

iv. Diabetes 

v. Iron deficiency 

vi. Osteoporosis 

vii. Other disease controls 

viii. Other (fill in box): 

d. Control group 2 (if applicable): 

i. Unselected – general population (e.g., blood donors, routine 

physical, etc.) 

ii. Patients with suspected celiac 

iii. Relatives of celiac patients 

iv. Diabetes 

v. Iron deficiency 

vi. Osteoporosis 

vii. Other disease controls 

viii. Other (fill in box): 
 A-32

e. Control group 3 (if applicable): 

i. Unselected – general population (e.g., blood donors, routine 

physical, etc) 

ii. Patients with suspected celiac 

iii. Relatives of celiac patients 

iv. Diabetes 

v. Iron deficiency 

vi. Osteoporosis 

vii. Other disease controls 

viii. Other (fill in box): 

f. Control group 4 (if applicable): 

i. Unselected – general population (e.g., blood donors, routine 

physical, etc.) 

ii. Patients with suspected celiac 

iii. Relatives of celiac patients 

iv. Diabetes 

v. Iron deficiency 

vi. Osteoporosis 

vii. Other disease controls 

viii. Other (fill in box): 

14. Reference test(s) for cases (i.e., how was celiac diagnosed): 

a. Biopsy (required): 

i. endoscopic 

ii. capsule 

1. list type: text box 

iii. how many samples taken (text box) 

b. Serology (check as many as applicable) 

i. AGA (date >1990) 

ii. EMA 

iii. tTG 

c. Comments: 

15. What test was conducted first 

a. Biopsy 

b. Serology 

c. Simultaneous 

d. Mixed 

e. Unsure/other: comment in box 

16. Reference test for control (s) 1-----2-----3-----4 

a. Include biopsy (required) 

b. Otherwise excluded 
 A-33

17. Detail biopsy criteria used to define celiac (ESPGAN, Marsh, Rostami) and state 

what grades were used (i.e., Marsh I and above? etc.) 

18. Was IgA deficiency assessed (if applicable): 

a. Yes 

b. No 

c. N/A 

d. Comments: text box) 

19. Overall number: 

20. Number of: 

a. Cases 1 

b. Cases 2 (if applicable): 

c. Control group 1: 

d. Control group 2 (if applicable): 

e. Control group 3 (if applicable): 

f. Control group 4 (if applicable): 

21. Intervention: (may be up to 8+ tests studied – distinguish IgG from IgA) 

 Results (4x4 table) 

Test name Methodology Cut-off (criteria) Group a b c d 

 

22. Stated results if raw data not given: 

Test name Sensitivity Specificity PPV NPV Prevalence 

 

23. Comments regarding study: test box 
 A-34

Notes for reference: 

Test name can be: 

1) Anti-htTG 

2) Anti-endomysial antibody (EMA) 

3) Anti-gliadin antibody (AGA) 

 BIOPSY (gold standard) 

 positive negative 

positive 

a b 

TEST: 

______________ 

negative 

c d 

Calculate automatically 

• Prevalence: (a+c)/(a+b+c+d) 

• Sensitivity: (a/(a+c)); 

• Specificity: d/(b+d); 

• PPV: a/(a+b) 

• NPV: d/(c+d) 

Celiac 1: HLA 

1. Paper #: 

2. Title: 

3. Author/year: 

4. Reference: 

5. Reviewer: 

6. Publication type: 

a. Journal 

b. Conference abstract 

c. Other: 

7. Is this a duplicate publication (state refid of duplicate): 

8. Country: 

9. Racial groups and % if different from country: list in box

10. Age groups (ped, adult, both):
 A-35

11. Mean age: 

12. Range of age: 

13. Percent female: 

14. Study type: 

d. Relevant clinical population: (cases and controls defined from the 

population based on the results of the test under study) 

e. Case control: (groups are predefined and may come from different 

populations: 

f. Cross-sectional screening study 

g. Other: (list) 

15. Type of population (applies to 14 a, c): 

a. Unselected – general population (e.g., blood donors, routine physical etc) 

b. Patients with suspected celiac 

c. Relatives of celiac patients 

d. Diabetes 

e. Iron deficiency 

f. Osteoporosis 

g. Other (fill in box): not part of extraction – background / discussion only 

16. Case and control group types (applies to 14b): 

h. Celiac group 1 

i. Untreated 

1. Classic 

2. Silent celiac 

3. Atypical celiac 

4. Other 

ii. Treated on GFD 

iii. Refractory (implies on GFD) / ulcerative jejuno-ileitis 

iv. Other/can’t tell: text box Celiac group 2 

i. Celiac group 2 – if applicable 

i. Untreated 

1. Classic 

2. Silent celiac 

3. Atypical celiac 

4. Other 

ii. Treated on GFD 

iii. Refractory (implies on GFD) / ulcerative jejuno-ileitis 

iv. Other/can’t tell: text box 

Note: Control groups must have had a negative biopsy otherwise should have 

been excluded at level 3
 A-36

j. Control group 1: 

i. Unselected – general population (e.g., blood donors, routine 

physical, etc.) 

ii. Patients with suspected celiac 

iii. Relatives of celiac patients 

iv. Diabetes 

v. Iron deficiency 

vi. Osteoporosis 

vii. Other disease controls 

viii. Other (fill in box): 

k. Control group 2 (if applicable): 

i. Unselected – general population (e.g., blood donors, routine 

physical, etc.) 

ii. Patients with suspected celiac 

iii. Relatives of celiac patients 

iv. Diabetes 

v. Iron deficiency 

vi. Osteoporosis 

vii. Other disease controls 

viii. Other (fill in box): 

l. Control group 3 (if applicable): 

i. Unselected – general population (e.g., blood donors, routine 

physical, etc.) 

ii. Patients with suspected celiac 

iii. Relatives of celiac patients 

iv. Diabetes 

v. Iron deficiency 

vi. Osteoporosis 

vii. Other disease controls 

viii. Other (fill in box): 

m. Control group 4 (if applicable): 

i. Unselected – general population (e.g., blood donors, routine 

physical, etc.) 

ii. Patients with suspected celiac 

iii. Relatives of celiac patients 

iv. Diabetes 

v. Iron deficiency 

vi. Osteoporosis 

vii. Other disease controls 

viii. Other (fill in box): 
 A-37

17. Reference test for cases 

n. Biopsy: 

i. endoscopic 

ii. capsule 

1. list type: text box 

o. Serology (check as many as applicable) 

i. AGA (date >1990) 

ii. EMA 

iii. tTG 

18. Reference test for control 1-----2------3-----4 

p. Biopsy 

q. Serology (list) 

r. Can’t tell 

19. Overall number: 

20. Number of: 

s. Cases 1 

t. Cases 2 (if applicable): 

u. Control group 1: 

v. Control group 2 (if applicable): 

w. Control group 3 (if applicable): 

x. Control group 4 (if applicable): 

21. HLA tested 

 Results (4x4 table) 

Test name Methodology Cut-off (criteria) Group a b c d 

 

22. Stated results if raw data not given: 

Test name Sensitivity Specificity PPV NPV Prevalence 

 

23. Narrative result if data not extractable: text box 
 A-38

24. Comments regarding study: text box 
 A-39

Celiac 2: Prevalence and Incidence of Celiac Disease 

1. Paper #: 

2. Title: 

3. Author/year: 

4. Reference: 

5. Reviewer: 

Patient population: 

6. Publication type: 

a. Journal 

b. Conference abstract 

c. Etc (your list) 

7. Is this a duplicated: list refid 

8. Study type: 

a. Cross-sectional prevalence 

b. Cohort 

c. Case control 

d. Incidence study 

e. Other: (list) 

9. Country: 

10. Racial groups and % if different from country: list in box

11. Type of patients screened: 

a. Unselected – general population (e.g., blood donors, routine physical etc) 

b. Patients with suspected celiac 

c. Relatives of celiac patients 

d. Diabetes 

e. Iron deficiency 

f. Osteoporosis 

g. Other (fill in box): not part of extraction – background / discussion only

12. Age groups (ped, adult or both): from level 2 database

13. Mean age: 

14. Range of age: 

15. Percent female: 

Intervention: 
 A-40

 Results 

Test 

name 

Methodology # screened Cases detected Incidence (time period) Prevalence 

 

Note: distinguish IgG from IgA. Also the screen may be single test, or combination of tests. So list each 

strategy used as a “test name” 

16. State control reference and methodology of incidence study: (fill in box) 

17. Confirmatory test 

a. None 

b. Biopsy 

c. Other serology 

d. Other: fill in box 

18. Was IgA deficiency assessed (if applicable): 

a. Yes 

b. No 

c. N/A 

d. Comments: (text box) 

19. Comments about study: text box 
 A-41

Celiac 3: Lymphoma 

1. Paper #: 

2. Title: 

3. Author/year: 

4. Reference: 

5. Reviewer: 

6. Publication type: 

a. Journal 

b. Conference abstract 

c. Etc (your list) 

7. Study type: 

a. Cross-sectional prevalence 

b. Case series 

c. Cohort 

i. Prospective 

ii. Retrospective 

d. Case control 

e. Other: (list) 

8. Country: from level 2 database

9. Racial groups and % if different from country: list in box

10. Study population type(s) – this is the population of “lymphoma” in case control 

OR the overall population in a screening/prevalence study and cohort studies: 

Check multiple if study included different populations 

a. Classic celiac: 

1) Treated celiac 

2) Untreated celiac 

3) Non-compliant 

4) Unclear about treatment 

b. Asymptomatic (silent celiac) 

c. Atypical celiac (found on basis of 

d. Latent celiac (normal histology) 

e. Refractory celiac 

f. Ulcerative jejuno-ileitis 

g. Other celiac complications 

h. Patients on Immunosuppression: 

i. Other: 

11. How were celiac patients identified (text box) 
 A-42

12. How were cases of lymphoma identified? (i.e., registry, administrative database, 

etc.) text box 

13. Group demographics 

 Overall population study type 

a, b, c 

Case group Control group 

Age groups 

Mean age 

Age range 

% female 

Disease duration 

14. For case control study: 

a. Control population type (those without lymphoma) 

i. Unselected general population 

ii. Other disease controls: state disease(s) 

iii. A celiac population 

1. Classic celiac: 

a. Treated celiac 

b. Untreated celiac 

c. Non-compliant 

d. Unclear about treatment 

2. Asymptomatic (silent celiac) 

3. Atypical celiac (found on basis of 

4. Latent celiac (normal histology) 

5. Refractory celiac 

6. Ulcerative jejuno-ileitis 

7. Other celiac complications 

iv. Patients on immunosuppression: 

b. # of cases: 

c. # of controls: 

d. Risk factor used to calculate odds ratio 

i. Celiac itself 

1. classic 

2. refractory 

3. ulcerative jejuno-ileitis 

ii. Compliance with diet 

iii. Disease duration 

iv. Other: state in text box 

e. Raw data (if possible) 

Table for case control study 

Risk factor Lymphoma present Lymphoma absent 

Present 

Absent 
 A-43

15. For cohort study

f. Length of F/U of cohort: 

g. Timeline: 

iii. Prospective cohort 

iv. Retrospective cohort: 

h. Risk factor used to calculate Relative Risk if one population used 

v. Celiac itself 

1. classic 

2. atypical 

3. silent 

4. refractory 

5. ulcerative jejuno-ileitis 

vi. Compliance with diet 

vii. Disease duration 

viii. Other: state in text box 

i. If a celiac cohort was compared to another population to obtain another 

risk estimate (i.e., standardized mortality or morbidity ratios). Describe 

control population. 

ix. Unselected general population 

x. Other disease controls: state disease(s) 

xi. A celiac population 

1. Classic celiac: 

a. Treated celiac 

b. Untreated celiac 

c. Non-compliant 

d. Unclear about treatment 

2. Asymptomatic (silent celiac) 

3. Atypical celiac (found on basis of 

4. Latent celiac (normal histology) 

5. Refractory celiac 

6. Ulcerative jejuno-ileitis 

7. Other celiac complications 

xii. Patients on immunosuppression 

xiii. Other: (fill in text box) 

j. Overall number in cohort: 

xiv. Number of cases identified: 

k. Number in control population (if applicable) 

xv. Number of lymphomas identified 

xvi. Raw data if available: 

16. Table for classic cohort study 
 A-44

Risk factor Lymphoma present Lymphoma absent 

Present 

Absent 

17. For cross sectional studies: study population in Q #10 

l. Overall number screened: 

m. Number of cases identified: 

18. Results (text boxes) 

n. Lymphoma type 

o. Prevalence of lymphoma in celiac: 

p. Incidence of lymphoma in celiac: 

q. Odds ratio (95% confidence interval) 

r. Relative risk (95% confidence interval): 

s. Standardized mortality ratio 

t. Standardized morbidity ratio 

u. Other risk estimate: 

19. Study comments: 
 A-45

Celiac 4: Consequences of Testing 

1. Paper #: 

2. Title: 

3. Author/year: 

4. Reference: 

5. Reviewer: 

Patient population: 

6. Publication type: 

a. Journal 

b. Conference abstract 

c. Etc (your list) 

7. Study type: 

a. Diagnostic test 

b. Cross-sectional prevalence 

c. Cohort 

d. Case control 

e. Other: (list) 

8. Country: from level 2 database

9. Racial groups and % if different from country: list in box

10. Type of patients tested (from level 2 database)

a. Unselected – general population (e.g., blood donors, routine physical, etc.) 

b. Patients with suspected celiac 

c. Relatives of celiac patients 

d. Diabetes 

e. Iron deficiency 

f. Osteoporosis 

g. Other (fill in box): 

11. Type of celiac patients identified: 

a. Classic celiac 

b. Asymptomatic 

c. Atypical celiac 

i. Fe deficiency 

ii. Osteoporosis 

iii. Other 

d. Complicated celiac 

i. Refractory 

ii. Jejuno-ileitis 

iii. Lymphoma) 
 A-46

e. Other 

12. Intervention: 

a. Test(s) used to identify celiac patients: 

i. Biopsy 

ii. AGA ELISA (publication date >1990) 

iii. AMA 

iv. tTG: 

13. Was IgA deficiency assessed (if applicable): 

a. Yes 

b. No 

c. N/A 

d. Comments: text box) 

14. Length of F/U: 

15. How were patients followed (if applicable): test box 

16. Outcomes: 

Outcome Result Notes 

Costs 

Cases diagnosed 

Patients complying with 

treatment 

Response to treatment 

Clinical outcome (reduced risk 

of complication, etc)

 

Other (fill in box) 

17. Comments regarding study: Fill in text box 
 A-47

Celiac 5: Promoting and Monitoring Adherence to Gluten-Free Diet 

1. Paper #: 

2. Title: 

3. Author/year: 

4. Reference: 

5. Reviewer: 

Patient population: 

6. Publication type: 

a. Journal 

b. Conference abstract 

c. Etc (your list) 

7. Study type: 

a. Diagnostic test 

b. Cross-sectional prevalence 

c. Cohort 

d. Case control 

e. Other: (list) 

8. Country: from level 2 database

9. Racial groups and % if different from country: list in box

10. Age groups (ped, adult, both): from level 2 database

11. Mean age: 

12. Range of age: 

13. Percent female: 

14. Disease duration: state in box 

15. Type of celiac studied 

a. Classic celiac 

b. Asymptomatic celiac 

c. Atypical celiac (Fe deficiency, osteoporosis, etc.) 

d. Refractory celiac 

e. Ulcerative jejuno-ileitis 

f. IgA deficient celiac 

g. Other: 

16. Does this refer to: 
 A-48

a. Promoting adherence 

b. Monitoring adherence 

c. Both 

17. What intervention was assessed? (if monitoring adherence) 

 Result (normalization of biopsy or drop in antibody titres - 

list result details) 

Biopsy 

Antibody testing 

(state test used) 

Other: ___________ 

18. Did this study determine the sensitivity/specificity of the intervention during 

follow-up or with different histologic grades: 

a. No 

b. Yes: detail in text box 

19. Was IgA deficiency assessed (if applicable): 

a. Yes 

b. No 

c. N/A 

d. Comments: text box 

20. What intervention was used? (if promoting adherence) – fill in box 

 

Intervention Result 

 

Comments about the study: fill in text box 
 A-49

Appendix D. Quality Assessment Forms 

QUADAS Checklist 

Item Yes No Unclear 

1. Was the spectrum of patients representative of the patients who 

will receive the test in practice? 

 

2. Were selection criteria clearly described? 

3. Is the reference standard likely to correctly classify the target 

condition? 

 

4. Is the time period between reference standard and index test 

short enough to be reasonably sure that the target condition did 

not change between the two tests? 

 

5. Did the whole sample or a random selection of the sample, 

receive verification using a reference standard of diagnosis? 

 

6. Did patients receive the same reference standard regardless of 

the index test result? 

 

7. Was the reference standard independent of the index test (i.e. 

the index test did not form part of the reference standard)? 

 

8a. Was the execution of the index test described in sufficient detail 

to permit replication of the test? 

 

8b. Was the execution of the reference standard described in 

sufficient detail to permit its replication? 

 

9a. Were the index test results interpreted without knowledge of the 

results of the reference standard? 

 

9b. Were the reference standard results interpreted without 

knowledge of the results of the index test? 

 

10. Were the same clinical data available when test results were 

interpreted as would be available when the test is used in 

practice? 

 

11. Were uninterpretable/ intermediate test results reported? 

12. Were withdrawals from the study explained? 
 A-50

Cross-Sectional/Prevalence Study Quality 

Item Yes No Unclear 

1) Define the source of information (survey, record review) 

2) List inclusion and exclusion criteria for exposed and 

unexposed subjects (cases and controls) or refer to previous 

publications 

 

3) Indicate time period used for identifying patients 

4) Indicate whether or not subjects were consecutive if not 

population-based 

 

5) Indicate if evaluators of subjective components of study were 

masked to other aspects of the status of the participants 

 

6) Describe any assessments undertaken for quality assurance 

purposes (e.g., test/retest of primary outcome measurements) 

 

7) Explain any patient exclusions from analysis 

8) Describe how confounding was assessed and/or controlled. 

9) If applicable, explain how missing data were handled in the 

analysis 

 

10) Summarize patient response rates and completeness of data 

collection 

 

11) Clarify what follow-up, if any, was expected and the 

percentage of patients for which incomplete data or follow-up 

was obtained 

 
 A-51

Newcastle–Ottawa Quality Assessment Scale: Cohort Studies 

Note: a study can be awarded a maximum of one star for each numbered item within 

the selection. A maximum of two stars can be given for comparability and selection. 

1) Representativeness of the exposed cohort 

a) truly representative of the average _____________ (describe) in the communityD

b) somewhat representative of the average _____________ in the community D

c) selected group of users e.g. nurses, volunteers 

d) no description of the derivation of the cohort 

2) Selection of the non exposed cohort 

a) drawn from the same community as the exposed cohort D

b) drawn from a different source 

c) no description of the derivation of the non exposed cohort 

3) Ascertainment of exposure 

a) secure record (e.g. surgical records) D

b) structured interview D

c) written self report 

d) no description 

4) Demonstration that outcome of interest was not present at start of study 

a) yes D

b) no 

Comparability 

1) Comparability of cohorts on the basis of the design or analysis 

a) study controls for _____________ (select the most important factor) D

b) study controls for any additional factor D (This criteria could be modified to indicate 

specific control for a second important factor.) 

Outcome 

1) Assessment of outcome 

a) independent blind assessment D

b) record linkage D

c) self report 

d) no description 

2) Was follow-up long enough for outcomes to occur 

a) yes (select an adequate follow up period for outcome of interest) D

b) no 

3) Adequacy of follow up of cohorts 

a) complete follow up - all subjects accounted for D

b) subjects lost to follow up unlikely to introduce bias - small number lost - > ____ % (select 

an adequate %) follow up, or description provided of those lost) D

c) follow up rate < ____% (select an adequate %) and no description of those lost 

d) no statement 
 A-52

Newcastle–Ottawa Quality Assessment Scale: Case Control Studies 

Note: a study can be awarded a maximum of one star for each numbered item within 

the selection and exposure categories. A maximum of two stars can be given for 

comparability. 

Selection 

1) Is the case definition adequate? 

a) yes, with independent validation D

b) yes, e.g. record linkage or based on self reports 

c) no description 

2) Representativeness of the cases 

a) consecutive or obviously representative series of cases D

b) potential for selection biases or not stated 

3) Selection of Controls 

a) community controls D

b) hospital controls 

c) no description 

4) Definition of Controls 

a) no history of disease (endpoint) D

b) no description of source 

Comparability 

1) Comparability of cases and controls on the basis of the design or analysis 

a) study controls for _______________ (Select the most important factor.) D

b) study controls for any additional factor D (This criteria could be modified to 

indicate specific control for a second important factor.) 

Exposure 

1) Ascertainment of exposure 

a) secure record (e.g. surgical records) D

b) structured interview where blind to case/control status D

c) interview not blinded to case/control status 

d) written self report or medical record only 

e) no description 

2) Same method of ascertainment for cases and controls 

a) yes D

b) no 

3) Non-Response rate 

a) same rate for both groups D

b) non respondents described 

c) rate different and no designation
 A-53

Appendix E. Summary ROC Curves 

Summary ROC curves as calculated by the methods of Moses and Shapiro (meta-analysis text). 

For all figures below, the middle curve is the summary ROC, the other curves are upper and 

lower 96% CI, and the vertical line is the point were sensitivity = specificity; dots are individual 

studies 

Figure 1. Summary ROC HLA average-risk with 95% CIs 

Figure 2. Summary ROC IgA-AGA–adults 
 A-54

Figure 3. Summary ROC IgG-AGA–adults 

Figure 4. Summary ROC IgA-EMA-EM–adults 
 A-55

Figure 5. Summary ROC IgA-EMA-HU–adults 

Figure 6. Summary ROC IgA-tTG-GP–adults 
 A-56

Figure 7. Summary ROC IgA-tTG-HR–adults 

Figure 8. Summary ROC IgA-AGA–child 
 A-57

Figure 9. Summary ROC IgG-AGA–child 

Figure 10. Summary ROC IgA-EMA-ME–child 
 A-58

Figure 11. Summary ROC IgA-EMA-HU–child 

Figure 12. Summary ROC IgA-tTG-GP–child 
 A-59

Figure 13. Summary ROC IgA-tTG-HR–child 

Figure 14. Summary ROC IgA-AGA–mixed-age populations 
 A-60

Figure 15. Summary ROC IgG-AGA–mixed-age populations 

Figure 16. Summary ROC IgA-EMA-ME–mixed-age populations 
 A-61

Figure 17. Summary ROC IgA-tTG-GP–mixed-age populations 
 A-62

Appendix F. Modified QUOROM Flow Chart 

Modified QUOROM Flow Charts 

Objective 1 – Sensitivity and Specificity of Tests for CD 

Objective 2 – Prevalence and Incidence of CD 

3814 Evaluated for inclusion 

3920 Failed to meet inclusion criteria: 

 3585 Not sensitivity or specificity of an 

identified test 

 21Review article 

 27 Serology <1990 

 4 Test-specific exclusion 

220 Improper control group 

 57 Unable to extract data 

 6 Unable to obtain full article 

168 Duplicate records removed 

3931 Records identified from bibliographic databases 

219 Nominated by reviewers 

62 Studies included for Question 1 

2116 Evaluated for inclusion 

1983 Failed to meet inclusion criteria: 

1843 No prevalence or incidence reported 

 11 Review article 

 50 Not a relevant geography location 

31 Serology screen <1990 

 14 Not a relevant screening test 

 32 Not a relevant screening population 

 2 Unable to obtain full article 

34 Duplicate records removed 

2051 Records identified from bibliographic databases 

99 Nominated by reviewers 

133 Studies included for Question 2 
 A-63

Objective 3 – Celiac Associated Lymphoma 

Objective 4 – Expected Consequences of Testing for CD 

379 Evaluated for inclusion 

 5 Duplicate records removed 

327 Records identified from bibliographic databases 

57 Nominated by reviewers 

10 Studies included for Question 3 

1199 Evaluated for inclusion 

1164 Failed to meet inclusion criteria: 

 1148 Not about consequences of testing 

 7 Review article 

 9 Could not obtain full article 

29 Duplicate records removed 

1121 Records identified from bibliographic databases 

107 Nominated by reviewers 

35 Studies included for Question 4 

369 Failed to meet inclusion criteria: 

 256 Not about celiac and GI lymphoma 

 35 Review article

 16 Does not address the question 

 16 Risk of CD in lymphoma 

 9 Pathogenesis only 

 31 Not a controlled study

 5 Double publication of included data 

 1 Unable to extract data
 A-64

Objective 5 – Promoting or Monitoring Adherence to a GFD 

502 Evaluated for inclusion 

467 Failed to meet inclusion criteria: 

 415 Not relevant to adherence 

 5Review article 

 18 No monitoring measure of interest 

 15 Monitoring not serology, EMA, tTG 

or biopsy based, or not promoting 

GFD adherence 

 14 Only mean scores reported 

11 Duplicate records removed 

320 Records identified from bibliographic databases 

193 Nominated by reviewers 

35 Studies included for Question 5 
A-65

Appendix G. Raw Pooled Data 

All raw pooled data by antibody test and study types showing number of studies and total patient 

numbers. 

AGA - ELISA 

Population Pooled Number IgA Pooled Number IgG 

 Studies Patients Sens Spec PPV NPV Prev Studies Patients Sens Spec PPV NPV Prev 

Case 

Control 

 

Adults 2 336 57.9 92.6 93.2 55.7 0.40 1 157 78.0 80.7 87.6 67.6 56.7 

Children 5 412 76.6 79.9 81.1 75.2 0.5 5 412 84.4 60.3 70.5 77.5 0.5 

Both 1 343 84.6 81.6 75.2 88.9 0.4 1 343 69.1 73.4 63.1 78.4 0.4 

Relevant 

CP 

 

Adults 8 946 71.0 81.1 61.7 86.8 0.35 6 652 65.6 85.7 70.7 82.7 31.9 

Children 14 1382 80.1 89.9 78.7 90.7 0.3 12 1189 89.3 83.6 68.1 95.2 0.3 

Both 3 737 68.2 92.7 91.5 71.5 0.5 3 737 83.8 79.5 82.6 80.9 0.5 

EMA – Monkey Esophagus IF 

Study 

Population Pooled Number IgA Pooled Number IgG 

 Studies Patients Sens Spec PPV NPV Prev Studies Patients Sens Spec PPV NPV Prev 

Case 

Control 

 

Adults 6 706 97.3 100.0 100.0 97.1 50.7 n/a n/a n/a n/a n/a n/a n/a 

Children 12 1038 96.5 98.7 98.6 96.6 0.5 1* 153 100 100 100 100 0.1 

Both 1 131 75.3 98.3 98.2 76.0 0.6 n/a n/a n/a n/a n/a n/a n/a 

Relevant 

CP 

 

Adults 5 692 95.0 99.4 98.1 98.5 22.4 1 89 39.3 98.4 91.7 77.9 0.14 

Children 6 868 93.2 95.4 88.3 97.4 0.3 n/a n/a n/a n/a n/a n/a n/a 

Both 3 737 87.9 99.7 99.7 87.6 0.5 n/a n/a n/a n/a n/a n/a n/a 

Note: *this study was conducted in CD patients known to be IgA-EMA negative, and 50% had IgA deficiency 

EMA – Human Umbilical Cord - IF 

Population Pooled Number IgA Pooled Number IgG 

 Studies Patients Sens Spec PPV NPV Prev Studies Patients Sens Spec PPV NPV Prev 

Case 

Control 

 

Adults 5 578 90.3 100.0 100.0 93.7 37.2 n/a n/a n/a n/a n/a n/a n/a 

Children 4 375 96.6 100.0 100.0 97.1 0.5 n/a n/a n/a n/a n/a n/a n/a 

Both 2 428 92.5 99.6 99.5 93.8 0.5 n/a n/a n/a n/a n/a n/a n/a 

Relevant 

CP 

 

Adults 1 92 87.5 100.0 100.0 98.8 7.6 n/a n/a n/a n/a n/a n/a n/a 

Children 2 172 70.5 86.7 64.6 89.5 0.3 n/a n/a n/a n/a n/a n/a n/a 

Both n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a n/a 

tTG - Guinea Pig Liver - ELISA 

Population Pooled Number IgA Pooled Number IgG 

 Studies Patients Sens Spec PPV NPV Prev Studies Patients Sens Spec PPV NPV Prev 

Case 

Control 

 

Adults 3 368 83.4 97.1 97.0 84.2 45.1 n/a n/a n/a n/a n/a n/a n/a 

Children 3 270 92.3 99.2 99.2 92.0 0.5 n/a n/a n/a n/a n/a n/a n/a 

Both 3 559 91.2 94.7 94.3 91.8 0.5 1 85 61.5 100.0 100.0 44.4 0.8 

Relevant 

CP 

 

Adults 2 327 100.0 94.2 66.7 100.0 15.6 n/a n/a n/a n/a n/a n/a n/a 

Children 2 176 95.1 93.0 87.9 97.3 0.3 n/a n/a n/a n/a n/a n/a n/a 

Both 1 111 91.7 98.4 97.8 93.9 0.4 1 111 22.9 98.4 91.7 62.6 0.4 
A-66

tTG – Human Recombinant - ELISA 

Population Pooled Number IgA Pooled Number IgG 

 Studies Patients Sens Spec PPV NPV Prev Studies Patients Sens Spec PPV NPV Prev 

Case 

Control 

 

Adults 1 63 95.2 100.0 100.0 97.7 31.7 n/a n/a n/a n/a n/a n/a n/a 

Children 2 115 95.3 98.0 98.4 94.3 0.6 n/a n/a n/a n/a n/a n/a n/a 

Both 1 85 90.8 100.0 100.0 76.9 0.8 1 85 67.7 100.0 100.0 48.8 0.8 

Relevant 

CP 

 

Adults 2 299 100.0 97.8 84.2 100.0 12.7 n/a n/a n/a n/a n/a n/a n/a 

Children 1 101 96.2 100.0 100.0 96.1 0.5 n/a n/a n/a n/a n/a n/a n/a 

Both 1 426 90.0 94.9 96.2 87.0 0.6 n/a n/a n/a n/a n/a n/a n/a 
A-67

Appendix H. Biopsy Results 

Relationship of Serology to Histology 

CD clearly exists in patients with histological grades milder than Marsh IIIa, and given that 

the sensitivity of biopsy is improved by using a lower grade as a cut-off, an important question 

arises—what test is most sensitive for detecting CD with mild histologic changes, biopsy or 

serology? 

Fasano,1

 in a large American prevalence study of CD in at risk and not at risk populations, 

found that only 34% of biopsied EMA-positive subjects had subtotal or total VA (modified 

Marsh IIIb or IIIc). In this study, no EMA-positive patient had a Marsh 1 lesion, 26% of EMApositive patients had a Marsh II lesion, and 40% had a Marsh IIIa lesion. All newly-diagnosed, 

EMA-positive CD patients with (n=98) or without (n=114) biopsy had HLA DQ2, DQ8 or both, 

as apposed to 59% of EMA-negative subjects (n=92). The results of this study once again 

suggest that applying a criterion of subtotal or total VA would miss 66% of CD patients. The 

absence of Marsh I lesions in EMA-screened subjects is not surprising (discussed below), given 

the lower sensitivity of this test in lower-grade histologic lesions of CD, suggesting that the CD 

may have been unrecognized in some EMA-negative subjects. Unfortunately, HLA was not 

evaluated in all subjects and assessment of the correlation with serology in the population at 

large or systematically with biopsy grade was not reported. 

Rostami et al.2

 evaluated the diagnostic value of IgA EMA and AGA in 101 untreated CD 

patients. The diagnosis of CD was made on the basis of “appropriate histopathological features” 

(Marsh IIIa or greater) and clinical improvement on a gluten-free diet (GFD). Sixteen firstdegree relatives with minor histologic abnormalities (Marsh I-II) were used as controls. Sixteen 

patients were excluded for not meeting diagnostic criteria, IgA deficiency, or undergoing 

serology while on GFD. 

Rostami et al.2 Marsh I-II (controls) Marsh IIIa Marsh IIIb Marsh IIIc 

Biopsy 16 29 (%) 23 (%) 17 (%) 

AGA 3 (21%) 9 (31%) 16 (70%) 14 (82%) 

EMA 0 9 (31%) 16 (70%) 17 (100%) 

The combination of the two tests showed an overall sensitivity of 76%. Unfortunately, the 

authors, as is commonly done, considered Marsh I-II as controls; it is unclear if any of these, 

particularly those who were AGA positive, actually have CD. As will be described below, there 

is a subset of patients with Marsh I-II who are serology negative who have CD. In any case, this 

study demonstrates an important finding, i.e., that the sensitivity of the studied serological 

markers varies with the severity of the histologic grade. Alarmingly, the sensitivity even for CD 

patients with Marsh IIIa lesions is close to 30%. This is partially at odds with the results of the 

Fasano study1

 where only 34% of the identified patients were found to have Marsh IIIb or greater 
A-68

grade lesions, with the rest having grade II to IIIa lesions. In both studies, no EMA-positive 

Marsh I lesions were found. The Fasano study, being a population-based screening study, 

obviously did not biopsy all screened patients. This begs the question of how many grade IIIb or 

less patients with CD were missed based on the findings of Rostami and Tursi (detailed below). 

Tursi et al.3

 assessed the relationship of the histologic grade of 119 consecutive adult patients 

with CD defined by characteristic duodenal biopsy and “permanent gluten-sensitive 

enteropathy.” The following table summarizes the main findings. 

Tursi et al.3 Marsh I Marsh II Marsh IIIa Marsh IIIb Marsh IIIc 

Biopsy 13 (11%) 24 (20%) 27 (23%) 31 (26%) 24 (20%) 

tTG positive 1 (8%) 8 (33%) 15 (56%) 26 (84%) 23 (96%) 

Mean tTG level 

UA/mL 

7.3 18.5 n/a 36 74.95 

In this study, 69% of CD patients had VA (Marsh IIIa or greater). The frequency of tTGpositivity (sensitivity) and mean tTG levels were greatest with the highest Marsh grade and 

dropped steadily with milder histologic grades, reaching a low of only 8%-positivity in CD 

patients with Marsh I lesions. Since these patients all have “permanent gluten-sensitive 

enteropathy,” it is clear that tTG would have missed 76% of this cohort of CD patients with 

Marsh I or II lesions who were picked up by biopsy. 

Tursi et al.,4

 also assessed 123 adult patients (possibly the same patients cohort from the 

above study) with either subclinical (equivalent to atypical in this review) or silent CD. All 

patients were biopsied and CD was diagnosed on the basis of “permanent-gluten sensitive 

enteropathy”, and histology was classified with the modified Marsh criteria. The subclinical 

group included patients with associated CD conditions such as iron deficiency but without GI 

symptoms, while silent CD patients were asymptomatic patients screened in at risk groups such 

as first-degree relatives or type 1 diabetes. EMA was positive in 77/96 (80.8%) of subclinical 

CD cases and 17/27 (63.0%) of silent CD cases. EMA was negative in patients with Marsh I 

lesions. Once again, assuming that all these patients with “permanent gluten-sensitive 

enteropathy” are truly CD patients, then EMA would miss 19% of subclinical CD patients, and 

37% of silent CD that were picked-up by biopsy. 

In what appears to be a partial duplicate publication, Tursi et al.5

 demonstrated similar results 

with AGA, and EMA in 115 patients with subclinical or silent CD. 
A-69

Patients with subclinical CD 

Tursi et al5

 Marsh I Marsh II Marsh IIIa Marsh IIIb Marsh IIIc 

Biopsy 2 10 18 25 30 

AGA pos. 0 3 (30%) 14 (77%) 21 (84%) 27 (90%) 

EMA pos 0 4 (40%) 16 (88.9%) 23 (92%) 29 (96.7%) 

Patients with silent CD 

Tursi et al5

 Marsh I Marsh II Marsh IIIa Marsh IIIb Marsh IIIc 

Biopsy 2 2 5 6 9 

AGA pos. 0 0 3 (60%) 4 (66.7%) 7 (77.8%) 

EMA pos 0 0 4 (80.0%) 5 (83.3%) 8 (88.9%) 

As before, in this group of CD patients, serology would miss patients that would be picked 

up by biopsy. 

Demir et al.6

 (Celiac 4) studied the presentation and clinical features of 104 newly diagnosed 

Turkish children. EMA and biopsy correlation was available for 72 children. Similar to what 

was described above, EMA was positive in 92% of children with Marsh III compared with 

66.6% of children with Marsh I-II. 

Kotze et al.7,8 assessed 47 symptomatic subjects with CD with intestinal biopsy, tTG and 

EMA antibodies. Forty were suspected of having CD (9 were children) and the investigations 

were performed together, while seven were biopsy-diagnosed CD who were already on a GFD. 

Both EMA and tTG antibodies were negative in these seven patients. The findings of the 40 

suspected CD patients are presented in the following table. 

Kotze et al7,8 

Normal biopsy 7 8 2 1 (child) 

Partial VA 1 1 

Total VA 1 3 7 8 (child) 8 

Mean tTG titer 8.14 11.87 41.5 181.7 356.3 307.4 432.8 

Mean EMA titer neg 1/2.5 1/5 1/10 1/20 1/40 1/80 

Notes: Titers of EMA and tTg antibodies of 1/2.5 and 20 U, respectively 

VA= VA 
A-70

The authors used an older histology grading system, and did not systematically report on the 

overall number of “normal biopsies” with raised IELs. They also did not report on the number of 

subjects with the Marsh II hyperplastic lesion, nor did they distinguish between Marsh IIIa and 

IIIb (lumped as “partial VA”). Nonetheless, the authors report that in the eight subjects with 

positive-EMA antibodies (>1/2.5) yet negative for tTG antibodies (<20), the mucosa showed 

normal villous structure but raised levels of IELs. These eight subjects responded to a GFD and 

were considered to have CD. The correlation between the two serological tests was high 

(Pearson’s Chi square [the large R is ‘accountable’ variance]; r=0.797). However, the same 

finding as in the previous studies is repeated again. CD occurred in eight patients with negative 

tTG antibodies, and the titres of both EMA and tTG antibodies correlated with histologic grade, 

once again suggesting that serology alone would miss CD patients who would be picked-up by 

biopsy. This is a very recent study and it would shed a great deal of light on the false-positive 

and negative-rate of biopsy if the authors would publish a follow-up study on: (1) the status of 

the three subjects who were positive for EMA and tTG antibodies yet had “normal” biopsies 

(IEL status not reported); (2) the seven subjects who were negative for all tests; and (3) the 

histologic and clinical response to GFD in those who were diagnosed with CD. 

Hoffenberg et al.9

 studied a group of children at risk of CD who were part of a large 

prospective study of the genetic and environmental factors associated with autoimmune diseases. 

For the CD portion, newborns were screened for the presence of HLA DR3/3, DR3/4, or DR3/x 

as markers for DQ2. In another group, at risk children with type I diabetes, first-degree relatives 

of type 1 diabetics, and first-degree relatives of CD patients, were studied. Thirty anti-tTG 

positive subjects among these screened patients were enrolled in the study (14 diabetics, 11 firstdegree relatives, and five HLA DR3). All 30 children underwent Marsh biopsy grading. No 

relationship was found between Marsh grade and the genetic risk factor leading to screening. A 

significant correlation was found between Marsh grade and anti-tTG (r=0.57, p<0.01). The 

calculated mean anti-tTG titers are presented in parentheses in the table below. 

Biopsy results of 30 tTG-positive children 

Hoffenberg et al9 Marsh 0 Marsh I Marsh II Marsh III 

Biopsy 5 (16.7%) 4 (13.3%) 2 (6.7%) 19 (63%) 

Mean tTG level UA/mL < 0.6 < 0.6 < 0.6 > 0.6 (0.70) 

Unlike the other studies presented in this series, this study selected patients at risk of CD who 

were anti-tTG positive. Unfortunately, this makes direct comparisons difficult, but in essence 

this study supports the notion of a greater sensitivity of tTG in high-grade histologic lesions 

through the finding that high-grade lesions are associated with higher anti-tTG titres. 

In a small case control study assessing the diagnostic value of EMA, Sategna-Guidetti,10 also 

found that in patients with documented CD, EMA positivity correlated with the severity of the 

histologic grade. In this study, EMA was falsely negative in 50% of CD patients without VA. 
A-71

Other Histological Features 

Several other histological features have been studied in an attempt to improve the accuracy of 

biopsy in the diagnosis of CD. Some of these features include: assessment of small bowel 

mucosal mast cells,11-14 mucosal fat,15 and endocrine cell hyperplasia.16 Discussion of these 

features is beyond the scope of this review. 

References 

 1. Fasano A, Berti I, Gerarduzzi T, Not T, Colletti RB, Drago S, et al. Prevalence of celiac 

disease in at-risk and not-at-risk groups in the United States: a large multicenter study. 

Archives of Internal Medicine 2003;163(3):286-92. 

 2. Rostami K, Kerckhaert J, Tiemessen R, von Blomberg BM, Meijer JW, Mulder CJ. 

Sensitivity of antiendomysium and antigliadin antibodies in untreated celiac disease: 

disappointing in clinical practice. American Journal of Gastroenterology 1999;94(4):888-

94. 

 3. Tursi A, Brandimarte G, Giorgetti GM. Prevalence of antitissue transglutaminase 

antibodies in different degrees of intestinal damage in celiac disease. Journal of Clinical 

Gastroenterology 2003;36(3):219-21. 

 4. Tursi A, Brandimarte G, Giorgetti GM. Sorbitol H2-breath test versus anti-endomysium 

antibodies for the diagnosis of subclinical/silent coeliac disease. Scand J Gastroenterol

2001;36(11):1170-2. 

 5. Tursi A, Brandimarte G, Giorgetti G, Gigliobianco A, Lombardi D, Gasbarrini G. Low 

prevalence of antigliadin and anti-endomysium antibodies in subclinical/silent celiac 

disease. American Journal of Gastroenterology 2001;96(5):1507-10. 

 6. Demir H, Yuce A, Kocak N, Ozen H, Gurakan F. Celiac disease in Turkish children: 

presentation of 104 cases. Pediatrics International - Official Journal of the Japan Pediatric 

Society 2000;42(5):483-7. 

 7. Kvedar JC, Pion IA, Bilodeau EB, Baden HP, Greco MA. Detection of substrates of 

keratinocyte transglutaminase in vitro and in vivo using a monoclonal antibody to 

dansylcadaverine. Biochemistry 1992;31(1):49-56. 

 8. Kotze Lorete Maria da Silva, Utiyama Shirley Ramos da Rosa, Nisihara RM, de C, V, 

Ioshii SO. IgA class anti-endomysial and anti-tissue transglutaminase antibodies in relation 

to duodenal mucosa changes in coeliac disease. Pathology 2003;35(1):56-60. 

 9. Hoffenberg EJ, Bao F, Eisenbarth GS, Uhlhorn C, Haas JE, Sokol RJ, et al. 

Transglutaminase antibodies in children with a genetic risk for celiac disease. Journal of 

Pediatrics 2000;137(3):356-60. 
A-72

 10. Sategna-Guidetti C, Bruno M, Pulitano R, Ferfoglia G. Disease specificity of IgA class 

anti-endomysium antibodies (IgA-EmA) in adult coeliac disease. Eur J Gastroenterol 

Hepatol 1991;3(3):251-4. 

 11. Kosnai I, Kuitunen P, Savilahti E, Sipponen P. Mast cells and eosinophils in the jejunal 

mucosa of patients with intestinal cow's milk allergy and celiac disease of childhood. 

Journal of Pediatric Gastroenterology and Nutrition 1984;3(3):368-72. 

 12. Strobel S, Busuttil A, Ferguson A. Human intestinal mucosal mast cells: expanded 

population in untreated coeliac disease. Gut 1983;24(3):222-7. 

 13. Suranyi Y, Freier S, Faber J, Dollberg L. Intestinal mast cells in different stages of celiac 

disease. Israel Journal of Medical Sciences 1986;22(5):370-5. 

 14. Dollberg L, Gurevitz M, Freier S. Gastrointestinal mast cells in health, and in coeliac 

disease and other conditions. Arch Dis Child 1980;55(9):702-5. 

 15. Variend S, Placzek M, Raafat F, Walker-Smith JA. Small intestinal mucosal fat in 

childhood enteropathies. Journal of Clinical Pathology 1984;37(4):373-7. 

 16. Johnston CF, Bell PM, Collins BJ, Shaw C, Love AH, Buchanan KD. Reassessment of 

enteric endocrine cell hyperplasia in celiac disease. Hepato-Gastroenterology

1988;35(6):285-8. 
A-73

Appendix I. Evidence Tables 

List of abbreviations used in the evidence tables 

Ab=antibody 

AGA=anti-gliadin antibodies 

ARA=antireticulin antibodies 

Bx=biopsy 

CD=celiac disease 

CI=confidence interval 

CO=control 

Dx=diagnosis 

EGD=esophagogastroduodenoscopy 

EIA=enzyme immunoassay 

EMA=anti-endomysium antibodies 

F=female 

GC=gluten challenge 

GCD=gluten-containing diet 

GERD=gastroesophageal reflux disease 

GFD=gluten-free diet 

GI=gastrointestinal 

GP=guinea pig 

Hb-hemoglobin 

HLA=human leukocyte antigens 

HU=human umbilical cord 

HUVEC= human umbilical vein endothelial cells 

JAB=human jejunal antibodies 

IBS=irritable bowel syndrome 

IDA=iron deficiency anemia 

IDDM=insulin-dependent diabetes mellitus 

IF=immunofluorescence 

M=male 

ME=monkey esophagus 

mos=months 

n=number of patients 

n/a=not applicable 

NHL=non-Hodgkin’s lymphoma 

n/r=not reported 

OR=odds ratio 

pt=patient 

RR=relative risk 

SD=standard deviation 

TGA=anti-thyroglobulin 

tTG=anti-tissue transglutaminase 

UTCD=untreated celiac disease 

VA=villous atrophy 

y=year 
A-74

Celiac 1: Sensitivity and Specificity of Tests for CD 

Serology Evidence Table 1: Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d Sens Spe

Altuntas, 

1998 

Turkey 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: 

• endoscopic biopsy 

First test: 

• serology test 

Controls biopsied: 

• yes 

Biopsy criteria: 

• subtotal or total VA, crypt 

hyperplasia, increased IEL 

Checked IgA def. 

• n/r 

Studied tests 

• IgA-AGA • IgG-AGA 

Methodology: • ELISA 

Cut-off: 

• levels between 25 and 50 

RU/mL were accepted as weakly positive and levels >50 RU/mL as strongly positive 

Celiac Group 1 • 26 shortstatured 

children with probable CD on biopsy 

• mean age: 

n/r 

• % F: n/r 

Group 1: • 21 shortstatured 

children without CD on biopsy; 

• median age: 

n/r 

• % F: n/r 

celiac 1 vs control 1 

IgA AGA 

celiac 1 vs control 1 

IgG AGA 

6 26 

20 0 

2 21 

19 

0 

23 

100 

90 0 
A-75

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d S

Artan, 

1998, 

Turkey 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: 

• biopsy 

First test: 

• simultaneous 

Controls biopsied: 

• yes 

Biopsy criteria: 

• ESPGAN 

Checked IgA def. 

• n/r 

Studied tests 

IgA-AGA; IgG-AGA; IgA and IgG; IgA or IgG 

Methodology: • ELISA Cut-off: 

• >25 arbitrary units 

(did not adjust for age) 

Celiac Group 1 • 24 children with 

CD by ESPGAN, out of 63 suspected CD pts 

• age: n/r 

• % F: n/r 

Group 1: • 39 of 63 with 

normal intestinal villous structure. 

• Age: n/r • % F: n/r 

celiac 1 vs control 1-IgA-AGA celiac 1 vs control 1-IgG-AGA IgA AND IgG IgA OR IgG 

1420 12 20 

10

4 

12 

4 

19 

16; 13; 25; 

20; 

23 26 14 
A-76

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d Sens S

Ascher, 

1996 

Sweden 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: 

• n/r 

First test: 

• biopsy and serum tests 

obtained simultaneously 

Controls biopsied: 

• yes 

Biopsy criteria: 

• ESPGAN 

Checked IgA def. 

• Yes 

Studied tests 

• EIA IgA; EIA IgG; DIG-ELISA 

IgA; DIG-ELISA IgG; ARA; Human JAB; Rat JAB; EMA 

Methodology: 

for EIA IgA and IgG: ELISA; for ARA: IF; for EMA, JAB: immunohistochemical method Cut-off: 

EIA IgA and IgG: 35 AU (arbitrary units) for children <5 y; and 20 AU for children >5 y; DIG-ELISA: IgA values >13 mm and IgG values >16 mm were considered positive in children <5 y; IgA values <11 mm and IgG values >14 mm - in children >5 y 

Celiac Group 1 • 55 pts with biopsy 

proven CD 

• mean age: n/r; <5 

y n=22; >5 y n=33 

• % female: n/r Celiac Group 2 

• 36 out of initial 55 

pts who were treated with GFD of 1 y; 

• mean age: n/r; <5 

y n=21; >5 y n=15 

• % female: n/r Celiac Group 3 

• 21 pts on a 

gluten-challenge diet of 3-6 mos 

• mean age: n/r; 

<5 y n=18; >5 y n=3; 

• % female: n/r 

NB: group 2: biopsy proven CD on a GFD of > 1 y; group 3: biopsy proven CD on a gluten challenge of 3-6 mos duration 

Group 1: 

• 65 disease 

controls with biopsy proven normal intestinal mucosa; 

• mean age: n/r; 

<5 y n=18; >5 

y n=47 

• % female: n/r 

group 1 vs control, EIA IgA group 1 vs control, EIA IgG group 1 vs control, DIG-ELISA IgA group 1 vs control, DIS-ELISA IgA group 1 vs control ARAgroup 1 vs control, Human JAB group 1 vs control, RAT JAB group 1 vs control, EMA group 3 vs control, EIA IgA group 3 vs control, EIA IgG group 3 vs control, DIG-ELISA IgA group 3 vs control, DIS-ELISA IgA group 3 vs control, ARA group 3 vs control, Human JAB group 3 vs control, RAT JAB group 3 vs control, EMA

50 53 50 48 48 55 55 54 20 19 17 15 18 21 18 19 

5 2 5 7 6 0 0 1 1 2 4 5 3 0 3 2 

1 

20 2 9 18 18 11 0 1 20 2 9 18 18 11 0 

64 45 63 56 47 47 54 65 64 45 63 56 47 47 54 65 

90.9 96.4 90.9 87.3 88.9 

100 100 

98.2 95.5 90.5 80.9 

75 

85.7 

100 

85.7 90.5 
A-77

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d Sens Spec 

Ascher, 

1990 

Sweden 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: 

• Watson capsule 

First test: 

• biopsy and serum 

tests obtained simultaneously 

Controls biopsied: 

• yes 

Biopsy criteria: ESPGAN Checked IgA def. Yes Studied tests 

• Pharmacia Gluten 

IgA-AGA measured by enzyme immunoassay (PG IgA-EIA) 

Methodology: • ELISA 

Cut-off: 

• 35 AU (arbitrary 

units) 

Celiac Group 1 • 36 pts with CD out of 

130 consecutive group of children who had a small intestinal biopsy due to symptoms suggestive of CD; out of 36 pts with CD, 28 have been verified according to ESPGAN criteria; 

• mean age: n/r • % female: n/r Celiac Group 2 • children with CD 

according to ESPGAN's criteria, differing with regard to gluten content of diet: first biopsy on a gluten-containing diet (n=29); at the second biopsy after 1 y on GFD (n=45); at the third biopsy after gluten-challenge (n=45); 

• mean age: n/r • % F: n/r Celiac Group 3 • children with an initial 

abnormal mucosa that normalized on a GFD but did not relapse after gluten challenge during 3-31 mos 

• mean age: n/r • % F: n/r 

Group 1: 

• 92 children 

taken from consecutive group of 130 children who 

did not have CD; 12 had other food intolerance, 1 had cystic fibrosis and 79 had no intestinal disorder 

group 1 vs control PG IgA-EIA 35 1 7 85 97 92 
A-78

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d Sens Spe

Bahia, 

2001 

Brazil 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• suspected CD 

Reference test: 

• Carey capsule 

First test: 

• n/r 

Controls biopsied: 

• yes 

Biopsy criteria: 

• severe VA 

Checked IgA def. 

• n/r 

Studied tests 

• IgA and IgG-AGA 

Methodology: • ELISA 

Cut-off: 

• mean+2 SD for a 

group of 20 normal children: 0.022 for IgA (mean=0.0065, SD=0.0076); and 0.103 for IgG (mean=0.0393, SD=0.032) 

Celiac Group 1 • 22 pts with CD • age (mos): 

mean/SD: 30.6+/-28.8; 

• % F: 54.5 • median 

w/range: 19.3 (6.0-135.6) 

• % female: 54.5 Celiac Group 2• 61 pts with 

other enteropathies (OE); 

• age (mos): 

mean/SD: 43.3+-38.1; 

• median 

w/range: 27.9 (4.8-156.5); 

• % F: 59 

Group 1: • 46 controls with 

biopsy-proven non-CD enteropathies (CO) 

• age (mos): 

mean/SD: 96.9+/-48.5; median w/range: 92.6 (12.2-170.8); 

• % F: 54.5 

IgA group 1 vs CO IgA group 1 vs OE+CO IgG group 1 vs CO IgG group 1 vs OE+CO 

21 21 

20 20 

1 1 2 2 

2 9 1 12 

46 98 45 95 

95.5 95.5 90.9 90.9 

95.91.97.88.
A-79

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d Sens Sp

Bardela, 

2001 

Italy 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• suspected CD 

Reference test: 

• endoscopic biospy 

First test: 

• n/r 

Controls biopsied: 

• yes 

Biopsy criteria: 

• Marsh, no grade 

reported 

Checked IgA def. 

• Yes and excluded 

Studied tests 

• IgA-AGA; IgAEMA; IgA-tTGA 

Methodology: • ELISA for AGA; 

ELISA for tTGA GP liver; IF for EMA ME 

Cut-off: 

• AGA: 12 AU/mL; 

tTGA: >10 AU/mL; EMA: antibody titre > 1:10 

Celiac Group 1 • 40 untreated 

biopsy-proven CD pts 

• age (y): mean 

38, range 16-77 

• % F: 72.5 Celiac Group 2 • 195 treated 

CD pts; biopsy proven on GFD 

• age (y): mean 

38, range 16-79 

• % F: 70.2 

Group 1: 

• 110 biopsy 

proven non-CD disease controls (CO): inflammatory bowel disease (n=22); IBS (n=29); peptic ulcer (n=7); diverticular disease (n=6); pancreatitis (n=5); non- ulcer dyspepsia(n=14); anemia not due to malabsorption (n=7); reflux esophagitis (n=3); atrophic gastritis (n=2); acute appendicitis (n=1) 

• age (y): mean 41, 

range 14-80 

• % F: 75.7; 

AGA group 1 vs CO EMA group 1 vs CO tTGA group 1 vs CO

384040 

2 0 0 

12

3 2 

98 

107108 

95 

100 100 

8

97

98
A-80

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d Sens 

Berger, 

1996 

Switzerland 

Publication type: • journal Study design: • case-control Ethnicity:

• n/a 

Population Type: 

• suspected CD 

Reference test: 

• endoscopic biopsy 

First test: 

• n/r 

Controls biopsied: 

• yes 

Biopsy criteria: 

• ESPGAN revised with complete VA 

Checked IgA def. 

• n/r 

Studied tests 

• 5 different AGA assays: Eurospital; 

Labodia; Pharmacia; FIST-IF; Granditsch; IgA EMA 

Methodology: • for AGA - ELISA; for EMA - IF 

Cut-off: 

For IgG Eurospital: index30-50; in 

Pharmacia units: 30-50 AU; Labodia: 30 U/mL; in Pharmacia units-18; Pharmacia: 20-100 AU; FIST: titer 1:20; in Pharmacia units-13 AU; Granditsch: 0.350 OD; in Pharmacia units: 70 AU; for IgA Eurospital: index 8-20; in Pharmacia units: 53-132 AU; Labodia: 15 U/mL; in Pharmacia units-28; Pharmacia: 20-35 AU; FIST: titer 1:20; in Pharmacia units-34 AU; Granditsch: 0.250 OD; in Pharmacia units: 38 AU 

Celiac Group 1 • 67 

biopsy proven CD pts 

• age: n/r • % F: n/r 

Group 1 (CO): 

• 54 biopsy 

proven nonCD pts: transient GI problems (n=39), ulcerative colitis (n=2), Crohn's disease (n=8), duodenal ulcer (n=3), short stature (n=2) 

• age: n/r • % F: n/r 

CD vs CO 

Eurospital IgG FIST IgG Granditsch IgG Labodia IgG Pharmacia IgG Eurospital IgA FIST IgA Granditsch IgA Labodia IgA Pharmacia IgA;

55565561464144535851 

121112

6 

21262314

9 

16 

2753464222

3 

49233518 

27

1 8 

123251

5 

311936 

82 84 82 91 69 61 66 79 87 76 
A-81

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d Sens Spe

Biagi, 

2001 

Italy 

Publication type: • journal Study design: • case-control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: 

• Carey capsule 

First test: 

• n/r 

Controls biopsied: 

• yes 

Biopsy criteria: 

• partial VA or greater 

Checked IgA def. 

• Only in EMA (neg) 

pts in CD group 

Studied tests 

• IgA-tTG • IgA-EMA 

Methodology: • TTG-GP; EMA -ME 

Cut-off: 

• on the basis of ROC 

analysis performed on the preliminary results (group of 30 controls) results >0.65 OD (optical density) were considered positive; <0.35 OD - negative and 0.35-0.65 OD - borderline 

Celiac Group 1 • 56 pts with 

biopsyproven CD 

• age (y): 

mean/SD: 39.2+-19.2; range 4-79 

• % F: 76 

Group 1: 

• 52 disease 

controls (biopsyproven non-SD enteropathies) with irritable bowel disease (n=29); Crohn’s disease (n=9); gastric lymphoma (n=7); Whipple disease (n=3); giardiasis (n=2); systemic mastocytosis (n=1); IgEmediated food sensitivity 

• mean age (y): 

40.4+-19.9; range 14-79; 

• % F: 

IgA TTG group 1 vs CO when considering borderline results as positive IgA-tTG group 1 vs CO 

when considering borderline results as negative IgA EMA group 1 vs CO 

55 49 53 

1 7 3 

8 1 0 

44 51 52 

98.2 87.5 94.6 

84.98.

100 
A-82

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d Sens S

Bode, 

1993 

Denmark 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: 

• n/r 

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: 

• typical biopsy and 

response to a GFD (likely ESPGAN) 

Checked IgA def. 

• yes 

Studied tests 

• serum IgG-AGA • serum IgA-AGA 

Methodology: 

• DIG-ELISA - 

diffusion in gel ELISA 

Cut-off: 

• 1) old limits: 

positive test for IgA AGA was defined as >10.5 mm and/or IgG level >14 mm; 2) new limits for children: for IgA >10 mm and for IgG >13 mm 

Celiac Group 1 

• 14 of 233 

consecutive children with untreated CD

• median age for 

the 233: 2.75; range 0.33-15.5)

• 117 males; 74 

females

Celiac Group 2a • T-CD - group 

2a) 47 children with CD on GFD 

• age (y): median 

11.83, range 1-17.92 

• % F: 61.7 Celiac Group 2b• 14 children with 

known CD on gluten challenge 

Group 1: 

• 177 children with 

non-CD diseases: postenteritis diarrhea (n=43), short stature (n=25), diarrhea (n=25), failure to 

thrive (n=22), food allergy (n=11), dissaccharide intolerance (n=8), dietary problems (n=8), giardiasis (n=4), ulcerative colitis (n=3), recurrent abdominal pain (3), constipation (n=2), recurrent infections (n=2), acute gastroenteritis (n=1), Crohn’s disease (n=1), other GI diseases (n=4), other nonGI diseases (n=15) 

Group 2: • 8 children not 

CD/GFD and gluten challenge 

• age (y): median 

2.5, range 1.17-7.5 

• % F: 37.5 

group 1 vs control 1, serum AGA-IgA; in brackets data according to new cut off group 1 vs control 1, serum AGA-IgG; in brackets data according to new cut off limits group 1 vs control 1, serum AGA-IgA/IgG; in brackets data according to new cut-off limits 

64 (79) 71 (93) 

86 (100) 

99 99 99 
A-83

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d Sens Sp

Bode, 

1994 

Denmark 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: 

• n/r 

First test: 

• n/r 

Controls biopsied: 

• yes 

Biopsy criteria: 

• Crypt hyperplasia, 

VA and increase inflammatory cells 

Checked IgA def. 

• n/r 

Studied tests 

• serum IgG-AGA • serum IgA-AGA 

Methodology: 

• DIG-ELISA - diffusion 

in gel ELISA 

Cut-off: 

• positive test for IgA 

AGA was >10.5 mm; for IgG - >14 mm; borderline levels for IgA was between 9.5 mm and 10.5 mm; and for IgG - between 13 mm and 14 mm 

Celiac Group 1 

• 100 consecutive 

adult pts admitted for a small intestinal biopsy on suspicion of CD 

• age (y): median 

51, range 17-81 

• % F: 64; 13 CD 

pts

Celiac Group 2 

• 118 adult pts 

with increased or borderline (gliadin antibodies) AGA 

• age (y): median 

48, range 19-95 

• % F: 72; • 55 children pts 

with increased or borderline (gliadin antibodies) AGA 

• age (y): median 

4, range 7 mos17 

• % F: 56 

Group 1: 

• 87 out of 100 

suspected of CD who did not have CD by biopsy 

group 1 IgA-AGA group 1 IgG-AGA group 1 IgA/IgG-AGA 

 46 

62 77 

999
A-84

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d Se

Bonamico, 

2001 

Italy 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: 

• biopsy 

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: 

• ESPGAN (severe VA and 

crypt hyperplasia) 

Checked IgA def. 

• Yes 

Studied tests 

• tTG-HR (RIA) • tTG-GP (ELISA) • IF-EMA 

Methodology: 

• tTG-HR • tTG-GP • EMA-ME IF 

Cut-off: 

• RIA anti-tTG Ab >0.05 index 

as selected on ROC plot analysis; ELISA anti-tTG Ab >7 AU; IF-EMA - n/r 

(appearance of fluorescence) 

Celiac Group 1 

• 62 pts; 

untreated with biopsy-proven celiac CD

• median age 7, 

age range 1-23

• % F: n/r

Celiac Group 2 

• 78 pts; GFD 

treated, at least 6 mos 

• median age, 

age range 

• % F: n/r 

Celiac Group 3

• 14 pts; on 

glutenchallenge at least 3 mos 

• median age, 

age range 

• % F: n/r 

Group 1: 

• 56 disease 

controls; chronic diarrhea, short stature, recurrent abdominal pain; age and sexmatched controls 

• median 

age, age range 

• % F: n/r 

RIA group 1 vs control RIA group 2 vs control RIA group 3 vs control ELISA group 1 vs control ELISA group 2 vs control ELISA group 3 vs control IF-EMA group 1 vs control IF-EMA group 2 vs control IF-EMA group 3 vs control 

62 34 14 56 

7 

11 59 

9 

13 

0 

44

0 6 

71

3 3 

69

1 

0 0 0 0 0 0 1 1 1 

56 56 14 56 56 56 

55 55 55 

1

43

1

90

9

78951192
A-85

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d Sens 

Bottaro, 

1997 

Italy 

Publication type: • journal Study design: • case-control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: 

• n/r 

First test: 

• n/r 

Controls biopsied: 

• yes 

Biopsy criteria: 

• ESPGAN 

Checked IgA def. 

• Yes 

Studied tests serum AGA-IgG serum AGA-IgA serum EMA-IgA serum ARA-IgA Methodology: 

• for AGA ELISA; for 

AGA-IgA IF; for EMA-IgA IF using ME or HU 

Cut-off: 

• AGA: for IgA 10% 

and for IgG 25%, resulting the mean+-SD of values obtained from children proven normal 

Celiac Group 1 

• 50 children with 

biopsy proven CD 

• age: median 

2.5 y, range 7 mos - 15 y 

• % F: 68 

Group 1: 

• 25 control group 

of children (CO) 

• age: median 3.0 

y, range 9 mos - 14 y 

• % F: 52 

group 1 vs control 1, serum AGA IgA group 1 vs control 1, serum AGA IgG group 1 vs control 1, serum EMA-IgA, HUC group 1 vs control 1, serum EMA-IgA, ME group 1 vs control 1, serum ARA IgA 

46 50 47 48 

4 

0 3 2 

8 

16 

0 1 

17 

9 

25 24 

92 

100 

94 96 
A-86

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b 

Carroccio

2002 

Italy 

Publication type: • journal Study design: • case-control Ethnicity:

• n/a 

Population Type: 

• suspected CD 

Reference test: children: Crosby capsule; adults: endoscopic biopsy First test: 

• n/r 

Controls biopsied: 

• yes 

Biopsy criteria: 

Marsh; CD was diagnosed as enlarged crypts and/or VA - with normalization on GFD 

Checked IgA def. 

• Yes 

Studied tests Serum AGA-IgG; Serum AGA-IgA; Serum EMA; Culture EMA; Culture EMA+gliadin Methodology: 

ELISA for AGA; indirect IF on ME for serum EMA; biopsy specimen incubation in a culture medium with gliadin peptide and further IF on ME Cut-off: 

AGA-results expressed as a % of reference serum: 20% was upper normal limit for IgG and 10% for IgA antibodies; EMA-semiquantified as follows: 0=not detectable; 1=positive at dilutions between 1/5 and 1/20; 2=positive between 1/40 and 1/80; 3=positive at 1/100; 4=positive at 1/200; 5=positive at >1/200; EMA in culture-same as serum EMA and for IgG 25%, resulting the mean+-SD of values obtained from children proven normal 

Celiac Group 1 

• 91 pts with 

biopsy proven CD 

• age (y): 

median 2; range 7 mos - 84 y 

• % F: 56 Celiac Group 2 

• 21 treated CD 

pts on a GFD with normal intestinal architecture 

• age (y): 

median 5, range 3-51 

• % F: 62 

Group 1: 

• 100 

subjects with a normal intestinal morphology or diseases other than CD (biopsy proven) 

• age (y): 

median 21 y, range 9 mos-76 y 

• % F: 56 

Group 2: 

• 22 disease 

controls (biopsyproven nonCD) with 

GERD-like symptoms 

• age (y): 

median 33, range 4-60 

• % F: 54.5 

group 1 vs control 1, serum AGA IgG group 1 vs control 1, serum AGA IgA group 1 vs control 1, serum EMA group 1 vs control 1, culture EMA group 1 vs control 1, culture EMA+gliadin group 2 vs control 2, culture EMA+gliadin 

69 61 80 82 87 10 

22 30 11 

9 4 

11 

25 10 

1 0 0 0 

799

11

2
A-87

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table 

Author, 

Year, 

Location Study Design 

Study 

Population Control Population Comparison a c b d Sens 

Carroccio 

1993 

Italy 

Publication type: • journal Study design: • case-control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: 

• Biopsy Watson 

capsule 

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: 

• Biopsies confirmed 

at diagnosis, on GFD, and rechallenge (severity grade-not reported) 

Checked IgA def. 

• n/r 

Studied tests IgA-AGA IgG-AGA IgA-EMA Methodology: 

• ELISA; IF likely ME Cut-off: 

• AGA mean +2 SD 

Celiac Group 1 

• infants with CD 

on gluten diet; biopsy proven 

• median age 

2.6; range 0.8-10 

• 21 males; 22 

females 

Group 1: 

• 60 infants disease 

controls; biopsy proven non-CD 

• median age 1.2; 

range 0.9-9 

• 32 males; 28 females 

celiac 1 vs control 31

40 45 

14 

5 0 

5 

32 

2 

55 28 58 

68 

88.9 

100 
A-88

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d 

Carroccio 

2002 

Italy 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: gastroduodenoscopy and biopsy 

First test: 

• simultaneously 

Controls biopsied: 

• yes 

Biopsy criteria: 

• Ferguson and Murray; partial or total VA 

Checked IgA def. yes (none of CD pts showed IgA deficiency 

Studied tests 

EMA-IgA; anti-GP-tTG IgA (GP used); anti-h-tTG IgA (HR) Methodology: 

for EMA - IF ME; for tTG–ELISA Cut-off: 

anti-h-tTG IgA-results were expressed as a % of the positive control serum. Normal values were taken as <7%, which represented a value >2 SD above the mean of 850 healthy individuals; anti-gptTG IgA-values >95th percentile of a control group were considered positive; 

Celiac Group 1 

• 24 

consecutive pts with untreated biopsy proven CD 

• age (y): 

median 30, range 18-80 

• % F: 58 

Group 1: 

• 183 

consecutive pts with biopsy proven non-CD disorders: IBS (n=70), esophagatis (n=45), peptic ulcers (n=41), Crohn's disease (n=15), Food intolerance (10), chronic liver disease (n=6), gastric cancer (n=2), right colon cancer (n=2), collagenous colitis (n=1), intestinal bacterial overgrowth syndrome (n=1), psoriasis (n=1) 

• age (y): median 

46, range 17-84 

• % F: 51 

CD vs CO: EMA CD vs CO: antiGP-tTG IgA CD vs CO: antih-tTG IgA 

24 24 24 

0 0 0 

0 

15 

6 

183 168 177 
A-89

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d Sens 

Cataldo, 

2000 

Italy 

Publication type: • journal Study design: • case-control Ethnicity:

• n/a 

Population Type: 

• IgA deficient adults 

and children 

Reference test: 

• n/r 

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: Original & revised criteria? Checked IgA def. 

• Yes 

Studied tests IgG-EMA IgA-EMA IgG-tTG IgA-tTG IgG-AGA IgA-AGA Methodology: 

• IgG-EMA, ME; IgGtTG, human serum 

albumin 

Cut-off: 

• n/a 

Celiac Group 1 

• 20 untreated 

CD (biopsy proven) with IgAD 

• age/gender: n/a Celiac Group 2 

• 11 untreated 

CD without IgAD 

• age/gender: n/a 

Group 1: 

• 10 healthy IgAD 

controls on GD (healthy controls (not biopsied - not used) 

• age: n/a • gender: adults 

and children 

Group 2 

•25 healthy 

controls on a GD, first degree relatives of CD pts, adult or paediatric pts with GI diseases i.e. mild protein intolerance, pstenteritis syndrome, Crohn’s disease, ulcerative colitis, or giardiasis 

•age/gender: n/a 

Celiac 1 vs control 1 20 

0 

20 

0 

20 

0 

0 

20 

0 

20 

0 

20 

0 0 2 0 0 0 

10 10 

8 

10 10 10 

100 

0 

100 

0 

100 

0 
A-90

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d Sens 

Chan, 

2001 

Canada 

Publication type: • journal Study design: • case-control Ethnicity:

• n/a 

Population Type: 

• suspected CD 

Reference test: 

• Carey capsule or 4 

to 6 duodenal biopsies at endoscopy 

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: Villous atrophy, crypt hyperplasia, increase lymphocytes Checked IgA def. 

• Yes 

Studied tests IgA-EMA; IgA-tTG Methodology: 

• EMA-ME; IgA tTG 

ELISA GP liver 

Cut-off: 

• EMA:≥1:10; tTG: 

>20 

Celiac Group 1 

• 9 untreated CD 

(biopsy + from a group of 77 children 

• age: 2 mos -16 

y 

Celiac Group 2 

• 12 suspected 

CD with DM from a group of 16 DMs 

• age: 3-18Y 

Celiac Group 3 

• 2 IgAD pts, 

one biopsy positive, (excluded in the analysis) 

Group 1: 

• 62 disease 

controls with negative biopsy with abdominal pain, diarrhea, failure to thrive/short stature, family history of CD, Crohn's disease, vomiting, abdominal distension, ulcerative colitis, autoimmune thyroiditis/short stature, trisomy, (from a total of 77) 

• age 2 mos to 16 

y 

Group 2 

•2 DM from a 

group of 16 DMs 

celiac 1 vs control 1 8 

8 

1 1 

2 4 

64 62 

89 89 
A-91

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table 

Author, 

Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d Sens 

Chartrand

1997 

Canada 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• suspected CD 

Reference test: 

• Biopsy - 

endoscopic 

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: ESPGAN - with flat mucosal biopsy Checked IgA def. 

• yes - 2 of false 

negatives were IgA def 

Studied tests IgA–AGA IgG-AGA IgG or IgA Methodology: 

• ELISA 

Cut-off: 

• 0.25 for IgA, 0.3 

for IgG (optical density) 

Celiac Group 1 

• 30 of 176 

children suspected of CD 

• mean age: 5.2; 

range 0.5-18; 

• % F: n/r 

Group 1: 

•146 with 

suspected CD - biopsy excluded 

•mean age: n/r 

•% F: n/r 

Celiac 1 vs Control 24 

25 28 

6 5 2 

12 31 42 

134 115 104 

80 83 93 
A-92

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d Sens 

Chirdo 

1999 

Argentina 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• suspected CD 

Reference test: 

• n/r 

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: Total or subtotal VA Checked IgA def. 

• n/a 

Studied tests IgG commercial gliadin; IgG ethanolic extract; IgG ωgliadins ; IgA commercial gliadin; IgA ethanolic extract; IgA IgG ω-Gliadins Methodology: 

• ELISA 

Cut-off: 

• n/r 

Celiac Group 1 

• 28 pts, biopsy 

proven untreated 

• mean age: 7 y; 

range 13 mos14 y 

• % F: 15 (54%) 

Group 1: 

•31 disease 

controls; chronic diarrhea, short stature, abdominal distension 

•mean age: 5.4 y, 

2-12 y 

•13 F, 18 M 

Celiac 1 vs Control 24 

23 25 21 18 24 

4 5 3 7 

10 

4 

6 8 5 4 3 1 

25 23 26 27 28 30 

85.7

82.189.3

75 

64.3

85.7 
A-93

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d Sens 

Chirdo 

2000 

Argentina 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: Intestinal biopsyFirst test: 

• biopsy 

Controls biopsied: 

• only group 3 

Biopsy criteria: ESPGAN Checked IgA def. 

• Yes 

Studied tests IgA w-AGA; IgG wAGA; not a commercial kit (not used) IgA-EMA (used) Methodology: 

• IgA-EMA-ME IF 

Cut-off: 

• cut-off value for 

each antigen by using the same set of samples. Five control samples used as reference to normalize the day-to-day variation 

Celiac Group 1 

• 105 untreated 

CD pts (biopsy proven) 

• mean age: 6.5 

y; range 16 mos-15 y 

• % F: n/r 

Group 1: 

• 45 healthy 

controls 

• mean age 8.5 y; 

range 3-14 y 

Group 2: 

• 36 healthy blood 

donors 

• mean age 36, 

range 22-45 y 

Group 3: 

• 46 biopsy 

negative disease control; presenting with short stature, chronic diarrhoea, parasitic infection 

• mean age 5.2 y; 

range 1.5-14 y this group used for analysis 

Group 4: 

• 27 disease 

controls with Crohn’s disease, ulcerative colitis, or Helicobacter pylori infection 

Celiac 1 vs control 3 94 

100

97 

11 

5 8 

5 9 0 

41 37 46 

89.5 95.2 92.4 
A-94

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d Sens 

Dahele 

2001 

Scotland 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• suspected CD 

Reference test: duodenal biopsyFirst test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: Included partial VA or greater Checked IgA def. 

• Yes 

Studied tests IgA AGA; IgG AGA; IgA EMA; IgA tTG Methodology: 

• IgA AGA, ELISA; 

IgG-AGA, ELISA; IgA-EMA, HU; IgAtTG ELISA GP liver 

Cut-off: 

• for IgA & IgG AGA: 

≥30 unit/mL & ≥45 

units/mL, respectively 

Celiac Group 1 

• 53 untreated 

CD pts (biopsy proven) 

• median age 51 

y; range 22-77 y 

• 39 F; 14 M 

Group 1: • 65 control pts • median age: 45 

y; range 17-90 y 

• 46 F; 19 M 

Celiac 1 vs Control 1 34 

44 40 

35; 

19 

8 

13 18 

10 14 

0 3 

55 51 65 62 

64 83 75 66 
A-95

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d Sens 

Dahele 

2001 

Scotland 

NB: update of Dahele et al., Dig Dis Sci; 2001;46:214 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• suspected CD 

Reference test: duodenal biopsyFirst test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: Included 6 with IEL, rest partial VA or greater Checked IgA def. 

• yes - 2 IgA 

deficient excluded (114/116 CD used) 

Studied tests IgA AGA; IgA AEM; IgA tTG Methodology: 

• IgA-AGA, ELISA; 

IgG-AGA, ELISA; IgA-EMA, HU; IgA tTG ELISA GP liver 

Cut-off: 

• for IgA & IgG AGA: 

≥30 unit/mL & ≥45 

units/mL, respectively 

Celiac Group 1 

• 116 untreated 

CD pts (biopsy proven) 

• median age: 

47 y; range 15-78 y 

• 74 F; 42 M 

Group 1: 

• 65 control pts 

(suspected CD pts with normal biopsy) 

• median age 45 

y; range 16-90 y 

• 45 F; 20 M 

Celiac 1 vs Control 1 69 

99 92 

45 15 22 

9 0 2 

56 65 63 

61 87 81 
A-96

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d S

Di Leo 

1999 

Italy 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: biopsyFirst test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: ESPGAN Checked IgA def. 

• yes 

Studied tests EIA-IgA; EIA-IgG; DIGELISA IgA; DIG-ELISA IgG; ARA; human JAB-IgA; Rat JAB; EMA-IgA Methodology: 

• for EIA-IgA and IgG-ELISA; 

for ARA-IF; for EMA, JABimmunohistochemical method

•Cut-off: 

EIA IgA and IgG: 35 AU (arbitrary units) for children <5 y; and 20 AU for children >5 y; DIG-ELISA: IgA values >13 mm and IgG values >16 mm were considered positive in children <5 y; IgA values <11 mm and IgG values >14 mm - in children >5 y 

Celiac Group 1 

• 45 untreated pts 

(biopsy proven untreated) 

• mean age: 6.11 

y; range 9 mos17 y 

• 32 F, 13 M 

Celiac Group 2 

• 18 GDF pts 

(celiac on GFD) 

• mean age: 13.2 

y; range 3 y 8 mos-16 y 6 mos 

• 13 F, 5 M 

Group 1: 

• 67 healthy 

controls 

• mean age: 8 

y. 9 mos; range 1 y. 4 mos-16 y. 9 mos 

• 43 F, 24 M 

group 1 vs control, EIA IgA group 1 vs control, EIA IgG group 1 vs control, DIGELISA IgA group 1 vs control, DISELISA IgA group 1 vs control, ARA group 1 vs control, Human JAB group 1 vs control, RAT JAB 

group 1 vs control, EMA group 3 vs control, EIA IgA group 3 vs control, EIA IgG group 3 vs control, DIGELISA IgA group 3 vs control, DISELISA IgA group 3 vs control, ARA group 3 vs control, Human JAB group 3 vs control, RAT JAB group 3 vs control, EMA 

50 53 50 48 48 55 55 54 20 19 17 15 18 21 18 19 

5 2 5 7 6 0 0 1 1 2 4 5 3 0 3 2 

1 

20 

2 9 

18 18 11 

0 1 

20 

2 9 

18 18 11 

0 

64 45 63 56 47 47 54 65 64 45 63 56 47 47 54 65 

999889998889
A-97

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table 

Author, 

Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d S

Dickey 

2001 

Northern 

Ireland 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: 

• n/a

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: VA Checked IgA def. 

• no 

Studied tests EMA (excluded); tTGA; EMA and/or tTGA Methodology: 

• EMA=ME; tTGa, ELISA GP liver

Cut-off: 

>30 as positive 

Celiac Group 1 

• 73 untreated 

biopsyproven CD pts 

• age 13-72 y • 45 F, 28 M 

Group 1: 58 disease controls; diarrhea, anaemia, family history of celiac and others 

Celiac 1 vs Control 1 55 

68 

185 

1 2 

5756 

79
A-98

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d S

FaithMagnusson 

1994 

Sweden 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• suspected CD 

Reference test: 

• Watson capsule or Stortz

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: ESPGAN+ Alexander grading IV, grade III to IV callenge Checked IgA def. 

• no 

Studied tests DIG - ELISA combined IgA & IgG; ELISA combined IgA & IgG Methodology: 

• ELISA; DIG-ELISA

Cut-off: 

DIG ELISA (mm) combined IgA+IgG ≥ 6 and /or; ≥10; 

≥12; ≥14; ≥16; ELISA (mm) 

for combined IgA+IgG ≥0.25; and; ≥0.8; ≥0.9; ≥1.0; ≥1.1 

Celiac Group 1 

• 116 pts; 

biopsied twice; median time on GFD pre 2nd biopsy 13 mos (10-24 mos) 

• age @ 1st 

biopsy median 13 mos, range 0.7-16.7 y, age @ 2nd biopsy 29 mos range 1.6-17.8 y 

• 73 F; 43 M 

Group 1: 

• 199 disease 

controls; poor weight gain; diarrhea; stature 

• median age 

22 mos range 0.7-16.8 y 

• 105 F; 94 M 

Celiac 1 vs Control 1 n/r n/r n/r n/r 9

9989888
A-99

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d S

Gilbert 

2000 

Canada 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• n/r 

Reference test: 

• biopsy

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: mild, moderate, severe VA Checked IgA def. 

• n/r 

Studied tests IgA-EMA; IgA-tTG Methodology: 

• EMA-HU

• tTG- HR

Cut-off: 

EMA:≥1:5; tTG: >400u 

Celiac Group 1 

• 21 CD adults • age: n/r • % F: n/r 

Group 1: 

• biopsied 

disease controls with CD excluded 

• age: n/r • % F: n/r 

Celiac 1 vs Control 21 

20 

0 1 

0 0 

42 42 

9
A-100

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d S

Gonczi 

1991 

Australia 

Publication type: • journal Study design: • cohort Ethnicity:

• n/r 

Population Type: 

• suspected celiac; single 

institution 1977-1983; mean age 3.97 (range 1 mos-16 y) 

Reference test: 

• biopsy technique not reported (likely capsule)

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: ESPGAN no details on biopsy findings Checked IgA def. 

• yes - 1 CD child 

Studied tests IgA AGA; IgG-AGA Methodology: 

• ELISA mean + 2 SD; IgA 25 

AU; IgG 46

Cut-off: 

20.2% 

Celiac Group 1 

• 20 children 

untreated biopsy-proven CD 

• age: n/r • % F: n/r 

Celiac Group 2 

• 25 untreated 

adults biopsyproven CD 

• age: n/r • % F: n/r 

Group 1: 

• 79 children 

biopsynegative controls w sx 

• age: n/r • % F: n/r 

Group 2: 

• 34 adult 

disease controls 

• age: n/r • % F: n/r 

celiac 1 vs control 1-IgA-AGA celiac 1 vs control 1-IgG – AGA celiac 1 vs control 1- IgA+IgG celiac 2 vs control 2-IgA-AGA celiac 2 vs control 2-IgG – AGA celiac 2 vs control 2- 

IgA+IgG 

19 20 20 23 25 25 

1 0 0 2 0 0 

6 6 1 4 

11 

1 

73 73 78 30 23 33 
A-101

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d S

Hallstrom 

1989 

Findland 

Publication type: • journal Study design: • case control Ethnicity:

• n/r 

Population Type: 

• n/a 

Reference test: 

• biopsy

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: Flat mucosa Checked IgA def. 

• yes 

Studied tests IgA - EMA Methodology: 

• EMA-MECut-off: 

n/r 

Celiac Group 1 

• 32 untreated 

adult CD pts 

• mean age 36 y; 

range 18-63 y) 

• % F: n/r 

Celiac Group 2 

• 18 children with 

untreated CD 

• mean age 1; 

range 2-16 

• % F: n/r 

Group 1: 

• 24 non-CD 

children by biopsy, with various abdominal symptoms 

• mean age 

7.5 y; range 1-15 

• % F: n/r 

celiac 1 vs control 1 celiac 2 vs control 1 

29 18 

3 0 

0 0 

24 24 

9
A-102

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d S

Hansson 

2000 

Sweden 

Publication type: • journal Study design: • case control Ethnicity:

• n/r 

Population Type: 

• n/a 

Reference test: 

• n/r

First test: 

• serology test 

Controls biopsied: 

• no 

Biopsy criteria: ESPGAN Checked IgA def. 

• no 

Studied tests IgA EMA; IgA serum; IgG AGA; IgA tTG; human erythrocyte tTG; tTG GP liver Methodology: 

• IgA-EMA-ME; tTG, ELISA 

(human)

Cut-off: 

n/r 

Celiac Group 1 

• 22 untreated 

pts (biopsy proven CD) 

• median age 3 

y; range 1-16 y 

• 14 F, 8 M 

Group 1: 

• 23 disease 

controls (note: no biopsy for the 5/23 control group); GI symptoms; inflammatory bowel disease; cow's milk protein intolerance; food intolerance; miscellaneous GI disorders 17 confirmed biopsy negatives 

• median age: 6 

y, range 1-16 y 

• 9 F, 13 M 

Celiac 1 vs Control 1 21 

21 18 21 22 20 

1 1 4 1 0 2 

0 6 4 1 0 1 

23 17 19 

22 23 22 

99899
A-103

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d S

Iltanen 

1999 

Finland 

Publication type: • journal Study design: • cohort Ethnicity:

• n/r 

Population Type: 

• 78 children with suspected 

CD 

Reference test: 

• biopsy

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: ESPGAN - CD confirmed at follow-up Checked IgA def. 

• n/r 

Studied tests IgA - EMA Methodology: 

• HU - IFCut-off: 

>=1:5 

Celiac Group 1 

• 23 CD children 

out of 78 evaluated for suspected CD 

• median age: 

overall group 6.5; range 0.5-15.8 

• % F: n/r 

Group 1: 

• 57 biopsy 

negative children who were suspected of CD 

• age: n/r • % F: n/r 

celiac 1 vs control 1 20 0 13 44 
A-104

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d S

Kaukinen, 

2000 

Finland 

Publication type: • journal Study design: • cohort Ethnicity:

• n/r 

Population Type: 

• pts suspected of CD with 

self reported symptoms upon gluten ingestion 

Reference test: 

• biopsy

First test: 

• simultaneous 

Controls biopsied: 

• yes 

Biopsy criteria: Villous height to crypt ration <2.0; IEL and HLA also tested Checked IgA def. 

• n/r 

Studied tests IgA EMA; IgA htTg; IgA AGA; IgG AGA Methodology: 

• IF-EMA-HU; Human 

recombinant TTG ELISA (from Enova Diagnostics web site); AGA ELISA

Cut-off: 

>1:5; >20 U; IgA-AGA >0.2 

EU/mL; IgG-AGA >10 EU/mL 

Celiac Group 1 

• 93 pts with 

self-reported suffering from GI symptoms upon gluten ingestion 

• mean age: 39 

y; range 17-73 y; 9 CD pts 

• % F: 70; 23 M 

Group 1: 

• 84 of 93 with 

negative biopsy 

• age: n/r • % F: n/r 

celiac 1 vs control 1 7 

8 

1 0 

0 0 

8484 

8
A-105

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d 

Kolho, 

1997 

Finland 

Publication type: • journal Study design: • case control Ethnicity:

• n/r 

Population Type: 

• suspected CD; or reason to 

exclude CD 

Reference test: 

• Biopsy either ingestible 

capsule technique or endoscopically

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: revised ESPGAN Checked IgA def. 

• yes – in pts with neg 

serology 

Studied tests EMA (HU); EMA (ME) Methodology: 

• EMA-ME• EMA-HU

Cut-off: 

cut off level was 20% for class IgA and IgG antibodies 

Celiac Group 1 

• 53 pts newly 

diagnosed CD (biopsy proven) 

• mean age: 

6.46 y (range 0.77-19.7 y) 

• gender: n/r 

Celiac Group 2 

• 22 pts with CD 

in remission (CD on GFD) 

• age (range 

0.77-19.7 y) 

• gender: n/r 

Celiac Group 3 

• 13 CD pts 

gluten challenge 

• age range: 

0.77-19.7 y 

• gender: n/r 

Group 1: 

• 48 pts 

children/adolescents GI complaints; disturbed growth or elevated AGA titres (normal biopsy) 

• median age 

5.39 y (age range 0.63-13.3 y) 

• % F: n/r 

Group 2: 

• 20 pts with 

cow’s milk sensitivity enteropathy n/r 

Group 3: • 23 pts with 

inflammatory bowel disease n/r 

Group 4: 

• 23 pts with 

diabetes mellitus n/r 

CD untreated and on gluten challenge (group 1) vs control groups 1-4 (combined in the study) CD gluten challenged vs control EMA 

50 50 13 13 

3 3 0 0 

0 0 0 0 

114 114 

13 13 
A-106

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d 

Kumar, 

1989 

USA, Israel 

Publication type: • journal Study design: • relevant clinical 

population and control cases 

Ethnicity:

• n/r 

Population Type: 

• suspected CD; 

asymptomatic family members 

Reference test: 

• Crosby-Kugler capsule

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: ESPGAN + Townley Checked IgA def. 

• no 

Studied tests IgA-EMA Methodology: 

• IgA EMA, IF studies; ME

Cut-off: 

n/r 

Celiac Group 1 

• 38 children (biopsy 

proven); untreated CD 

• age: n/r • gender n/r Celiac Group 2 

• 37 pts; GFD 

treated. 

• age: n/r • gender: n/r 

Celiac Group 3 

• 30 suspected CD; 

on gluten diet 

Celiac Group 4 • 30 suspected cd on 

GFD 

Group 1: 

• 106 

asymptomatic family members 

• age & gender: 

n/r 

Group 2: 

• 52 children 

with chronic diarrhea; 30 ulcerative colitis; 65 Crohn's disease; 21 liver disease; 34 recurrent abdominal pain 

• age & gender: 

n/r 

Group 3: • 87 healthy 

subjects 

• age & gender: 

n/r 

CD untreated and suspected untreated and 8 biopsy + family members vs Control 1 (106-8), 2, 3 

73 3 11 376 
A-107

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d 

Ladinser, 

1994 

Italy 

Publication type: • journal Study design: • case control Ethnicity:

• n/r 

Population Type: 

• n/r 

Reference test: 

• endoscopic biopsy; IgA EMA

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: revised ESPGAN Checked IgA def. 

• IgA deficiency excluded 

by serum testing 

Studied tests IgA EMA Methodology: 

• IgA-EMA, IF studies HU 

smooth muscle; IgA-EMA, IF studies ME

Cut-off: 

n/r 

Celiac Group 1 

• 20 biopsy-proven 

CD pts 

• mean age: 35 y 

(range 5-68) 

• % F: 67%; 20 on 

gluten-containing diet 

Celiac Group 2 

• 10 pts GFD (subset 

of original 30). 

• age: n/r • gender: n/r 

Group 1: 

• 35 pts (CD on 

GFD) with positive AGA serum samples no histological abnormalities 

• Mean age: 40 y 

(range 3-65) 

• % F: 57% 

Group 2: 

• 40 non-celiac pts 

without GI disorder with AGA below average range (IgA<5 and IgG <15) 

• mean age: 37 y 

(range 5-65) 

• % F: 50% 

20 active untreated cases vs control group; IgA-EMA (HU) 20 active untreated cases vs control group 

IgA-EMA (ME) 

20 18 

0 2 

0 0 

75 75 
A-108

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d 

Lerner, 

1994 

USA, Israel 

NB: duplicate of Pacht et al., Isr J Med Sci 1995;31:218 (used data from Lerner et al, 1994 since more complete and larger control group) 

Publication type: • journal Study design: • case control Ethnicity:

• n/r 

Population Type: 

• n/r 

Reference test: 

• Crosby capsule

First test: 

• simultaneous Biopsy & 

serology 

Controls biopsied: 

• yes 

Biopsy criteria: criteria of Townley modified by Ingkaran Checked IgA def. 

• no 

Studied tests IgA -AGA; IgG-AGA; IgAARA (rat kidney); IgA-ARA (mouse kidney); IgA-EMA ME Methodology: 

AGA=ELISA; ARA=IF rat & mouse kidney; EMA=IF ME

Cut-off: 

ELISA 2 SD above the mean of normal value considered positive 

Celiac Group 1 

• 34 biopsy proven 

CD 

• mean age: 9.6 

(range 1.7-17 y) 

• male:female: 

0.6:1.0 

Group 1: 

• 9 pts abnormal 

biopsy pathological control grade IIIV atrophy; (3) Giardia lamblia (3) protracted diarrhea (1) Crohn's (1) HSP (1) intestinal lymphangectasis (1) hypogammaglobulinaemia 

• mean age 9.3 y 

(range 2-16 y) 

• male:female 

1.2:1 

Group 2: 

• 32 pts with 

normal intestinal morphology (GCD) 

• mean age: 8.4 y 

(range 1-16 y) 

• male:female 

0.9:1 

CD1 vs CO IgAAGA CD1 vs CO IgGAGA CD1 vs CO IgAARA-r CD1vs CO IgAARA-m CD1 vs CO IgAEMA; 
A-109

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d 

Lindberg, 

1985 

Sweden 

NB: 

duplicate 

Jardas et 

al., Pol J Immunol 

1994;19:49 

Publication type: • journal Study design: • cohort Ethnicity:

• n/r 

Population Type: 

• suspected malabsorption 

Reference test: 

• biopsy duodenojejunal 

flexure Watson pediatric capsule EMA

First test: 

• biopsy & serology 

simultaneous (sera collected ± 2 weeks of biopsy) 

Controls biopsied: 

• yes 

Biopsy criteria: ESPGAN and Alexander grades; reported sensitivity and specificity for pts with severely damaged mucosa Checked IgA def. 

• yes 

Studied tests IgA-AGA; IgG-AGA; combined IgA/IgG Methodology: 

• DIG-ELISACut-off: 

11 mm IgA; 14mm IgG combined 

Celiac Group 1 

• 25 pts untreated 

CD; 29 pts probable CD 

• mean age: 12 

months (range 7-132 mos) 

• gender: n/r • 58 pts in total used 

(with severely damaged mucosa) 

Celiac Group 2 

• 32 pts CD treated 

GFD (2nd biopsy) 

• mean age: 30 mos 

(range 18-168 mos) 

• gender: n/r 

Celiac Group 3 

• 37pts confirmed 

CD challenged period with gluten 

• mean age: 36 mos 

(range 16-192 mos) 

• gender: n/r 

Group 1: 

• 121 pts with 

other GI disorders i.e., unspecified diarrhea, cow's milk protein intolerance, 

multiple food allergies, post infectious diarrhea, diarrhea caused by Yersinia enterocolitica 

• mean age 14 

mos (7-130 mos) 

• gender: n/r 

Group 2: 

• 23 pts short 

stature no GI symptoms 

• mean age: 48 

mos (range 12-180 mos) 

• gender: n/r 

NB: the study combined control 1 and control 2 (132 pts) 

Author reports groups as: CD severely damaged intestinal mucosa vs control IgA AGA CD severely damaged intestinal mucosa vs control IgG AGA CD severely damaged intestinal mucosa vs control IgA/IgG AGA 
A-110

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d 

Lindquist, 

1994 

Sweden 

Publication type: • journal Study design: • cohort Ethnicity:

• n/r 

Population Type: 

• suspected CD 

Reference test: 

• paediatric Watson capsule

First test: 

• Simultaneous biopsy & 

serology 

Controls biopsied: 

• yes 

Biopsy criteria: ESPGAN; subtotal or partial VA Checked IgA def. 

• yes 

Studied tests IgA-EMA IgA-AGA Methodology: 

IgA-EMA, indirect IF & ME; IgA-AGA, DIG-ELISA

Cut-off: 

IgA-AGA >11mm regarded as positive 

Celiac Group 1 

• 42 confirmed CD 

pts (meets ESPGAN criteria) 

• mean age: 2.7 y 

(range 5 mos-14.4 y) 

• % F: 48 

Celiac Group 2 

• 10 suspected CD 

pts with characteristic biopsy but repeat biopsy on GFD was pending 

• mean age: 2.7 y 

(range 5 mos-14.4 y) 

• % F: 48 

Group 1: 

• 25 pts with other 

pathology (CD excluded) 

• mean age: 2.7 y 

(range 5 mos14.4 y) 

• % F: 48 

Celiac 1 & 2 vs control 1 EMA Celiac 1 & 2 vs control 1 IgA 

51 45 

1 7 

3 3 

38 

39 
A-111

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d 

Maki, 1991 

Finland 

Publication type: • journal Study design: • cohort Ethnicity:

• n/r 

Population Type: 

• suspected celiac 

Reference test: 

• paediatric Watson capsule

First test: 

• Simultaneous Biopsy & 

serology 

Controls biopsied: 

• yes 

Biopsy criteria: ESPGAN; subtotal or partial VA Checked IgA def. 

• yes 

Studied tests IgA-EMA IgA-AGA Methodology: 

IgA-EMA, indirect IF & ME; IgA-AGA, DIG-ELISA

Cut-off: 

IgA-AGA > 11mm regarded as positive 

Celiac Group 1 

• 42 confirmed CD 

pts (meets ESPGAN criteria) 

• mean age: 2.7 y 

(range 5 mos-14.4 y) 

• % F: 48 

Celiac Group 2 

• 10 suspected CD 

with characteristic biopsy but repeat biopsy on GFD was pending 

• mean age: 2.7 y 

(range 5 mos-14.4 y) 

• % F: 48 

Group 1: 

• 25 pts with other 

pathology (CD excluded) 

• mean age: 2.7 y 

(range 5 mos-14.4 y) 

• % F: 48 

Celiac 1 & 2 vs control 1 EMA Celiac 1 & 2 vs control 1 IgA 

51 45 

1 7 

3 3 

38 

39 
A-112

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table 

Author, 

Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d 

McMillan, 

1991 

Ireland 

Publication type: • journal Study design: • cohort Ethnicity:

• n/r 

Population Type: 

• suspected celiac 

Reference test: 

• Crosby capsule "muzzle loaded"

First test: 

• simultaneous Biopsy & 

serology 

Controls biopsied: 

• yes 

Biopsy criteria: revised ESPGAN Checked IgA def. 

• yes 

Studied tests IgG-AGA; IgA-AGA; IgGAGA; IgA-AGA; IgG-EMA; IgA-EMA; IgA jejunum; IgG jejunum Methodology: 

• AGA by indirect IF; AGA 

by ELISA; EMA by IF, ME; jejunum, IF with sections of black hooded rat jejunum as antigen

Cut-off: 

titre of one in 20 or greater were considered positive 

Celiac Group 1 

• 23 biopsy proven 

CD + 5 probable CD = 28 pts 

• Adults age (y): 16-

89 

• % F: n/r 

Group 1: 

• 7 pts 2 did not 

respond to GFD 4 had ulcerative colitis (1 of those pts had partial VA); 1 had IBS 

• mean age: n/r • % F: n/r 

Group 2: 

• 61 normal results 

of jejunal biopsies 

Celiac group 1 vs control group 2 

21 21 16 28 11 25 15 21 

7 7 

12 

0 

17 

3 

13 

7 

4 0 9 0 

1 0 0 0 

57 61 52 61 60 61 61 61 
A-113

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d 

Meini, 1996 

Italy 

Publication type: • journal Study design: • cohort Ethnicity:

• n/r 

Population Type: 

• 65/85 IgA-def pts seen in 

single immunology clinic 1989-93 (76.5%) 

Reference test: 

• Watson capsule

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: partial VA or total VA Checked IgA def. 

• yes 

Studied tests IgA-AGA; IgG-AGA Methodology: 

ELISA

Cut-off: 

25 AU/dL 

Celiac Group 1 

• 5 pts; untreated; 

IgA-deficient 

• mean age: 8.8 y; 

range 7-11 y 

• % F: 80 

Group 1: 

• 60 biopsynegative IgAdeficient 

celiac 1 vs control 1 0 

5 

5 0 

0 

11 

55 44 
A-114

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d 

Picarelli, 

2000 

Italy 

Publication type: • journal Study design: • case control Ethnicity:

• n/r 

Population Type: 

• suspected CD 

Reference test: 

• EMA; biopsy (EGD) 2 biopsies

First test: 

• EMA serology 

Controls biopsied: 

• yes 

Biopsy criteria: ESPGAN Checked IgA def. 

• yes 9 of 18 IgA deficient 

Studied tests IgG-EMA; IgA-AGA; IgGAGA Methodology: 

EMA, indirect IF ME; AGA, in house ELISA

Cut-off: 

0.9 for AGA-IgA and 1.1 for AGA-IgG 

Celiac Group 1 

• 30 EMA neg 

suspected CD; 18 confirmed cases CD 

• mean age: 10.6 y 

(age range 2-16 y) 

• % F: 60 

Group 1: 

• 60 disease 

control (other GI diseases) 

• mean age: 

11.3 y (age range 4-16) 

• % F: 55 

Group 2: • 63 healthy 

children 

• mean age 

10.5 y (age range 3-16 y) 

• % F: 52 - this 

group not biopsied so not used 

Group 3: 

• 12 suspected 

CD pts biopsy negative

celiac 1 vs control 1 and EMA celiac 1 vs control 3 for IgA-AGA IgG-AGA 

18 4 6 

0 

14 12 

0 4 5 

135 8 7 
A-115

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d 

Poddar, 

2002 

India 

Publication type: • journal Study design: • cohort Ethnicity:

• n/r 

Population Type: 

• suspected CD 

Reference test: 

• biopsy - endoscopic

First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: ESPGAN (VA and unequivocal response to GFD) Checked IgA def. 

• n/r 

Studied tests IgA–AGA Methodology: 

ELISA 

Cut-off: 

5U/mL 

Celiac Group 1 

• 50 CD children of 

100 biopsied for suspected CD 

• mean age: 6.3; 

range 2.5-12 y 

• % F: n/r 

Group 1: 

• 44 biopsynegative 

controls who were suspected of CD 

celiac 1 vs control 1 47 3 4 43 
A-116

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d 

Rich, 1990 

USA 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: pediatric suction biopsy technique under fluoroscopic control First test: 

• n/r 

Controls biopsied: 

• yes 

Biopsy criteria: n/r - state "severe" lesion Checked IgA def. 

• n/r 

Studied tests xylose; IgA-AGA; IgG-AGA Methodology: 

D-xylose absorption test; for AGA - ELISA 

Cut-off: 

xylose <25 mg/dL was 

considered abnormal; AGA - Ab levels >2 SD above the mean of the reference group of normal subjects were considered to be abnormal 

Celiac Group 1 

• 15 biopsy-proven 

CD pts out of 60 consecutive group of children suspicious of having CD 

• age: n/r • % F: n/r 

Group 1: 

• 45 non-CD 

biopsies out of 60 consecutive group of children suspicious of having CD 

• age: n/r • % F: n/r 

celiac vs CO: Xylose celiac vs CO: IgG AGA celiac vs CO: IgA AGA 

14 15 

8 

1 0 7 

24 19 

3 

21 26 42 
A-117

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d 

Russo, 

1999 

Canada 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: endoscopic biopsy First test: 

• n/r 

Controls biopsied: 

• yes 

Biopsy criteria: ESPGAN Checked IgA def. yes (1 pts with CD were found to be IgA deficient) Studied tests AGA-IgA; AGA-IgG; EMA ME; EMA HU Methodology: 

for AGA-IgA and IgG ELISA; for EMA - IF on either ME, or HU Cut-off: 

for AGA-gA cut-off was 0.25 EU and for AGA-IgG 0.3 EU; for EMA positive results were considered when a characteristic honeycomb pattern was observed around the smooth muscle 

Celiac Group 1 

• 24 pediatric 

pts with CD (biopsy proven) diagnosed by evaluating consecutive group of 95 children with suspected CD 

• age: mean 3.5 

y, range 7 mos-11 y 

• % F: 50 

Group 1: 

• 71 children 

with biopsy proved nonCD enteropathies or normal mucosa 

• age: n/r • % F: n/r 

celiac vs control IgG-AGA celiac vs control IgA-AGA; celiac vs control EMA ME celiac vs control EMA HU parallel series 

 
A-118

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d 

Salmaso, 

2001 

Italy 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: consecutive CD Dx 1996-99 Reference test: 

• no info on biopsy

First test: 

• biopsy? 

Controls biopsied: 

• yes 

Biopsy criteria: grades 1-1V Marsh with response to GFD Checked IgA def. yes; IgA deficients were excluded Studied tests IgA-EMA; IgA-tTG Methodology: 

UC EMA; GP-tTG antigen 

Cut-off: 

tTG=20 AU 

Celiac Group 1 

• 23 adult untreated 

CD pts 

• median age: 50; 

range 27-96 

• % F: 56.5 Celiac Group 2 

• 59 children with 

untreated CD 

• median age: 8.2 y; 

range 2-14 

• % F: 37.3 

Group 1: 

58 adult agematched biopsynegative controls Group 2: 48 children agematched biopsyneg controls 

celiac 1 vs control 1 celiac 2 vs control 2 

20 20 59 56 

3 3 0 3 

0 2 0 0 

58 56 48 48 
A-119

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d 

SategnaGuidetti, 

1995 

Italy 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: endoscopic biopsy First test: 

• n/r 

Controls biopsied: yes, except pts with ulcerative colitis Biopsy criteria: Roy-Choudhury criteria; partial or total VA Checked IgA def. yes Studied tests AGA-IgA; AGA-IgG; Ig AGA total Ig; EMA IgA (ME); JAB IgA Methodology: 

for AGA-IgA and IgG: ELISA; for IgAGA, EMA, JAB: IF Cut-off: 

for AGA-IgA and IgG: mean±2 SD of control absorbance index values; for Ig AGA: endpoint still generating a pertubular and a periglomerular reticular pattern; for EMA: results considered when a characteristic honeycomb pattern was observed around the smooth muscle; for JAB: IF at a dilution of 1:5 in phosphate-buffered saline 

Celiac Group 1 

• 100 untreated 

biopsy-proven CD pts 

• age (y): 

mean/median n/r; range 14-79 

• % F: 71 

Group 1: 

• 52 healthy 

volunteers recruiting among medical and nursing staff 

• Group 2: • 57 pts with 

non-CD conditions: Crohn's disease (n=38), ulcerative colitis (n=5), lymphoma (n=7), Whipple's disease (n=1), irritable bowel disease (n=6) 

• age: n/r 

celiac vs CO EMA celiac vs CO JAB celiac vs CO IgA-AGA celiac vs CO IgG-AGA celiac vs CO Ig-AGA 

100 100 

55 78 92 

0 0 

45 22

8 

0 0 0 

18 

5 

109 109 109 

91 

104 
A-120

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d 

Sblaterro, 

2000 

Italy 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: n/r First test: 

• biopsy 

Controls biopsied: ESPGHAN Biopsy criteria: ESPGHAN Checked IgA def. yes Studied tests EMA-IgA; GP-tTG IgG and IgA; HR tTG Methodology: 

for tTG: ELISA; for EMA: IF 

Cut-off: 

normal values for IgA HR-tTG were taken as <13% and for IgG HR-tTG <30%; normal values for IgA GP-tTG were taken as <7% and <16% 

Celiac Group 1 

• 65 pts with 

biopsy proven CD 

• age (y): 

median 12, range 2-60 

• % F: 52.3 

Group 1: 

• 150 healthy 

donors and 20 pts with Crohn's disease (biopsy proven non-CD enteropathies or normal mucosa) 

• age: 

mean/media n/r; range 12-60 y 

• % F: 44 

celiac vs CO EMA celiac vs CO IgG GP-tTG celiac vs CO IgA GP-tTG IgG/IgA GP-tTG celiac vs CO IgG HR-tTG celiac vs CO IgA HR-tTG IgG/IgA HR-tTG 

60 40 53 58 44 59 64 

5 

25 

12 

7 

21 

6 1 

0 3 3 6 7 1 8 

170 167 167 164 163 169 162 
A-121

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b d 

Sulkanen, 

Collin, et 

al. 1998 

Finland 

N.B: used 

adult 

group of 

Sulkanen, 

Collin, et 

al., 1998; 

more 

complete 

data 

located in 

Sulkanen, 

Halttunen

, et al. 

1998 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: n/r First test: 

• n/r 

Controls biopsied: 

• yes 

Biopsy criteria: 

subtotal or severe partial VA, crypt hyperplasia, increased IEL 

Checked IgA def. 

yes (4 pts with CD and 1 CO had IgA deficiency) 

Studied tests 

HU IgA; HU IgG; ARA IgA and IgG; AGA IgA and IgG Methodology: 

for AGA ELISA; for ARA IF; for HU IF using HU 

Cut-off: 

HU-Ab positivity included a specific honey-comb IF around the smoothmuscle fibres; AGA IgA - cut off level0.2 EU/mL; AGA IgG cut off level - 10.0 EU/mL; ARA test was considered positive when the characteristic R1-type ARA pattern was found 

Celiac Group 1 

• 92 

consecutive adult pts with biopsyproven CD 

•age (y): 

median 43; range 20-72 

• % F: 71.7 

Group 1: 

• 95 disease 

controls with biopsy proven non-CD enteropathies: 52 undergoing gastroscopic exam for dyspepsia; 14 with Crohn's disease, 29 with ulcerative colitis 

• age (y): 

median 44; range 16-76 

celiac vs control IgA-HU celiac vs control IgG-HU celiac vs control IgA-ARA celiac vs control IgG-ARA celiac vs control IgA-AGA celiac vs control IgG-AGA 

78 11 72 12 74 35 

12 81 20 80 18 57 

0 0 0 2 

13 

3 

95 95 95 93 82 92 
A-122

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b 

Sulkanen, 

Halttunen

, et al. 

1998 

Finland 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population type: 

• n/a 

Reference test: Watson capsule First test: 

• n/r 

Controls biopsied: 

• yes 

Biopsy criteria: ESPGAN Checked IgA def. yes (n=14) Studied tests 

IgA tTG; IgA EMA; IgA-ARA; IgAAGA; IgG-AGA Methodology: 

tTG-source n/r ELISA; IgA-EMAHU; IgA and IgG-AGA-ELISA; IgA ARA-IF) 

Cut-off: 

for IgA tTG cut off level-10 AU 

Celiac Group 1 

• 136 consecutive 

pts with untreated CD (biopsy proven) 

• age (y): median 

10.7, range 0.8-69.3 

• % F: n/r 

Celiac Group 2 

• 38 pts with CD 

on GFD of a median duration 48 mos 

• age: median, 

range n/r 

• % F: n/r 

Celiac Group 3 

• 18 pts on a 

glutenchallenge 

• age: median, 

range n/r 

• % F: n/r • 11 pts after 

reintroduction of a GFD (group 4) 

• age (y): median, 

range n/r 

• % F: n/r 

Group 1: 

• 154 disease 

CO with suspicion of CD but biopsy proven nonCD 

• age (y): 

median 10, range 0.8-76.0 

• % F: n/r 

CD group1 vs CO IgA-tTG CD group1 vs CO IgA-EMA 

CD group1 vs CO IgA-ARA CD group1 vs CO IgA-AGA CD group1 vs CO all IgGAGA 

129 126 125 115 

94 

7 

1011 21 42 

13 

1 8 

3855 

12111
A-123

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b 

Tesei, 

2003 

Argentina 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: endoscopic biopsy First test: Simultaneously Controls biopsied: yes Biopsy criteria: Marsh 2 to 4 - with confirmation Checked IgA def. yes (11 pts were diagnosed as IgA deficient having dermatitis herpetiformis) Studied tests HU-anti-tTG IgA-HR; EMA-IgA; AGA-IgA; AGA-IgG Methodology: 

for HU-anti-tTG, ELISA; for EMA, ME IF; for AGA, ELISA 

Cut-off: 

for HU-anti-tTG - 7 AU/mL; for AGA - 20 AU/mL; for EMA - florescence at dilution of 1:5 

Celiac Group 1 

• 250 

consecutive pts with biopsy proven CD 

• age (y): mean 

39, range 13-79 

• % F: 74 

Group 1: 

• 176 biopsy 

proven nonCD disease controls: chronic diarrhea (n=78), chronic microcitic anemia (n=33), firstdegree relatives of index cases (n=32), healthy individuals (n=11), malabsorption (n=4), miscellaneous (n=12), undernutrition (n=6) 

• age (y): mean 

40, range 17-83 

• % F: 75 

CD vs CO: HU-anti-tTG IgA CD vs CO: EMA CD vs CO: AGA IgA CD vs CO: AGA IgG 

225 214 159 210 

25 36 91 40 

9 0 

14 25 

111

1
A-124

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table 

Author, 

Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b 

Troncone, 

1999 

Italy 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: n/r First test: 

• n/r 

Controls biopsied: 

• yes 

Biopsy criteria: ESPGAN Checked IgA def. yes (none of celiac or CO suffered from IgA deficiency) Studied tests 

anti-tTG IgA; anti-tTG IgG; IgA EMA Methodology: 

for tTG-GP, ELISA; for EMA, ME IF 

Cut-off: 

for anti-tTG - at the 97th percentile of the control group (9% of the reference serum for IgA and 60% - for IgG); for EMA - as the highest dilution giving a positive result (a thin fluorescent network around the smooth muscle fibres) 

Celiac Group 1 

• 48 biopsy 

proven CD pts 

• age (y): mean 

5.7, range 0.9-20 

• % F: 58 

Celiac Group 2 

• 33 pts who 

were on GFD of at least 2 y 

• age (y): mean 

7.3, range 4.3-18 

• % F: 60.6 

Celiac Group 3 

• 10 pts from 

group 2 who were reintroduced to glutencontaining diet 

Group 1: 

• 63 biopsy 

proven non-CD disease controls: chronic diarrhea (n=16), failure to thrive (n=14), Crohn's disease (n=10), cow's milk protein allergy (n=5), GERD (n=5), recurrent abdominal pain (n=4), sideropenic anemia (n=4), hepatatis C (n=3), Cystic fibrosis (n=2) 

• age (y): mean 

4.2, range 1.1-17 

• % F: 49 

CD vs CO: anti-tTG IgA CD vs CO: anti-tTG IgG 

44 11 

4 

37 

1 1 

66
A-125

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

Author, 4X4 table 

Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b 

Valdimarsson, 

1996 

Sweden 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: Watson capsule in 91 pts; fiberoptic endoscopy - in 65 pts First test: 

• biopsy 

Controls biopsied: 

• yes 

Biopsy criteria: Alexander's classification; partial or subtotal VA Checked IgA def. yes (5 had IgA deficiency) Studied tests 

IgA AGA; IgA EMA Methodology: 

for AGA, ELISA; for EMA, IF ME 

Cut-off: 

for AGA-IgA, 30 units (>92nd percentile in healthy blood donors); for AGA-IgG, 20 units (>91.3th percentile in healthy blood donors); for IgA EMA, characteristic honeycomb pattern was observed around the smooth muscle 

Celiac Group 1 

• 19 pts with CD 

(biopsy-proven) out of 156 pts referred for symptoms suspicious for CD 

• age: n/r • % F: n/r 

Group 1: 

• 137 pts with 

biopsy proven non-CD; 5 had IgA deficiency and 7-dermatitis herpetiformis 

• age: n/r • NB: pts with IgA 

deficiency and dermatitis herpetiformis were excluded from the analysis of sensitivity, specificity, so that CO group was composed of 125 pts 

celiac vs CO IgA EMA celiac vs CO IgA AGA 

14 15 

5 4 

0 

38 
A-126

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b 

Valentini, 

1994 

Italy 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: multipurpose biopsy tube, endoscopic First test: 

• simultaneously 

Controls biopsied: 

• yes 

Biopsy criteria: partial VA or greater Checked IgA def. n/r Studied tests 

IgA-AGA; IgG-AGA; IgA-EMA ME Methodology: 

for IgA/IgG AGA, ELISA; for IgA-EMA, IF 

Cut-off: 

lower limit of AGA positive was 1 EU, based on the mean+-2 SD of the results obtained in a large series of healthy adults; IgA-EMA identified by their reticulinlike staining of the smooth muscle; sera containing antibody at a titre of 1:5 or greater were considered to be positive 

Celiac Group 1 

• 100 

consecutive adult untreated pts with CD (biopsy proven) 

• age (y): mean 

37.4+-15.4, range 17-79 

• % F: 77 

Celiac Group 2 

• 33 pts out of 

100 group 1 who were on GFD of at least 6 mos (mean 9.9 mos, range 6-12 mos); 

Group 1: 

• 30 disease 

controls (CO) with biopsy proven non-CD conditions: ulcerative colitis (n=8), gastric lymphoma (n=8), Crohn's disease (n=5), Whipple disease (n=3), IBS (n=3), giardiasis (n=2), Graves disease (n=1) 

• age (y): mean 

40+-13, range 18-60 

• % F: 47 

celiac vs CO IgA EMA celiac vs CO IgA/IgG AGA 

99 92 

1 8 

0 3 

32
A-127

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design Study Population 

Control 

Population Comparison a c b d 

Vitoria, 2001 

Italy 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: n/r First test: 

• n/r 

Controls biopsied: 

• yes 

Biopsy criteria: subtotal VA Checked IgA def. n/r Studied tests 

IgA tTG-ab; IgA EMA Methodology: 

tTG-HR, ELISA; IgA-EMA, IF ME 

Cut-off: 

for tTG, values of 9 U/mL and more were considered positive; for EMA, reticular pattern of fluorescence in the muscular mucosa at a dilution of serum 1:5 were considered positive 

Celiac Group 1 

• 42 biopsy 

proven CD pts 

• age: mean 

4.2±4.2 y 

• % F: n/r 

Group 1: 

• 28 biopsy proven 

non-CD disorders 

• age: mean 6.1+-

5.2 y 

• % F: n/r 

celiac vs CO: tTG celiac vs CO: EMA 

40 42 

2 0 

0 0 

28 28 
A-128

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table 

Author, 

Year, 

Location Study Design Study Population Control Population Comparison a c b d 

Vogelsang, 

1995 

Austria 

Publication type: • journal Study design: • cohort Ethnicity:

• n/r 

Population Type: 

• suspected CD 

Reference test: biopsy First test: 

• endoscopic biopsy distal 

duodenum or Baumgartner-Classen capsule from duodenojejunal flexure 

Controls biopsied: 

• yes 

Biopsy criteria: modified ESPGAN; flat mucosa; crypt hyperplasia raised IELs Checked IgA def. yes; no cases found Studied tests 

IgA-AGA; IgG-AGA; IgAEMA Methodology: 

ELISA; >95th percentile; ME 

Cut-off: 

AGA 0.2 AU/mL 

Celiac Group 1 

• 49 untreated 

biopsy-proven CD 

• age: median 35; 

range 17-75 

Group 1: 

• 53 biopsy-neg 

controls; median age 31; range 15-79; Crohn's (17); IBS (16); lactase def (7); fibroma (1); duodenitis (1); gastroparesis (3); gastritis (2); chron pancr (1); UC (1); coll colitis (1) 

celiac 1 vs control 1 40 

36 49 

9 

13 

0 

9 

14 

0 

44 39 53 
A-129

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b 

Volta, 

1995 

Italy 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: n/r First test: 

• n/r 

Controls biopsied: 

• only disease CO 

Biopsy criteria: Roy-Choudhury criteria Checked IgA def. n/r Studied tests 

IgA-EMA on ME; IgA-EMA on HU Methodology: 

IF 

Cut-off: 

staining of the endomysium around the smooth muscle was considered as a positive result 

Celiac Group 1 

• 60 untreated 

pts with biopsy-proven CD 

• age (y): 

median 41, range 14-68 

• % F: 70 

Celiac Group 2 

• 36 pts with CD 

on GFD of 12 mos duration 

Group 1: 

• 100 disease CO 

(biopsy proven non-CD in disease CO): ulcerative colitis (n=25), Crohn's disease (n=35), various other GI diseases (n=40) 

• age (y): median 

44, range 25-70 

• % F: 68 

Group 2: 

• 100 healthy CO 

(not biopsied) 

• age: median, 

range n/r 

• % F: n/r 

celiac vs CO IgA-EMA ME celiac vs CO IgA-EMA HU 

57 57 

3 3 

0 0 

11
A-130

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b 

Whelan, 

1996 

Ireland 

Publication type: • journal Study design: • case control Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: n/r First test: 

• n/r 

Controls biopsied: 

• only disease CO 

Biopsy criteria: subtotal VA Checked IgA def. n/r Studied tests 

HUVEC IgA - human umbilical vein endothelial cells; EMA IgA; (ME) ARA IgA (rat liver); only EMA used for analysis Methodology: 

HUVEC - IF; EMA - IF; ARA - IF 

Cut-off: 

n/a 

Celiac Group 1 

• 25 untreated 

CD (biopsyproven) – (UTCD) 

• age: median, 

range n/r 

• % F: n/r 

Celiac Group 2 

• 16 treated CD 

on GFD – TCD 

• age: median, 

range n/r 

• % F: n/r 

Group 1: 

• 20 disease CO 

(biopsy proven non-CD in disease CO) - 10 pts with ulcerative colitis and 10 - with Crohn's disease 

• age: median, 

range n/r 

• % F: n/r 

Group 2: 

• 16 CO with 

normal intestinal mucosa 

• age: median, 

range n/r 

• % F: n/r 

UTCD vs CO: HUVEC UTCD vs CO: EMA ME UTCD vs CO: ARA 

25 25 21 

0 0 4 

0 0 0 

333
A-131

Evidence Table 1 (cont’d): Included studies of the sensitivity and specificity of serology for CD 

Results 

 4X4 table Author, Year, 

Location Study Design 

Study 

Population 

Control 

Population Comparison a c b 

Wolters, 

2002 

Netherlands 

Publication type: • journal Study design: • cohort Ethnicity:

• n/a 

Population Type: 

• n/a 

Reference test: endoscopic biopsy First test: 

• n/r 

Controls biopsied: 

• yes 

Biopsy criteria: subtotal VA with crypt hyperplasia Checked IgA def. n/r Studied tests 

IgA-AGA; IgG-AGA; IgAEMA; IgA-GP-tTG; IgA-HUtTG Methodology: 

for AGA-ELISA; for EMA–IF ME; for tTG - ELISA 

Cut-off: 

for AGA: Ab titers were considered positive if IgAAGA exceeded 4 U/mL and IgG-AGA exceeded 150 U/mL; for EMA - fluorescence in the muscularis mucosa at a serum dilution equal to or greater than 1:5 

Celiac Group 1 

• 52 pediatric 

pts with biopsy proven CD 

• age: mean 4.0 

y, range 1.1-14.4 y 

• % F: 73 

Group 1: 

• 49 disease CO 

pts with biopsy proven nonCD 

• age: mean 5.1 

y, range 0.8-19.2 y 

• % F: 41 

CD vs CO: IgA AGA CD vs CO: IgG AGA CD vs CO: IgA EMA CD vs CO: anti-GP-tTG IgA CD vs CO: anti-h-tTG IgA 

43 43 48 50 50 

9 9 4 2 2 

10 

7 5 4 0 

34444
A-132

HLA DQ2/DQ8 Evidence Table 2: Case-control study evidence for the use of HLA as a marker of CD 

Results 

Con

Author, 

Year, 

Location Study Design Study Population Control Population Celiac Group Group 1 

Iltanen, 

1999, 

Finland 

• case control • monoclonal 

antibodies used to stain jejunal IELs and mucosal HLADR; DQA1*0501 and DQB1*0201 alleles determined 

• 21 children with 

biopsy-confirmed CD

• CD criteria: 

ESPGAN

• mean age: 6.1 y, 

range 0.5-16.3 y

• % F: n/r

• ethnicity: n/r 

Group 1: 

• 67 ethnically-, agematched pts with 

biopsy-negative CD

• ethnicity: n/r 

• DQ2: 19 (90.48) • DQ8: n/a • DQ2 or 8: n/a 

Prevalence of CD: 0.24 

• DQ2: 29.85 

Sens: 0.90 Spec: 0.70 PPV: 0.49 NPV: 0.96 

• DQ8: n/a • DQ2 or 8: n/a 
A-133

Evidence Table 2 (cont’d): Case-control study evidence for the use of HLA as a marker of CD 

Results 

Con

Author, 

Year, 

Location Study Design Study Population Control Population Celiac Group Group 1 

Sacchetti, 

1998,

Southern 

Italy 

• case control • used PCR to 

examine prevalence of HLA heterodimer and HLA DRB104 alleles in healthy subjects, in CDaffected children, and in other agematched subjects affected by confounding disease 

• 122 children with 

biopsy-confirmed CD

• CD criteria: 

ESPGAN 

• ethnicity: Italian 

Group 1: 

• 32 age-matched pts 

with GI symptoms but negative biopsy for CD

• Ethnicity: Italian Group 2: • 116 ethnicallymatched healthy adult 

controls 

• DQ2: 106 (86.89%) • DQ8: n/a • DQ2 or 8: n/a 

• prevalence of CD: 0.79 • DQ2: 6 (18.75%) 

Sens: 0.87 Spec: 0.81 PPV: 0.95 NPV: 0.62 

• DQ8: n/a • DQ2 or 8: n/a 
A-134

Celiac 2: Incidence and Prevalence of CD 

Incidence of CD in the General Population Evidence Table 3. Incidence of CD in the general population

Study, 

year; 

country Group at risk Case ascertainment Incidence Other observations 

Bode, 

1996 

Denmark 

Region: County of Copenhagen Period: 1976-1991 retrospective Age groups: all adults>15 Size: 480,581 in 1976; 503,283 in 1992 

Institution(s): sole 3 teaching hospitals + clinic of region Register(s): Discharged Dx w ICD 269-0.01; all small bowel biopsy from path depts; case register of all celiacsVerification of accuracy: review of case records Dx Criteria: at least 1 biopsy; good response to GFD; gluten challenge with re-biopsy if Dx uncertain % capture: 

Outcome measures: cumulative incidence avg incidence rates adjusted for age/sex Results: # cases: 101 (64F/37M) Characteristics of cases: median age at Dx: 40.1 y (range 16-81) crude incidence: 1.27/100,000 cumulative incidence: 19 y: 198/1000 births 

Women: Crude incidence: 1.55/100,000 Lifetime cumulative incidence: 55.8/100,000 Men: Crude incidence: 0.96/100,000 Lifetime cumulative incidence: 35.3/100,000 Prevalence (1992): 45.9/100,000 
A-135

Evidence Table 3 (cont’d). Incidence of CD in the general population

Study, 

year; 

country Group at risk Case ascertainment Incidence Other observations 

Collin 

1997 

Finland 

Region: Tampere City Period: 1975-94 Age groups: Adult Size: 121,000 in 1970; 147,000 in 1994 Note: Screening of high-risk groups in effect Systematic small bowel biopsy during gastroscopy 

Institution(s): Sole 3 centers that perform gastroscopy; The University Hospital. The City Hospital and the local health centre Register(s): Membership list of local Coeliac Society Verification of accuracy: All case records and specimen of CD pts were verified Dx Criteria: Subtotal or severe partial VA and crypt hyperplasia; clinical or histological improvement on GFD % capture: NR

Outcome measures: Prevalence: All adult CD pts living in Tampere on Dec 31 1994 per 100 000 population. 5-y Incidence: All adult CD pts dx’ed between 1975 and 1994 per 100,000 pop. Results: # cases: 301 cases (222 F/79 M) Characteristics of cases: Crude incidence (/100,000 pop/yr): 1975-79: 1.6 1980-84: 6.8 1985-89: 13 1990-94: 17.2 Cumulative incidence: NR

Median age at Dx: 39 y (range 1-80)Prevalence in 1994: 204/100,000 (95% CI 181-231) Mode of presentation: Apparent symptoms: 24% Minor symptoms: 37% Screening: 27% Chance at endoscopy: 13% Causes for increased incidence: 

Use of serologic screening Performance of small bowel biopsy on all pts undergoing gastroscopy Ability of all GP to refer pts to gastroscopy 
A-136

Evidence Table 3 (cont’d). Incidence of CD in the general population

Study, 

year; 

country Group at risk Case ascertainment Incidence Other observations 

Corrao, 

1996 

Italy 

Region: Provinces of Turin, Cuneo, Brescia, Umbria region, Sardinia region Period: 1990-91 prospective vs retrospective Age groups: All ages Size: Italian population census in 1991 6,339,194 in 1991 (11.0% Italy); 107,048 live births (9.4% Italy) 

Institution(s): Dx lists of peds, med, GI depts in all hosp; Dx lists leading Italian hosp

Register(s): National Health Service records; local Italian Coeliac Society Verification of accuracy: capture-recapture method Dx Criteria: biopsy without challenge in 47.2% ESPGAN in 52.8% % capture: 85.6% Exclusion(s): pts residing outside Dx area 

Outcome measures: crude incidence: #new Dx/yr/100,000 pop cumulative incidence: #cases over period/100,000 births Results: # cases: 270 (181F/89M) Characteristics of cases: mean age at Dx: children 3.7; adults 34; overall 21 Crude incidence: 2.13/100,000/y Cumulative incidence (/10,000 births): 2 y: 5.75 5 y: 8.08 10 y: 10.30 15 y: 11.42 

RR according to gender (95% CI): Male: 1.0 Female: 1.90 (1.48, 2.45) RR according to age (95% CI): 0-15: 1.0 16-39:0.33 (0.25-0.44) 40-59:0.21 (0.15-0.30) >60: 0.11 (0.06-0.18) 
A-137

Evidence Table 3 (cont’d). Incidence of CD in the general population

Study, 

year; 

country Group at risk Case ascertainment Incidence Other observations 

Hawkes, 

2000 

England 

Region: South Glamorgan Period: 1980-95 retrospective Age groups: all ages Size: Registrar General mid-yr estimates for total pop, pop <16yr, total live births415,900 in 1995 

Institution(s): sole 3 teaching hospitals in Cardiff Register(s): Local Celiac Society, letters to GP from consultants Verification of accuracy: pathology & dietetic records from the 3 Cardiff teaching hospitalsDx Criteria: ESPGAN % capture: 100% 

Outcome measures: Crude incidence: age-weighed avg/100,000 pop Results: # cases: 137 (98F/39M) Characteristics of cases: mean age at Dx: children 5.3 yrs (range 0.9-14.9); adults 49.1 yrs (range 19.9-88.2) Crude incidence: children (/100,000/yr): 1981-85: 2.08 1986-90: 2.53 1991-95: 2.15 adults (/100,000/yr):1981-85: 1.32 1986-90: 2.15 1991-95: 3.08 Cumulative incidence: NR 
A-138

Evidence Table 3 (cont’d). Incidence of CD in the general population

Study, 

year; 

country Group at risk Screening Incidence Other observations In

Hoffenberg

2003 

US 

Region: Denver Colorado Period: 1993-99 prospective Age groups: Birth to 7 y; 987 for at least 1 y; 386 for at least 5 y Size: Sample from 22 346 newborns screened for HLA, i.e. 987 infants from one institution (St Joseph’s Hospital). Ethnicity: 56% non Hispanic white 30% Hispanic 7% African American 2% Asian American 5% biracial/other Genotypes: HLA-DR3/3; DR3/4, DQB1*0302; DR4, DQ8; DR5/7 

Intervention: HLA type newborn; followup of selected genotypes Follow-up: CD serology at 9, 15 and 24 months of age, then yearly. If positive tTG on 2 separate occasions, or if positive tTG plus clinical suspicion, evaluation for small bowel biopsy. CD serology: EMA IgA 1993-98; tTG IgA 1998-99; Retesting of EMA positive samples with tTG once test available; Total IgA; tTG IgG used on IgA deficients. Dx criteria: Either positive tTG plus biopsy (Marsh 2 or greater), or two consecutive tTG positives 6 months apart

Outcome measures: Time to the event of evidence of CD; Cumulative probability of being event-free for the entire population; Cumulative incidence of evidence of CD, stratified by genotype (DR3/3; DR3/x, DRx/x); RR evidence of CD by genotype Results: # cases: 40 tTG pos at least once; 19 with evidence of CD; 10 biopsy-confirmed; 9 with pos tTG at least twice Characteristics of cases: 13F/6M Mean age 4.6 (range 2.6-6.5) 84% non-hispanic whites Crude incidence: NR Cumulative incidence at age 5: 9/1000 births (95% CI 4-20) Cumulative incidence at age 5 according to genotype: HLA-DR3/3: 32/1000 (95% CI 10-110) HLA-DR3/x: 34/1000 (95% CI 30-117) HLA-DR3 neg: 3/1000 (95% CI 0-27) 

RR according to gender: Female: 3.34 (95% CI 1.00-10.9) RR according to ethnicity: Non-hispanic whites: 3.33 (0.7-12.5) RR according to genotype (Compared to HLA DR3 negatives): HLA-DR3/3: 9.1 (95% CI 1.7-48) HLA-DR3/x: 5.6 (95% CI 1.5-21) 
A-139

Evidence Table 3 (cont’d). Incidence of CD in the general population

Study, 

year; 

country Group at risk Case ascertainment Incidence Other observations 

Ivarsson, 

2003, 

Sweden 

Duplicate: 

Ivarsson 

Acta 

Paediatrica 

2000;89:165 

Region: Entire Sweden Period: 1973-97 prospective and retrospective Age groups: Children 

• 0-2 y • 2-15 y 

Size: 258,683 in 1973; 623,439 in 1991 Dx Criteria: ESPGAN 

Institution(s): Prospective reporting from 9 departments of pediatricsRegister(s): Sweden's National Child health program; central register of CD cases in children <15; Statistics Sweden Verification of accuracy: local registers% capture: 

Outcome measures: Incidence rate: #new cases/100,000 PYs; cumulative incidence: # cases up to age/1000 birth in same cohort Results: # cases of CD: 2151 (1340F/811M) Characteristics of cases: Crude incidence (/100,000PY): 1973-84: 0-2: 65 (57-74) 1987-94: 0-2: 198 (186-210) 1997: 0-2: 51 (36-70) Cumulative incidence at 2 y: 1995: 1.7 (95% CI 1.3-2.1)/1000 births 

RR according to age: 0-2 y: 1.0 2-15: 0.031 (0.022-0.043) RR according to genderM: 1.0 F: 1.9 (1.7-2.1) RR according to period: 1973-84: 1.0 1985-95 1.7 (1.2-2.5) 1996-97 6.8 (4.5-10) 
A-140

Evidence Table 3 (cont’d). Incidence of CD in the general population

Study, 

year; 

country Group at risk Case Ascertainment Incidence Other observations 

Jansen, 

1993 

Netherlands 

Region: Entire country Period: 1975-91 retrospective Age groups: all ages Size: Central Bureau for statistics14,892,574 in 1990 

Institution(s): Register(s): Dutch Coeliac Disease Society for 1992 Verification of accuracy: Dx criteria: at least 1 biopsy % capture: 97% 

Outcome measures: Incidence: # new cases/100,000 pop/yr; Prevalence rate: # cases/100,000 Results: # cases: 1983 Characteristics of cases: Crude incidence (/100,000/yr): 1981-88: 0.65 1988-90: 0.8 1991-92: 1.0 

Prevalence 1990: 7.9/100,000 (95% CI 6.7-9.3) 1991: 11.3/100,000 (95% CI 9.5-1.0) 1992: 12.7/100,000 (95% CI 11.0-14.
A-141

Evidence Table 3 (cont’d). Incidence of CD in the general population

Study, 

year; 

country Group at risk Case ascertainment Incidence Other observations 

Lopez 

Rodriguez, 

2003 

Spain 

Region: Caceres, southwest Spain Period: 1981-99 retrospective Age groups: Children 0-14 y; Spanish National Statistics Institute Size: 65 137 children in 1998; 98 641 in 1986 66 496 in 1996 

Institution(s): San pedro de Alcantara hospital, Province referral center for biopsy Register(s): Verification of accuracy: clinical records Dx Criteria: ESPGAN % capture: 

Outcome measures: crude incidence: # cases/100,000 pop/yr Results: # cases: 157 (90F/67M) Characteristics of cases: mean age at Dx: 

1981-90: 37.4+/-47.4 mo 1991-99:43.9+/-43.7 mo 

Crude incidence (/100,000/yr): 

1981-90: 6.87 (5.26-8.83) 1991-99: 16.04 (12.99-19.59) 

RR according to period: 

1981-90: 1 1991-99: 2.31 (1.61-3.31) 

RR according to age: 

4-15 y: 1.0 0-4 y (1981-90): 18.2 0-4 y (1991-99):42.04 

% with typical clinical presentation: 

1981-90: 83.6% 1991-99: 58.3% 

Significant positive correlation between age at Dx and age of introduction of gluten: 

1981-90: r=0.296 , p=0.0211 1991-99: r= 0.293, p=0.0037 
A-142

Evidence Table 3 (cont’d). Incidence of CD in the general population

Study, 

year; 

country Group at risk Case ascertainment Incidence Other observations 

Magazzu, 

1994 

Sicily 

Region: Entire country Period: 1975-89 retrospective Age groups: children Size: 69,945 births in 1989 

Institution(s): All 4 Sicilian centers of pediatric GI in Catania, Messina and Palermo Register(s): Registrations from all 62 Sicilian health authorities; pt list of each GI pediatric centers; pt list of gluten-free products consumption Verification of accuracy: Chart review of cases; personal interviews; contact of family pediatrician Dx Criteria: ESPGAN % capture: Exclusion(s): no proof of remission on GFD; at least subtotal VA on biopsy; pts not traced back (1.5%) 

Outcome measures: cumulative incidence rate by birth cohort: #new cases/#live birth in same birth cohort (95%CI); incidence density: # cases/(#birth in cohort/#yrs of follow up)/15 y obs period Results: # cases: 1074 (607F/467M) Characteristics of cases: 99.4% Caucasian Crude incidence: Cumulative incidence: 1980 birth year: 1.19/1000 child.yr, 95% CI 0.96-1.45 1984 birth yr: 1.16/1000 child.yr, 95% CI 0.92-1.42 1989 birth yr: 0.13 /1000 child.yr, 95% CI 0.06-0.23 
A-143

Evidence Table 3 (cont’d). Incidence of CD in the general population

Study, 

year; 

country Group at risk Case ascertainment Incidence Other Observations 

Maki, 

1990 

Finland 

Region: Tampere City Period: 1961-84 Age groups: Children Size: 131,394 live births 1960-84 Exclusion(s): Cases not born in a certain strict area around the city 

Institution(s): Department of Paediatrics, University Central Hospital of Tampere Register(s): nil Verification of accuracy: Questionnaire to pts and their parents; hospital medical records; Child health center charts Dx Criteria: Small bowel biopsy; ESPGAN in 44% % capture: NR 

Outcome measures: Crude incidence: # cases/100,000pop/yr Results: # cases: 96 Characteristics of cases: Crude incidence: 1964-73: 10.12/100,000 PYs 1974-83: 3.46/100,000 PYs 1960-84: 2.28/100,000 PYs Cumulative incidence: 

Significant correlation between the age at Dx and duration of breastfeeding Decreased incidence in 0-2; increased incidence in 2-15; increased subclinical presentation in children 
A-144

Evidence Table 3 (cont’d). Incidence of CD in the general population

Study, 

year; 

country Group at risk Case Ascertainment Incidence Other Observations 

Talley, 

1994 

US 

Region: Olmstead County Period: 1960-90 retrospective all ages Age groups: Size: 

Institution(s): Register(s): Rochester Epidemiology Project

Verification of accuracy: Medical records reviewed; biopsy reviewed Dx Criteria: % capture: Exclusion(s): living outside territory at time dx 

Outcome measures: Results: # cases: 28 (19F/9M) Characteristics of cases: Crude incidence: Overall: 1.2 1960-69: 0.9 1970-79: 0.7 1980-90: 1.7 Cumulative incidence: 

0-14:0.4/100,000PYs 15-44:0.7 45-64:2.5 >65 2.1 prevalence 1991: 21.8/100 000 Median age at Dx: median 50 (interQ range 35-62) 
A-145

Evidence Table 3 (cont’d). Incidence of CD in the general population

Study, 

year; 

country Group at risk Case ascertainment Incidence Other Observations 

Weile, 

1993 

Denmark 

Region: Copenhagen County Period: 1960-88 retrospective Age groups: children Size: 1,972,864 live births Dx criteria: Biopsy-proven (90%); clinically suspected CD (10%) 

Institution(s): Register(s): National Central register of Diagnosis 1977-87 Local register of pts admitted for SB biopsy Celiac Patient Society Verification of accuracy: Data twice thoroughly evaluated % capture: 

Outcome measures: Cumulative incidence: #cases/1000 birth in birth cohort Results: # cases: 176 (103F/73M) Characteristics of cases: Crude incidence: 1988: 0.102/1000 births Cumulative incidence: median: 0.089/1000 live births (range 0-0.182) age 5: 0.118/1000 births 
A-146

Prevalence and Incidence in the General Population—Different Geographic and RPopulations Evidence Table 4: Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Borch, 

2000 

Sweden 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

biopsy; IgA & IgG-AGA; IgAEMA MEBiopsy criteria/description: Alexander GradeConfirmatory test: n/r Checked IgA def. 

n/r 

Ethnicity:

459 Swedish; 17 Northern Europeans; outside of Northern EuropePatient type/# screened: 

n=2,000 healthy adults invited to participate in endoscopy study of relation of H.pylori to duodenitis; 482 agreed to participate 

Demographics: age range: 34-75 y Incidence: 

first serology: 96 

confirmation serology: 7 biopsy proven: 9 

 
A-147

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Carlsson, 

2001 

Sweden 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

AGA, cut-off at 25AU; indirect IF EMA, cut-off at titre >5; biopsy using Watson capsule

Biopsy criteria/description: 

used Waston capsule; revised ESPGAN? for classification: normal, subnormal (villous length/crypt length<2, increased number of inflammatory cells in the muscosa with or without damage to the surface epithelium and the brush border), or total VA (flat mucosa) 

Confirmatory test: 

biopsy 

Checked IgA def. 

n/r 

Ethnicity:

n/aPatient type/# screened: 

unselected; all children born July 1992 through June 1993 Demographics: n=690 (out of 1287/3007 children initially contacted, excluding 22 known CD cases) mean age: 32 mos; range: 27-41 mos Incidence: 

5.1% (35/690) had either EMA or AGA positive; (13/690) EMA alone: by biopsy: 1.6% (11/35/690) serology positives underwent jejunal biopsies, 11 of them became biopsyconfirmed CDs 
A-148

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Catassi, 

1996, 

Italy 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

IgA or IgG-AGA Biopsy criteria/description: ESPGANConfirmatory test: 

EMA and biopsy 

Checked IgA def. 

n/r 

Ethnicity:

n/aPatient type/# screened: 

School age children 

Demographics: n=17,201; age range: 6-15 y Incidence: 

1289/17201 (7.5%) AGAIgG or IgA pos; confirmed with EMA=111/17201; biopsy on 98/111 was pos in 75 + 7 who had no biopsy but CD by various investigations 
A-149

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Catassi, 

2000, 

Italy 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

IgG-AGA (7 AU); IgA-AGA (15 AU); IgA-EMA indirect IF (1:5 dilution); biopsy

Biopsy criteria/description: 

ESPGAN; Marsh; grade I = isolated increase gamma delta IEL count, grade II= increase gamma delta lymphocyte count with shortened villi/crypt hyperplasia, grade III= subtotal VA 

Confirmatory test: 

biopsy 

Checked IgA def. 

yes, 6 found 

Ethnicity:

n/aPatient type/# screened: 

general public, students Demographics: n=2,096; pedi age range: 11-15 y % F: 49.5 Incidence: 

0.86% (18/2,096) 
A-150

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Collin, 

2002 

Finland 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

biopsy

Biopsy criteria/description: 

ESPGAN 

Confirmatory test: 

biopsy 

Checked IgA def. 

n/r 

Ethnicity:

n/aPatient type/# screened: 

1. GERD group: regurgitation or heartburn; 2. dyspepsia group; 3. suspected CD Demographics: n=9,971; adolescent and adult median age: 58 y; range: 12-93 y % F: 63.5 Incidence: 

GERD: 0.61% (18/2974) 

dyspepsia: 0.77% (41/5347) 

CD: 5.33% (88/1650) 
A-151

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Corazza, 

1997 

Republic 

of San 

Marino 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

indirect IF EMA titre >1:5; biopsy

Biopsy criteria/description: 

n/r 

Confirmatory test: 

biopsy 

Checked IgA def. 

no, but mentioned as such that it could have caused some misclassification of pts, but the effect should be minimal given the powerful sensitivity and specificity of EMA test 

Ethnicity:

n/aPatient type/# screened: 

random sample stratified for age and sex Demographics: n=2,237; adult median age: 44 y; range, 20-87 y % F: 53.2 Incidence: 

by both EMA and biopsy: 1 in 559 pts, or 1.79 per 1,000 (0.18%) 
A-152

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Csizmadia 

1999 

Netherlands 

Duplicate: 

no 

Publication type: Journal (research letter) Study design: cross-sectional prevalence 

Test/methodology: 

IgA-EMA (methodology n/r)

Biopsy criteria/description: 

n/r 

Confirmatory test: 

small bowel biopsy, subset of 27 had HLA typing for DQ2 

Checked IgA def. 

n/r 

Ethnicity:

n/aPatient type/# screened: 

6,127 children between ages of 2-4 y general population Demographics: 

6,127 pediatric pts age: range 2-4 y % F: n/r 

Incidence: Time period: between May 1997-June 1998 

1.2% (75/6127) by IgA-EMA, 18/75 refused small bowel biopsy; 0.51% (31/75/6127) VA (CD) 

 
A-153

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Dickey 

1992, 

Ireland 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

IgA-AGA

Biopsy criteria/description: no biopsy performedConfirmatory test: n/r Checked IgA def. 

n/r 

Ethnicity:

n/aPatient type/# screened: 

healthy blood donors 

Demographics: n=443; adults, age range 18-65 y Incidence: 

By first serology: 5 
A-154

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Fasano, 

2003, 

USA 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

EMA-IF; ME or HUC; positive at 1:10; all positive EMA tested with human tTG ELISA positive at 2 SD above mean of healthy controls; HLA DQ2 and DQ8

Biopsy criteria/description: Confirmation test: 

htTG; biopsy; also small subset 98 EMA positive and 114 EMA neg had HLA DQ2/8 tested 

Checked IgA def. 

• n/r 

Ethnicity:

94% White; 3% Black; 1.5% Hispanic, 1% Asian, 0.5% otherPatient type/# screened: 

9,019 at risk of CD; 4,126 not at risk Demographics: at risk: symptoms of CD (1,326 children, 1,909 adults); CD associated disorders; 4,508 1st deg relatives; 1,275 2nd deg relatives; not at risk: 2,000 blood donors (mean age 39 y, range 19-65 y); 1,119 school children (mean age 12.3 y, range 6-18 y); 1,007 adults and children for routine physical (mean age 39 y, and 13.7 y, range 19-71 y and 2-18 y, respectively) Incidence: 

1) at risk: a) 1st deg relatives-205/4508 (4.55%); children-54/1294 (4.17%); adults-151/3214 (4.70%); b) symptomatic adults-28/1910 (1.47%); children-53/1326 (4.00%) 2) not at risk-1/4126 (0.75%); adults-27/2845 (0.95%); children4/1281(0.31%); biopsy in EMA pos-Marsh I-0%; II30/116 (25.9%); IIIa-46/116 (39.7%); IIIb-24/116 (20.7%); IIIc-16/116 (13.8%); HLA DQ2-76/98 (78%); DQ8-16/98 (16%); DQ2 and 8-6/98 (6%); all EMA pos were also tTG pos 

 
A-155

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Green, 

2000 

USA 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

EGD, biopsy Biopsy criteria/description: n/r Confirmatory test: n/r Checked IgA def. 

n/r 

Ethnicity:

n/aPatient type/# screened: 

n=1,749 adults; suggestive endoscopic features of CD while undergoing routine endoscopy 

Demographics: n/r Incidence: 

Biopsy proven: 9 
A-156

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Grodzinsky, 

1996 

Sweden 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

IgA-AGA; both IgA- and IgG-AGABiopsy criteria/description: n/rConfirmatory test: ? Checked IgA def. 

n/r 

Ethnicity:

n/aPatient type/# screened: 

healthy adult blood donors 

Demographics: n=1,866; median age 38.5 y, range 18-64 y Incidence: 

By first serology: 124 by confirmation serology: 11 by biopsy: 7 

 
A-157

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Hovdenak, 

1999 

Norway 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

IgA and IgG-AGA, ELISA, cut-off levels: for IgA >0.35 

and for IgG >0.90; IgA-EMA, 

IF, cut-off n/r

Biopsy criteria/description: 

endoscopic biopsy; at least 3 biopsy specimens taken; classification as either normal, partial VA or subtotal VA 

Confirmatory test: 

biopsy Checked IgA def. n/r 

Ethnicity:

n/aPatient type/# screened: 

2,069 healthy blood donors screened for CD; 1st level of screening: measuring of IgA and IgG AGA; 2nd level of screening: measuring IgA-EMA in AGA positives; 3rd level of screening - biopsy in IgA EMA positives Demographics: n=2,069; age: median 39 y, range 18-67 y M/F ratio: 1.65 Incidence: 

Prevalence of CD in the screening group was 1:340 (7/2069); prevalence of test positivity: 83 of 2069 were positive for AGA; EMA was positive in 8 of these 83 pts; biopsy proven CD was diagnosed in 7 of these 8 pts 

 
A-158

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Ivarsson, 

1999 

Sweden 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgA and IgG AGA - ELISA, cut-off n/r; IgA EMA - IF on a ME, cut-off dilution level varied from 1/20 to 1/320; positive if presence of characteristic reticulin-like staining pattern; serum IgA level measurement using routine nephelometric method, level below 0.05 gL was defined as IgA deficient

Biopsy criteria/description: 

criteria for the diagnosis of CD was biopsy demonstrating enteropathy grade III to IV according to Alexander 

Confirmatory test: 

endoscopic biopsy 

Checked IgA def. 

yes, using routine nephelometric method; 0.2% (4/1892) pts were found to have IgA deficiency 

Ethnicity:

n/aPatient type/# screened: 

1,894 individuals taken randomly from 1994 WHO MONICA study population and screened for CD Demographics: n=1,894 age (y): median 50, range 25-74 % F: 50 Incidence: 

Prevalence of CD was 5.3 per 1000 (10/1894); prevalence of newly diagnosed CD was at least 4 per 1000 (8/1892) - (1 woman with positive IgA EMA refused biopsy); as for the prevalence of test positivity: IgA and/or IgG AGA - positive in 23% (438/1892); IgA EMA - positive in 0.5% (9/1892); all CD pts had elevated IgA EMA 

 
A-159

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 Com

Jager, 

2001 

Germany 

Duplicate: 

no 

Publication type: Journal Study design: Cross-sectional prevalence 

Test/methodology: 

IDDM-associated antibodies: islet cell antibodies (ICA) - detected by IF, insulin autoantibodies (IAA) - radioimmunoassay, anti-IA-2 antibodies, and anti-GAD65 antibodies (anti-GADA) - both radioligand binding; thyroid disease-associated antibodies: anti-thyroid peroxidase (anti-TPO) and anti-thyroglobulin (anti-TG) - both ELISA; pernicious anemia-associated antibodies: anti-gastric parietal cell antibodies (antiGPC) - IF; adrenalitisassociated antibodies: antiadrenal cortex antibodies - IF; celiac disease-associated antibodies: IgA AGA, IgG AGA, IgA-tTG - all ELISA Biopsy criteria/description: n/r Confirmatory test: none Checked IgA def. 

n/r 

Ethnicity:

n/aPatient type/# screened: 

197 pts with a new onset of IDDM diagnosed according to WHO criteria; 882 first-degree relatives; 150 healthy controls without a family history of IDDM 

Demographics: 197 pts with IDDM (age (y): median 16, range 5-27, 43% F); 882 first-degree relatives - 485 were parents (age (y): median 43, range 22-59), 382 siblings and 15 offspring of IDDM pts (age (y): median 16, range 2-41) Incidence:

Recentonset IDDM (n=197): IgG AGA - 10.2%; IgA AGA - 7.6%; antitTG IgA - 9.7%; at least 1 antibody positive - 16.8% 

First-degree relatives (n=882): IgG AGA - 5.6%; IgA AGA - 2.6%; antitTG IgA - 3.2%; at least 1 antibody positive7.3% 

Healthy control subjects (n=150): IgG AGA - 3.2%; IgA AGA -2.0%; antitTG IgA - 2.6%; at least 1 antibody positive4.6% 

IDDM associated antibodiesignificantly more frequent group and first-degree rela(p<0.05); the relevance of was significantly higher in IDDM compared to first de(p<0.05), but the difference relatives and controls did nsignificance; the overall freantibodies did not differ sig

as for coexistence of antib

presented with 27% of the positive-specific for 2 or mcompared with 3.1% in the and 0% of control populatio

IDDM (n=197): IDDM-asso82.1%; anti-GADA - 76.0%IAA - 37.8%; at lease 1 andisease-associated antibod- 18.4%; pernicious anemiaGPC - 5.6%; adrenalitis-asadrenal cortex antibodies - (n=882): IDDM-associated GADA - 7.6%; anti-IA-2 anlease 1 antibody - 11.6%; Tantibodies: anti-TPO+-TG anemia-associated antibodadrenalitis-associated antib

antibodies - 1.1%; healthy IDDM-associated antibodie2.6%; anti-IA-2 antibodies antibody - 4.0%; Thyroid danti-TPO+-TG antibodies - associated antibodies: antiassociated antibodies: anti0.7% 
A-160

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Johnston, 

1998 

UK 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgA AGA - ELISA, normal range of 0-99 (97.5th percentile); IgA EMA - IF on a ME, positive was taken at a titre of 1:5

Biopsy criteria/description: enteropathy consistent with CD was considered to include severe partial VA, sub-total or total VA Confirmatory test: 

biopsy; Watson-Crosby capsule; biopsy done in 51 out of 87 pts in MONICA 1991 survey pts and in 20 out of 72 pts in MONICA 1983 survey group 

Checked IgA def. 

n/r 

Ethnicity:

n/aPatient type/# screened: 

1) MONICA 1991 survey study: 89 subjects tested positive for CD serology taken from 1823 subjects randomly tested for CD (2 pts were excluded from further analysis because they had CD diagnosis prior to follow-up of the screening program, but included in the assessment of prevalence); 2) MONICA 1983 survey study: 72 CD pts out of 102 who consented to a follow-up of 11.2 y (range 11.3-11.9) Demographics: 

MONICA 1991: 89 subjects with positive CD serology; age (y): mean 50.9, range n/r, 49.4% F; age- and sex-matched 89 controls: age (y): mean 51.1, range n/r, 49.4% F MONICA 1983: 72 with a known CD; age (y): mean 58.1, range n/r, 53% F; no controls were included in this survey 

Incidence:

MONICA 1991: 0.82% [15 (2 with a CD prior to screening program and 13 - screening revealed CD pts) out of 1823] biopsy proven CD making a prevalence of 1:122 

MONICA 1983: the estimated prevalence for CD from this survey is 4/1206, or 1:301; if the 2 deceased subjects are included prevalence raises to 6/1206, or 1:201 

 
A-161

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Kolho, 

1998 

Finland 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

EMA – IF HUC; methodology n/r

Biopsy criteria/description: 

capsule or endoscopic biopsy; ESPGAN criterias; CD3-positive T cell calculation (limit for high cell number was 77 cells/mm; limit for a moderate cell number was 63 cells/mm); gamma/delta T-cell receptorbearing cell calculation (limit for a high cell number was 8.2 cells/mm) 

Confirmatory test: 

capsule or endoscopic biopsy 

Checked IgA def. 

n/r 

Ethnicity:

n/aPatient type/# screened: 

not at risk: 1,070 adults of Finnish ancestry screened for CD Demographics: 1,070 adult population with no clinical signs of CD screened at Helsinki University General Hospital during 1996 Incidence: 

11 out of 1,070 were positive for IgA EMA; 8 out of these 11 were found to have CD on biopsy, giving the prevalence of CD in this group 1:130 

 
A-162

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Maki, 

2003 

Finland 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgA-tTG, Celikey assay with low-cut off of 5U/mL; IgGtTG, ELISA; IgA- and IgGEMA, IF; total serum IgA - nephelometerical determination with serum levels of <0.05 g/L indicative of IgA deficiency; HLA- DR; DQ2 and DQ8

Biopsy criteria/description: 

endoscopic biopsy; the ratio of villous height and crypt depth less than 2 was considered to be indicative of CD 

Confirmatory test: 

biopsy in children with IgA EMA and IgA-tTG positivity (in 2001) 

Checked IgA def. 

yes 

Ethnicity:

n/aPatient type/# screened: 

3,654 schoolchildren Demographics: asymptomatic schoolchildren median age: 12 y, range 7-16 y at the time of 1st sampling (1994) Incidence: 

Prevalence of CD was 1:99 (37/3654); prevalence of test positivity for CD was 56/3654; 10 of these were identified by symptoms, and of remaining 46, 27 had abnormal biopsy. all but two (52) of antibody pos pts had either HLA-DQ2 or the HLA-DQ8 haplotype; Prevalence of combination of antibody positivity and CD-associated HLA haplotype was 1 in 67 

 
A-163

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Mazzeti, 

1992 

Italy 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

IgA-AGA; biopsy Biopsy criteria/description: atrophic or completely absent villi Confirmatory test: n/r Checked IgA def. 

n/r 

Ethnicity:

n/rPatient type/# screened: 

n=3,022; Roman school children 

Demographics: age range: 13-15 y olds Incidence: 

By first AGA-IgA: 19 

biopsy proven: 18 

 
A-164

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Not, 1998, 

USA 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgG and IgA-AGA - ELISA (goat immunoglobulin) cut-off was above mean ± 2 SD; IgAEMA (IgA-AGA or IgG-AGA) - indirect IF on either ME or HU, cut-off n/r

Biopsy criteria/description: 

n/r 

Confirmatory test: 

no biopsy in the 96 IgA/IgG pos or 8 EMA positive pts; HLA haplotype typed in 4 EMA-positive and 23 EMAnegative donors; all 4 EMApositives carried CDassociated alleles: 3 had DQA1*0501 and DQB1*0201 haplotype and 1 - DQA1*03 and DQB1*0302 

Checked IgA def. 

yes; none of 86 donors with positive IgG AGA and negative IgA AGA/EMA had IgA deficiency 

Ethnicity:

1,740 Caucasians (87%), 230 African-American (11.5%), and 30 Asians (1.5%)Patient type/# screened: 

2,000 healthy blood donors Demographics: mean age: 39 y % F: 48 Incidence: 

Prevalence of test positivity: 4.8% (96/2000) for IgA and/or IgG; 0.4% (8/2000) for EMA 

 
A-165

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Pittschieler, 

1996 

Italy 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgA- & IgG-AGA; IgA-EMA; biopsy

Biopsy criteria/description: partial or total VAConfirmatory test: ? Checked IgA def. 

n/r 

Ethnicity:

2,778 German; 1,837 ItalianPatient type/# screened: 

healthy consenting adults 

Demographics: n=4,615; median age (y) 36.6; range 18-82 Incidence: 

By first serology: 140 By confirmation serology: 9 By biopsy: 9 
A-166

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Riestra, 

2000 

Spain 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

IgG/IgA-AGA-ELISA; values above 25 (children) and 34 (adults) AU for IgA or above 46 (children) and 42 (adults) AU for IgG were considered positive; IgA-EMA, IF, sera manifesting fluorescence at a titre of at least 1:5 was considered positive; The study was conducted as a 1) two step (determination of IgA/IgG AGA, if positive measuring IgA-EMA); and a 2) one-step protocol (measuring IgA-EMA)Biopsy criteria/description: endoscopic biopsy; Marsh Confirmatory test: EMA- indirect IF ME; titre≥1/5; biopsy in IgA and 

IgG pos/IgG AGA pos with IgA deficiency or isolated EMA positives; HLA DQ2 Checked IgA def. 

yes; none were found to have IgA deficiency 

Ethnicity:

n/aPatient type/# screened: 

1,170 randomly selected individuals from general population Demographics: age (y): mean 44.9+-20.9; range 2-89; 55.3% F Incidence:

overall prevalence of CD was 2.6:1000; in twostep screening prevalence rate was 0.8:1000 (1/1170, 95% CI 0-55%); in one-step screening prevalence was 1.7:1000 (2/1170, 95% CI 0-6.9%); as for test positivity: IgA or IgG AGA was positive in 15% (174/1170); 1/174 confirmed with EMA and biopsy; 1 CD biopsy proven CD was confirmed even if AGA and EMA were negative; HLA-DQ2 allele was found in 2/3 new CD pts 
A-167

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Rostami, 

1999 

Netherlands 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

IgA-EMA, IF; IgAnephelometry; methodology n/r Biopsy criteria/description: EPSGAN; Marsh Confirmatory test: endoscopic biopsy; endoscopically guided capsule (Fujinon) Checked IgA def. 

yes; none were found to have IgA deficiency 

Ethnicity:

n/aPatient type/# screened: 

1,000 healthy blood donors 

Demographics: n/r 

Prevalence of CD in a healthy donors was 1 in 330 (3/1000); as for the prevalence of test positivity: 3/1000 were positive for EMA; biopsy in all of these 3 confirmed CD: 2/3 Marsh IIIb; 1/3 Marsh II 

 
A-168

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Rutz, 2002 

Switzerland 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

IgA-EMA, indirect IF on ME; IgA-tTG- ELISA with lower threshold value 0.2 g/L; IgG-AGA and IgA-AGA Biopsy criteria/description: Marsh criteria; endoscopic biopsy Confirmatory test: endoscopic biopsy Checked IgA def. 

yes (0/1450) 

Ethnicity:

n/aPatient type/# screened: 

1,450 students 

Demographics: age range 12-18 y; 871 (60.1%) F 

Prevalence of CD was 1 in 132 (0.75%; 11/1450); as for the prevalence of test positivity: 11/1450 EMA/tTG positive; 10/11 (1refusal) EMA/TTG/AGA/AGG positive (second level of screening); 9/10 (1 refusal) biopsied: 8/9 Marsh III 

 
A-169

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Sanders, 

2003 

UK 

Duplicate: 

no 

Publication type: Journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgG and IgA - ELISA; EMAindirect IF of ME; methodology n/r Biopsy criteria/description: Revised Marsh Confirmatory test: biopsy Checked IgA def. 

yes 

Ethnicity:

n/aPatient type/# screened: 

1,200 randomly selected individuals divided in 2 groups: visitors and pts: 1) 609 pts with a non CD-related symptoms in 338; 2) visitor group 591 individuals with a non-CD associated symptoms found in 409 (69.2%) 

Demographics: 1) pts group: age (y): median 48, range 16-91; 64.4% F; 2) visitors group: age (y): median 45, range 18-85; 61.1% F Incidence:

Prevalence of CD in primary care population was 1% (12/1200; 95% CI 0.4-1.3%); as for the prevalence of test positivity: 13.5% (162/1200) were antibody positives: 139 - IgG AGA positive, 10 - IgA AGA positive; 4 both IgA/IgG AGA positive, 3 - only EMA positive, 4 - EMA and IgG AGA positive; 2 all antibody positive; 23 pts were eligible for biopsy; out of 22 biopsies (1 pts refused) CD was confirmed in 12 pts 

 
A-170

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Sjoberg, 

1994 

Sweden 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgG AGA- ELISA, cut-off 330; IgA AGA- cut-off 8.5; (arbitrary cut-off values adopted based on normal samples)

Biopsy criteria/description: 

Marsh; Watson Capsules 

Confirmatory test: 

biopsy 

Checked IgA def. 

n/a 

Ethnicity:

n/aPatient type/# screened: 

1) 1,537 consecutive healthy blood donors; 2) 384 school children; 3) 944 women Demographics: 1) age (y): mean 38, range 19-70; 27.3% F; 2) 12 y; 51% F; 3) 57 y women only Incidence: 

Prevalence of CD in blood donors was at least 1 in 1,500; as for test positivity: 22/1537 (1.43%) pts were positive for IgG and IgA AGA; 13 of these 22 pts were biopsied and 1 of 13 had biopsy confirmed CD 

12 y old children15/384 (3.9%) were positive for IgG and/or IgA AGA 

57 y old women11/944 (1.17%) were positive for IgG and/or IgA AGA; 
A-171

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Sjoberg, 

1999 

Sweden 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgA-AGA, ELISA values above 8.5 arbitrary units were considered positive; IgGAGA, ELISA values above 330 arbitrary units were considered positive; EMA, IF ME

Biopsy criteria/description: 

subtotal and total VA considered diagnostic of CD. Infiltrative lesions, i.e., increased level of IELs were also considered as CD 

Confirmatory test: 

small bowel biopsy 

Checked IgA def. 

n/r 

Ethnicity:

n/aPatient type/# screened: 

1,970 blood donors Demographics: 685 women 1,285 men (adults) mean age: 41.2 y, range 18-70 y % F: 35 Incidence: Time period: between Oct. 1996-Feb.1997 (4 mos) 

Positive results from 1970 pts IgG AGA- 60/1970 (3%) IgA AGA- 150/1970 (7.6%); both IgA and IgG- were 25/210 for a total of 185/1970 (9.4%) who had either IgA or IgG. Those 185 serum samples were analysed for EMA 3/185 positive 3 had small bowel Bx, 2 subtotal VA, 1- total VA. One had classic CD and 2 had infiltrative lesions and were on GFD with improvement. Thus prevalence rate for confirmed CD 4:1970 (0.20%) if infiltrative lesions regarded as CD prevalence 6:1970 (0.30%) 
A-172

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Trevisol, 

1999 

Italy 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgA-EMA; biopsyBiopsy criteria/description: subtotal or total VA

Confirmatory test: ? Checked IgA def. 

n/r 

Ethnicity:

White CaucasiansPatient type/# screened: 

healthy adult blood donors 

Demographics: n=4,000; mean age 35 y;

range 18-60 Incidence: 

By first serology: 10 By biopsy: 10 
A-173

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 Group 4 

Overall at risk 18/240 were EMA positive and confirmed positive with intestinal biopsy (7.5%) 

Stature growth defect 8:105 (7.6%) 

Recurrent abdominal pain 3:45 (6.6%) 

Sideropenic anemia 4:17 (23.5%) 

Group 5 Group 6 Group 7 Group 8 

Ventura, 

2001 

Italy 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: IgA-EMA , indirect IF using HU 

Biopsy criteria/description: 

ESPGAN a single specimen from the duodenal junction with a Watson capsule 

Confirmatory test: 

intestinal biopsy 

Checked IgA def. 

yes 

Ethnicity:

n/aPatient type/# screened: 

19,791 children visiting family pediatrician over a 2 y period. Inclusion criteria "at risk": short stature; recurrent abdominal pain; IDA; enamel hypoplasia; recurrent aphthous stomatitis; autoimmune disease (such as IDDM, juvenile arthritis, autoimmune thyroiditis), occult hypertransaminasemia, IgA deficiency Down syndrome or CD in a first degree relative 240 met criteria; first-degree relatives of newly diagnosed CDs of this study (n=17?) Demographics: 240 (103 male 43%) mean age 4.8 y Incidence: Time period: Oct. 31, 1995- Oct. 31, 1997 

Autoimmune disease 1:19 (5.2%) 

Down syndrome 1:11 (9.0%) 

CD firstdegree relative 1:14 (7.1%) 
A-174

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Volta, 2001 

Italy 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgA-EMA-HUBiopsy criteria/description: Roy-Choudhry; Subtotal villous strophyConfirmatory test: ? Checked IgA def. 

n/r 

Ethnicity:

Northern ItaliansPatient type/# screened: 

3,483 general population 

Demographics: n=3,483; 12-65 y, only 784 in 12-25 group Incidence: 

By EMA: 0.57% (20/3483); by biopsy: 0.49% (17/3483) 

 
A-175

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Weile, 

2001 

Denmark 

& Sweden 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

serum IgA; IgG-AGA; IgAAGA, cut-off >40 units; EMA; in cases of IgA <0.07g/L, IgGAGA was analyzed

Biopsy criteria/description: 

n/a 

Confirmatory test: 

biopsy in the Swedish sample only 

Checked IgA def. 

yes; prevalence in both population of blood donors was 0.3% 

Ethnicity:

n/aPatient type/# screened: 

blood donors Demographics: Denmark: 

n=1,573 adults mean age: 41.4 y, range >18 y % F 40.9 

Sweden: 

n=1,866 adults mean age = 37.6 y, range >18 y % F: 31.7 

Incidence:

Denmark: by IgAAGA 4% (61/1573), by EMA 0.25% (4/1573) 

Sweden: by IgAAGA 3.2% (60/1866), by EMA 0.27% (5/1866); by biopsy 0.27% (5/1866) 
A-176

Evidence Table 4 (cont’d): Prevalence/incidence of CD in the general population 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

West, 2003 

UK 

Duplicate: 

no 

Publication type: Journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgA EMA, indirect IF on commercial ME using 1:10 dilution; tTGA, ELISA >3 U/mL considered positive Biopsy criteria/description: no biopsy done Confirmatory test: tTGA (no confirmatory test conducted i.e. biopsy) Checked IgA def. 

yes 

Ethnicity:

n/aPatient type/# screened: 

7,550 general practice unselected 

Demographics: 7,527 adults aged 45-76 y not previously diagnosed with CD, mean age 59 y; 4,444 (59% F) Incidence:

Time interval: 1990-1995 

EMA positive 87/7527 (1.2%); EMA pos and abnormal tTGA 77/87 (89%) 

 
A-177

Prevalence of CD in Associated Clinical Conditions—Patients with Suspected CD Evidence Table 5: Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Agardh, 

2001 

Sweden 

Duplicate: 

yes, 

Celiac 1 

(Carlsson 

et al., 

Pediatrics 

1999;103:

1248) 

Publication type: journal Study design: 

retrospective crosssectional prevalence Test/methodology: 

tTG; HLA DQB1; AGA >25 

AU; EMA titres >1:5, 

biopsies Biopsy criteria/description: as described in Carlsson et al., 1999 (Pediatrics 103:1248) Confirmatory test: biopsy Checked IgA def. 

n/r 

Ethnicity:

n/aPatient type/# screened: 

Group 1: IDDM (three were known and treated CD cases) Group 2: generally healthy subjects Demographics: IDDM group: (n=165) with CD: median age 7 y, age range=1-13 y; 64% F Without CD: median age=10 y, age range 2-19 y, 44% F control group: (n=277) age range 11-16 y, 53% F Incidence: n/a 

IDDM group: by AGA: 6.8% (11/162); by EMA: 4.9% (8/162); by biopsy: 3.7% (6/162); by IgAtTG: 5.6% (9/162); by IgG-tTG: 6/162 (3.7%) 

control group: by AGA: 8.7% (24/277); by EMA: 0% (0/277); by IgAtTG: 0% (0/277); by IgG-tTG: 0% (0/277) 

 
A-178

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Annibale, 

2003 

Italy 

Duplicate: 

no 

Publication type: journal Study design: 

prospective prevalence Test/methodology: 

IgA-tTG, ELISA normal values were < 7UA/mL Biopsy criteria/description: Marsh Confirmatory test: Biopsy, antral, gastric body, and duodenal biopsy collected Checked IgA def. 

n/r 

Ethnicity:

n/aPatient type/# screened: 

IDA in premenopausal women Demographics: n=59 premenopausal women; age range 22-54 y with IDA Hb<12g/dLF Incidence: Time period: March-July 2000 

7/59 (11.9%) had positive anti-tTG antibodies titre; biopsyconfirmed: 8.5% (5/59) 

 
A-179

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Bardella 

1991 

Italy 

Duplicate: 

no 

Publication type: journal Study design: 

prevalence Test/methodology: 

IgA-AGA Biopsy criteria/description: n/r Confirmatory test: Checked IgA def. 

Ethnicity:

n/rPatient type/# screened: 

suspected CD: iron-deficient, bowel disturbances, chronic intermittent diarrhea, severe malabsorption, tiredness and wt loss, mineral metabolism deficiencies, glutenintolerance in childhood not further investigated Demographics: n=60; median age 28 (range 15-69); 41 F/19 M Incidence: 

26 
A-180

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Bardella 

2001 

Italy 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

IgA-tTG >10 AU/mL using GP liver; AGA >12 AU/mL; indirect IF EMA titre>1:10; biopsy Biopsy criteria/description: n/a? didn't mentioned the biopsy results, not used for case diagnosis Confirmatory test: none Checked IgA def. yes, one found 

Ethnicity:

n/aPatient type/# screened: 

suspected CD, confirmed and treated CD pts (to be excluded), disease control group (to be excluded) Demographics: n=80 suspected CD; adult; mean age 39 y; age range 17-79 y; 70% F Incidence: 

50% (40/80) 
A-181

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Bode 

1993 

Denmark 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

AGA, IgG, IgA Biopsy criteria/description: all biopsied Confirmatory test: all biopsied criteria not stated Checked IgA def. no 

Ethnicity:

n/rPatient type/# screened: 

suspected CD; all children Demographics: n=191; 74 F/117 M; median age: 2.75 y (range 0.33-15.5 y) Incidence: 

14 cases (7.3%) 
A-182

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Carroccio, 

2002 

Italy 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional prevalence Test/methodology: 

serum EMA; serum anti-GPtTG; serum anti-human-tTG Biopsy criteria/description: ESPGAN? Three groups: normal, partial VA or subtotal/total VA; positive for CD if partial or total VA Confirmatory test: biopsy Checked IgA def. Yes, none found 

Ethnicity:

n/aPatient type/# screened: 

adult pts with suspected CD Demographics: n=207; adult; median age 42 y; age range 17-84 y; 52.3% F Incidence: 

By GP-tTG: 18.8% (39/207); by h-tTG: 14.5% (30/207); by biopsy: 11.6% (24/207) 
A-183

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 

Chan, 

2001 

Canada 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

GP-tTG; EMA; biopsy Biopsy criteria/description: Carey capsule, or 4-6 duodenal biopsies at time of endoscopy; no grade provided, a diagnosed case=increased number of IELs with associated subtotal or total VA Confirmatory test: biopsy Checked IgA def. Yes, two found 

Ethnicity:

n/aPatient type/# screened: 

77 pediatric pts with suspected CD; 16 type I diabetes Demographics: n=93; mean age: n/r; range 2 mos to 18 y; % F: n/r Incidence: 

GI group: 12% (9/77) DM group: 75% (12/16) 
A-184

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Chartrand, 

1997 

Canada 

Duplicate: 

no 

Publication type: journal Study design: 

prevalence Test/methodology: 

biopsy Biopsy criteria/description: ESPGAN Confirmatory test: Checked IgA def. 

Ethnicity:

n/rPatient type/# screened: 

suspected CD; n=179 Demographics: all children; mean age 5.2 y, range 0.5-18.1 y Incidence: 

30 (17%); mean age 3.7 y (range 0.6-11.2); 17 F/13 M 
A-185

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Csizmadia 

1999, 

Netherlands 

Duplicate: 

no 

Publication type: journal (research letter) Study design: 

cross-sectional Prevalence Test/methodology: 

IgA-EMA (methodology n/r) Biopsy criteria/description: n/r Confirmatory test:

Small bowel biopsy, subset of 27 had HLA typing for DQ2 Checked IgA def. n/r 

Ethnicity:

n/rPatient type/# screened: 

6,127 children between ages of 2-4 y general population Demographics: 6,127 pediatric pts between 2-4 y; gender:n/r Incidence: Time period: between May 1997-June, 1998 

1.2% (75/6127) by IgA-EMA, 18/75 refused small bowel biopsy; 0.51% (31/75/6127) VA 

 
A-186

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Day, 2000 

New 

Zealand 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

IgA, IgG-AGA, EMA Biopsy criteria/description: single pathologist, Marsh Confirmatory test: biopsy on EMA pos Checked IgA def.

yes 

Ethnicity:

n/rPatient type/# screened: 

pediatric input or output; single center; suspected CD: failure to thrive, short stature, chronic GI symptoms; DM; histological findings of CD; 6 mos-15 y Demographics: mean age: 63 mos (range 6 mos-15 y); % M: 58 Incidence: 

27/36 EMA+; 5/11 biopsy confirmed 
A-187

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Fasano, 

2003 

USA 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

EMA-IF; ME or HU; positive at 1:10 ; all positive EMA tested with human tTG ELISA positive at 2 SD above mean of healthy controls; HLA DQ2 and DQ8 Biopsy criteria/description: single pathologist, Marsh Confirmatory test: htTG; biopsy; also small subset 98 EMA positive and 114 EMA neg had HLA DQ2/8 tested Checked IgA def.n/r 

Ethnicity:

94% White; 3% Black; 1.5% Hispanic, 1% Asian, 0.5% other Patient type/# screened: 

9,019 at risk of CD; 4,126 not at risk Demographics: at risk: symptoms of CD (1,326 children, 1,909 adults); CD associated disorders; 4,508 1st deg relatives; 1,275 2nd deg relatives; not at risk: 2,000 blood donors (mean age 39 y range 19-65 y); 1,119 school children (mean age 12.3 y, range 6-18 y); 1,007 adults and children for routine physical (mean age: 39 y, and 13.7 y; range: 19-71 y, and 2-18 y, respectively) Incidence: 

1) At risk: a) 1st deg relatives-205/4,508 (4.55%); children54/1,294 (4.17%); adults-151/3,214 (4.70%); b) symptomatic adults: 28/1,910 (1.47%); children: 53/1326 (4.00%) 2) Not at risk: 1/4,126 (0.75%); adults27/2,845 (0.95%); children4/1281(0.31%); biopsy in EMA+ Marsh I-0%; Marsh II30/116 (25.9%); IIIa46/116 (39.7%); IIIb24/116 (20.7%); IIIc16/116 (13.8%); HLA DQ2-76/98 (78%); DQ8-16/98 (16%); DQ2 and 8-6/98 (6%); all EMA pos were also tTG pos 
A-188

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Fitzpatrick 

2001 

Canada 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence; authors state that the study is a case-control (doubtful) Test/methodology: 

IgA-EMA-IF using ME; positive when characteristic fluorescence pattern was produced Biopsy criteria/description: not performed Confirmatory test: None Checked IgA def.n/r 

Ethnicity:

n/rPatient type/# screened: 

92 pts with recurrent abdominal pain screened for EMA positivity; 81 healthy children also screened for EMA positivity Demographics: 92 pts with recurrent abdominal pain; age: n/r; 62% F; 81 healthy controls; age: n/r; 42% F Incidence: 

The prevalence of IgA-EMA positivity in children with recurrent abdominal pain was 1 in 92 (1%, 95% CI 0-6) 

The prevalence of IgA-EMA positivity in controls was 1 in 81 (1%, 95% CI 0-7) 
A-189

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Hill 2000 

USA 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

IgA-EMA, IF on ME, methodology n/r; IgA and IgG-AGA, ELISA, methodology n/r Biopsy criteria/description: Marsh Confirmatory test: biopsy Checked IgA def.yes 

Ethnicity:

n/rPatient type/# screened: 

1,200 pediatric group of individuals at risk of CD; pts were assigned to one of 7 groups: 1) chronic diarrhea (n=182); 2) abdominal pain (n=316); 3) IDDM (n=81); 4) short stature (n=259); 5) failure to thrive (n=123); 6) miscellaneous (Down's syndrome, thyroiditis, anemia, unexplained elevation of liver enzymes) (n=47); 7) asymptomatic relatives (n=192) Demographics: 1,200 pediatric group of individuals at risk of CD; age: mean n/r; range: 6 mos-20 y; % F n/r Incidence: 

Prevalence of CD in pts at risk was 1 in 57 (21/1200); prevalence of test positivity: 2.8% (34/1200) was both EMA and AGA positive; 26 of pts (19 EMA positive) underwent biopsy and 21 were diagnosed with CD 

 
A-190

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Hin 1999 

UK 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional Prevalence Test/methodology: 

EMA (ME); biopsy of positives; IgA levels, IgGAGA for IgA deficient Biopsy criteria/description: Crosby capsule, EGD distal duod in 2 cases Confirmatory test: biopsy; 100% positive; IEL: 1/30; mild VA: 1/30; partial VA: 1/30; subtotal VA: 14/30; total VA: 13/30 Checked IgA def.yes 

Ethnicity:

n/aPatient type/# screened: 

entry criteria: IBS, anemia, histological findings of CD, malabsorption symptoms, diarrhea, fatigue, thyroid disease, DM, wt loss, short stature, failure to thrive, epilepsy, infertility, arthralgia, eczema; 1,000 screened Demographics: n=271 M, mean age: 49.9 y (range 1-84); n=729 F, mean age: 45.2 y, range 6 mos-85 y); 5.3% <10 y, 3.1% aged 80-90 y; % F: 73 Incidence: 

# New cases: 30 pts (8 M:22 F) +ve EMA and +ve biopsy 

Time period: 30/1 y Control popn: 7 /preceding 1 y in absence of case finding 

Prevalence of CD in pts at risk was 1 in 57 (21/1200); prevalence of test positivity: 2.8% (34/1200) was both EMA and AGA positive; 26 of pts (19 EMA positive) underwent biopsy and 21 were diagnosed with CD 

 
A-191

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Hoffenberg 

2003 

USA 

Duplicate: 

no 

Publication type: journal Study design: 

prospective stratified cohort study Test/methodology: 

IgA tTG Biopsy criteria/description: Marsh score of 2 (enlarged crypts and increased numbers of intraepithelial lymphocytes) or 3 (any degree of VA) was considered evidence of CD Confirmatory test: TG autoantibody seropositivity on two separate occasions at least 6 mos apart; biopsy Checked IgA def.yes 

Ethnicity:

non-Hispanic white 56%, Hispanic 30%, AfricanAmerican 7%, AsianAmerican 2%, or biracial/other 5% Patient type/# screened: 

987 infants with high-risk genotypes: HLA DR3-3; DR3/4, DQB1*0302; DR4, DQ8 DR5/7 (since 2000) Demographics: 987 infants (tested over 5 y span) gender n/r Incidence: Time period: newborns between Dec 1993-Sept 1999 

 40/987 tested positive 

for tTG; 19/40 met criteria for CD (10 with intestinal biopsy and 9 with persistent tTG autoantibody seropositivity) 

 
A-192

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Hogberg, 

2003 

Sweden 

Duplicate: 

no 

Publication type: journal Study design: 

longitudinal follow-up, incidence & prevalence Test/methodology: 

IgA-AGA, ELISA cut-off for a positive outcome 42.5 units; IgA-EMA, indirect IF using ME, antibody titre defined as the highest serum dilution yielding positive fluorescence; IgA-TGA, commercially available ELISA, highest cut-off value for positive results >30 units. Biopsy criteria/description: revised ESPGAN. Grade 1 normal; Grade 2 mild; Grade 3 moderate, Grade 4 total VA Confirmatory test: Small bowel biopsy Checked IgA def.yes, 5 cases found 

Ethnicity:

n/aPatient type/# screened: 

120 first degree relatives of CD pts Demographics: n=56 parents (adults), mean age 53.6 y, range 43-78 y; n=44 siblings (ped and adult), mean age 27.4 y, range 15-49 y; n=20 offspring, mean age 6.5 y, range 1-16 y; gender n/r Incidence: Time period: 20 y follow-up study. Original study period Sept 1975-Feb 1981 

10/120 (8.3%) prevalence, 2 were diagnosed in the original study 20 y prior, 8 new cases from the present follow-up study group. (biopsy confirmed); serum results: IgAAGA 8/120 pos; IgAEMA 0.5% (6/120) pos; IgA-TGA 3.8% (4/104) pos (3 pts with positive biopsy were not tested for IgA TGA) 

 
A-193

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Pittschieler, 

2003 

Italy 

Duplicate: 

no 

Publication type: journal Study design: 

prospective prevalence Test/methodology: 

EMA, HUC examined by fluorescence. Absence of binding was considered a negative test; HLA typing was done exclusively once diagnosis of CD was confirmed (microlymphocytotoxic technique) Biopsy criteria/description: Small intestinal biopsy of first jejunal loop. Ferraris Watson capsule. Normal values being <3.2 cells/mm γ/δ T-cell receptors by immuno-histology Confirmatory test: biopsy, HLA typing Checked IgA def.

yes, none found 

Ethnicity:

n/a Patient type/# screened: 

92 first-degree relatives of CD pts. Yearly testing over 12 y period Demographics: n=92 at risk (first-degree relatives; 18 offspring and 74 siblings); aged 2-18 y Incidence: Time period: 12 y time period Jan 1990-Dec 2001 

6.5% (6/92) confirmed CD by both serology & biopsy within a few months of CD diagnosis in one of their relatives. 5 total VA and 1 partial VA; over 2-5 y a further 5.8% (5/86) confirmed positive with both HUC EMAIgA and biopsy 1 partial VA and 4 total VA; combined prevalence=12% (11/92); 11/11 were carriers of HLA DQ2/ heterodimers 

 
A-194

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Thomas, 

1992 

England 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional prevalence 

Test/methodology: 

biopsy Biopsy criteria/description: normal histology; mild enteropathy; moderate enteropathy; severe enteropathy; response to GFD Confirmatory test: n/r Checked IgA def. 

yes 

Ethnicity:

n/rPatient type/# screened: 

pediatric pts presenting with chronic diarrhea 

Demographics: n=381; 64% <2 y; 20% 2-5 y; 16% 5-15 y; % F: 41.5 Incidence: 

2/97 mild enteropathy; 1/38 moderate enteropathy; 27/34 severe enteropathy=7.9% 
A-195

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Tursi, 

2003 

Italy 

Duplicate: 

no 

Publication type: journal Study design: prevalence 

Test/methodology: 

IgA IgG, ELISA lower limit of positivity of IgA 0.2 EU/mL and IgG 10.0 EU/mL; IgA-EMA, indirect IF on ME; IgA-tTG, ELISA using GP liver substrate, lower limit of positivity was 7 UA/mL Biopsy criteria/description: Marsh criteria 6 biopsies from small bowel from the second part of duodenum. Marsh Type I -'infiltrative' lesions with >30 lymphocytes/100 epithelial cells; Type II- 'infiltrative/hyperplastic' lesions; Type III-

'partial (sub)total VA; partial VA Marsh IIIa); subtotal VA Marsh IIIb); and total VA as Marsh IIIc) Confirmatory test: Biopsy Checked IgA def. 

yes 

Ethnicity:

n/rPatient type/# screened: 

111 first-degree relatives of pts with CD 

Demographics: at risk n=111 firstdegree relatives: mean age 28.7 y, range (10-65 y); 38 M, 73 F Incidence: n/r 

CD diagnosed in 49/11 screened relatives (44.14%) prevalence; Prevalence AGA 36.73%; EMA 38.78% ; anti-tTG 44.89% 

 
A-196

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

van Mook, 

2001 

Netherlands 

Duplicate: 

no 

Publication type: journal Study design: retrospective prevalence 

Test/methodology: 

EGD; upper digestive tract endoscopy in 10/35; duodenal biopsies taken in 15/35 Biopsy criteria/description: Marsh Confirmatory test: biopsy Checked IgA def. 

no 

Ethnicity:

n/rPatient type/# screened: 

35 pts with IDA, anaemia defined as Hb <8.0 mmol/L in men or < 7.4 mmol/L in women. Iron deficiency defined as a serum ferritin level <20 μg/L for men or 

<10 μg/L in women; or 

serum iron concentration <45 μg/dL with a transferrin saturation of 10% or less, or the absence of iron stores in bone marrow biopsy specimens. 

Demographics: n=35 pts: median age 71 y, range 22-89 y; 22 F (63%) and 13 M (37%), Incidence: n/r 

2.9% (1/35) Marsh IIIc on both biopsy and endoscopy 
A-197

Evidence Table 5 (cont’d): Prevalence of CD in patients with suspected CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Overall at risk 18/240 were EMA positive and confirmed positive with intestinal biopsy (7.5%); 

Stature growth defect 8/105 (7.6%) 

Recurrent abdominal pain 3/45 (6.6%) 

Group 4 Group 5 Group 6 Sideropenic anemia 4/17 (23.5%) 

Group 7 

Ventura, 

2001 

Italy 

Duplicate: 

no 

Publication type: journal Study design: cross-sectional Prevalence 

Test/methodology: 

IgA EMA, indirect IF using HUC Biopsy criteria/description: ESPGAN a single specimen from the duodenal junction with a Watson capsule Confirmatory test: intestinal biopsy Checked IgA def. 

yes 

Ethnicity:

n/rPatient type/# screened: 

19,791 children visiting family pediatrician over a 2 y period. Inclusion criteria "at risk": short stature; recurrent abdominal pain; IDA; enamel hypoplasia; recurrent aphthous stomatitis; autoimmune disease (such as IDDM, juvenile arthritis, autoimmune thyroiditis),occult hypertransaminasemia, IgA deficiency Down’s syndrome or CD in a first degree relative; 240 met criteria; first-degree relatives of newly diagnosed CDs of this study (n=17?) 

Demographics: n=240: mean age 4.8 y; 103 M (43%) Incidence: Time period: Oct. 31, 1995- Oct. 31, 1997 

CD first degree relative 1/14 (7.1%) 

Autoimmune disease 1/19 (5.2%) 

Down syndrome 1/11 (9.0%) 
A-198

Prevalence of CD in High-Risk Patients—Type I Diabetes Evidence Table 6: Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Agardh, 

2001 

Sweden 

Duplicate: 

yes, 

Celiac 1 – 

Carlsson 

et al., 

Pediatrics 

1999;103: 

1248 

Publication type: journal Study design: 

retrospective crosssectional prevalence Test/methodology: 

tTG; HLA-DQB1; AGA>25 

AU; EMA titres> 1:5, 

biopsies Biopsy criteria/description: as described in Carlsson et al., 1999 Pediatrics 103:1248 Confirmatory test: biopsy Checked IgA def. 

n/r 

Ethnicity:

n/aPatient type/# screened: 

1. IDDM (3 were known and treated CD cases); 2. generally healthy subjects Demographics: ped; 1. IDDM group (n=165)-with CD: median age 7 y, age range 1-13 y, 64% F; without CD: median age 10 y, age range 2-19 y, 44% F. 2. control group (n=277)- age range 11-16 y, 53% F Incidence: 

IDDM group: by AGA: 6.8% (11/162); by EMA: 4.9% (8/162); by biopsy: 3.7% (6/162); by IgAtTG: 5.6% (9/162); by IgG-tTG: 6/162 (3.7%) 

Control group: by AGA: 8.7% (24/277); by EMA: 0% (0/277); by IgAtTG: 0% (0/277); by IgG-tTG: 0% (0/277) 

 
A-199

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Gro

Arato, 

2002 

Hungary 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

EMA, indirect IF; serum IgA measured to avoid false-negative IgA-EMA tests in cases of IgA deficiency (serum IgA<0.2g/L); jejunal biopsy using Crosby capsule for EMA positives; intraepithelial gamma/delta 

T-cells elevated if >7 cells/mm (95% CI) Biopsy criteria/description: other: not described Confirmatory test: jejunal biopsy Checked IgA def. 

yes; none found 

Ethnicity:

n/aPatient type/# screened: 

type I diabetes Demographics: n=205; randomly selected ped pts with IDDM; mean age 11.6 y; age range 2.0-17.0 y; 42.9% F Incidence:n/a 

By EMA: 11.7% (24/205); by biopsy: 8.3% (17/205) 

 
A-200

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Gro

Bao, 1999 

USA 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

tTG (ELISA) >0.05=positive; IgA-EMA using indirect IF; HLA genotype DQ B1 typing of peripheral WBCs with PCR amplification and hybridization; DQ alphatyping performed with ampliType; DQ2, DQ8 Biopsy criteria/description: Other: not described Confirmatory test: *consent to biopsies in only 20 of the 98 tTG positives Checked IgA def. 

no, not mentioned 

Ethnicity:

n/aPatient type/# screened: 

type I diabetes Demographics: n=847; children and adult; mean age 14.5 y; range 0.7-77.7 y; % F? Incidence:n/a 

By tTG only: 11.6% (98/847); by tTG & EMA: 5.8% (49/847); by biopsy: 1.8% (15/20/98/847) 

 
A-201

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Gro

Barera, 

1991 

Italy 

Duplicate: 

no 

Publication type: journal Study design: 

Test/methodology: 

AGA IgA then if negative, IgG AGA Biopsy criteria/description: subtotal VA Confirmatory test: none Checked IgA def. 

Ethnicity:

n/aPatient type/# screened: 

type I diabetes Demographics: n=498; children Incidence:n/a 

By first AGA-IgA: 30 Biopsy proven: 16 

 
A-202

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Gro

Barera, 

2002 

Italy 

Duplicate: 

no 

Publication type: journal Study design: 

prospective cohort; 6 years follow-up [did not give incidence measures, only prevalence] Test/methodology: 

EMA, indirect IF; serum IgA <0.05 g/L in the presence of normal IgG and IgM were regarded as selective IgA deficiency; duodenojejunal biopsy in >8 y children with positive EMA; upper endoscopy for younger children, mucosal histology Biopsy criteria/description: Marsh; three types of lesions: 1. Infiltrative lesion normal mucosa, 2. 

Hyperplastic lesion with enlarged crypts infiltrated by IELs, 3. Some degree of VA with inflammation and hyperplastic crypts; diagnosis considered positive with demonstration of type 2 or 3 lesion Confirmatory test: biopsy Checked IgA def. 

yes, 2 selective IgA deficiency 

Ethnicity:

n/aPatient type/# screened: 

type I diabetes Demographics: n=273; children; mean age 8.28 y, age range 0.6-18.7 y; 42.5% F Incidence:n/a 

By 1 EMA only: 5.5% (15/273); after second EMA: 3.7% (10/273); by biopsy: 3.3% (9/10/273); if add the 1 excluded case (because diagnosed CD before developed IDDM): 3.6% (10/274) 

 
A-203

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Gro

Calero, 

1996 

Spain 

Duplicate: 

no 

Publication type: journal Study design: 

Test/methodology: 

IgA-AGA if positive on two occasions Biopsy criteria/description: subtotal VA Confirmatory test: none Checked IgA def. 

Ethnicity:

n/aPatient type/# screened: 

type I diabetes Demographics: n=141; children Incidence:n/a 

By first AGA-IgA: 12 Biopsy proven: 4 
A-204

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Gro

Cronin, 

1997 

Ireland 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

EMA; biopsy Biopsy criteria/description: other: not mentioned Confirmatory test: biopsy Checked IgA def. no, not mentioned

Ethnicity:

n/aPatient type/# screened: 

IDDM pts Demographics: n=101 diabetic pts and n=51 controls; adolescent and adult; age range for diabetic pt 15-59 y. Other info n/a Incidence:n/a 

By EMA: 7.9% (8/101) By biopsy: 5.0% (5/101) 
A-205

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Gro

De Block, 

2001 

Belgium 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional Prevalence] Test/methodology: 

islet cell antibodies (ICA) - IF, cut-off level was >12 JDF; antibodies to glutamic acid decarboxilase-65 (GADA) - radiobinding assay, cut-off level was >2.6% tracer bound GADA; tyrosine phosphate antibodies (IA2A) - radiobinding assay, cut-off level was >0.5% tracer bound IA2A; thyroid peroxidase antibodies (aTPO) - radiobinding assay, cut-off was >100 U/mL; parietal cell antibodies (PCA) - IF, positivity at >1:20 dilution; antibodies to intrinsic factor (AIF) - radiobinding assay; anti-adrenal antibodies (AAA) - IF; 

anti-EMA - IF on a ME, positivity at >1:10 dilution; HLA DQ Biopsy criteria/description: no biopsy performed Confirmatory test: none Checked IgA def. 

n/r 

Ethnicity:

all CaucasiansPatient type/# screened: 

399 pts with IDDM screened for different autoimmune diseases (176 children <18 y; 223 adults) Demographics: 399 pts with IDDM screened for different autoimmune diseases; age (y): mean 26±16, range n/r; 53% F Incidence:n/a 

Prevalence of CD in 399 pts with IDDM was 0.75% (3/399); prevalence of test positivity: 1) ICA - 39% (157/399); GADA - 70% (278/399); IA2A - 44% (177/399); aTPO - 22% (87/399); PCA - 18% (73/399); AAA - 1% (5/399); IgA EMA - 2% (9/399) 

 
A-206

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Gro

De Vitis, 

1996 

Italy 

Duplicate: 

no 

Publication type: journal Study design: 

Test/methodology: 

IgA, IgG then IgA EMA Biopsy criteria/description: Marsh VA Confirmatory test: biopsy Checked IgA def. 

Ethnicity:

n/aPatient type/# screened: 

type I diabetes Demographics: n=1,114; children & adults Incidence:n/a 

By first IgA: 121 Biopsy proven: 63 

 
A-207

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Fasano, 

2003 

USA 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional prevalence Test/methodology: 

EMA, IF ME or HU; positive at 1:10 ; all positive EMA tested with human tTG ELISA positive at 2 SD above mean of healthy contols; HLA DQ2 and DQ8 Biopsy criteria/description: single pathologist, Marsh Confirmatory test: htTG; biopsy; also small subset 98 EMA-positive and 114 EMA-neg had HLA DQ2/8 tested Checked IgA def.

n/r 

Ethnicity:

94% White; 3% Black; 1.5% Hispanic, 1% Asian, 0.5% other Patient type/# screened: 

9,019 at risk of CD; 4,126 not at risk Demographics: at risk: symptoms of CD (1,326 children, 1,909 adults); CD-associated disorders; 4,508 1st deg relatives; 1,275 2nd deg relatives; not at risk: 2,000 blood donors (mean age 39 y range 19-65 y); 1,119 school children (mean age 12.3 y, range 6-18 y); 1,007 adults and children for routine physical (mean age 39 y, and 13.7 y, range, 19-71 y, and 2-18 y) Incidence: 

1) At risk - a) 1st deg relatives - 205/4,508 (4.55%); children - 54/1,294 (4.17%); adults - 151/3,214 (4.70%); b) symptomatic adults - 28/1,910 (1.47%); children - 53/1,326 (4.00%); 2) Not at risk - 1/4126 (0.75%); adults - 27/2,845 (0.95%); children - 4/1281(0.31%); biopsy in EMA pos - Marsh 1- 0%; 2 -30/116 (25.9%); 3a - 46/116 (39.7%); 3b - 24/116 (20.7%); 3c - 16/116 (13.8%); HLA DQ2-76/98 (78%); DQ8 - 16/98 (16%); DQ2 and 8 - 6/98 (6%); all EMA pos were also tTG pos 
A-208

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

FrazerReynolds, 

1998 

Canada 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional prevalence Test/methodology: 

IgA EMA - IF using ME, positive if staining at a dilution of 1:10; total serum IgA, measured using rate nephelometry Biopsy criteria/description: Carey capsule; Marsh criteria Confirmatory test: biopsy Checked IgA def.yes; none of IDDM pts had IgA deficiency; 3 pts in suspected malabsorption group were found to have IgA deficiency 

Ethnicity:

94% white; 3% Black; 1.5% Hispanic, 1% Asian, 0.5% other Patient type/# screened: 

236 pts with IDDM screened for CD; 56 pts who underwent intestinal biopsy for suspected malabsorption Demographics: 236 pts with IDDM; age (y): mean n/r, range 1-18; 50% F; 56 pts with GI complaints; age (y): mean n/r, range n/r; 43% F Incidence: 

Estimated prevalence of CD in 236 pts with IDDM was 5.1% (12/236; 95% CI 2.7-8.8); as for test positivity: none were IgA deficient; 19 pts were IgA EMA positive; 2 refused biopsy; of 17 pts with IgA EMA, 12 had CD on biopsy 

Estimated prevalence of CD in 56 pts with suspected malabsorption was 9% (5/56); as for test positivity: 3 pts were EMA positive and all had biopsy proven CD; 3 pts were IgA deficient and EMA negative and 1 of them was found to have CD on biopsy; 1 of 50 IgA-sufficient and EMA negative pts had biopsy proven CD 

 
A-209

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Gillett, 

2001 

Canada 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional prevalence Test/methodology: 

IgA EMA, IF on HU, starting dilution 1:5; positive sample were tested at increased dilutions until fluorescence disappeared; IgA tTG, ELISA; reference range of 140 AU/mL or less was calculated to include 3 SD above the mean (99% confidence limit) Biopsy criteria/description: endoscopic biopsy; ESPGAN criteria; 4 biopsy specimens from distal duodenum; elevated IEL count was defined as more than 40 IELs per 100 enterocytes Confirmatory test: biopsy Checked IgA def.yes; using Nor-Partigen Total IgA Kit; 1 pt was found to be IgA-deficient 

Ethnicity:

209 White, 12 East Indian, 7 Asian, 4 First Nation, 1 African Patient type/# screened: 

233 pts with IDDM screened for CD Demographics: 233 pts with IDDM screened for CD; age (y): median 12.9, range 1.3-19.2; 46% F Incidence: 

Prevalence of CD in IDDM pts was 7.7% (18/233); prevalence of test positivity: 8.2% (19/233) was both EMA and AGA positive and all were white; 18 of these 19 pts underwent biopsy (1 was previously diagnosed with CD and was not offered biopsy); CD was confirmed in 14 of these 18 pts 
A-210

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Hansen, 

2001 

Denmark 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional prevalence Test/methodology: 

IgA AGA - ELISA, cut-off n/r; IgA EMA - IF on a ME; IgA tTG - ELISA; thyroid antibodies: thyroid peroxidase (TPO) and thyroglobulin (TG), using radioimmunoassay Biopsy criteria/description: endoscopic biopsy; CD was diagnosed when mucosa showed partial or total VA, crypt hyperplasia and IEL infiltration Confirmatory test: endoscopic biopsy Checked IgA def.yes; none was IgA deficient 

Ethnicity:

n/a Patient type/# screened: 

106 pts with IDDM screened for CD; 106 aged-, and sexmatched healthy controls Demographics: 106 pts with IDDM screened for CD; 2 had been previously diagnosed with CD; age (y): median 12.8, range 2.3-18.2; 47% F; median duration of IDDM 4.8 y, range 0.2-13.3 y; 1 pt had a second-degree relative with CD; 106 aged-, and sexmatched healthy controls; age (y): median 12.9, range 1.3-18.3; 47% F; none had relatives with CD Incidence: 

Screening revealed 9 biopsy proven CD in the 104 pts with IDDM, giving a prevalence of CD 10.4% (95% CI 4.6-16.2%), (11/106 - 2 pts had CD prior to screening); as for test positivity: of 104 tested pts 7 had IgA AGA, 19 - IgG AGA, and 10 - IgA EMA+ IgA tTG; 9 out of 10 EMA+tTG positive pts underwent biopsy (1 refused) and were found all of them to have CD 

Control: none had been diagnosed with CD; as for test positivity: 1 had IgA AGA, 9 - IgG AGA, none - EMA or tTG 

 
A-211

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Jager, 

2001 

Germany 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional prevalence Test/methodology: 

DDM-associated antibodies: islet cell antibodies (ICA) - detected by IF, insulin autoantibodies (IAA) - radioimmunoassay, anti-IA-2 antibodies, and anti-GAD65 antibodies (anti-GADA) - both radioligand binding; thyroid disease-associated antibodies: anti-TPO and anti-TG - both ELISA; pernicious anemiaassociated antibodies: antigastric parietal cell antibodies (anti-GPC) - IF; adrenalitisassociated antibodies: antiadrenal cortex antibodies - IF; CD-associated antibodies: IgA AGA, IgG AGA, IgA-tTG - all ELISA Biopsy criteria/description: n/r Confirmatory test: none Checked IgA def.n/r 

Ethnicity:

n/a Patient type/# screened: 

197 pts with a new onset of IDDM diagnosed according to WHO criteria; 882 first-degree relatives; 150 healthy controls without a family history of IDDM; Demographics: 197 pts with IDDM (age (y): median 16, range 5-27, 43% F); 882 first-degree relatives - 485 were parents (age (y): median 43, range 22-59), 382 siblings and 15 offsprings of IDDM pts (age (y): median 16, range 2-41) Incidence: 

Recent-onset IDDM (n=197): IgG AGA - 10.2%; IgA AGA - 7.6%; anti-tTG IgA - 9.7%; at least 1 antibody positive - 16.8% 

First-degree relatives (n=882): IgG AGA - 5.6%; IgA AGA - 2.6%; anti-tTG IgA - 3.2%; at least 1 antibody positive7.3% 

Healthy control subjects (n=150): IgG AGA - 3.2%; IgA AGA -2.0%; anti-tTG IgA - 2.6%; at least 1 antibody positive- 4.6% 
A-212

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Kaukinen, 

1999 

Finland 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional prevalence Test/methodology: 

IgA EMA - IF, screening dilution of 1:5 was considered as a positive; IgA and IgG AGA - ELISA, for IgA AGA lower limit of positivity was 0.2 EU/mL and for IgG AGA - 10.0 EU/mL Biopsy criteria/description: endoscopic biopsy; ESPGAN criteria; 7 forceps biopsy specimens; histological classification as 1) normal; 2) mild partial VA; 3) severe partial VA; 4) subtotal VA; 3 and 4 were considered as CD Confirmatory test: endoscopical biopsy; performed in 6 (10%) previously diagnosed CD and in 28 pts without the diagnosis of CD; (23 refused biopsy, 3 - lost to follow-up, 2 - died); HLA DR and HLA DQ alleles in a dilution of 1:1500 using PCR/RFLP method Checked IgA def.n/r 

Ethnicity:

n/a Patient type/# screened: 

62 adult pts with more than one autoimmune endocrinologic disorder Demographics: 67% F); ATD+addison's disease - 4 (age (y): median 52, range 34-53; 50% F); APECED - 4 (age (y): median 26, range 17-51; 25% F); IDDM+alopecia areata - 3 (age (y): median 20, range 17-30; 67% F); ATD+alopecia areata - 3 (age (y): median 48, range 33-57; 100% F); ATD+addison's disease+alopecia areata - 1 (age (y): median 42; 0% F); IDDM+addison's disease - 1 (age (y): median 32; 100% F) Incidence: 

In total 7 (11%) out of 62 pts were diagnosed to have biopsy-proved CD; 6 (10%) were previously diagnosed with CD, and 1 (3.6%) of the 28 pts undergoing biopsy also was diagnosed with CD; EMA was positive in 1 (3.6%) pts with a newly diagnosed CD; IgA AGA - in 7 (25%), and IgG AGA - in 1 (3.6%); 14 of 26 subjects were HLA-DQ2 positive, in addition 4 had a celiac-type DQ8 haplotype; thus, 18 (69%) had celiactype and 8 (31%) - a non-celiac genetic background; 

 IDDM 

diabetautoim(includor Graautoimpolyencetodeprevaldepict in pts autoimwere tclinic, 

bias 
A-213

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Kordonouri, 

2000 

Germany 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional prevalence Test/methodology: 

IgA anti-tTG - ELISA antibody titers above 15 were considered positive; EMA - IF, fluorescence at 1:5 dilution was considered as a positive; IgA and IgG AGA - ELISA, for both methods a level above 35 AU were considered as a positive Biopsy criteria/description: endoscopical biopsy; Marsh criteria Confirmatory test: endoscopical biopsy; Marsh criteria (stated as a reference 9); done in 13 CD pts out of 23 suspected CD pts (7 lost to follow-up, 3 - refused biopsy); 9 were found to have biopsy proven CD; IEL per 100 enterocytes counted after immunohistochemical staining for CD8+ cells (normal values in children up to 26 IEL per 100 enterocytes) Checked IgA def.yes; 9 pts out of initial 529 had below normal IgA levels and were excluded from further analysis 

Ethnicity:

n/a Patient type/# screened: 

520 pts with IDDM and no clinical signs of CD Demographics: 520 pts with IDDM; age (y): median 14.2, range 1.6-27.3; 47% F; medium duration of IDDM 4.0 y, range 0-23.6 y Incidence: 

23 (4.4%) of the 520 pts with IDDM were found to be positive for IgA anti-tTG; 18 (3.5%) - for EMA; and 18 (3.5%) - for IgA AGA; prevalence of biopsy proven CD in the whole group of IDDM pts was at least 1.7% (9/520), because in 10 pts with increased IgA anti-tTG levels biopsy was not performed; all 9 pts with biopsy confirmed CD were positive for anti-tTG, and 8 - for EMA 

 Study 

elevatwhen occasthan Eform opositivthe inchistolobiopsy calculabiopsygroup 
A-214

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Lampasona, 

1999 

Italy 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional Prevalence Test/methodology: 

human tissue transglutaminase C - TGCA IgA and TGC IgG; the threshold for positivity was the upper first percentile of normal controls, respectively 0.9 AU for IgG TGCA and 0.3 for the IgA TGCA; typing of HLA for 128 pts with IDDM either using the standard microcytotoxicity test on lymphocytes isolated by immuno-magnetic beads or by sequence specific PCR on DNA extracted from blood mononuclear cells; subjects grouped as DR3/X, DR4/Y, DR3/4, or DRX/Y Biopsy criteria/description: endoscopical biopsy; Marsh criteria Confirmatory test: n/r Checked IgA def.

n/r 

Ethnicity:

n/a Patient type/# screened: 

287 pts with a new onset IDDM; 119 pts with NIDDM; 213 pediatric controls with no family history of diabetes Demographics: 287 pts with IDDM; age (y): median 10, range 0.8-33; 41% F; 119 pts with NIDDM; age (y): median 65, range 42-87; 45% F; 213 controls; age (y): median 4.4, range 0.1-11.2; 49% F Incidence: 

Increased levels of TGCA were detected in 122 of 287 pts with IDDM (43%; CI 37-48%); of the pts 25 (9%; CI 6-13%) had raised levels of IgA TGCA and 121 (42%; CI 36-48%) - IgG TGCA; in 24 pts (8%; CI 5-12%) both IgA and IgG TGCA were found 

In the NIDDM group 2 pts had low levels of IgG TGCA only; as for HLA typing, 34 had DR3/4 genotype, 41 - DR3/X, 38 - DR4/Y and 15 - DRX/Y; increased TGCA were found in 22 (65% CI 46-80%) with the DR3/4 genotype, 19 of those with DR4/Y (50%; CI 33-67%), 16 with DR3/X (39%; CI 24-55%) and in 3 with DRX/Y (20%; CI 4-48%) 

 Almos

autoimanotheTGCA prevalinvolvepathog

transgautoancell de
A-215

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Li Voon 

Chong, 2002 

UK 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional prevalence Test/methodology: 

IgA EMA - IF; IgA AGA - ELISA; total serum IgA Biopsy criteria/description: n/r Confirmatory test: biopsy Checked IgA def.yes 

Ethnicity:

n/a Patient type/# screened: 

509 pts with IDDM assessed during 1998; treated autoimmune thyroid disease - AITD - present in 28 (5.5%); 7 (1.4%) out of 509 had known CD; 38 pts with coexisting IDDM and AITD, but without known CD studied during 1999; and 112 pts with IDDM alone and without known CD assessed during 1999 Demographics: age (y): mean 29.4, range 16-45; 41% F; 38pts with coexisting IDDM and AITD screened for CD: age (y): mean 35.6, range 17-53; 66% F; 112 pts with IDDM alone screened for CD: age (y): mean 30.6+-9, range 16-57; 43% F Incidence: 

1) prevalence of known CD in 509 IDDM pts was 1.4% (7/509); 2 of these 7 pts later on developed AITD 

2) in the 38 pts with coexisting IDDM and AITD screening revealed 1 pts with increased IgA EMA, but normal IgA AGA levels; none were diagnosed with biopsy proven CD, making a prevalence of CD 0% in this group 

3) in the 112 pts with IDDM alone screening for CD revealed 2 pts with increased IgA EMA and normal IgA AGA, 1 of whom had biopsy confirmed CD, making a prevalence of CD in this group 0.9% 

UndiaIDDM compaalone; known develoauthorknown annua
A-216

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Lorini, 1996 

Italy 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional prevalence Test/methodology: 

IgA and IgG AGA: ELISA; levels more than 2 SD were considered abnormal - for IgA >10 AU; for IgG - >7500 AU; R1-ARA: IF on rat kidney and liver; IgA EMA: IF on a distal ME; HLA-DR3, HLA-DR4, HLA-DR7 Biopsy criteria/description: n/r Confirmatory test: intestinal biopsy in 6 pts with constantly elevated IgA AGA during a follow-up Checked IgA def.

n/r 

Ethnicity:

n/a Patient type/# screened: 

133 pts with IDDM; 45 age-matched, apparently normal controls Demographics: 133 IDDM - age (y): mean 14.1, range 1.4-28.4; 47.3% F; 53 pts were considered at the onset of IDDM and 49 of them were also investigated for a 1-10 y follow-up; 45 agedmatched controls (CO); age: mean, range n/r Incidence: 

IDDM pts: 3.75% (5/133) 

IDDM pts: 3.75% (5/133) 

 At the 

AGA w(17/53decreain 13 pAGA ndiagnoIgA AGa folloAGA pR1-ARalso inlevels transieimmunnot prethey sprimara diagunless presenDR4 wwith Apositiv
A-217

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Not, 1998, 

USA 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgG and IgA-AGA - ELISA (goat immunoglobulin) cut-off was above mean ± 2 SD; IgAEMA (IgA AGA or IgG AGA) - indirect IF on either ME or HU, cut-off n/r

Biopsy criteria/description: n/rConfirmatory test: 

no biopsy in the 96 IgA/IgG pos or 8 EMA positive pts; HLA haplotype typed in 4 EMA-positive and 23 EMAnegative donors; all 4 EMApositives carried CDassociated alleles: 3 had DQA1*0501 and DQB1*0201 haplotype and 1 - DQA1*03 and DQB1*0302 

Checked IgA def. 

yes; none of 86 donors with positive IgG AGA and negative IgA AGA/EMA had IgA deficiency 

Ethnicity:

1,740 Caucasians (87%), 230 African-American (11.5%), and 30 Asians (1.5%)Patient type/# screened: 

2,000 healthy blood donors Demographics: mean age: 39 y % F: 48 Incidence: 

Prevalence of test positivity: 4.8% (96/2,000) for IgA and/or IgG; 0.4% (8/2,000) for EMA 

 
A-218

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Page, 

1994, 

UK 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgA-AGA-in-house ELISA; titers of >90 U/L were considered abnormal

Biopsy criteria/description: n/aConfirmatory test: 

Biopsy 

Checked IgA def. 

yes (8 pts had IgA deficiency and 1 was found to have CD ) 

Ethnicity:

n/aPatient type/# screened: 

1,785 diabetic pts (43% with IDDM and 57% with NIDDM) Demographics: n/r Incidence: 

Prevalence of test positivity: IGA-AGA was positive in 4.1% (73/1785); 49 of these 73 pts were biopsied; CD was diagnosed in 13 of 49 biopsied pts; in 8 out of 1,765 pts IgA and 1 pt was diagnosed with CD; in general, prevalence of newly diagnosed CD was at least 0.78% (14/1785); the overall prevalence of CD in the whole group (4 pts were previously diagnosed with CD) was at least 1% (18/1789); 0.4% (8/2000) for EMA 

 
A-219

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Gro

Rensch, 

1996 

USA 

Duplicate: 

no 

Publication type: journal Study design: 

Test/methodology: 

EMA Biopsy criteria/description: Loss of villous architecture, crypt hyperplasia, and increased IELs Confirmatory test: none Checked IgA def. 

Ethnicity:

n/aPatient type/# screened: 

type I diabetes Demographics: n=47; adults Incidence:n/a 

By first EMA: 3 Biopsy proven: 3 
A-220

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Gro

Roldan, 

1998 

Spain 

Duplicate: 

no 

Publication type: journal Study design: 

Test/methodology: 

IgA, IgG AGA (and known cases, and some tested with EMA) Biopsy criteria/description: ESPGAN Confirmatory test: none Checked IgA def. 

Ethnicity:

n/aPatient type/# screened: 

type I diabetes Demographics: n=117; children Incidence:n/a 

By first IgA: 19 Biopsy proven: 7 

 
A-221

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Rossi, 

1993, 

USA 

Duplicate: 

no 

Publication type: journal Study design: 

Test/methodology: EMA 

Biopsy criteria/description: ESPGAN Confirmatory test: 

none 

Checked IgA def. 

Ethnicity:

Patient type/# screened: 

type I diabetes 

Demographics: 

n=211; children 

Incidence: 

By first EMA: 10 Biopsy proven: 3 

 
A-222

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

SategnaGuidetti, 

1994 

Italy 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgA EMA - IF ME

Biopsy criteria/description: Roy-Choudhury capsule from upper jejunum; criteria of RoyChoudhury

Confirmatory test: 

endoscopic biopsy and RoyChoudhury capsule 

Checked IgA def. 

no 

Ethnicity:

n/aPatient type/# screened: 

383 consecutive IDDM adults; 151 CD pts (as true positives) and 250 healthy and diseased controls (as true negatives) to assess IgA EMA test sensitivity and specificity Demographics: IDDM - age (y): mean 39, range 16-84; 43.9% F Incidence: 

Prevalence of test positivity: CD pts -145/151 (96%) EMA positive(1:50-1:>2000); sensitivity of IgA EMA was 96% 

Prevalence of biopsy proven CD in IDDM group was at least 2.6% (10/383): 2 pts out of 12 IgA EMA positives refused biopsy; prevalence of IgA EMA positivity was 3% (12/383) 

Controls0/437 EMA positive; specificity of IgA AGA was 100% 
A-223

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Saukkonen, 

1996 

Finland 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

gA- reticulin-indirect IF goat anti-human antiserum; IgA and IgG AGA - ELISA cutoff >30% of an intralaboratory standard (intra and inter-assay CV of 5.6% and 10.5% for IgA, and 6.9% and 16.1% - for IgG, respectively)

Biopsy criteria/description: n/rConfirmatory test: 

Biopsy for all pts with abnormally high levels of antibodies but not for those with initially (diagnosis of IDDM) positive antibodies but negative at follow-up (6, 12, 18, 24 and 36 mos) 

Checked IgA def. 

no 

Ethnicity:

n/aPatient type/# screened: 

776 IDDM children Demographics: children less than 16 y Incidence: 

Prevalence of CD in IDDM pts was at least 2.4% (19/776); prevalence of test positivity: at the diagnosis of IDDM and or at 24/36 months follow-up 76/775 positive for IgA-ARA and or IgA-AGA; 35 of these 76 pts were biopsied; in 17 of 35 pts biopsy confirmed CD was found; 2 pts out of 76 pts with a negative antibodies/symptomatic/ were diagnosed by biopsy; overall, 19/776 biopsy confirmed cases; 19/19 positive IgA-ARA; 14/18 genotyped for HLA DR positive for DR3 and 10 (56%) positive for DR4; DQB2 present in 17/18 (94%) 

 
A-224

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Schober, 

2000 

Austria 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

EMA - indirect IF of ME, any positive reading at a dilution of 1:10 was considered as a positive; IgG-AGA and IgA-AGA - ELISA; cut-off for IgG AGA was ->30 AU; for IgA-AGA - >25 AU

Biopsy criteria/description: Modified Marsh and Crowe; Watson-type capsuleConfirmatory test: 

Biopsy 

Checked IgA def. 

yes 

Ethnicity:

n/aPatient type/# screened: 

403 children and adolescents with type I diabetes Demographics: age (y): mean 12.4, range 1-22; 47.9% F Incidence: 

Overall prevalence of biopsy proven CD was 1.49% (6/403); as for prevalence of test positivity: 12 pts had increased IgA EMA; 11 of these 12 were biopsied (1 refusal); on biopsy: 3 (0.74%) had Marsh I; 2 (0.49%) - Marsh 0; 1 - Marsh IIIa/c and 5 Marsh IIIc (1.49%) 
A-225

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Sigurs, 1993 

Sweden 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgA- AGA - ELISA, cut off level at least 25 AU; IgA and IgG ARA - IF; titers equal to or diluted more than 1:5 were considered positive

Biopsy criteria/description: Watson CapsuleConfirmatory test: 

Biopsy 

Checked IgA def. 

yes (3 cases) 

Ethnicity:

n/aPatient type/# screened: 

436 children with IDDM Demographics: age (y): mean 13.6+-4.1, range 2-21 y, 46.3% F Incidence: 

Minimum prevalence of CD in IDDM pts was 4.6% (21/459); prevalence of newly diagnosed CD was 3.4% (15/436); as for prevalence of test positivity: 4.3% (19/436) were IgA AGA positive; 18 of these 19 pts were biopsied; minimum PPV for IgA ARA was 77% (13 of 17) 
A-226

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Sjoberg, 

1998 

Germany 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

IgA-AGA - ELISA, titre > 8.5 AU was considered positive; IgG-AGA - ELISA, titre > 330 AU was considered positive

Biopsy criteria/description: Marsh; Watson Capsule or gastroscopy and biopsyConfirmatory test: 

EMA-indirect IF of ME- titre ≥ 5; biopsy 

Checked IgA def. 

no 

Ethnicity:

n/aPatient type/# screened: 

1,664 diabetes pts (848 IDDM; 745 NIDDM; 71 secondary diabetes) Demographics: IDDM - age (y): mean 46.1, range 17-86; 52.8% F; NIDDM - age (y): mean 61.7, range 24-92; 47.3 F; secondary diabetes - age (y): mean 53.9, range 33-77, 9.8% F Incidence: 

Prevalence of biopsy proven CD was 1.8% (15/848): 8 out of 848 were previously diagnosed with CD; as for prevalence of test positivity: 258/848 were positive for IgA and/or IgG-AGA; 22/258 were positive for EMA giving a prevalence of 2.6%; 7/20 were biopsy positive (14/20 potential CD:4 death; 3 refused biopsy) 

NIDDM- 1/745 previously diagnosed CD; 1/745 EMA positive; prevalence in total 0.27% 

Secondary diabetes group3/71 IgG-AGA positive; no EMA positives; no previously diagnosed CD; prevalence of CD was 0% 
A-227

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Spiekerkoetter, 

2002 

Germany 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

human tTG: IgA/IgG assay cut-off of 9.0 units, IgG-tTGA cut-off 7.0 units, IgA-tTGA cut-off 8.3 units

Biopsy criteria/description: Marsh

Confirmatory test: 

biopsy 

Checked IgA def. 

no, not mentioned 

Ethnicity:

n/aPatient type/# screened: 

ped IDDM pts Demographics: n=205; ped; median age=12 y 7 mos; age range=3-19.5 y; 47.3% F Incidence: 

By IgA/IgG-tTG: 6.3% (13/205); by IgG-tTG: 5.4% (11/205); by biopsy 2.9% (6/8/13/205) [only 8 of the 13 with elevated tTGA levels agreed to biopsy] 
A-228

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Talal, 1997 

USA 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

EMA, cut-off at dilution >

1:10; biopsy

Biopsy criteria/description: ESPGANConfirmatory test: 

small bowel biopsy 

Checked IgA def. 

yes 

Ethnicity:

n/aPatient type/# screened: 

adult diabetic pts Demographics: n=185; adult; other info n/a Incidence: 

By EMA: 4.9% (9/185); by biopsy 2.2% (4/5/9/185) [only 5 of the 9 EMA positives underwent biopsy] 
A-229

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Valerio, 2002 

Italy 

Duplicate: 

Yes (see Celiac 1) 

Publication type: journal Study design: Prevalence 

Test/methodology: 

IgA AGA, ELISA; IgG AGA, ELISA; IgA EMA, indirect IF (substrate n/r) 

Biopsy criteria/description: ESPGANConfirmatory test: 

small bowel biopsy 

Checked IgA def. 

yes 

Ethnicity:

n/aPatient type/# screened: 

383 type 1 diabetes pts Demographics: 383 Type 1 diabetics (194 M, 189 F, 49% F) age < 18 y Incidence:Time period: from January 1992 to December 2000 

Type 1 diabetics 32/383 (8.3%); 2 out of 32 had IgA deficiency 
A-230

Evidence Table 6 (cont’d): Prevalence/incidence of CD in patients with diabetes

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Vitoria, 1998 

Spain 

Duplicate: 

no 

Publication type: journal Study design: Prevalence 

Test/methodology: 

AGA; EMA; intestinal biopsy; IAA, GAD65, IA2, ICA tests to assess IDDM-related pancreatic autoimmunity among CD pts 

Biopsy criteria/description: ESPGANConfirmatory test: 

biopsy 

Checked IgA def. 

yes, none found 

Ethnicity:

n/aPatient type/# screened: 

confirmed CD pts and IDDM pts; exclude confirmed CD pts for data extraction, irrelevant data Demographics: 93 IDDM: pedi; mean age=10.5 y; ?% F Incidence:

IDDM group: by AGA 17.2% (16/93); by EMA 7.25% (7/93); by biopsy 6.5% (6/93) 

 
A-231

Prevalence of CD in High-Risk Patients—Relatives Evidence Table 7: Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Parents: 14.7% Siblings: 21.3% 

Group 4 Group 5 

Book, 

2003 

USA 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

IgA-EMA; tTG-ELIZA; HLA DQA1, DQB1 Biopsy criteria/description: n/a Confirmatory test: biopsy; diagnosis based on positive biopsy or had positive EMA and tTG serologies Checked IgA def. 

n/a 

Ethnicity:

n/a; but all families were CaucasianPatient type/# screened: 

Relatives of CD pts Demographics: n=163 first-degree relatives, n=82 second-degree relatives, n=47 first cousins; ped & adult; mean age=?; age range=2-78 y; % F? Incidence: 

Second-degree relatives: 19.5% 

First cousins: 17.0% 

Offspring: 14.7% 
A-232

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Corazza, 

1997 

Italy 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

AGA Biopsy criteria/description: Some VA Confirmatory test: n/a Checked IgA def. 

n/a 

Ethnicity:

n/aPatient type/# screened: 

Relatives of CD pts Demographics: n=328 first-degree relatives Incidence: 

4% 
A-233

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Farre, 

1999 

Spain 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional prevalence Test/methodology: 

IgA EMA - IF either on a ME (n=550), or HU (n=119); positive ab 1:5 dilution and characteristic honeycomb staining pattern; IgA AGA - ELISA; values over 40 AU were considered positive; HLA-DQ2 (DQA1*0501 and DQB1*0201 alleles) were assayed in 169 pts; typing performed by PCR amplification Biopsy criteria/description: Watson-Crosby capsule; classification: 1) total VA; 2) severe partial VA with crypt hyperplasia; 3) minor non-specific abnormalities; 4) morphologically normal; 1 and 2 were diagnostic criterias for CD Confirmatory test: Watson-Crosby capsule; HLA-DQ2 typing performed in 169 first-degree relatives of CD pts, in 60 CD pts and in 50 ethnically matched controls from the general population Checked IgA def. 

yes, results were not explicitly given in the text. Presumably there was no case of IgA deficiency found because the alternative IgG test for such pts were not used or mentioned in the results section 

Ethnicity:

n/aPatient type/# screened: 

675 first-degree relatives in 227 families of CD probands (149 pediatric and 78 adult pts) Demographics: 669 first-degree relatives in 227 families of CD probands (149 pediatric and 78 adult pts) screened for CD (6 were diagnosed with CD prior to screening and excluded from the study, but accounted for overall prevalence); out of 669 relatives: 331 were parents (163 fathers, 168 mothers), 260 siblings (123 brothers and 137 sisters), and 78 children (42 sons and 36 daughters) Incidence: 

The prevalence of unrecognised CD in first-degree relatives of CD pts was 4.6% (31/669); the overall prevalence of CD in this group is 5.5% (37/675 - 6 relatives of CD pts were diagnosed with CD prior to the study); as for test positivity: IgA EMA was positive in 39/669 (5.8%) and IgAAGA - in 13/669 (1.9%) relatives; simultaneous positivity occurred in 12 of 669 relatives (1.8%); of 39 EMA-positive relatives, biopsy has been done in 32 pts (7 refused) and CD were found in 31 individuals 

 
A-234

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Fasano, 

2003 

USA 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional prevalence Test/methodology: 

EMA - IF; ME or HU; positive at 1:10; all positive EMA tested with human tTG ELISA positive at 2 SD above mean of healthy controls; HLA DQ2 and DQ8 Biopsy criteria/description: single pathologist, Marsh Confirmatory test: htTG; biopsy; also small subset 98 EMA positive and 114 EMA neg had HLA DQ2/8 tested Checked IgA def.

n/a 

Ethnicity:

94% white; 3% black; 1.5% Hispanic, 1% Asian, 0.5% other Patient type/# screened: 

9,019 at risk of CD; 4,126 not at risk Demographics: at risk - symptoms of celiac (1326 children, 1909 adults); CD associated disorders; 4,508 1st deg relatives; 1,275 2nd deg relatives; Not at risk – 2,000 blood donors (mean age 39 range 19-65); 1,119 school children (mean age 12.3, range 6-18); 1,007 adults and children for routine physical (mean age 39, and 13.7, range, 19-71, and 2-18) Incidence: 

1) At risk - a) 1st deg relatives - 205/4,508 (4.55%); children - 54/1,294 (4.17%); adults - 151/3,214 (4.70%); b)symptomatic adults - 28/1,910 (1.47%); children - 53/1,326 (4.00%); 2) Not at risk - 1/4126 (0.75%); adults - 27/2,845 (0.95%); children - 4/1,281(0.31%); biopsy in EMA pos - Marsh 1- 0%; 2 -30/116 (25.9%); 3a - 46/116 (39.7%); 3b - 24/116 (20.7%); 3c - 16/116 (13.8%); HLA DQ2-76/98 (78%); DQ8 - 16/98 (16%); DQ2 and 8 - 6/98 (6%); all EMA pos were also tTG pos 
A-235

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Hill 2000 

USA 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional prevalence Test/methodology: 

IgA-EMA - IF on ME, methodology n/a; IgA and IgG-AGA - ELISA, methodology n/a Biopsy criteria/description: Marsh Confirmatory test: Biopsy Checked IgA def.yes 

Ethnicity:

n/aPatient type/# screened: 

1,200 pediatric group of individuals at risk of CD; pts were assigned to one of 7 groups: 1) chronic diarrhea (n=182); 2) abdominal pain (n=316); 3) IDDM (n=81); 4) short stature (n=259); 5) failure to thrive (n=123); 6) miscellaneous (down's syndrome, thyroiditis, anemia, unexplained elevation of liver enzymes) (n=47); 7) asymptomatic relatives (n=192) Demographics: 1,200 pediatric group of individuals at risk of CD; age (y): mean n/a, range 6 mos - 20 y; % F n/a Incidence: 

Prevalence of CD in pts at risk was 1 in 57 (21/1200); prevalence of test positivity: 2.8% (34/1200) was both EMA and AGA positive; 26 of pts (19 EMA positive) underwent biopsy and 21 were diagnosed with CD 

 
A-236

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Hogberg, 

2003 

Sweden 

Duplicate: 

no 

Publication type: journal Study design: 

longitudinal follow-up, incidence & prevalence Test/methodology: 

IgA-AGA, ELISA cut off for a positive outcome 42.5 units; IgA-EMA, indirect IF using ME the antibody titre was defined as the highest serum dilution yielding positive fluorescence; IgA-TGA, commercially available ELISA, highest cut-off value for positive results >30 units. Biopsy criteria/description: revised ESPGAN. Grade 1 normal; Grade 2 mild; Grade 3 moderate, Grade 4 total VA Confirmatory test: Small bowel biopsy Checked IgA def.

yes, 5 cases found 

Ethnicity:

n/aPatient type/# screened: 

120 first degree relatives of CD pts Demographics: 56 parents (adults) mean age 53.6 range (43-78); 44 siblings (ped and adult) mean age 27.4 y age range (15-49); offspring 20 mean age 6.5 y age range (1-16). Gender not reported Incidence: Time period: 20 y follow-up study. Original study period Sept. 1975- Feb. 1981 

10/120 (8.3%) prevalence, 2 were diagnosed in the original study 20 y prior, 8 new cases from the present follow-up study group. (biopsy confirmed); Serum results; IgA AGA 8/120 pos; IgA EMA 0.5% (6/120) pos; IgA TGA 3.8% (4/104) pos (3 pts with positive biopsy were not tested for IgA TGA) 

 
A-237

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Holm, 

1993 

Finland 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

biopsy Biopsy criteria/description: Some VA Confirmatory test: n/a Checked IgA def. 

n/a 

Ethnicity:

n/aPatient type/# screened: 

Relatives of celiac pts Demographics: n=121 first-degree relatives Incidence: 

10.7% 
A-238

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Prevalence of CD in the whole screened population was 8.3% (83/997); prevalence for first-degree relatives in total: 8.6% (80/943) 

parents: 4.2% (22/521) 

Group 4 Group 5 

KorponaySzabo, 

1998 

Hungary 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional Prevalence Test/methodology: 

IgA EMA - IF using ME and human duodenum as substrate; serum total IgA, deficiency was defined as total serum IgA<0.1 g/L Biopsy criteria/description: Watson capsule; histological evaluation according to the grading of Fontaine and Navarro; ESPGAN criteria for CD Confirmatory test: biopsy; Watson-Crosby capsule; biopsy done in 77 out of 81 pts with positive IgA EMA Checked IgA def.

yes; 2.1% (21/997) of all family members studied were IgA deficient; among CD diagnosed pts 10.8% (9/83) were IgA deficient 

Ethnicity:

n/aPatient type/# screened: 

997 family members of 396 pts with CD screened for CD Demographics: 997 family members of 396 pts with CD screened for CD (521 parents, 368 siblings, 54 children and 54 seconddegree relatives); age: mean/median, range n/a Incidence: # New cases: 75 new cases of CD; incidence of CD was 7.6% (75/989) 

children: 12.9% (7/54); 

second-degree relatives: 5.6% (3/54) 

siblings: 13.8% (51/368) 
A-239

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Kotze, 

2001 

Brazil 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

EMA Biopsy criteria/description: n/a Confirmatory test: n/a Checked IgA def. 

n/a 

Ethnicity:

n/aPatient type/# screened: 

Relatives of celiac pts Demographics: n=115 first-degree relatives Incidence: 

3.5% 
A-240

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Mustalahti, 

2002 

Finland 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional Prevalence Test/methodology: 

IgA-EMA- indirect IF on a HU, serum dilution of at least 1:5 was considered positive; IgA and IgG AGA - ELISA, level of AGA was considered positive when mean+-2 SD of healthy controls; IgA-tTG-ELISA, values at least 20 AU were considered positive Biopsy criteria/description: Small-bowel biopsies with pediatric or adult Watson capsule or forceps from the distal duodenum Confirmatory test: Biopsy; DQ2 and DQ8 typing on PCR Checked IgA def.n/a 

Ethnicity:

n/aPatient type/# screened: 

466 healthy first-degree family members of CD pts Demographics: 466 healthy first-degree family members of CD pts; age (y): median 41, range 2-90 Incidence: 

Prevalence of CD in healthy, first-degree relatives of CD pts was 6.2% (29/466); as for test positivity: 72/466 pts (44 EMA pos 9.4% and 48 IgA pos 10.3%) were positive for EMA and IgA; IgA-tTG was positive in 12.9% (60/466) pts; IgAEMA detected 97% of CD (28/29) and IgAAGA detected - 51% (15/29); all 44 IgA EMA and 19/28 AGA positive pts were positive for DQ2; all 29 newly diagnosed CD pts were DQ2 positive 

 
A-241

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Pittschieler, 

2003 

Italy 

Duplicate: 

no 

Publication type: journal Study design: 

Prospective prevalence Test/methodology: 

EMA, HUC examined by fluorescence. Absence of binding was considered a negative test; HLA typing was done exclusively once diagnosis of CD was confirmed= microlymphocytotoxic technique Biopsy criteria/description: Small intestinal biopsy of first jejunal loop. Ferraris Watson capsule. Normal values being less than 3.2 cells/mm γ/δ T-cell 

receptors by immunohistology Confirmatory test: biopsy, HLA typing Checked IgA def.yes, none found 

Ethnicity:

n/a Patient type/# screened: 

92 first-degree relatives of CD pts. Yearly testing over 12 year period Demographics: 92 at risk (first-degree relatives; 18 offspring and 74 siblings) aged 2-18 y Incidence: Time period: 12 year time period January 1990- December 2001 

6.5% (6/92) confirmed CD by both serology & biopsy within a few months of CD diagnosis in one of their relatives; 5 total VA and 1 partial VA; over 2-5 y a further 5.8% (5/86) confirmed positive with both HU EMA IgA and biopsy 1 partial VA and 4 total VA; combined prevalence=12% (11/92); 11/11 were carriers of HLA DQ2/ heterodimers 

 
A-242

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Prevalence of DQA1*0501 and DQB1*0201 positivity in CD index group: 100% (31/31) CD index pts were positive; relative risk for having at least two alleles 156 Group 4 

Polvi, 1996 

Finland 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional Prevalence Test/methodology: 

DQA1*0501 and DQB1*0201 Biopsy criteria/description: n/a Confirmatory test: n/a Checked IgA def.n/a 

Ethnicity:

n/aPatient type/# screened: 

31 CD index pts; 14 silent CD pts; 29 healthy siblings of CD index pts; 32 controls; Demographics: n/a Incidence: 

prevalence of DQA1*0501 + DQB1*0201 in cadaver organ donors: 28% (9/32) controls 

Prevalence of DQA1*0501 and DQB1*0201 positivity in silent CD group: 100% (14/14) silent CDs 

Prevalence of DQA1*0501 anDQB1*0201 positivity in siblings of indeCD pts: 48% (14/29) healthy sibs 
A-243

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Robinson, 

1971 

UK 

Publication type: journal Study design: 

Cross-sectional prevalence Test/methodology: 

small bowel biopsy, Crosby capsule Biopsy criteria/description: Other: normal, convoluted, and flat; either partial or subtotal VA represents confirmed CD Confirmatory test: biopsy Checked IgA def.n/a 

Ethnicity:

n/aPatient type/# screened: 

relatives of celiac pts Demographics: 1) n=68, first-degree relatives=parents & siblings; 2) n=164, second-degree relatives=uncles & aunts, 50.6% F; 3) n=238, thirddegree relatives=cousins, 52.1% F Incidence: 

First-degree: 4.4% (3/68) 

Second-degree: 0% (0/164) 

Third-degree: 0(0/238) 
A-244

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Rolles, 

1974 

UK 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

biopsy Biopsy criteria/description: n/r Confirmatory test: n/a Checked IgA def. 

n/a 

Ethnicity:

n/aPatient type/# screened: 

Relatives of CD pts-CD child in family Demographics: n=72 first-degree relatives Incidence: 

5.6% 
A-245

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Rostami, 

2000 

Netherlands 

Publication type: journal Study design: 

Cross-sectional prevalence Test/methodology: 

IgA-EMA- indirect IF on a primate ileum; min 1:5 and 1:100; IgA-AGA- ELISA, >25 AU/mL was considered positive; IgA by nephelometry Biopsy criteria/description: EPSGAN; Marsh 1992 Confirmatory test: biopsy in all pts with positivity of symptoms and/or serology tests Checked IgA def.yes; 3 individuals were found to have IgA deficiency 

Ethnicity:

n/aPatient type/# screened: 

388 first-degree relatives of CD pts Demographics: age (y): mean 39, range 1-80; 60% F Incidence: # New cases: 17 new cases of CD; incidence of 5% (17/338) 

Overall prevalence of CD in the first-degree relatives of CD pts was 11% (37/338); there were 17 new and 20 previously diagnosed CD cases; as for the prevalence of test positivity: 28% (96/338) were positive for clinical complaints + lab tests (4 pts) and serology screening; 17/96 (18%) biopsy positive; 6/17 Marsh IIIc; 5/17 Marsh IIIa; 6/17 strongly positive EMA and AGA 
A-246

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Fathers: 10.3% (4/39) 

Mothers: 2.3% (1/43) 

Brothers: 7.4% (5/68) 

Group 4 Group 5 Group 6 Sisters: 17.3% (13/75) 

Group 7 

Stokes, 

1976 

UK 

Duplicate: 

no 

Publication type: journal Study design: 

Cross-sectional Prevalence Test/methodology: 

biopsy Biopsy criteria/description: biopsy result must be grade III to be considered confirmed CD: subtotal VA Confirmatory test: biopsy Checked IgA def.n/a; no serology done; not mentioned 

Ethnicity:

n/aPatient type/# screened: 

Relatives of CD pts Demographics: n=326; children and adult; other info n/a Incidence: # New cases: 17 new cases of CD; incidence of 5% (17/338) 19.2% (35/182 total biopsied) 

Sons: 8.3% (5/60) Daughters: 17.1

(7/41) 
A-247

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Tursi, 

2003 

Italy 

Duplicate: 

no 

Publication type: journal Study design: Prevalence 

Test/methodology: 

IgA IgG AGA, ELISA lower limit of positivity of IgA 0.2 EU/mL and IgG 10.0 EU/mL; IgA EMA, indirect IF on ME; IgA tTG, ELISA using GP liver substrate lower limit of positivity of these antibodies was 7 UA/mL Biopsy criteria/description: Marsh criteria 6 biopsies from small bowel from the second part of duodenum. Marsh Type I -'infiltrative' lesions with >30 lymphocytes/100 epithelial cells; Type II- 'infiltrative/hyperplastic' lesions; Type III-'partial (sub)total VA; partial VA Marsh IIIa); subtotal VA Marsh IIIb); and total VA as Marsh IIIc) Confirmatory test: Biopsy Checked IgA def. 

yes 

Ethnicity:

n/aPatient type/# screened: 

111 first-degree relatives of pts with CD 

Demographics: at risk 111 first degree relatives 38 M, 73 F, mean age 28.7 y, range (10-65 y); 65.8% F Incidence: n/a 

CD diagnosed in 49/11 screened relatives (44.14%) prevalence; prevalence AGA 36.73%; EMA 38.78% ; anti-tTG 44.89% 

 
A-248

Evidence Table 7 (cont’d): Prevalence of CD in relatives of patients with CD

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Fathers: by IgA-AGA: 11.7% (21/180), by IgG-AGA: 13.9% (25/180), by EMA: 0% (0/180), by biopsy: 0.56% (1/180) 

Mothers: by IgAAGA: 9% (18/200), by IgG-AGA: 8.5% (17/200), by EMA: 2.5% (5/200), by biopsy: 2.5% (5/200)) 

Group 4 Group 5 

Vitoria, 1994 

Spain 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional Prevalence 

Test/methodology: 

IgA-AGA>0.085 AU in children, >0.128 AU in adults; IgG-AGA>0.45 AU in children, >0.317 AU in adults; EMA titre>1:5 

Biopsy criteria/description: ESPGAN Confirmatory test: biopsy Checked IgA def. 

n/a 

Ethnicity:

n/aPatient type/# screened: 

first degree relatives of celiac pts 

Demographics: n=642 (380 parents, 249 siblings, 13 offspring); ped and adult; mean age= 27 y; age range=1-64 y; 52.3% F Incidence: 

Sisters: by IgA-AGA: 12.4% (16/129), by IgG-AGA: 15.5% (20/129), by EMA: 5.4% (7/129), by biopsy: 6.2% (8/129) 

Offspring: by IgAAGA: 15.4% (2/13), by IgG-AGA: 23.1% (3/13), by EMA: 7.7% (1/13), by biopsy: 7.7% (1/13) 

Brothers: by IgA-AGA: 8.3% (10/120), by IgG-AGA: 9.2% (11/120), by EMA: 3.3% (4/120), by biopsy: 2.5% (3/120) 
A-249

Prevalence of CD in Associated Clinical Conditions—Anemia Evidence Table 8. Prevalence of CD in patients with anemia

Prevalence Author, Year, 

Location Study Design Patient Characteristics Group 1 Group 2 Group 3 

Akerman, 

1996 

Israel 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

EGD/Biopsy Biopsy criteria/description: subtotal or greater VA

Confirmatory test: n/a Checked IgA def. 

n/a 

Ethnicity:

n/aPatient type/# screened: 

out pts with IDA (50% symptomatic) Demographics: 93 pts; mostly adults although some teens Incidence: 

By biopsy: 13 
A-250

Evidence Table 8 (cont’d): Prevalence of CD in patients with anemia

Prevalence Author, Year, 

Location Study Design Patient Characteristics Group 1 Group 2 Group 3 

Annibale, 

2001 

Italy 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

antral (n=3 per pt)/body(n=3)/duodenal(n=2) biopsies; assessment of gastritis according to Sydney system; March classification for CD; colonoscopy for suspicious lesions; refusal of colonoscopy led to doublecontrast barium enema; NOTE: no serology done Biopsy criteria/description: n/a Confirmatory test: Biopsies Checked IgA def. 

no, not mentioned 

Ethnicity:

n/aPatient type/# screened: 

iron deficiency Demographics: 81 pts; adult; median age 54; range 23-87; 74% F Incidence: 

By biopsy: 6% (4/71); 71 pts formed the final sample of completely examined subjects. Note: no serology done 

 
A-251

Evidence Table 8 (cont’d): Prevalence of CD in patients with anemia

Prevalence 

Author, 

Year, 

Location Study Design Patient Characteristics Group 1 Group 2 Group 3 

Annibale, 

2003 

Italy 

Duplicate: 

no 

Publication type: journal Study design: 

Prospective prevalence Test/methodology: 

IgA tTG, ELISA normal values were <7 UA/mL Biopsy criteria/description: Marsh Confirmatory test: Biopsy - antral, gastric body, and duodenal biopsy collected Checked IgA def. 

n/a 

Ethnicity:

n/aPatient type/# screened: 

IDA in premenopausal women Demographics: 59 premenopausal women age range 22-54 y with IDA Hb < 12g/dLF Incidence: Time period: March-July 2000 

7/59 (11.9%) had positive tTG antibodies titre; biopsy-confirmed: 8.5% (5/59) 

 
A-252

Evidence Table 8 (cont’d): Prevalence of CD in patients with anemia

Prevalence 

Author, 

Year, 

Location Study Design Patient Characteristics Group 1 Group 2 Group 3 

Corazza, 

1997 

Republic 

of San 

Marino 

Duplicate: 

no 

Publication type: journal Study design: Cross-sectional prevalence 

Test/methodology: 

indirect IF EMA titre >1:5; biopsy

Biopsy criteria/description: 

n/a 

Confirmatory test: 

biopsy 

Checked IgA def. 

no, but mentioned as such that it could have caused some misclassification of pts, but the effect should be minimal given the powerful sensitivity and specificity of EMA test 

Ethnicity:

n/aPatient type/# screened: 

random sample stratified for age and sex Demographics: n=2,237; adult median age: 44 y; range: 20-87 y % F: 53.2 Incidence: 

By both EMA and biopsy: 1 in 559 pts, or 1.79 per 1000 [0.18%] 
A-253

Evidence Table 8 (cont’d): Prevalence of CD in patients with anemia

Prevalence Author, Year, 

Location Study Design Patient Characteristics Group 1 Group 2 Group 3 

Dickey, 

1997 

UK 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

EMA; AGA; methodology and cut-off levels n/a Biopsy criteria/description: endoscopic biopsy; criteria n/a; finding of VA and IELs in duodenal biopsy Confirmatory test: Biopsy Checked IgA def. 

n/a 

Ethnicity:

n/aPatient type/# screened: 

41 pts with IDA and no specific GI symptoms or evidence of a bleeding on FOBT or upper GI and colonic endoscopy screened for achlorhydric gastric atrophy and CD Demographics: 41 pts with IDA screened for achlorhydric gastric atrophy and CD; age (y): mean 59, range 15-84; 61% F Incidence: 

prevalence of CD in IDA pts was 10% (4/41); EMA was positive in 3 (75%) of 4 these pts; prevalence of EMA and/or AGA being positive was 10% (4/41) 

 
A-254

Evidence Table 8 (cont’d): Prevalence of CD in patients with anemia

Prevalence Author, Year, 

Location Study Design Patient Characteristics Group 1 Group 2 Group 3 

Howard, 

2002 

UK 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

IgA/IgG-AGA and EMA then biopsy

Biopsy criteria/description: 

n/a Confirmatory test: n/a Checked IgA def. 

n/a 

Ethnicity:

n/aPatient type/# screened: 

IDA identified through lab Demographics: 

258 adult pts with IDA, folate Incidence: 

By first serology: 28 by biopsy: 12 
A-255

Evidence Table 8 (cont’d): Prevalence of CD in patients with anemia

Prevalence Author, Year, 

Location Study Design Patient Characteristics Group 1 Group 2 Group 3 

Kepczyk, 

1995 

USA 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

EGD/biopsyBiopsy criteria/description: VA, crypt hyperplasia, inflammatory infiltrate

Confirmatory test: n/a Checked IgA def. 

n/a 

Ethnicity:

n/aPatient type/# screened: 

Mostly symptomatic out pts with IDA Demographics: 

39 adult pts with IDA 

Incidence: 

By biopsy: 4 
A-256

Evidence Table 8 (cont’d): Prevalence of CD in patients with anemia

Prevalence Author, Year, 

Location Study Design Patient Characteristics Group 1 Group 2 Group 3 

McIntyre, 

1993 

UK 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

duodenal biopsy performed in 50 pts; upper GI endoscopy performed in 108 pts Biopsy criteria/description: n/a Confirmatory test: prevalence of biopsy proven CD was at least 6% (3/50) Checked IgA def. 

No serology tests done. Results based on clinical findings of upper & lower GI symptoms. Prevalence was calculated only in biopsy-performed group of pts that consisted of 50 individuals. 

Ethnicity:

n/aPatient type/# screened: 

111 pts with IDA Demographics: 111 pts with IDA; age (y): mean 63+-17.3, range 20-86; 61.3% F Incidence: 

Prevalence of biopsy proven CD was at least 6% (3/50) 

 
A-257

Evidence Table 8 (cont’d): Prevalence of CD in patients with anemia

Prevalence Author, Year, 

Location Study Design Patient Characteristics Group 1 Group 2 Group 3 

Oxentenko, 

2002 

USA 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

endoscopic biopsy of second and third parts of duodenum Biopsy criteria/description: CD was defined as total or partial VA with IELs Confirmatory test: Biopsy Checked IgA def. 

NA 

Ethnicity:

n/aPatient type/# screened: 

113 pts with IDA Demographics: age (y): mean 55.6+-15.3, median 54, range 20-86; 71.7% F Incidence: 

Prevalence of CD was 15% (17/113); 10 of these 17 pts had positive endoscopic markers suggestive of CD; 8 pts with endoscopic markers present did not have CD on biopsy 

 
A-258

Evidence Table 8 (cont’d): Prevalence of CD in patients with anemia

Prevalence Author, Year, 

Location Study Design Patient Characteristics Group 1 Group 2 Group 3 

Ransford, 

2002 

UK 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

IgA-EMA-ME, titers> 1:5 was considered positive; IgA tTG- ELISA, cut-off n/a Biopsy criteria/description: revised ESPGAN; duodenal histologic changes were graded according to Marsh criteria Confirmatory test: Biopsy Checked IgA def. 

No 

Ethnicity:

n/aPatient type/# screened: 

484 anemic pts; 498 age and sex matched controls Demographics: n/a Incidence: 

Prevalence of newly diagnosed CD in anemic pts was at least 2.2% (11/484)prevalence of CD in "EMA positive pts" was 1 in 28; prevalence of CD in "definite celiac + ↑IELs alone+not biopsied group" was 1 in 30; prevalence of CD in "definite celiac and ↑IELs alone group" was 1 in 35; prevalence of CD in "definite celiac group" was 1 in 44 

Prevalence of newly diagnosed CD in age & sex matched nonanemic pts was 0.2% (1/484); prevalence of CD in "EMA positive group" was 1 in 83; prevalence of CD in "definite celiac +↑IELs alone+ not biopsied group" was 1 in 100; prevalence of CD in "definite celiac & ↑IELs alone group" was 1 in 166; prevalence of CD in "definite celiac group" was 1 in 498 

 
A-259

Evidence Table 8 (cont’d): Prevalence of CD in patients with anemia

Prevalence Author, Year, 

Location Study Design Patient Characteristics Group 1 Group 2 Group 3 

Unsworth, 

2000 

UK 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

plasma diluted 1:5 IgA EMA using HU as substrate. Seropositives tested for IgA and IgG AGA ELISA and tTG ELISA using GP liver tTG Biopsy criteria/description: n/a Confirmatory test: small bowel biopsy Checked IgA def. 

n/a 

Ethnicity:

n/aPatient type/# screened: 

110,937 blood donors, 1,380 anaemic donors, 483 with haemaglobin(<11 g/dL for women; <13.5 g/dL for men) Demographics: 1,380 anemic adult blood donors 87% women (age range n/a) 483 anemic pts meeting criteria 84% women Incidence: 

IgA EMA positive 32/483 (6.6%); 25/32 had small bowel biopsy (4 pts lost to follow-up and 3 refused further testing) 22/25 had positive small bowel biopsy(88%) Subsequent results 22/32 cases IgA AGA positive; 26/32 cases were either IgA or IgG AGA pos; 31/32 cases pos using ME as substrate rather than HU; 31/32 were IgA tTG antibody pos 

Prevalence of newly diagnosed CD in age & sex matched nonanemic pts was 0.2% (1/484); prevalence of CD in "EMA positive group" was 1 in 83; prevalence of CD in "definite celiac +↑IELs alone+ not biopsied group" was 1 in 100; prevalence of CD in "definite celiac & ↑IELs alone group" was 1 in 166; prevalence of CD in "definite celiac group" was 1 in 498 

 
A-260

Evidence Table 8 (cont’d): Prevalence of CD in patients with anemia

Prevalence 

Author, 

Year, 

Location Study Design Patient Characteristics Group 1 Group 2 Group 3 

van Mook, 

2001 

Netherlands 

Duplicate: 

no 

Publication type: journal Study design: retrospective prevalence 

Test/methodology: 

EGD; upper digestive tract endoscopy in 10/35; duodenal biopsies taken in 15/35 Biopsy criteria/description: Marsh Confirmatory test: biopsy Checked IgA def. 

no 

Ethnicity:

n/aPatient type/# screened: 

35 pts with IDA, anaemia defined as Hb below 8.0 mmol/L in men or below 7.4 mmol/L in women. Iron deficiency defined as a serum ferritin level equal to or below 20 ug/L for men equal to or below 10 ug/L ; or serum iron concentration equal to or below 45 ug/dl with a transferrin saturation of 10% or less, or the absence of iron stores in bone marrow biopsy specimens. 

Demographics: 35 pts, 22 F (63%) and 13 M (37%), median age 71 y range (22-89 y) Incidence: n/a 

2.9% (1/35) Marsh III(C) on both biopsy and endoscopy 
A-261

Prevalence of CD in Associated Clinical Conditions—Low Bone Mineral Density (BEvidence Table 9: Prevalence of CD in patients with low BMD 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Gro

Gonzalez, 

2002 

Argentina 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

IgA and IgG-AGA, ELISA; cut-off levels: for IgA, 15 AU/mL; for IgG, 20 AU/mL; IgA-EMA, IF on ME; positive if fluorescence at 1:5 dilution; 1st level of screening: measuring of IgA and IgG-AGA; 2nd level of screening: measuring of IgA and IgGEMA and total serum IgA if AGA positive; 3rd level of screening: biopsy in EMA positives Biopsy criteria/description: endoscopic biopsy; CD was diagnosed when mucosa showed VA, crypt hyperplasia and intraepithelial lymphocytic infiltration (>30%) Confirmatory test: EMA; biopsy Checked IgA def. 

yes; 2 controls were found to have very low IgA level 

Ethnicity:

n/aPatient type/# screened: 

127 consecutive postmenopausal pts with verified osteoporosis screened for CD; 747 controls screened for CD taken from a population-based study aiming to determine the prevalence of CD in Argentina Demographics: n=127 postmenopausal pts with osteoporosis; age: mean 68 y, range 50-82 y; n=747 controls; age: mean 29 y, range 16-79 y Incidence:Time period: prevalence of CD in 127 

postmenopausal pts with osteoporosis was 1/127, or 7.9x1000 (95% CI 0.2-43.1); as for test positivity: AGA was found in 8 of 127 pts on level 1; 1 of these 8 pts was EMA-positive on the 2nd level and eligible for biopsy which established a diagnosis of CD Control popn: estimated prevalence of 

CD in control women population was 6/747, or 8x1000 (95% CI 3.3-18.3); as for test positivity: AGA was found in 96 of 747 (12.8%) pts on level 1; 4 pts were EMA-positive and 2 other pts had very low serum IgA on the 2nd level and all 6 were eligible for biopsy which established a diagnosis of CD in all cases 

Prevalence of CD in 127 postmenopausal pts with osteoporosis was 1/127, or 7.9x1000 (95% CI 0.2-43.1); as for test positivity: AGA was found in 8 of 127 pts on level 1; 1 of these 8 pts was EMApositive on the 2nd level and eligible for biopsy which established a diagnosis of CD 

 
A-262

Evidence Table 9 (cont’d): Prevalence of CD in patients with low BMD 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Lindh, 

1992 

Sweden 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

IgA-AGA, micro ELISA method; cut-off point was selected to be a 2 SD above the mean in a healthy population of blood donors Biopsy criteria/description: endoscopic biopsy; methodology and criteria of CD diagnosis n/r Confirmatory test: endoscopic biopsy Checked IgA def. 

n/r 

Ethnicity:

n/aPatient type/# screened: 

92 consecutive pts with idiopathic osteoporosis screened for CD Demographics: n=92 consecutive pts with idiopathic osteoporosis screened for CD; 91% F (mean age 66±12 y)/ 9% M (mean age 50±12 y); Incidence:prevalence of CD was 3% (3/92); IgA-AGA was positive in 11 of 92 pts and biopsy was performed in 6 pts 

Prevalence of CD was 3% (3/92) 
A-263

Evidence Table 9 (cont’d): Prevalence of CD in patients with low BMD 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Mather, 

2001 

Canada 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

IgA-EMA, IF of ME Biopsy criteria/description: increased number of IELs with associated subtotal or total VA Confirmatory test: biopsy Checked IgA def. 

yes 

Ethnicity:

n/aPatient type/# screened: 

96 consecutive idiopathic low BMD pts Demographics: n=96: mean age 57 y; range 18-86 y; 81.3% (78) F, 18.7% M (18) Incidence:n/a 

7 (7.3%) of 96 pts were EMA pos at titers of ≥1:10; all biopsies were negative; prevalence of 0% 
A-264

Evidence Table 9 (cont’d): Prevalence of CD in patients with low BMD 

Prevalence Author, Year, 

Location Study Design 

Patient 

Characteristics Group 1 Group 2 Group 3 

Nuti, 2001 

Italy 

Duplicate: 

no 

Publication type: journal Study design: 

cross-sectional prevalence Test/methodology: 

IgA-AGA, ELISA cut-off level of 10 U/mL-1 Biopsy criteria/description: intestinal biopsy criteria n/r Confirmatory test: TG-ab-ELISA with cut-off 22 AU; intestinal biopsy Checked IgA def. 

no 

Ethnicity:

n/aPatient type/# screened: 

255 females with osteoporosis Demographics: mean age 66.6 y, range 36-65 y Incidence:n/a 

53/255 pos IgG-AGA; 24/53 pos TG-ab (9.4%); intestinal biopsy in 10/24 resulted in 6 confirmed CDs 
A-265

Celiac 3: Risk of Lymphoma in CD 

Evidence Table 10: Risk of lymphoma in patients with CD

Author, year, 

country Methods Participants Outcomes 

Measures of risk 

(lymphoma) 

Askling, 2002, 

Sweden 

Other reports of 

same cohort: 

Peters et al., 

Arch Int Med 

2003;163:1566 

Retrospective Cohort Study Study Dates: 1964-1994 Group selectionPts with CD: All 

individuals discharged at least once with a Dx CD (ICD 7-9) Controls: (5-y)Age/sex 

and (1 y) calendar period matched cancer incidence rate and mortality rate for the entire Swedish population Institution: All hospitals in Sweden (Swedish input register) Ascertainment of outcomeCancer register, register of causes of death, population register, register of population changes. Pathology report from Cancer Registry for lymphomas Dx’ed 1990 or after Blinding n/rFollow-up See ascertainment of outcome. 3.4% excluded with incomplete/non matching ID numbers 

CD pts: n = 11,019 Mean age at CD Dx: 17.4 (range 0->70) Mean follow-up: 9.8 y (range 0-32) 97236 PYs Proportion of females: 59% Proportion on GFD: n/r % refractory CD: n/r Clinical presentation: symptomatic (admission to hospital) 

Lymphoma # lymphomas 38 Lymphoma types: NHLs Dead patients Mean age at death: 68.6 Time from CD Dx: n/r Death from NHL #Ls in celiacs: 33 # expected lymphomas:2.9 Death from all causes # deaths 828 # expected 419.3 Exclusions Were lymphomas occurring prior to CD Dx included? NO Were lymphomas occurring within 12 months of CD Dx included? NO Were incidental lymphomas found at autopsy included? NO 

SIR NHL 6.3 95% CI 4.2-125 SIR 1-4 y Dx: 9.7 95% CI 6.3-14 SIR >5 y Dx: 3.8 95% CI 2.2-6 SIR age 0-59: 6.0 95% CI 3.7-9.5 SIR age >60: 5.8 95% CI 3.7-8.5 SIR childhood Dx (age 0-19): 1.995% CI 0.4-5.5 SIR adult Dx (age 20-59):7.7 95% CI 4.9-12 SIR late Dx (age >60): 6.3 95% CI 3.8-9.8 SIR 1970-79: 12 (3.8-28) 

SIR 1980-89: 8.5 (5.5-13) SIR 1990-95: 3.4 (1.9-5.7) P (linear trend) 1964-95 0.025 

SM95% SMSMSMP(trSM11.4 
A-266

Evidence Table 10 (cont’d): Risk of lymphoma in patients with CD

Author, year, 

country Methods Participants Outcomes 

Measures of risk 

(lymphoma) 

Collin, 1996, 

Finland 

Other reports of 

same cohort: 

Collin et al. Gut 

1994;35:1215 

Prospective cohort study (Collin et al. Gut 1996;38:528) Study dates: 1970-1993 Case-control study (Collin et al. Gut 1994;35:1215) Group selectionPts with CD: All consecutive 

biopsy-proven CD (ESPGAN criteria) Controls: age/sex matched 

for Finnish population (database not stated) Controls(2): age/sex and year matched outputs for upper endoscopy Institution: single tertiary care institution Ascertainment of outcomeFinnish cancer registry, Statistics Finland Blinding n/rFollow-up See ascertainment of outcome. 290 pts available for biopsy 6-12 mos post Dx 

CD pts: n = 383 Mean age at CD Dx: 41.8 (range 16-78) Mean follow-up: 8.1 y 3107 PYs Mean follow-up (casecontrol) 3.1 (range 0.5-11) Proportion of females: 73% Proportion on GFD: 

Strict GFD 75% Partial GFD 8% Normal diet 6% Unknown 11% 

Compliance monitoring: control bx and dietary assessment 6-12 mos after Dx Clinical presentation: 

82% symptomatic 18% serology Dx 

Lymphoma # lymphomas 1 Lymphoma types: # expected lymphomas 0.4 Death from all causes # deaths: 31 (8.1%) # expected: see graph p1217 of Collin et al. Gut 1994;35:1215 Exclusions Were lymphomas occurring prior to CD Dx? NO Were lymphomas occurring within 12 months of CD Dx? YES Were incidental lymphomas found at autopsy included? PROBABLY NOT 

SIR NH 2.66 95% CI 0.07-14.8 
A-267

Evidence Table 10 (cont’d): Risk of lymphoma in patients with CD

Author, year, 

country Methods Participants Outcomes 

Measures of risk 

(lymphoma) 

Corrao, 2001 

Italy 

Other reports of 

same cohort: 

none 

Prospective Cohort Study Dates: 1962-1994 Group selectionPts with CD: All 

consecutive biopsyproven CD (ESPGAN criteria) Controls: (5-y) age/sex 

and calendar year matched national life tables and regional mortality rates Institution: 11 GI units throughout Italy selected for quality of record keeping; mostly tertiary Ascertainment of outcomephone interview (pts, relatives); death certificates, Italian National Institute of Statistics Blinding n/rFollow-up see ascertainment of outcome. 8 pts or their relative not tracked down; excluded. 50 pts lost to follow-up 

CD pts: n = 1,072 Mean age at CD Dx: 35.7 (range 18->50) Median Dx delay 17 months Mean follow-up: 6.0 y 6444 PYs Proportion of females: 76% Proportion on GFD: 59% 

Strict GFD: 59% Not likely: 15% Unknown: 27% 

Compliance monitoring: control biopsy and phone interview 1999 % refractory CD: none Clinical presentation: 

55% symptomatic 39% mild symptoms 6% serology Dx 

Death from NHL # lymphomas: 16 lymphoma types: # expected lymphomas 0.2 Death from all causes # deaths 53 # expected 25.9 Exclusions Were lymphomas occurring prior to CD Dx included? NO Were lymphomas occurring within 12 months of CD Dx included? YES Were incidental lymphomas found at autopsy included? PROBABLY NOT 

SIR NHL SM

95SM95SM0.9SM0.9SM(0.SM(1.SM2.6SMSMSMSM1.5 SM2.6 

SM3.8 SMSM(0.SM7.0SMSMSM
A-268

Evidence Table 10 (cont’d): Risk of lymphoma in patients with CD

Author, 

year, 

country Methods Participants Outcomes 

Measures of 

risk 

(lymphoma) 

Cottone, 

1999, Sicily 

Other 

reports of 

same 

cohort: 

none 

Retrospective cohort study Study dates: 1980-1997 Group selectionCD pts: All biopsy-proven CD 

Controls: Age and sex-matched 

reported mortality from same period and region; cancer registry of the city of Ragusa in Sicily 1983-1987 Institution: Single institution; referral basis for all of Sicily Ascertainment of outcome

Hospital medical records were reviewed; pathology specimen reviewed Blinding n/rFollow up 5% incomplete records 

CD pts: n = 228 Mean age at CD Dx: 34.7 

adult Dx: 98% Range of age: n/r 

Mean follow-up: 73 mos (range 1-204) #PYs: n/r Proportion of females: 76% Proportion on GFD: 100% Compliance monitoring: serial EMA % refractory CD: n/r Clinical presentation: 

Anemia 60% Malabsorbtion 20% Other 10% Asymptomatic 10% % inputs: 29% 

Marsh grade: n/r 

Lymphoma #NHLs in celiacs: 7 Lymphoma types: ETCL (4), Bcell (2), other NHL(1) # expected lymphomas: 1.824 % silent: n/r % Dx’ed during childhood : 0 Lymphoma patients Mean age: 59.4 Time from CD Dx: 78 mos % compliant to diet: 100 incidence NHL: 3% expected incidence: 0.8 Death from lymphoma # death from lymphoma in celiacs: 5 # expected death from lymphomas: n/r Death from all causes # death CD: 12 # expected deaths: 3.12 # deaths within 4 y of Dx: 8 # expected: 1.48 Exclusions Were lymphomas occurring prior to Dx of CD included? NO Were lymphomas occurring within 6 months of CD Dx included? NO Were incidental lymphomas found at autopsy included? No such cases 

SIR NHL 3.75P<0.01 
A-269

Evidence Table 10 (cont’d): Risk of lymphoma in patients with CD

Author, year, 

country Methods Participants Outcomes 

Measures of risk 

(lymphoma) 

Delco, 1999 US 

Other reports of 

same cohort: 

none 

Case-control study Study Dates: 1986-1995 Group selectionPts with CD: all consecutive 

pts discharged with CD Dx (ICD 579.0) Controls: 5 randomly 

selected controls from same annual data file per case Institution: All US VA hospitals Ascertainment of outcomePt Treatment File of the VA. Validity of records checked with 7 pt files Blinding n/rFollow-up See ascertainment of outcome. 

CD pts: n = 458 Controls: n=2692 Mean age: celiacs: 63.8 +/- 12.4 controls: 59.7 +/- 14.8 p< 0.0001 Proportion of females: celiacs 4% controls 2% p=0.105 Race: celiacs: 93% whites controls: 74% p<0.0001 Proportion on GFD: n/r Compliance monitoring: n/a % refractory celiac: n/r Clinical presentation: 

100% symptomatic (all discharged Dx) 

Lymphoma # lymphomas n/r Lymphoma types: n/r # expected lymphomas n/r Death from all causes # deaths: n/r Exclusions Were lymphomas occurring prior to CD Dx included? NO Were lymphomas occurring within 12 mos of CD Dx included? LIKELY Were incidental lymphomas found at autopsy included? LIKELY Pts with repeated admission within 1 y were excluded 

OR NHL 4.53 95% CI 2.01-10.23 
A-270

Evidence Table 10 (cont’d): Risk of lymphoma in patients with CD

Author, year, 

country Methods Participants Outcomes 

Measures of risk 

(lymphoma) 

Green, 2003, 

US (New York) 

Other reports of 

same cohort: 

none 

Prospective Cohort Study Dates: 1981-2000 Group selectionPts with CD: All 

consecutive biopsyproven CD (ESPGAN criteria) Controls: (5-y) age/sex 

and calendar year matched site-specific incidence rates from the National Cancer Institute’s Surveillance, Epidemiology and End Results Program for whites Institution: single tertiary care institution Ascertainment of outcomept interview, review of pathology records Blinding n/rFollow-up pts not followed-up excluded; # n/r 

CD pts: n = 381 Mean age at CD Dx: 44 +/- 18 y Duration of CD symptoms prior to Dx: 5y +/- 8 Mean follow-up: 6 +/- 11 y 1977 PYs Proportion of females: 64% Proportion on GFD: 100% of NHLs after Dx Compliance monitoring: clinical interview, yearly AGA and EMA after 1993 % refractory celiac: n/r Clinical presentation: n/r 

NHL 1 mos after CD Dx # lymphomas 5 # expected lymphomas n/r Age at Dx cancer 62+/- 8 y Mean duration from celiac Dx 5+/- 4 y Mean follow-up 16+/- 17 y NHL before/1 mos after CD Dx* # NHLs: 4 # expected: 0.7 NHL any time before/after Dx celiac* # NHLs: 9 # expected: 1 Lymphoma types: B-cell(3), T-cell (4 – ETCL 3), large cell (2) Exclusions Were lymphomas occurring prior to Dx of celiac included? YES* Were lymphomas occurring within 1 months of celiac Dx included? YES* Were incidental lymphomas found at autopsy included? n/r *separate analysis 

SIR NHL 6.2 95% CI 2.9-14 SIR NHL before/1 mos after Dx celiac:* 5.3 (2.3-13) incidence NHL 135/100 00PYs expected 14.8/100 000 PYSIR NHL any time before/after Dx celiac:*9.1 (4.7-13) 
A-271

Evidence Table 10 (cont’d): Risk of lymphoma in patients with CD

Author, year, 

country Methods Participants Outcomes Measures of 

Holmes, 1989, 

England 

Other reports of 

same cohort: 

Holmes et al. 

Gut 

1976;17:612; 

Harris et al, Am 

J Med 

1967;42:899 

Prospective cohort study Study Dates: 1941-1985 Group selectionPts with CD: All biopsyproven CD 

Controls: Age/sex matched 

incidence for 2 calendar periods standardized to ICD 8,200 and 202, in West Midlands region Institution: Single institution Ascertainment of outcomeDirect pt interview, case notes, GP, Birmingham and West Midlands cancer registry, autopsy results, death certificates, pathology specimen reviewed Blinding n/r Follow-upUse of the family Practitioner Committee records and National Health Service Central Register at Southport; 2% drop outs 

CD pts: n = 210 Mean age at CD Dx: n/r Adult Dx: 80%* (*from Harris et al, Am J Med 1967;42:899) Mean follow-up: 17.4 PYs for men, 19.4 PYs for women; minimum 13 y Proportion of females: 55.2% Proportion on GFD: 51% 

strict GFD 51% reduced gluten 27% normal diet 22% 

Compliance monitoring: direct interview; repeat biopsy in 86 pts % refractory CD: 17 poor response to GFD Clinical presentation: n/r 

Lymphoma #NHLs in celiacs: 9 lymphoma types: n/r # expected lymphomas: 0.21 Lymphoma patients Mean age: n/r Time from CD Dx: n/r % compliant to diet: 

2 NHL in strict GFD 7 NHL in gluten diet 

Death from lymphoma Not calculated Death from all causes Not calculated Exclusions Were lymphomas occurring prior to Dx of CD included? NO Were lymphomas occurring within 12 months of CD Dx included? NO Were incidental lymphomas found at autopsy included? No such cases 

SIR NHL 42.795% CI 19.6-81.4 SMR from NHL n/r SMR all causes Not calculated SMR 4 y from Dx n/r SIR NHL Strict gluten-free Gluten diet 100 
A-272

Evidence Table 10 (cont’d): Risk of lymphoma in patients with CD

Study Methods Participants Outcomes Measures of 

Logan, 1989, 

Scotland 

Other reports of 

same cohort: 

Celiac 2; Logan 

et al. 

Gastroenterol 

1986;90:334 

Celiac 2; Logan 

et al. BMJ 

(Clinical 

research ed) 

1983;286:95 

Prospective cohort study Study dates: 1979-1986 Group selectionPts with CD: All biopsyproven CD entered in 

register for Edinburgh and the Lothians Controls: Age/sex matched 

mortality for Scotland and corresponding person-years over 5 calendar periods standardized to ICD 8 200- 203, in Scotland Institution: All hospitals in Edinburgh and the Lothian region, postal survey of all GPs, Scottish in-pt Statistics 1961-1977, local branch of Celiac Society Ascertainment of outcomeDeath certificates Blinding n/rFollow-up National Health Service Central Record, death certificates, Scottish national death records. 6% lost to follow-up 

CD pts: n = 653 Mean age at CD Dx: n/r Mean follow-up: 13.5 y 8823 PYs Proportion of females: 60% Proportion on GFD: n/r % refractory CD: n/r Clinical presentation: n/r 

Lymphoma # lymphomas: n/r Lymphoma types: most lymphosarcomas or reticulum-cell sarcomas, 2 Hodgkins Dead patients Mean age at death: 60.8 Time from CD Dx: n/r Death from lymphoma #s in celiacs: 17 #expected lymphomas: 0.55 Death from all causes # deaths 115 # expected 61.8 Exclusions Were lymphomas occurring prior to CD Dx included? NO Were lymphomas occurring within 12 months of CD Dx included? YES Were incidental lymphomas found at autopsy included? NO 

SIR NHL: n/r SMR from lympho31 p<0.001 SMR(L) 0-1 y Dx: SMR(L) 2-4 y Dx: SMR (L) 5-49 y DxSMR all causes 195% CI 1.5-2.2 SMR <1 y from DxSMR 1-2 y from DSMR 3-4 y from DSMR 5-9 y from DSMR 10-14 y from SMR childhood D

95% CI 0.4-3.7 SMR adult Dx: 1.9 95% CI 1.5-2.3 SMR late Dx:* 1.7 95% CI 0.02-4.8 *obvious CD sympduring childhood 
A-273

Evidence Table 10 (cont’d): Risk of lymphoma in patients with CD

Author, year, 

country Methods Participants Outcomes 

Measures of risk 

(lymphoma) 

Selby, 1979 

Australia 

Other reports of 

same cohort: 

none 

Retrospective cohort study dates: 1959-1978 Group selectionPts with CD: All consecutive 

biopsy-proven CD (ESPGAN criteria) Controls: ?age/sex and 

period matched incidence New South Wales Central cancer Registry Institution: Single tertiary care institution Ascertainment of outcomedirect call or via medical officer Blinding n/rFollow-up Direct call or via medical officer. 21% lost to follow-up 

CD pts: n = 93 Mean age at diagnosis celiac: 40 (range 14-70) Duration of Sx of celiac prior to Dx: 3yrs (range 2 wks to 26 y) Mean follow-up: 6 y (max 9 y) Proportion of females: 67% Proportion on GFD: 100% of NHLs after Dx Compliance monitoring: n/r % refractory CD: none of the lymphoma pts Clinical presentation: 100% malabsorption: 18% malabsorption during childhood 

Lymphomas # lymphomas 4 # expected lymphomas 0.081 Age at cancer Dx: 47.5 Mean duration from CD symptoms: 11 y (range 2-26 y) Mean follow-up: n/r Lymphoma types: ETCL (2), lymphosarcoma (1), histiocytic medullary reticulosis (1) Exclusions Were lymphomas occurring prior to Dx of celiac included? NO Were lymphomas occurring concomitantly with celiac Dx included? NO Were incidental lymphomas found at autopsy included? n/r 

SIR NHL 4.94p< 0.0005 symptom duration (cancnone): not significant age Dx (cancer vs nonesignificant 
A-274

Celiac 4: Consequences of Testing for CD 

Evidence Table 11: Consequences of testing for CD 

Study, Year 

Country Methods Participants Outcomes Results 

Addolorato, 

2001 

Italy 

Study type - 1996-1998 Population-group selection Celiacs – newly diagnosed CD selected from outpatient clinic of 234 adult CD Controls - healthy asymptomatic controls - matched for age, sex and SES Loss to follow-up -8 Setting - Tertiary 

Celiac - n=43 enrolled Controls - n=59 Proportion F – 60% Mean follow-up - 1 y Mean age: 29.8 ± 7.4 

Before/after GFD Anxiety State and Trait Anxiety Inventory test Depression SDS self rating depression scale 

Before – CD 71.4% showed high levels of state anxiety, 25.7% showed anxiety as a trait and 57.1% positive for depression compared to 23.7%, 15.2% and 9.6% of controls Post GFD – 25.7% still affected by state anxiety, 17% trait anxiety, and 45.7% depressed Significant decrease in state anxiety (p<0.001) No significant changes in trait anxiety or depression - anxiety in CD predominantly reactive 

Sto R
A-275

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author, 

Year 

Country Methods Participants Outcomes Results 

Amin, 

2002 

UK 

Study type - case controlled longitudinal 1994-1998 Population-group selection Celiacs – 11 pts, EMA + and biopsy diagnosed CD out of 230 pts screened from diabetic clinic Controls – 22 matched for age, sex and duration of diabetes, with negative serology Institution – diabetic clinic – tertiary care hospital 

Celiacs: n=11 (6 had repeat small bowel Bx on GFD) Controls: n=22 Age: 8.1 (1.2-16.1) cases, 7.4 (1.3-14.8) controls Proportion of females: 54.5% Duration of type 1 diabetes: 4.2 y Mean follow-up - 4 y BMISDS -1.2 

± 0.1 (SEM) vs -0.1 

± 0.1 WtSDS - 0.7 vs 0.5 HbgA1c – 8.3 cases 9.8 controls Insulin units – 0.8 

BMI Hgba1c Insulin regimens 

Cases: 1.1 

± 0.1 

Controls: 1 

± 0.1 

Cases: 8.3 

± 0.2 

Controls: 10 

± 0.2 

Insulin regimens increased but did not differ significantly between Insulin units 1.0 All reverted to antibody negative 
A-276

Evidence Table 11 (cont’d): Consequences of testing for CD 

Study, Year 

Country Methods Participants Outcomes Results 

Annibale, 

2001 

Italy 

Study type - prospective 1994- May 1997 Population-group selection Celiacs190 consecutive adults with iron deficiency anemia, 26 pts were diagnosed with CD after duodenal biopsy 

Celiac n= 26 of 190 pts with IDA Proportion F - 92% Mean age - 31.3 Mean follow-up – 24 mos 77% had total VA, 23% had subtotal atrophy 11 did not have symptoms apart from anemia 42% BMI 

Iron Deficiency (Hgb<14 for men and 12 for women, MCV <80, low serum iron and low serum ferritin Ferritin Nutritional parameters Repeat endoscopy – 6 mos 

6 mos 77.8% recovered IDA, but only 5 of 18 (27.8%) developed normal ferritin levels 12 mos – 94.4% recovered from anemia and 50% from iron deficiency – all pts had normal RDW 24 mos, 55% recovered from iron deficiency 

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author, 

Year 

Country Methods Participants Outcomes Results 

Arato, 

2002 

Hungary 

Study type – longitudinal – own controls Population-group selection Celiacs selected from 205 children with type 1 diabetes randomly selected, screened with EMA and then confirmed with biopsy Controls – no controls 

Celiacs: n=17 % Females -59% Mean follow-up – 3 mos BMI 14.2 vs 16.3 for controls 11 had silent CD, 6 had mild GI symptoms 

BMI HbA1c Insulin requirements 

Before 

16.8 <0.05 

7.82 NS 

0.48 

After GFD 

0.64 <0.05 
A-277

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author, 

Year 

Country Methods Participants Outcomes Results 

Bardella, 

1985 

Italy 

Study type - prospective Population-group selection Celiacs- adults with biopsy confirmed disease (Grade II or IV – Scott/Losowsky) and malabsorption Controls ---none 

Celiacs - n=26 Proportion F - 81% Mean age - 42.2 Mean follow-up– 55.4 mos on GFD (range 13-137 mos) 

Clinical Symptoms CBC, biochemical parameters Repeat biopsy (17/26) 

8 pts good health and norblood tests and 18 had soclinical or biochemical abnormalities, 4 pts had recurrent abd pain, meteoand diarrhea, 2 isolated episodes of diarrhea and meteorism alone present, pts had one more of anemmoderate abnormal of calcium, alkaline phosphaphosphorus 13 showed grade II, and 4 grade III – all improved by 2 grades but none returnenormal 

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author, 

Year 

Country Methods Participants Outcomes Results 

Bardella, 

2000 

Italy 

Study type - case control 1962-1994 Population-group selection Celiacs not clear how selected 33.4% asymptomatic Controls – 2/pt matched for age and sex 

Cases 71 out of 212 43 diagnosed as children, 28 as adults Control - n=142 Proportion F - 72% 

Weight BMI Fat mass Lean mass 

Lower than controls 55.5 vs 58.7 kg (p=0.004) 20.9 vs 22.4, p=0.03 22.9 vs 27.5, p<0.05 38.8 vs 40.5 (p<0.03) 
A-278

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author, 

Year 

Country Methods Participants Outcomes Results 

At baseline, weight, fat mass, BMD, mass of limbs all lower in the pts vecontrols, after 1 y no significant diffein body composition between pts ancontrols 

Barera, 

2000 

Italy 

Study type - case control prospective Population-group selection Celiacs – biopsy confirmed CD, 4 classic symptoms, remainder atypical Controls - age and sex matched healthy controls 

Celiac cases - n=29 Control - n=29 Age - 9.54 + 3.42 Proportion F: 51.7% Mean follow-up – 1.20 ±

0.15 Compliance – EMA ab 

Body composition - DEXA Weight (kg) Height (cm) BMI (kg/m2) Lean Mass 

Untreated 

30.3 + 11.5kg 

134.9 + 19 

16.7 +4.5 

166.8 

Tre

34.7 + 1

140.9 + 

17.3 + 179.9 +

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author, 

Year 

Country Methods Participants Outcomes Results 

Boersma, 

Netherlands 

2002 

Study type - 1994-1995 prospective study Population-group selection Celiacs-children with newly diagnosed celiac (symptoms and biopsy confirmed) CD patients acted as own controls 

Celiacs - 28 Proportion F - 68% Mean follow-up - 3 y BMI 

BMI BMI-SDS Height SDS 

BMI - SDS for CD improved significantly after a GFD over  1st half year. (P<0.001) 

Height for SDS for CD showed a continuous significant increment over the first 3 y of GFD (p<0.001) 

With insincreaselevels of 3 rise 
A-279

Evidence Table 11 (cont’d): Consequences of testing for CD 

Study, Year 

Country Methods Participants Outcomes Results 

Ciacci, 

1996 

Italy 

Study type - case control Before after Population-group selection Celiacs Untreated CD had a least one pregnancy when symptoms leading to diagnostic workup for CD were present Controls (treated) had at least one pregnancy after 1 y of GFD Setting- Tertiary clinic 

Celiac - n=94 Controls - n= 31 12 separate women acted as own control for before after study to assess impact of the GFD (not included in other analysis). Mean age at diagnosis of untreated older than treated (37.3 vs 22.4) Mean follow-up of treated celiacs 9.2 

± 1.4 

Mean weight of treated 50.6 vs 50 Mean BMI 20.1 vs 19.4 Clinical symptoms of untreated group 33% did not have diarrhea, 24.5% did not have anemia 

Number of pregnancies/woman Number of abortions/woman Abortion to pregnancy ratio Low birth weight baby to pregnancy ratio 

2.72 in untreated vs 1.36 in controls 0.489 

± 0.08 untreated vs 0.032 

± 0.032 treated (17.8% vs 2.4%) 0.153 

± 0.027 vs 0.024 

± 0.024 

0.126 

± 0.037 vs 0.024 

± 0.024 

(prevalence 12.7% vs 2.4% in treated) *controls not age matched – cases significantly older 

RR 1.1RR 5.812Did groco
A-280

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author, 

Year 

Country Methods Participants Outcomes Results 

Fabiani, 

1996 

Italy 

Study type - longitudinal Population-group selection Celiacs – biopsy proven CD from screening of adolescents (n = 6,315) Controls - none Loss to follow-up – 5 

Celiacs – n=28 adolescents (age 11-14) Proportion F -74% Mean F/U 23 ± 7 mos 

Compliance 52% on strict GFD 

47% partial adherence weight gain 12/23 (52%), height gain (11/25) 

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author, 

Year 

Country Methods Participants Outcomes Results 

Fabiani, 

2000 

Italy 

Study Type – case control 1992-1994 Population-group selection Celiacs – selected from screening program for CD ages 11-14, Group A and second group B from pts diagnosed due to typical symptoms (biopsy proven ESPGAN) Loss to follow-up: Group A 5 pts, Group B 2 pts 

Celiacs Group A n = 22 pts, asymptomatic Group B n = 22 pts symptomatic Mean follow-up – 5 y Age at diagnosis of CD: Group A 13 y, Group B 4.3 y 

Compliance – FFQ conducted by dietician Anthropometric assessment 

Adherence to treatment lower in Group A (23%) asymptomatic versus Group B (68%) p value sig BMI no differences between groups 
A-281

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author, Year, 

Country Methods Participants Outcomes Measures of risk 

Fickling, 2001, 

UK 

Retrospective case-control study Group selectionCD pts: All individuals with 

CD who attended gastroenterology output depart and those with CD who were member of local celiac society Controls: Age/sex 

matched controls/ one per case selected from database of normal adults who had a bone densitometry performed with the same machine Institution: District general hospital Ascertainment of outcome:By questionnaire on fracture history with attempt to verify by case notes Blinding: n/rFollow-up: 

CD pts: n=75; 15 with metabolic bone disease and CD Controls: n=75 Mean age of CD pts: 52 y Proportion on GFD: full details n/r Median duration of GFD: 3.4 y Proportion of females: 80% Clinical presentation: n/r BMI: n/r 

Fractures: CD pts: 16/75 (21%), 

10 before Dx, 6 after Dx Controls: 2/74 (3%) 

BMD-DXA 6 pts had histomorphometry- 3 pts had osteomalacia 

RR: 7.0 (95% CI 4.2-125) Increased history of past fractures in subjects with CD. (p<0.001) No difference in BMD in those with and without fractures, but pts who had a fracture were older (56.3 vs 50.3) 
A-282

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author, 

Year 

Country Methods Participants Outcomes Results 

Greco, 

1997 

Italy 

Study type- cohort PopulationCeliac – biopsy confirmed pts (92.8%) consecutively recruited from a celiac clinic, 22 pts diagnosed on basis of immunological and clinical findings 

Celiac - 306 adolescent/young adults Cases of CD Mean age – 15.9 (range 10-27) Proportion F - 60.8% Mean follow-up BMI 

Compliance – one month retrospective questionnaire 

Three groups 1. Strict GFD 73% 2. Occasional relapse 15% 3. Full gluten containing 12% Females more compliant (80% vs 64% of males) 

88on oldAv24pe11

Evidence Table 11 (cont’d): Consequences of testing for CD 

Study, Year 

Country Methods Participants Outcomes Results 

Johnston, 1998 

N. Ireland 

Study type-case control Longitudinal follow-up of cases 1983-1998 Population-Group Selection- population survey Celiacs -screening detected CD of 1823 subjects with serology (n=113)- 3% also had inflammatory bowel disease Controls – 89 age and sex matched randomly selected from survey – antibody negative Ascertainment of outcome – death certificates 

Celiac n= 89 (72 followed) – 20 biopsied and 13 untreated detected Controls 89 Proportion F – 53 % Mean follow-up – 11.6 y 

Mortality- overall and cancer Number of deaths compared to Registrar General’s reports 1983-1994 

13 subjects with positive serology died, 4 with malignant disease No increase in all-cause mortality or number of cancer-related deaths in screening detected cases of CD 
A-283

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author 

Year 

Country Methods Participants Outcomes Results 

Kemppainen, 

1998 

Finland 

Study type - cohort Duration: 1988-1990 Population-group selection Celiacs: newly diagnosed biopsy confirmed, symptomatic, all started on GFD Partial (8), subtotal (17) and total VA (15) Controls –none Institution – Tertiary care Kuopio University Hospital Follow-up – 6 pts lost to follow-up 

Celiacs – 40 pts Age – 47 for men and 44 for women Proportion F - 70% Proportion on GFD -100% Mean follow-up: 1 y Duration of CD symptoms – males 15.8, women 13.1 BMI 25 in men, and 24 in women 

Nutritional status examined by food records, and BMI Ferritin/biochemical values Biopsy 

BMI increased after GFD, decreased intakes of fibre, thiamine Most of abnormal biochemical values improved, in 1 pt with subtotal atrophy – low Hgb, in pts with subtotal VA – 7 pts had low Hgb and 5 low ferritin After GFD – VA improved in all patients 29 pts had partial VA, 2 subtotal, 3 normal villi 

Bloaa
A-284

Evidence Table 11 (cont’d): Consequences of testing for CD 

Study, year, 

location Methods Participants Outcomes Measures of risk 

Moreno, 

2004, 

Argentina 

Case-control, cross sectional Group selection CD pts: unselected 

53% classic symptoms, 36% subclinical, 11% silent by screening Controls: 296 age and sex 

matched diagnosed with functional disorders Institution: 2 different tertiary referral centres Ascertainment of fracture: in-person interview 

CD pts: n=148 unselected CD Controls: n=296 (2:1) Mean age CD pts: 

Classic: 44 y Subclinical/silent: 38 y 

Age at diagnosis: 

Classic: 42 y Subclinical/silent: 36 y 

BMI: 22/22.1 Proportion females: 79 

% Clinical presentation:

53% classical CD; 35% subclinical, and 11% silent 

Fractures: classic symptoms vs subclinical overall -51pts Fractures-peripheral 47% symptomatic CD vs 15% controls 20% subclinical/silent CD vs 14% controls Mean BMD femoral neck 

OR 3.6 (95% CI 1.7-7.5) OR for symptomatic pts 5.2 (95% CI 2.8-9.8) OR 1.7 (0.7-4.4) Fractures not any greater in subclinical cases of CD vs controls Higher for subclinical/silent cases vs classical p<0.05 (T score -0.6 vs -1.5) Pts with CD–sig more fractures in 5th/6th decade; also sig more low trauma fractures than controls 

CfuFra
A-285

Evidence Table 11 (cont’d): Consequences of testing for CD 

Study, Year 

Country Methods Participants Outcomes 

Measures of risk - 

mortality 

Nielsen, 

1985 

Denmark 

Study type - retrospective cohort Study dates 1964-82 Population-group selection Celiacs – histologic diagnosis of CD - 100 Ascertainment of outcomeCentral person register, cancer registry Tertiary hospital 

Celiac pts - 98 Proportion F - 61 % Median age at diagnosis – 41 (F) and 42 (M) Mean follow-up - 18 y % refractory CD - 24% treated with prednisone since did not respond to GFD Compliance – not described how assessed 

Mortality 5-y survival 88%, 10-y 

survival 68.5% (23 deaths, 4 deaths attributed to malignancy) 8 pts developed cancer Responders to GFD – 2.2 extra mortality factor Non-responders to GFD - 5.8 Compliance with diet – 3.2 Non compliant – 4.5 

S

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author, 

Year 

Country Methods Participants Outcomes Results 

Poddar, 

2002 

India 

Study type – case control longitudinal Period – 09/1997 – 12/1998 Population-group selection Celiacs-104 children with 

clinical symptoms evaluated for celiac disease, 57 biopsy confirmed. Excluded those who did not have good response to diet Controls –Those who did not have celiac on biopsy of the initial 104 

Celiacs - n= 57 Controls - n=47 Proportion F - Mean follow-up - 19.6 ± 8 mos 

17% poor compliance 

Height Weight gain Symptoms 

Height 88 ± 5% of expected vs 94 ± 5% of expected 

baseline and follow-up (p=ns) 66% ± 14 vs 86% ± 11 of 

expected (p<0.001) Improved in 16 ± 9.8 days 

34% had poor compliance to diet 
A-286

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author, 

Year 

Country Methods Participants Outcomes Results 

Rea, 

1996 

Italy 

Study type - case control longitudinal Study dates 1992-1994 Population-group selection Celiacs - newly diagnosed children, biopsy confirmed Controls-age and sex matched healthy controls 

Celiacs: n= 23 Controls: n=23 Proportion of F - 65.2% Mean age 4.7 ± 0.76 

Mean follow-up - 1 y Co-interventions All patients received vitamin D 1000 IU If iron was low, received iron supplementation 

Height, BMI Weight, fat area index Triceps subscapular skin fold Biochemical values 

Height. BMI, triceps skinfold, fat area index, and weight for height index all improved significantly. Hgb, iron, protein, albumin, triglycerides, calcium and zinc significantly improved Transferring, cholesterol, phosphorus and alk phos were not different 
A-287

Evidence Table 11 (cont’d): Consequences of testing for CD 

Study, Year 

Country Methods Participants Outcomes Results 

SategnaGuidetti, 

2001 

Italy 

Study type - longitudinal case control 1996-1998 Population-group selection Celiacs consecutive newly diagnosed CD patients, biopsy proven Controls – age, sex matched healthy volunteers recruited among medical and nursing staff, blood donors or pts affected by COPD, peptic ulcer disease, no past history of thyroid dysfunction Excluded conditions that could affect thyroid function, excluded CD by means of EMA or biopsy Setting- 5 Italian centres 

Celiac - 241 Proportion F – 73% Controls – 212 Mean follow-up- 1 y Clinical presentation Typical in 49%, atypical in 44% and silent in 16% 

BMI Thyroid function (serum fT3 and fT4 by RIA, TSH by IRA and thyroid microsomal antibodies 

Similar in patients with and without thyroid disease Thyroid dysfunction in 73/241 (30.3%) vs 11.3% (p<0.0005) Thyroid disease 3 Χ higher than controls Hypothyroidism diagnosed in 12.9% vs 4.2% of controls (p<0.003) 128 pts reassessed at 1 y 91 had normal thyroid, 37 some impairment Subclinical hypothyroidism improved in 71% patients with nonautoimmune thyroid disease 

ImnaG(crenth5thud
A-288

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author, 

Year 

Country Methods Participants Outcomes Results 

Saukkonen, 

2002 

Finland 

Study type - longitudinal Population-group selection Celiacs, screened 776 children with type 1 diabetes with serology/biopsy (over 2.7 y period) – own controls Controls - none 

Celiacs/type 1 diabetes n = 18 Mean onset of diabetes – 8.0 ±4.5 y Proportion F – 50% Mean follow-up – 1 y 

HbA1c GI symptoms 

No change in HbA1c levels with GFD Symptoms which were reported in a retrospective questionnaire resolved in all but 2 pts 

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author, 

Year 

Country Methods Participants Outcomes Results 

Smecuol, 

1997 

Argentina 

Study type - longitudinal Dates – 1991-1993 Population-group selection Celiacs unselected consecutive patients with newly diagnosed CD, all were symptomatic, and biopsy confirmed acted as own controls 

Celiac – 47 and 25 pts reevaluated in 1995 Proportion F - Mean follow-up - 37 mos Compliance- 15 pts – strict GFD, 10 partial GFD BMI 

Fat and bone mass Lean tissue mass Weight and tricep skin fold thickness Mid arm circumference and muscle mass 

Significant increase in fat/bone mass No change in lean tissue mass Increases in body weight/triceps skinfold thickness 
A-289

Evidence Table 11 (cont’d): Consequences of testing for CD 

Study, year, 

location Methods Participants Outcomes Measures of risk 

Thomason, 

2003, UK 

Case-control study Self-report data from questionnaire. Group selection:CD pts: all biopsy-proven CD 

(also clinical/serology) from population based registers for Derby and Nottingham (less than 7% did not have a bx) Only pts born prior to 1950 included. Controls: age/sex matched 

random sample from Nottingham family health services. Ascertainment of fractures:

Self-report of low trauma and non low trauma fractures Blinding: Investigator who categorized fractures as low trauma or not was blinded to whether case or control

CD pts: n = 244 (70% females) Controls n=161 Mean age: 

CD: 60.2 y (10.1) Controls: 61.2 y 

Mean BMI:

CD: 23.9 Controls: 25.8 

Proportion of females: 70% Proportion on GFD: n/r Clinical presentation: n/r Dx of osteoporosis: 7.4% of cases versus 3.1% of controls Smokers: 

CD: 52.5% Controls: 43.3% 

Cointerventions:

4% of CD pts reported taking calcium HRT: 31% vs 21% of controls (significant), adjusted for HRT use in analysis 

Fractures – low trauma (fall from a standing height or less) Any fracture: 

CD: 82 (34.5%) Control: 53 (33.3%) 

Forearm/wrist:

CD: 39 (16.4) Control: 22 (13.8) 

Low trauma fracture: 

CD: 37 (15.7%) Control: 21 (13.8%) 

(20 reported first fracture before diagnosis of CD and 10 pts reported first fracture after diagnosis) Logistic regression to estimate odds ratio for fracture – adjusted for sex and age group Cox’s proportional Hazard model was used and only first low trauma fracture was included. 

OR 1.05 (0.68-1.02) OR1.21 (0.66-2.25) OR 1.16 (0.65-2.10) When adjusted age, sex, BMD and smoking the OR 1.13 (95% CI 0.6-2.12) Before Dx: HR 1.24 (95% CI 0.65 – 2.39) Small but statisticallysignificant increase in risk of fractures 
A-290

Evidence Table 11 (cont’d): Consequences of testing for CD 

Study, year, 

location Methods Participants Outcomes Measures of risk 

Vasquez, 

2000, 

Argentina 

Cross-sectional casecontrol study Retrospective historical review Group selection

CD pts: All biopsy-proven 

celiac disease, and clinical picture, excluded those with secondary osteoporosis other than celiac Controls: 165 subjects 

selected from output clinic and selected if their final diagnosis was a functional disorder. Excluded cases with known metabolic bone disorders Institution: Single institution Buenos Aires –tertiary hospital Ascertainment of fracturePt interview, case report Vertebral fractures –X-ray of lumbar spine (not thoracic) in all CD and 62% of controls Did not have medical records of trauma events Blinding: n/r 

CD pts: n=165 Median Age:CD: 40 (16-74) y; 23% over 50 y Mean age of controls: 41 y Median time from symptoms to diagnosis: 7 y Proportion of females:86.6% Proportion on GFD: 69% 

Strict GFD: 44.8% Reduced gluten: 24% Untreated: 31% 

Mean BMI: 21.4 Clinical presentation:malabsorption or subclinical Post-treatment biopsy:histological improvement in 38 pts Serology: negative or reduced titres in all with positive serology 

Fractures Peripheral: Cases: 41 (25%) 

Controls: 14 (8%) 

Total number of fractures: 51 in celiacs/15 in controls BMD: Lower in those with fractures (non-significant) Exclusions: Only lumbar spine X-rays from 68 pts and 78 controls were considered to be of adequate quality 

OR: Peripheral fractures (25%) 

of CD pts and (8%) of controls; 3.5 (95% CI 1.8-7.2) p<0.0001, wrist most commonVertebral fractures 4/78 (5%) of controls versus 9/68 (13%); OR 2.8 (0.7, 1.15) incomplete ascertainment X-rays: 68 pts and 78 controls were adequate quality Most fractures observed prediagnosis Only 7% of pt developed fractures after starting GFD 
A-291

Evidence Table 11 (cont’d): Consequences of testing for CD 

Study, 

Year, 

Location Methods Participants Outcomes Measures of risk 

Vestergard, 

2002, 

Denmark 

Retrospective cohort study, population based Study dates: 1983-1996 Group selectionCD pts: All individuals 

admitted/ discharged with a CD Dx (ICD -8) Controls: 3 controls per 

case population age and sex matched Institution: Danish hospitals Ascertainment of fractureNational pt discharge register–any fracture registered during hospitalization Confounders: not examinedBlinding: n/r Comorbidity examined by assessing hospital admissions for conditions that may alter risk of fractures. (2.8% in CD vs 2.6% in controls) 

CD pts: n=1,021; 7,774 PY Controls: n=23; 316 PY Mean age at diagnosis:31.5 y (24.7) Mean follow-up: 7,774 PYs cases; 23,316 controls Proportion of females:58% Proportion on GFD: n/r Compliance: n/r Clinical presentation:symptomatic (admission to hospital) BMI: n/r Age at first fracture after diagnosis: 40.2 y Exclusions ? output diagnosis of CD 

All Fractures: CD vs controlBefore diagnosis: 24/7774 PY vs 103/23,316 PY After diagnosis: 65/6,675 vs 223/21,468 PY Spine Rib Pelvis Osteoporosis 

Incidence rate ratio (ALL) Before Dx: 0.70 (0.45,1.09)After Dx: 0.94 (0.71, 1.24) (spine, rib, pelvis) IRR 2.14 (0.70, 6.57) pre IRR 1.07 (0.39, 2.95) post IRR 3.00 (0.21,41.9) pre IRR 1.29 (0.4, 4.09) post
A-292

Evidence Table 11: Consequences of testing for CD 

Study, 

Year, 

Location Methods Participants Outcomes Measures of risk 

West, 2003, 

UK 

Retrospective matched cohort study Study dates: 1987-2002 Group selectionPts with CD: All recorded Dx 

of CD recorded 1-yr after beginning of the GPRD record; no biopsy data Controls: matched by age, 

sex, general practice and follow-up time, excluded any who had record of a glutenfree prescription Primary care database: GPRD established in 1987 Ascertainment of fracture: Admin database Blinding: n/r Examined potential confounders 

CD pts: n=4,732 observ. time (27,116) Controls: n=23,620 (149,896 y of risk) Mean age at diagnosis celiac: 43.5 y Range of age: n/r Proportion of females:

67% Proportion smoke: 13% 

(controls 15.4%) Mean follow-up: 5.7 y, # PYs: 27,116 10% of cohort did not receive a prescription for GFD, 36% 0-10 and 54≥10 

BMI: Celiacs: <25 – 47% 

Controls: <25: 30.6% 

≤18.5; 4.2% vs 1.2% of controls 

Fracture: CD vs control Any fracture: 356/4732 vs 1524/23616 137.9/10,000 PYs vs 105.9/10,000 in controls Hip: 8.9/10,000 PY versus 4.7/10,000 PY Ulna/radius fracture: 24.9/10,000 versus 14.1/10,000 No difference in risk of fracture in period after diagnosis compared to before diagnosis 

HR: 1.30 (95% CI, 1.16,1.46) (report prevalent and incident) HR 1.9 (1.20,3.02) HR 1.77 (1.35,2.34) Absolute diff in overall fracture rate was 3.2/1000 person y 0.97/1000 for hip fracture in those >45 y 

Evidence Table 11 (cont’d): Consequences of testing for CD 

Author, 

Year 

Country Methods Participants Outcomes Results 

Westman 

1999 

Australia 

Study typePopulation-coexisting type 1 diabetics and CD identified from database of Diabetes Center-biopsy proven Controls- 40 matched for age and sex and duration of IDDM 

Cases 20 Control 40 Duration of diabetes: 7.2 vs 7.3 y controls % F - 75% Mean follow-up Compliance with FFQ 

Height SDS Weight SDS BMI SDS HbA1c Compliance 

No difference in heighSDS, weight SDS or BSDS 8.48 ± 0.98% for CD v

8.87 ± 1.46 for contro

30% strict GF, 30% trgluten and 40% signifamt of gluten 
A-293

Celiac 5: Promoting or Monitoring Adherence to a GFD 

Evidence Table 12: Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design Study Population Time 1 Time 2 Time 3 Time 4 

Baseline 

Biopsy AGA EMA 

Anson, 

1990, 

Israel 

Publication type: journal Study design: Parental questionnaire Ethnicity:

n/r 

Population type: 

Jewish children with CD 

Biopsy criteria: 

n/r 

Checked IgA def. no Serologic tests: 

Test name:

n/a Methodology:n/a Cut-off:n/a 

Celiac Group 1 

• 31 children judged 

GFD compliant based on symptoms and/or serology and/or biopsy 

• age: n/r • %F: n/r 

Celiac Group 2 

• 12 children 

judged noncompliant with GFD 

• age: n/r • %F: n/r 

tTG
A-294

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design Study Population Time 1 Time 2 Time 3 Time 4 

Baseline 

Biopsy AGA Group 1 95%; Group 2 100%; Group 3 40.9%; Group 4 16.2%; Control 10.9%EMA 100%; 100%; 54.5%; 9.5%; 2.7%

Bardella, 

2001, 

Italy 

Publication type: journal Study design: case-control Ethnicity:

n/r 

Population type: 

CD: details of diagnosis n/r 

Biopsy criteria: 

Marsh 

Checked IgA def. Yes, excluded Serologic tests: 

Test name:

IgA-AGA; IgAEMA; IgA-tTG Methodology:n/r; ME; GP liver Cut-off:12 AU/mL; 1:10; 10 AU/mL 

Celiac Group 1 • 40 pts, untreated CD • mean age: 38 y (range 

16-77 y) 

Celiac Group 2 • 25 CD; poor GFD 

compliance 

• age: n/r • gender: n/r Celiac Group 3 • 22 CD. Compliant 

GFD<2 y 

• age: n/r • gender: n/r Celiac Group 4 • 148 CD. Compliant GFD 

>2 y 

• age: n/r gender: n/r Control • 110 non-CD controls • age: nr • gender: n/r 

tTG

100%; 100% 63.6%; 14.2% 1.8% 
A-295

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 

Biopsy AGA Group 1 3 (17%); Group 2 11 (92%)EMA 

Bartholomeus, 

1990, 

Australia 

Publication type: journal Study design: cohort Ethnicity:

n/r 

Population type: 

CD: details of diagnosis n/r 

Biopsy criteria: 

Adults partial VA, subtotal VA, total VA; children ESPGAN 

Checked IgA def. No Serologic tests: 

Test name:

IgA-AGA Methodology:n/r Cut-off:

n/r 

Celiac Group 1 • 17 CD. GFD >6 

mos adults and children 

• age: n/r • gender: n/r Celiac Group 2 • 12 adults and 

children with CD on gluten 

• age: n/r • gender: n/r 

tTG
A-296

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline GC 36 to 90 d GC 3 to 12 mos GC > 3 y Biopsy AGA 23% IgA-AGA 97% 5% 49% EMA 13% EMA 65% 84% 93% 

BurginWolff, 

1991, 

Switzerland 

Publication type: journal Study design: case-control Ethnicity:

n/r 

Population type: 

Classic CD 

Biopsy criteria: 

CD if subtotal VA, total VA 

Checked IgA def. no Serologic tests: 

Test name:

IgA-AGA ; IgA-EMA Methodology:n/r; ME Cut-off:n/r; 1:10 

Celiac Group 1 • 134 children 

CD on GFD 

• mean age: n/r 

(range 3-18 y) 

• gender: n/r 

tTG
A-297

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline GFD 3 mos GFD 6 mos GFD 12 m

Biopsy 12 partial VA; 21 subtotal VA; 21 total VA 

 20 normal

Marsh 1 (hIEL); 22 partial VA; total VA or subtotal VA 

AGA EMA 100% 42% 25% 

0% norma0% Marsh 2 (9%) parVA; 3 (30%subtotal/toVA 

Dickey, 

2000, 

Northern 

Ireland 

Publication type: journal Study design: prospective cohort Ethnicity:

n/r 

Population type: 

Adults with classic CD 

Biopsy criteria: 

Marsh 

Checked IgA def. Yes. Excluded Serologic tests: 

Test name:

IgA EMA Methodology:ME Cut-off:>1:5 

Celiac Group 1 • 53 pts • mean age: 55; 

range 16-80 y 

• 74% F 

tTG
A-298

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 

Biopsy AGA EMA 

Fabiani, 

1996, 

Italy 

Publication type: journal Study design: retrospective cohort Ethnicity:

n/r 

Population type: 

CD identified by screen 

Biopsy criteria: 

no description 

Checked IgA def. No Serologic tests: 

Test name:

IgA AGA; IgA EMA Methodology:n/r Cut-off:n/r 

Celiac Group 1 • 12 children 

reporting strict GFD 

• age: n/r • gender: n/r Celiac Group 2 • 11 children 

reporting noncompliance 

• age: n/r • gender: n/r 

tTG
A-299

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 

Biopsy AGA EMA 

Fabiani, 

2000, 

Italy 

Publication type: journal Study design: case-control Ethnicity:

n/r 

Population type: 

CD identified in a mass screen 

Biopsy criteria: 

ESPGAN 

Checked IgA def. No Serologic tests: 

Test name:

n/a Methodology:n/a Cut-off:n/a 

Celiac Group 1 • 22 children CD 

identified by screen 

• mean age: 17.9 

y; range: n/r 

• 59% F Control • 22 children with 

classic CD on GFD 

• mean age: 16 

y; range: n/r 

• 59% F 

tTG
A-300

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 

Biopsy Group 1: 

0 Marsh 1, 29 (16%) Marsh 2, 145 (84%) Marsh 3 

Group 2: n/a Control: n/a AGA EMA 

Fabiani, 

2001, 

Italy 

Publication type: journal Study design: case-control Ethnicity:

n/r 

Population type: 

Classic CD 

Biopsy criteria: 

Marsh 

Checked IgA def. Yes. Excluded Serologic tests: 

Test name:

IgA-tTG Methodology:GP liver Cut-off:7 AU 

Celiac Group 1 • 176 pt new 

diagnosis CD 

• mean age: 16.4 

y; range 0.3-87.4 y 

• 65% F Celiac Group 2 • 172 CD on 

GFD > 1 

• mean age: 17.6 

y; range 0.3 -89.8 y 

• 66% F Control • 206 healthy 

and non-CD 

• mean age: 

15.6 y; range 0.4-78 y 

• 50% F 

tTGGroup 1: 

mean tTG Marsh 2 16 AU, Marsh 3 22 AU 

Group 2: 

strict GFD 4.2 AU, GFD transgressions 9.9 AU Control: 2.7 AU 
A-301

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline GFD 12 mos GC 6 mos 

Biopsy n/r 100% Marsh 0 or 1 

(breakdown not given ) 

All Marsh 2 or 3 (breakdown not given ) 

AGA IgG AGA 100%; 90% IgA AGA 

40% IgG AGA; 0% IgA AGA 

100% IgG: 90% IgA 

EMA 100% 0% 90% 

Fotoulaki, 

1999, 

Greece 

Publication type: journal Study design: prospective cohort Ethnicity:

n/r 

Population type: 

Classic and atypical CD 

Biopsy criteria: 

ESPGAN 

Checked IgA def. yes Serologic tests: 

Test name:

IgG AGA; IgG AGA; IgA EMA Methodology:n/r; ME Cut-off:0.3 control; 0.3 control; 1:2.5 

Celiac Group 1 • 30 CD • mean age: n/r; 

range 1-24 y 

• 57% F Celiac Group 2 • median age: 

(range: ) 

• % F: 

tTG
A-302

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design Study Population Time 1 Time 2 Time 3 Time 4 

Baseline 

Biopsy AGA EMA 

Hogberg, 

2003, 

Sweden 

Publication type: journal Study design: retrospective cohort Ethnicity:

n/r 

Population type: 

Classic CD 

Biopsy criteria: 

ESPGAN 

Checked IgA def. no Serologic tests: 

Test name:

IgG-EMA; IgA-EMA; tTG Methodology:ME; GP Cut-off:1:10;1:10;>25 AU 

Celiac Group 1 • 29 adults 

diagnosed as a child 

• mean age: 26 y; 

range 19-34 y 

• 69% F 

tTG
A-303

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 

Biopsy AGA EMA 

Jackson, 

1985, 

Ireland 

Publication type: journal Study design: questionnaire Ethnicity:

n/r 

Population type: 

Classic CD 

Biopsy criteria: 

CD if severe VA and gluten response 

Checked IgA def. no Serologic tests: 

Test name:

n/a Methodology:n/a Cut-off:n/a 

Celiac Group 1 • 50 children CD • median age: 

9.9 y; range 1.5-19 y 

• 58% F 

tTG
A-304

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 

GFD median 1 y 

Biopsy 60 (69%) Marsh 0-II; 27 (31%) Marsh III AGA EMA 7 (26%) in Marsh III 

Kaukinen,

2002, 

Finland 

Publication type: journal Study design: prospective cohort Ethnicity:

n/r 

Population type: 

Classic CD 

Biopsy criteria: 

Marsh 

Checked IgA def. Yes. Excluded Serologic tests: 

Test name:

IgA-EMA; IgA-tTG Methodology:HU; GP liver Cut-off:1:5; 1:20 

Celiac Group 1 • 87 pts on GFD • mean age: 49 y; 

range 22-73 y 

• 72% F 

tTG11 (41%) in Marsh III 
A-305

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design Study Population Time 1 Time 2 Time 3 Time 4 

Baseline 

Biopsy AGA EMA 

Lamontagne, 

2001, 

Canada 

Publication type: journal Study design: questionnaire Ethnicity:

n/r 

Population type: Biopsy criteria: Checked IgA def. Serologic tests: 

Test name:

n/a Methodology:n/a Cut-off:

n/a 

Celiac Group 1 • 234 CD. 

Members of Quebec Celiac Foundation 

• mean age: 49 y; 

range 18-84 y 

• 75% F 

tTG
A-306

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 1-14 y after initial Dx: 

only 12 pts re-biopsied; 31/39 had serology 

Biopsy Normal 8 (21%); partial VA 27 (69%); total VA 4 (10%); IEL/epithelial cells 61 

IEL/100 epithelial cells38; villous height to crypt ratio improved in all but one; none normalized 

AGA 7; IgG only 4; IgG and 

IgA in 3 

EMA 1 of 31 

Lee, 2003, 

USA 

Publication type: journal Study design: retrospective cohort Ethnicity:

n/r 

Population type: 

Classic CD 

Biopsy criteria: 

Normal, partial VA or total VA 

Checked IgA def. n/r Serologic tests: 

Test name:

IgG AGA; IgA AGA; IgA AMA Methodology:n/r Cut-off:n/r 

Celiac Group 1 • n=39 pts on 

GFD 

• mean age: 52 

y; range 20-74 y 

• 60% F 

tTG
A-307

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 

Biopsy AGA EMA 

Ljungman,

1993, 

Sweden 

Publication type: journal Study design: questionnaire Ethnicity:

n/r 

Population type: 

Classic CD 

Biopsy criteria: 

ESPGAN 

Checked IgA def. n/r Serologic tests: 

Test name:

n/a Methodology:n/a Cut-off:n/a 

Celiac Group 1 • 47 children 

born between 1973-78 

• mean age: n/r • gender: n/r 

tTG
A-308

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 

(at diagnosis) 

GFD 1 y +/- 1mos 

Biopsy 6 (6%) Marsh 2; 95 (95%) Marsh3 

12 (12%) normal; 51 (50%) Marsh 1; 38 (38%) Marsh 2 or 3 

AGA n/a n/a EMA n/a Concordance (both 

biopsy/EMA + or both) 48% 

Martini, 

2002 

Italy 

Publication type: journal Study design: prospective cohort Ethnicity:

n/r 

Population Type: 

Classic CD 

Biopsy criteria: 

Marsh 

Checked IgA def. n/r Serologic tests: 

Test name:

IgA-EMA; IgA-tTG-1; tTG-2, tTG-3, tTG4, tTG-GP Methodology:ME; HU; HU; HU; HU; GP Cut-off:1:5; n/r 

Celiac Group 1 • 109 CD on 

GFD 1 y 

• median age: 

37 y; range 21-72 y 

• 78% F 

tTGn/a Concordance 29%; 

65%;14%; 16%; 19% 
A-309

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 

Biopsy Group 1- 16 (44%) normal. 20 (56%) slight mucosal damage; controls all normal AGA EMA 

McNichol, 

1976, 

Ireland 

Publication type: journal Study design: cohort Ethnicity:

n/r 

Population type: 

Classic CD 

Biopsy criteria: 

Normal, slight, moderate, severe mucosal damage 

Checked IgA def. n/r Serologic tests: 

Test name:

n/a Methodology:n/a Cut-off:n/a 

Celiac Group 1 • 36 children on 

GFD (mean 6 y) 

• mean age: n/r; 

range 2.75-11 y 

• gender: n/r Control • 25 normal 

siblings 

• mean age: 9.9; 

range: 4-18 

• gender: n/r 

tTG
A-310

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, Year, 

Location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 

22 GCD;17 GFD 

Biopsy n/r; histology available on 5 on GFD - all normal AGA EMA 22/22 GCD EMA+; 0/17 GFD EMA+ 

Pacht 

1995, 

Israel 

Publication type: journal Study design: retrospective cohort Ethnicity:

n/r 

Population Type: 

Classic CD 

Biopsy criteria: 

ESPGAN 

Checked IgA def. n/r Serologic tests: 

Test name:

IgA EMA Methodology:ME Cut-off:>1:2.5 

Celiac Group 1 • 39 CD, 22 GCD 

and 17 GFD 

• mean age: 10 

y; range: n/r 

• % F: 46% Celiac Group 2 • median age: 

(range: ) 

• % F: 

tTG
A-311

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline GFD 8-30 mos 

Biopsy 0 normal; 1 (2.1%) partial VA; 11 (23%) subtotal VA; 35 (74%) total VA 

9 (19%) normal ; 23 (49%) partial VA; 13 (28%) subtotal VA ;2 (4%) total VA 

AGA 39 (83%) AGA measured in 39; 

Bx normal: 1/7 AGA+; partial VA: 7/20; subtotal VA: 5/10; total VA: 2/2 

EMA 47 (100%) Bx normal: 0 EMA+; 

partial VA: 5/23; subtotal VA: 3/13; total VA: 1/2 

SategnaGuidetti, 

1996, 

Italy 

Publication type: journal Study design: prospective cohort Ethnicity:

n/r 

Population Type: 

CD: details of diagnosis not reported 

Biopsy criteria: 

Normal, partial VA, subtotal VA, total VA 

Checked IgA def. Yes, excluded Serologic tests: 

Test name:

total AGA; IgA EMA Methodology:n/r; ME Cut-off:

n/r 

Celiac Group 1 • 47 pts • mean age: n/r; 

range: 18-68 y 

• 55% F 

tTGn/a 
A-312

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 

(at diagnosis) 

GFD for 6 mos 

Biopsy n/r n/a AGA EMA 0 EMA+ 2/16 (12.5%) reporting 

strict GFD EMA+; 5/45 (11.1%) admitting dietary mistakes EMA+ 

Scalici, 

2003, 

Italy 

Publication type: journal Study design: prospective cohort Ethnicity:

n/r 

Population type: 

Classic CD 

Biopsy criteria: 

ESPGAN 

Checked IgA def. n/r Serologic tests: 

Test name:

IgA EMA Methodology:n/r Cut-off:n/r 

Celiac Group 1 • 61 CD pts • mean age: n/r; 

age range 2-27 y 

• %F: n/r Celiac Group 2 • median age: 

(range: ) 

• % F: 

tTG
A-313

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, Year, 

Location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 39 Codex diet; 50 no detectable gluten Biopsy 18/39 (46%) VA; 20/50 (40%) VA AGA EMA 

Selby, 

1999 

Australia 

Publication type: journal Study design: cross sectional Ethnicity:

n/r 

Population Type: 

Classic CD 

Biopsy criteria: 

Normal, partial VA, subtotal VA, total VA 

Checked IgA def. n/r Serologic tests: 

Test name:

n/a Methodology:n/a Cut-off:n/a 

Celiac Group 1 • 89 pts CD on 

GFD mean 8.3 y 

• mean age: 47 

y; range: 20-75 

• 82% F 

tTG
A-314

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, Year, 

Location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 

Biopsy Group 1 4/4 normal; Group 2 3/6 high IEL, 1/6 VA; Group 3 5/6 high IEL 3/6 VA; Group 4 7/7 VA AGA EMA Group1 0/4; Group 2 1/6; Group 3 3/6; Group 4 7/7 

Troncone, 

1995 

Italy 

Publication type: journal Study design: cohort Ethnicity:

n/r 

Population Type: 

CD : details of diagnosis not reported 

Biopsy criteria: 

Normal, partial VA, subtotal VA, total VA 

Checked IgA def. n/r Serologic tests: 

Test name:

IgA EMA Methodology:ME Cut-off:>1:5 

Celiac Group 1 • 4 CD on strict 

GFD (23 in overall study 

• mean age: 14.5 

y; range 10-19 y 

• 35% F) Celiac Group 2 • 6 pts <0.5 g/d 

gluten 

• median age: 

n/r; range: n/r 

• % F: n/r Celiac Group 3 • 6 pts 0.5-1.0 

g/d gluten 

• median age: 

n/r; range: n/r 

• % F: n/r 

Celiac Group 4 • 7 pts>2 g/d 

gluten 

• median age: 

n/r; range: n/r 

• % F: n/r 

tTG
A-315

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, Year, 

Location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 

(39% strict GFD) 

Biopsy n/a AGA EMA 2.5% strict GFD; 37% minor transgression; 86% major transgression 

Vahedi, 

2000 

France 

Publication type: abstract Study design: cross sectional Ethnicity:

n/r 

Population type: 

CD: details of diagnosis not reported 

Biopsy criteria: 

no description 

Checked IgA def. Yes. Excluded Serologic tests: 

Test name:

IgA EMA; IgA tTG Methodology:n/r Cut-off:1:5; n/r 

Celiac Group 1 • 137 CD on 

GFD>1 y - median 75 mos 

• median age: 46 

y; range 18-74 y 

• 76% F 

tTG3% strict GFD; 31% minor transgression; 77% major transgression 
A-316

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 

GFD > 6 mos 

Biopsy 8 normal; 21 partial VA; 4 subtotal VA AGA EMA 9 (27%). Of 73% EMA negative, 7 normal,14 partial VA,3 subtotal VA 

Valentini, 

1994, 

Italy 

Publication type: journal Study design: prospective cohort Ethnicity:

n/r 

Population Type: 

Classic and atypical CD 

Biopsy criteria: 

Normal, partial VA, subtotal VA 

Checked IgA def. n/r Serologic tests: 

Test name:

IgA EMA Methodology:ME Cut-off:>1:5 

Celiac Group 1 • 33 CD pts on 

GFD >6 mosmean 9 mos 

• mean age: n/r; 

range: n/r 

• % F: n/r 

tTG
A-317

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, Year, 

Location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline 

Biopsy at 20-45 d, all had moderate or severe VA AGA 16/17 (94%) after 15 - 35 d gluten challenge EMA 

Valetta, 

1990 

Italy 

Publication type: journal Study design: prospective cohort Ethnicity:

n/r 

Population type: 

CD: details of diagnosis not reported 

Biopsy criteria: 

N,slight VA, moderate VA, severe VA 

Checked IgA def. n/r Serologic tests: 

Test name:

IgA AGA Methodology:n/r Cut-off:>3 SD controls 

Celiac Group 1 • 17 pts given 

gluten challenge 

• mean age: n/r; 

range 3 – 11 y 

• 59% F 

tTG
A-318

Evidence Table 12 (cont’d): Promoting or monitoring adherence to a GFD 

Outcomes Author, 

year, 

location Study Design 

Study 

Population Time 1 Time 2 Time 3 Time 4 

Baseline GFD <2 years GFD 2-5 years GFD >5 year

Biopsy 59 (37%) Marsh 3a; 59 (37%) 3b; 40 (25%) 3c 

88% 3a recovery to 0-2; 58% 3b recovery ; 81% 3c recovery 

98% 3a recovery to 0-2; 78% 3b recovery; 81% 3c recovery 

98% 3a recoveto 0-2; 88% 3b recovery; 86% recovery 

AGA EMA 

Wahab, 

2002, 

unknown 

Publication type: journal Study design: retrospectve cohort Ethnicity:

n/r 

Population type: 

Classic CD 

Biopsy criteria: 

Marsh 

Checked IgA def. No Serologic tests: 

Test name:

n/a Methodology:n/a Cut-off:n/a 

Celiac Group 1 • 158 pts • mean age: 44 

y; range 0 – 74 y 

• 91% F Celiac Group 2 • median age: 

(range: n/r ) 

• % F: 

tTG
A-288

Listing of Included Studies 

Ackerman Z, Eliakim R, Stalnikowicz R, Rachmilewitz D 

(1996) Role of small bowel biopsy in the endoscopic 

evaluation of adults with iron deficiency anemia. Am J 

Gastroenterol 91: 2099-2102 

Addolorato G, Capristo E, Ghittoni G, Valeri C, Masciana 

R, Ancona C, Gasbarrini G (2001) Anxiety but not 

depression decreases in coeliac patients after one-year 

gluten-free diet: a longitudinal study. Scand J Gastroenterol 

36: 502-506 

Agardh D, Nilsson A, Tuomi T, Lindberg B, Carlsson AK, 

Lernmark A, Ivarsson S-A (2001) Prediction of silent 

celiac disease at diagnosis of childhood type 1 diabetes by 

tissue transglutaminase autoantibodies and HLA. Pediatr 

Diabetes 2: 58-65 

Altuntas B, Kansu A, Ensari A, Girgin N (1998) Celiac 

disease in Turkish short-statured children and the value of 

antigliadin antibody in diagnosis. Acta Paediatr Jpn 40: 

457-460 

Amin R, Murphy N, Edge J, Ahmed ML, Acerini CL, 

Dunger DB (2002) A longitudinal study of the effects of a 

gluten-free diet on glycemic control and weight gain in 

subjects with type 1 diabetes and celiac disease. Diabetes 

Care 25: 1117-1122 

Annibale B, Capurso G, Chistolini A, D'Ambra G, 

DiGiulio E, Monarca B, DelleFave G (2001) 

Gastrointestinal causes of refractory iron deficiency anemia 

in patients without gastrointestinal symptoms. Am J Med 

111: 439-445 

Annibale B, Lahner E, Chistolini A, Gallucci C, Di Giulio 

E, Capurso G, Luana O, Monarca B, Delle FG (2003) 

Endoscopic evaluation of the upper gastrointestinal tract is 

worthwhile in premenopausal women with iron-deficiency 

anaemia irrespective of menstrual flow. Scand J 

Gastroenterol 38: 239-245 

Annibale B, Severi C, Chistolini A, Antonelli G, Lahner E, 

Marcheggiano A, Iannoni C, Monarca B, Delle FG (2001) 

Efficacy of gluten-free diet alone on recovery from iron 

deficiency anemia in adult celiac patients. Am J 

Gastroenterol 96: 132-137 

Anson O, Weizman Z, Zeevi N (1990) Celiac disease: 

parental knowledge and attitudes of dietary compliance. 

Pediatrics 85: 98-103 

Arato A, Korner A, Veres G, Dezsofi A, Ujpal I, Madacsy 

L (2002) Frequency of coeliac disease in Hungarian 

children with type 1 diabetes mellitus. Eur J Pediatr 162: 1-

5 

Artan R (1998) Antigliadin antibody measurement as a 

screening test for childhood coeliac disease. Int Med J 5: 

209-212 

Ascher H, Hahn-Zoric M, Hanson LA, Kilander AF, 

Nilsson LA, Tlaskalova H (1996) Value of serologic 

markers for clinical diagnosis and population studies of 

coeliac disease. Scandinavian Journal of Gastroenterology 

31: 61-67 

Ascher H, Lanner A, Kristiansson B (1990) A new 

laboratory kit for anti-gliadin IgA at diagnosis and followup of childhood celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 10: 443-450 

Askling J, Linet M, Gridley G, Halstensen TS, Ekstrom K, 

Ekbom A (2002) Cancer incidence in a population-based 

cohort of individuals hospitalized with celiac disease or 

dermatitis herpetiformis. Gastroenterology 123: 1428-1435 

Bahia M, Rabello A, Brasileiro FG, Penna FJ (2001) Serum 

antigliadin antibody levels as a screening criterion before 

jejunal biopsy indication for celiac disease in a developing 

country. Brazilian Journal of Medical and Biological 

Research = Revista Brasileira De Pesquisas Medicas E 

Biologicas / Sociedade Brasileira De Biofisica ...Et Al 34: 

1415-1420 

Bao F, Yu L, Babu S, Wang T, Hoffenberg EJ, Rewers M, 

Eisenbarth GS (1999) One third of HLA DQ2 homozygous 

patients with type 1 diabetes express celiac diseaseassociated transglutaminase autoantibodies. J Autoimmun 

13: 143-148 

Bardella MT, Fredella C, Prampolini L, Molteni N, Giunta 

AM, Bianchi PA (2000) Body composition and dietary 

intakes in adult celiac disease patients consuming a strict 

gluten-free diet. Am J Clin Nutr 72: 937-939 

Bardella MT, Molteni N, Cesana B, Baldassarri AR, 

Binanchi PA (1991) IgA antigliadin antibodies, 

cellobiose/mannitol sugar test, and carotenemia in the 

diagnosis of and screening for celiac disease. Am J 

Gastroenterol 86: 309-311 

Bardella MT, Molteni N, Quatrini M, Velio P, Ranzi T, 

Bianchi PA (1985) Clinical, biochemical and histological 

abnormalities in adult celiac patients on gluten-free diet. 

Gastroenterol Clin Biol 9: 787-789 

Bardella MT, Trovato C, Cesana BM, Pagliari C, Gebbia C, 

Peracchi M (2001) Serological markers for coeliac disease: 

Is it time to change? Dig Liver Dis 33: 426-431 
A-289

Barera G, Bianchi C, Calisti L, Cerutti F, Dammacco F, 

Frezza E, Illeni MT, Mistura L, Pocecco M, Prisco F 

(1991) Screening of diabetic children for coeliac disease 

with antigliadin antibodies and HLA typing. Arch Dis 

Child 66: 491-494 

Barera G, Bonfanti R, Viscardi M, Bazzigaluppi E, Calori 

G, Meschi F, Bianchi C, Chiumello G (2002) Occurrence 

of celiac disease after onset of type 1 diabetes: a 6-year 

prospective longitudinal study. Pediatrics 109: 833-838 

Barera G, Mora S, Brambilla P, Ricotti A, Menni L, Beccio 

S, Bianchi C (2000) Body composition in children with 

celiac disease and the effects of a gluten-free diet: a 

prospective case-control study. Am J Clin Nutr 72: 71-75 

Bartholomeusz RC, Labrooy JT, Davidson GP, Hetzel P, 

Johnson RB, Shearman DJ (1990) Polymeric IgA antibody 

to gliadin in the serum of patients with coeliac disease. J 

Gastroenterol Hepatol 5: 675-681 

Berger R, Schmidt G (1996) Evaluation of six anti-gliadin 

antibody assays. Journal of Immunological Methods 191: 

77-86 

Biagi F, Pezzimenti D, Campanella J, Vadacca GB, 

Corazza GR (2001) Endomysial and tissue 

transglutaminase antibodies in coeliac sera: a comparison 

not influenced by previous serological testing. 

Scandinavian Journal of Gastroenterology 36: 955-958 

Bode S, Gudmand-Hoyer E (1994) Evaluation of the 

gliadin antibody test for diagnosing coeliac disease. 

Scandinavian Journal of Gastroenterology 29: 148-152 

Bode S, Gudmand-Hoyer E (1996) Incidence and 

prevalence of adult coeliac disease within a defined 

geographic area in Denmark. Scand J Gastroenterol 31: 

694-699 

Bode S, Weile B, Krasilnikoff PA, Gudmand-Hoyer E 

(1993) The diagnostic value of the gliadin antibody test in 

celiac disease in children: a prospective study. J Pediatr 

Gastroenterol Nutr 17: 260-264 

Boersma B, Houwen RHJ, Blum WF, van Doorn J, Wit JM 

(2002) Catch-up growth and endocrine changes in 

childhood celiac disease. Endocrine changes during catchup growth. Horm Res 58: 57-65 

Bonamico M, Tiberti C, Picarelli A, Mariani P, Rossi D, 

Cipolletta E, Greco M, Tola MD, Sabbatella L, Carabba B, 

Magliocca FM, Strisciuglio P, Di Mario U (2001) 

Radioimmunoassay to detect antitransglutaminase 

autoantibodies is the most sensitive and specific screening 

method for celiac disease. American Journal of 

Gastroenterology 96: 1536-1540 

Book L, Zone JJ, Neuhausen SL (2003) Prevalence of 

celiac disease among relatives of sib pairs with celiac 

disease in U.S. families. Am J Gastroenterol 98: 377-381 

Borch K, Grodzinsky E, Petersson F, Jonsson K-A, Mardh 

S, Valdimarsson T (2000) Prevalence of coeliac disease 

and relations to Helicobacter pylori infection and 

duodenitis in a Swedish adult population sample: A 

histomorphological and serological survey. 

Inflammopharmacology 8: 341-350 

Bottaro G, Volta U, Spina M, Rotolo N, Sciacca A, 

Musumeci S (1997) Antibody pattern in childhood celiac 

disease. Journal of Pediatric Gastroenterology and 

Nutrition 24: 559-562 

Burgin-Wolff A, Gaze H, Hadziselimovic F, Huber H, 

Lentze MJ, Nussle D, Reymond-Berthet C (1991) 

Antigliadin and antiendomysium antibody determination 

for coeliac disease. Arch Dis Child 66: 941-947 

Calero P, Ribes-Koninckx C, Albiach V, Carles C, Ferrer J 

(1996) IgA antigliadin antibodies as a screening method for 

nonovert celiac disease in children with insulin-dependent 

diabetes mellitus. J Pediatr Gastroenterol Nutr 23: 29-33 

Carlsson AK, Axelsson IE, Borulf SK, Bredberg AC, 

Ivarsson SA (2001) Serological screening for celiac disease 

in healthy 2.5-year-old children in Sweden. Pediatrics 107: 

42-45 

Carroccio A, Iacono G, D'Amico D, Cavataio F, Teresi S, 

Caruso C, Di Prima L, Colombo A, D'Arpa F, Florena A, 

Notarbartolo A, Montalto G (2002) Production of antiendomysial antibodies in cultured duodenal mucosa: 

usefulness in coeliac disease diagnosis. Scandinavian 

Journal of Gastroenterology 37: 32-38 

Carroccio A, Iacono G, Montalto G, Cavataio F, Soresi M, 

Kazmierska I, Notarbartolo A (1993) Immunologic and 

absorptive tests in celiac disease: can they replace intestinal 

biopsies? Scandinavian Journal of Gastroenterology 28: 

673-676 

Carroccio A, Vitale G, Di Prima L, Chifari N, Napoli S, La 

Russa C, Gulotta G, Averna MR, Montalto G, Mansueto S, 

Notarbartolo A (2002) Comparison of antitransglutaminase ELISAs and an anti-endomysial antibody 

assay in the diagnosis of celiac disease: a prospective study. 

Clin Chem 48: 1546-1550 

Cataldo F, Lio D, Marino V, Picarelli A, Ventura A, 

Corazza GR (2000) IgG(1) antiendomysium and IgG 

antitissue transglutaminase (anti-tTG) antibodies in coeliac 

patients with selective IgA deficiency. Working Groups on 

Celiac Disease of SIGEP and Club del Tenue. Gut 47: 366-

369 
A-290

Catassi C, Fabiani E, Ratsch IM, et al. (1996) The coeliac 

iceberg in Italy. A multicentre antigliadin antibodies 

screening for coeliac disease in school-age subjects. Acta 

Paediatr 412: 29-35 

Catassi C, Fanciulli G, D'Appello AR, El Asmar R, 

Rondina C, Fabiani E, Bearzi I, Coppa G, V (2000) 

Antiendomysium versus antigliadin antibodies in screening 

the general population for coeliac disease. Scand J 

Gastroenterol 35: 732-736 

Chan AW, Butzner JD, McKenna R, Fritzler MJ (2001) 

Tissue transglutaminase enzyme-linked immunosorbent 

assay as a screening test for celiac disease in pediatric 

patients. Pediatrics 107: E8 

Chartrand LJ, Agulnik J, Vanounou T, Russo PA, Baehler 

P, Seidman EG (1997) Effectiveness of antigliadin 

antibodies as a screening test for celiac disease in children. 

CMAJ 157: 527-533 

Chirdo FG, Rumbo M, Carabajal P, Castagnino N, 

Mavromatopulos E, Cirincione V, Anon MC, Fossati CA 

(1999) Analysis of anti-gliadin antibodies by immunoblot 

analysis and enzyme-linked immunosorbent assay using 

gliadin fractions as antigens. Journal of Pediatric 

Gastroenterology and Nutrition 29: 171-177 

Chirdo FG, Rumbo M, Carabajal P, Mavromatopulos E, 

Castagnino N, Anon MC, Fossati CA (2000) Determination 

of anti-omega-gliadin antibodies in serologic tests for 

coeliac disease. Scandinavian Journal of Gastroenterology 

35: 508-516 

Ciacci C, Cirillo M, Auriemma G, Di Dato G, Sabbatini F, 

Mazzacca G (1996) Celiac disease and pregnancy outcome. 

Am J Gastroenterol 91: 718-722 

Collin P, Reunala T, Rasmussen M, Kyronpalo S, 

Pehkonen E, Laippala P, Maki M (1997) High incidence 

and prevalence of adult coeliac disease. Augmented 

diagnostic approach. Scand J Gastroenterol 32: 1129-1133 

Collin P, Syrjanen J, Partanen J, Pasternack A, Kaukinen 

K, Mustonen J (2002) Celiac disease and HLA DQ in 

patients with IgA nephropathy. American Journal of 

Gastroenterology 97: 2572-2576 

Corazza GR, Andreani ML, Biagi F, Corrao G, Pretolani S, 

Giulianelli G, Ghironzi G, Gasbarrini G (1997) The smaller 

size of the 'coeliac iceberg' in adults. Scand J Gastroenterol 

32: 917-919 

Corrao G, Corazza GR, Bagnardi V, Brusco G, Ciacci C, 

Cottone M, Sategna GC, Usai P, Cesari P, Pelli MA, 

Loperfido S, Volta U, Calabro A, Certo M (2001) Mortality 

in patients with coeliac disease and their relatives: a cohort 

study. Lancet 358: 356-361 

Corrao G, Usai P, Galatola G, Ansaldi N, Meini A, Pelli 

MA, Castellucci G, Corazza GR (1996) Estimating the 

incidence of coeliac disease with capture-recapture 

methods within four geographic areas in Italy. J Epidemiol 

Community Health 50: 299-305 

Cottone M, Termini A, Oliva L, Magliocco A, Marrone C, 

Orlando A, Pinzone F, Di Mitri R, Rosselli M, Rizzo A, 

Pagliaro L (1999) Mortality and causes of death in celiac 

disease in a Mediterranean area. Dig Dis Sci 44: 2538-2541 

Cronin CC, Feighery A, Ferriss JB, Liddy C, Shanahan F, 

Feighery C (1997) High prevalence of celiac disease among 

patients with insulin-dependent (type I) diabetes mellitus. 

Am J Gastroenterol 92: 2210-2212 

Csizmadia CGDS, Mearin ML, Von Blomberg BME, 

Brand R, Verloove-Vanhorick SP (1999) An iceberg of 

childhood coeliac disease in the Netherlands. Lancet 353: 

813-814 

Dahele A, Kingstone K, Bode J, Anderson D, Ghosh S 

(2001) Anti-endomysial antibody negative celiac disease: 

does additional serological testing help? Digestive Diseases 

and Sciences 46: 214-221 

Dahele A, V, Aldhous MC, Humphreys K, Ghosh S (2001) 

Serum IgA tissue transglutaminase antibodies in coeliac 

disease and other gastrointestinal diseases. Q J Med 94: 

195-205 

Day AS, Cook HB, Whitehead M, Abbott GD (2000) Antiendomysial and anti-gliadin antibodies in screening for 

coeliac disease in children at greater risk of developing 

coeliac disease. N Z Med J 113: 412-413 

De Block CE, De L, I, Vertommen JJ, Rooman RP, Du 

CM, V, Van Campenhout CM, Weyler JJ, Winnock F, Van 

Autreve J, Gorus FK (2001) Beta-cell, thyroid, gastric, 

adrenal and coeliac autoimmunity and HLA-DQ types in 

type 1 diabetes. Clin Exp Immunol 126: 236-241 

De Vitis, I, Ghirlanda G, Gasbarrini G (1996) Prevalence of 

coeliac disease in type I diabetes: a multicentre study. Acta 

Paediatr 412: 56-57 

Delco F, El Serag HB, Sonnenberg A (1999) Celiac sprue 

among US military veterans: associated disorders and 

clinical manifestations. Dig Dis Sci 44: 966-972 

Di Leo M, Weisz G, Ansaldi BN (1999) Serum and 

salivary antiendomysium antibodies in the screening of 

coeliac disease. Panminerva Medica 41: 68-71 

Dickey W, Hughes DF, McMillan SA (2000) 

Disappearance of endomysial antibodies in treated celiac 

disease does not indicate histological recovery. Am J 

Gastroenterol 95: 712-714 
A-291

Dickey W, Kenny BD, McMillan SA, Porter KG, 

McConnell JB (1997) Gastric as well as duodenal biopsies 

may be useful in the investigation of iron deficiency 

anaemia. Scand J Gastroenterol 32: 469-472 

Dickey W, McMillan SA, Bharucha C, Porter KG (1992) 

Antigliadin antibodies in blood donors in Northern Ireland. 

Eur J Gastroenterol Hepatol 4: 739-741 

Dickey W, McMillan SA, Hughes DF (2001) Sensitivity of 

serum tissue transglutaminase antibodies for endomysial 

antibody positive and negative coeliac disease. 

Scandinavian Journal of Gastroenterology 36: 511-514 

Fabiani E, Catassi C (2001) The serum IgA class anti-tissue 

transglutaminase antibodies in the diagnosis and follow up 

of coeliac disease. Results of an international multi-centre 

study. International Working Group on Eu-tTG. Eur J 

Gastroenterol Hepatol 13: 659-665 

Fabiani E, Catassi C, Villari A, Gismondi P, Pierdomenico 

R, Ratsch IM, Coppa G, V, Giorgi PL (1996) Dietary 

compliance in screening-detected coeliac disease 

adolescents. Acta Paediatr 412: 65-67 

Fabiani E, Taccari LM, Ratsch IM, Di Giuseppe S, Coppa 

G, V, Catassi C (2000) Compliance with gluten-free diet in 

adolescents with screening-detected celiac disease: a 5-year 

follow-up study. J Pediatr 136: 841-843 

Falth-Magnusson K, Jansson G, Stenhammar L, 

Magnusson KE (1994) Serum food antibodies analyzed by 

enzyme-linked immunosorbent assay (ELISA) and 

diffusion-in-gel (DIG)-ELISA methods in children with 

and without celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 18: 56-62 

Farre C, Humbert P, Vilar P, Varea V, Aldeguer X, 

Carnicer J, Carballo M, Gassull MA (1999b Serological 

markers and HLA-DQ2 haplotype among first-degree 

relatives of celiac patients. Catalonian Coeliac Disease 

Study Group. Dig Dis Sci 44: 2344-2349 

Fasano A, Berti I, Gerarduzzi T, Not T, Colletti RB, Drago 

S, Elitsur Y, Green PHR, Guandalini S, Hill ID, Pietzak M, 

Ventura A, Thorpe M, Kryszak D, Fornaroli F, Wasserman 

SS, Murray JA, Horvath K (2003) Prevalence of celiac 

disease in at-risk and not-at-risk groups in the United 

States: a large multicenter study. Arch Intern Med 163: 

286-292 

Fickling WE, McFarlane XA, Bhalla AK, Robertson DA 

(2001) The clinical impact of metabolic bone disease in 

coeliac disease. Postgrad.Med J 77: 33-36 

Fitzpatrick KP, Sherman PM, Ipp M, Saunders N, 

Macarthur C (2001) Screening for celiac disease in children 

with recurrent abdominal pain. J Pediatr Gastroenterol Nutr 

33: 250-252 

Fotoulaki M, Nousia-Arvanitakis S, AugoustidouSavvopoulou P, Kanakoudi-Tsakalides F, Zaramboukas T, 

Vlachonikolis J (1999) Clinical application of 

immunological markers as monitoring tests in celiac 

disease. Dig Dis Sci 44: 2133-2138 

Fraser-Reynolds KA, Butzner JD, Stephure DK, Trussell 

RA, Scott RB (1998) Use of immunoglobulin Aantiendomysial antibody to screen for celiac disease in 

North American children with type 1 diabetes. Diabetes 

Care 21: 1985-1989 

Gillett HR, Freeman HJ (2000) Comparison of IgA 

endomysium antibody and IgA tissue transglutaminase 

antibody in celiac disease. Canadian Journal of 

Gastroenterology = Journal Canadien De Gastroenterologie 

14: 668-671 

Gillett PM, Gillett HR, Israel DM, Metzger DL, Stewart L, 

Chanoine JP, Freeman HJ (2001) High prevalence of celiac 

disease in patients with type 1 diabetes detected by 

antibodies to endomysium and tissue transglutaminase. Can 

J Gastroenterol 15: 297-301 

Gonczi J, Skerritt JH, Mitchell JD (1991) A reliable 

screening test for coeliac disease: enzyme-linked 

immunosorbent assay to detect anti-gliadin antibodies in 

serum. Australian and New Zealand Journal of Medicine 

21: 723-731 

Gonzalez D, Sugai E, Gomez JC, Oliveri MB, Gomez AC, 

Vega E, Bagur A, Mazure R, Maurino E, Bai JC, Mautalen 

C (2002) Is it necessary to screen for celiac disease in 

postmenopausal osteoporotic women? Calcif Tissue Int 71: 

141-144 

Greco L, Mayer M, Ciccarelli G, Troncone R, Auricchio S 

(1997) Compliance to a gluten-free diet in adolescents, or 

"what do 300 coeliac adolescents eat every day?". Ital J 

Gastroenterol Hepatol 29: 305-310 

Green PH, Shane E, Rotterdam H, Forde KA, Grossbard L 

(2000) Significance of unsuspected celiac disease detected 

at endoscopy. Gastroenterol Int 51: 60-65 

Green PHR, Fleischauer AT, Bhagat G, Goyal R, Jabri B, 

Neugut AI (2003) Risk of malignancy in patients with 

celiac disease. Am J Med 115: 191-195 

Grodzinsky E (1996) Screening for coeliac disease in 

apparently healthy blood donors. Acta Paediatr 412: 36-38 

Hallstrom O (1989) Comparison of IgA-class reticulin and 

endomysium antibodies in coeliac disease and dermatitis 

herpetiformis. Gut 30: 1225-1232 

Hansen D, Bennedbaek FN, Hansen LK, Hoier-Madsen M, 

Hegedu LS, Jacobsen BB, Husby S (2001) High prevalence 

of coeliac disease in Danish children with type I diabetes 

mellitus. Acta Paediatr 90: 1238-1243 
A-292

Hansson T, Dahlbom I, Hall J, Holtz A, Elfman L, 

Dannaeus A, Klareskog L (2000) Antibody reactivity 

against human and guinea pig tissue transglutaminase in 

children with celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 30: 379-384 

Hawkes ND, Swift GL, Smith PM, Jenkins HR (2000) 

Incidence and presentation of coeliac disease in South 

Glamorgan. Eur J Gastroenterol Hepatol 12: 345-349 

Hill I, Fasano A, Schwartz R, Counts D, Glock M, Horvath 

K (2000) The prevalence of celiac disease in at-risk groups 

of children in the United States. J Pediatr 136: 86-90 

Hin H, Bird G, Fisher P, Mahy N, Jewell D (1999) Coeliac 

disease in primary care: case finding study. BMJ 318: 164-

167 

Hoffenberg EJ, MacKenzie T, Barriga KJ, Eisenbarth GS, 

Bao F, Haas JE, Erlich H, Bugawan TL, Sokol RJ, Taki I, 

Norris JM, Rewers M (2003) A prospective study of the 

incidence of childhood celiac disease. J Pediatr 143: 308-

314 

Hogberg L, Falth-Magnusson K, Grodzinsky E, 

Stenhammar L (2003) Familial prevalence of coeliac 

disease: A twenty-year follow-up study. Scand J 

Gastroenterol 38: 61-65 

Hogberg L, Grodzinsky E, Stenhammar L (2003) Better 

dietary compliance in patients with coeliac disease 

diagnosed in early childhood. Scand J Gastroenterol 38: 

751-754 

Holm KH (1993) Correlation of HLA-DR alleles to jejunal 

mucosal morphology in healthy first-degree relatives of 

coeliac disease patients. Eur J Gastroenterol Hepatol 5: 35-

39 

Holmes GK, Prior P, Lane MR, Pope D, Allan RN (1989) 

Malignancy in coeliac disease--effect of a gluten free diet. 

Gut 30: 333-338 

Hovdenak N, Hovlid E, Aksnes L, Fluge G, Erichsen MM, 

Eide J (1999) High prevalence of asymptomatic coeliac 

disease in Norway: a study of blood donors. Eur J 

Gastroenterol Hepatol 11: 185-187 

Howard MR, Turnbull AJ, Morley P, Hollier P, Webb R, 

Clarke A (2002) A prospective study of the prevalence of 

undiagnosed coeliac disease in laboratory defined iron and 

folate deficiency. J Clinl Path 55: 754-757 

Iltanen S, Holm K, Partanen J, Laippala P, Maki M (1999) 

Increased density of jejunal gammadelta+ T cells in 

patients having normal mucosa--marker of operative 

autoimmune mechanisms? Autoimmunity 29: 179-187 

Iltanen S, Rantala I, Laippala P, Holm K, Partanen J, Maki 

M (1999) Expression of HSP-65 in jejunal epithelial cells 

in patients clinically suspected of coeliac disease. 

Autoimmunity 31: 125-132 

Ivarsson A, Persson LA, Juto P, Peltonen M, Suhr O, 

Hernell O (1999) High prevalence of undiagnosed coeliac 

disease in adults: a Swedish population-based study. J 

Intern Med 245: 63-68 

Ivarsson A, Persson LA, Nystrom L, Hernell O (2003) The 

Swedish coeliac disease epidemic with a prevailing twofold 

higher risk in girls compared to boys may reflect gender 

specific risk factors. Eur J Epidemiol 18: 677-684 

Jackson PT, Glasgow JF, Thom R (1985) Parents' 

understanding of coeliac disease and diet. Arch Dis Child 

60: 672-674 

Jaeger C, Hatziagelaki E, Petzoldt R, Bretzel RG (2001) 

Comparative analysis of organ-specific autoantibodies and 

celiac disease--associated antibodies in type 1 diabetic 

patients, their first-degree relatives, and healthy control 

subjects. Diabetes Care 24: 27-32 

Jansen Th TLA, Mulder CJJ, Karssen PHZ, Wagenaar CGJ 

(1993) Epidemiological survey of the Dutch Coeliac 

Disease Society: An update 1992. Eur J Gastroenterol 

Hepatol 5: 73-78 

Johnston SD, Watson RG, McMillan SA, Sloan J, Love AH 

(1998) Coeliac disease detected by screening is not silent--

simply unrecognized. Q J Med 91: 853-860 

Kaukinen K, Collin P, Mykkanen AH, Partanen J, Maki M, 

Salmi J (1999) Celiac disease and autoimmune 

endocrinologic disorders. Dig Dis Sci 44: 1428-1433 

Kaukinen K, Turjanmaa K, Maki M, Partanen J, 

Venalainen R, Reunala T, Collin P (2000) Intolerance to 

cereals is not specific for coeliac disease. Scandinavian 

Journal of Gastroenterology 35: 942-946 

Kaukinen K, Sulkanen S, Maki M, Collin P (2002) IgAclass transglutaminase antibodies in evaluating the efficacy 

of gluten-free diet in coeliac disease. Eur J Gastroenterol 

Hepatol 14: 311-315 

Kemppainen TA, Kosma VM, Janatuinen EK, Julkunen RJ, 

Pikkarainen PH, Uusitupa M, I (1998) Nutritional status of 

newly diagnosed celiac disease patients before and after the 

institution of a celiac disease diet--association with the 

grade of mucosal villous atrophy. Am J Clin Nutr 67: 482-

487 

Kepczyk T, Kadakia SC (1995) Prospective evaluation of 

gastrointestinal tract in patients with iron-deficiency 

anemia. Dig Dis Sci 40: 1283-1289 
A-293

Kolho KL, Farkkila MA, Savilahti E (1998) Undiagnosed 

coeliac disease is common in Finnish adults. Scand J 

Gastroenterol 33: 1280-1283 

Kolho KL, Savilahti E (1997) IgA endomysium antibodies 

on human umbilical cord: an excellent diagnostic tool for 

celiac disease in childhood. Journal of Pediatric 

Gastroenterology and Nutrition 24: 563-567 

Kordonouri O, Dieterich W, Schuppan D, Webert G, 

Muller C, Sarioglu N, Becker M, Danne T (2000) 

Autoantibodies to tissue transglutaminase are sensitive 

serological parameters for detecting silent coeliac disease 

in patients with Type 1 diabetes mellitus. Diabet Med 17: 

441-444 

Korponay-Szabo I, Kovacs J, Lorincz M, Torok E, Goracz 

G (1998) Families with multiple cases of gluten-sensitive 

enteropathy. Z Gastroenterol 36: 553-558 

Kotze LM, Utiyama SR, Nisihara RM, Zeni MP, de Sena 

MG, Amarante HM (2001) Antiendomysium antibodies in 

Brazilian patients with celiac disease and their first-degree 

relatives. Arq Gastroenterol 38: 94-103 

Kumar V, Lerner A, Valeski JE, Beutner EH, Chorzelski 

TP, Rossi T (1989) Endomysial antibodies in the diagnosis 

of celiac disease and the effect of gluten on antibody titers. 

Immunological Investigations 18: 533-544 

Ladinser B, Rossipal E, Pittschieler K (1994) Endomysium 

antibodies in coeliac disease: an improved method. Gut 35: 

776-778 

Lamontagne P, West GE, Galibois I (2001) Quebecers with 

celiac disease: analysis of dietary problems. Canadian 

Journal of Dietetic Practice and Research - a Publication of 

Dietitians of Canada = Revue Canadienne De La Pratique 

Et De La Recherche En Dietetique - Une Publication Des 

Dietetistes Du C 62: 175-181 

Lampasona V, Bonfanti R, Bazzigaluppi E, Venerando A, 

Chiumello G, Bosi E, Bonifacio E (1999) Antibodies to 

tissue transglutaminase C in type I diabetes. Diabetologia 

42: 1195-1198 

Lee SK, Lo W, Memeo L, Rotterdam H, Green Peter HR 

(2003) Duodenal histology in patients with celiac disease 

after treatment with a gluten-free diet. Gastrointest Endosc 

57: 187-191 

Lerner A, Kumar V, Iancu TC (1994) Immunological 

diagnosis of childhood coeliac disease: comparison 

between antigliadin, antireticulin and antiendomysial 

antibodies. Clinical and Experimental Immunology 95: 78-

82 

Li Voon Chong JSW, Leong KS, Wallymahmed M, 

Sturgess R, MacFarlane IA (2002) Is coeliac disease more 

prevalent in young adults with coexisting Type 1 diabetes 

mellitus and autoimmune thyroid disease compared with 

those with Type 1 diabetes mellitus alone? Diabet Med 19: 

334-337 

Lindberg T, Nilsson LA, Borulf S, Cavell B, Fallstrom SP, 

Jansson U, Stenhammar L, Stintzing G (1985) Serum IgA 

and IgG gliadin antibodies and small intestinal mucosal 

damage in children. Journal of Pediatric Gastroenterology 

and Nutrition 4: 917-922 

Lindh E, Ljunghall S, Larsson K, Lavo B (1992) Screening 

for antibodies against gliadin in patients with osteoporosis. 

J Intern Med 231: 403-406 

Lindquist BL, Rogozinski T, Moi H, Danielsson D, Olcen 

P (1994) Endomysium and gliadin IgA antibodies in 

children with coeliac disease. Scandinavian Journal of 

Gastroenterology 29: 452-456 

Ljungman G, Myrdal U (1993) Compliance in teenagers 

with coeliac disease--a Swedish follow-up study. Acta 

Paediatr 82: 235-238 

Logan RF, Rifkind EA, Turner ID, Ferguson A (1989) 

Mortality in celiac disease. Gastroenterology 97: 265-271 

Lopez-Rodriguez MJ, Canal Macias ML, Lavado Garcia 

JM, Sanchez BM, Robledo AP, Pedrera Zamorano JD 

(2003) Epidemiological changes in diagnosed coeliac 

disease in a population of Spanish children. Acta Paediatr 

92: 165-169 

Lorini R, Scotta MS, Cortona L, Avanzini MA, Vitali L, 

De Giacomo C, Scaramuzza A, Severi F (1996) Celiac 

disease and type I (insulin-dependent) diabetes mellitus in 

childhood: follow-up study. J Diabetes Complications 10: 

154-159 

Magazzu G, Bottaro G, Cataldo F, Iacono G, Di Donato F, 

Patane R, Cavataio F, Maltese I, Romano C, Arco A (1994) 

Increasing incidence of childhood celiac disease in Sicily: 

results of a multicenter study. Acta Paediatr 83: 1065-1069 

Maki M, Holm K (1990) Incidence and prevalence of 

coeliac disease in Tampere. Coeliac disease is not 

disappearing. Acta Paediatrica Scandinavica 79: 980-982 

Maki M, Holm K, Lipsanen V, Hallstrom O, Viander M, 

Collin P, Savilahti E, Koskimies S (1991) Serological 

markers and HLA genes among healthy first-degree 

relatives of patients with coeliac disease. Lancet 338: 1350-

1353 
A-294

Maki M, Mustalahti K, Kokkonen J, Kulmala P, Haapalahti 

M, Karttunen T, Ilonen J, Laurila K, Dahlbom I, Hansson 

T, Hopfl P, Knip M (2003) Prevalence of Celiac disease 

among children in Finland. New Engl J Med 348: 2517-

2524 

Martini S, Mengozzi G, Aimo G, Giorda L, Pagni R, 

Guidetti CS (2002) Comparative evaluation of serologic 

tests for celiac disease diagnosis and follow-up. Clin Chem 

48: 960-963 

Mather KJ, Meddings JB, Beck PL, Scott RB, Hanley DA 

(2001) Prevalence of IgA-antiendomysial antibody in 

asymptomatic low bone mineral density. Am J 

Gastroenterol 96: 120-125 

Mazzetti dP, Giorgetti GM, Gregori M, De Simone M, 

Leonardi C, Barletta PA, Ricciardi MM, Sandri G (1992) 

Subclinical coeliac disease. Ital J Gastroenterol 24: 352-354 

McIntyre AS, Long RG (1993) Prospective survey of 

investigations in outpatients referred with iron deficiency 

anaemia. Gut 34: 1102-1107 

McMillan SA, Haughton DJ, Biggart JD, Edgar JD, Porter 

KG, McNeill TA (1991) Predictive value for coeliac 

disease of antibodies to gliadin, endomysium, and jejunum 

in patients attending for jejunal biopsy. Bmj (Clinical 

Research Ed.) 303: 1163-1165 

McNicholl B, Egan-Mitchell B, Stevens F, Keane R, Baker 

S, McCarthy CF, Fottrell PF (1976) Mucosal recovery in 

treated childhood celiac disease (gluten-sensitive 

enteropathy). J Pediatr 89: 418-424 

Meini A, Pillan NM, Villanacci V, Monafo V, Ugazio AG, 

Plebani A (1996) Prevalence and diagnosis of celiac 

disease in IgA-deficient children. Annals of Allergy, 

Asthma & Immunology - Official Publication of the 

American College of Allergy, Asthma, & Immunology 77: 

333-336 

Moreno ML, Vazquez H, Mazure R, Smecuol E, Niveloni 

S, Pedreira S, Sugai E, Maurino E, Gomez JC, Bai JC 

(2004) Stratification of bone fracture risk in patients with 

celiac disease. Clin Gastroenterol.Hepatol. 2: 127-134 

Mustalahti K, Sulkanen S, Holopainen P, Laurila K, Collin 

P, Partanen J, Maki M (2002) Coeliac disease among 

healthy members of multiple case coeliac disease families. 

Scand J Gastroenterol 37: 161-165 

Nielsen OH, Jacobsen O, Pedersen ER, Rasmussen SN, 

Petri M, Laulund S, Jarnum S (1985) Non-tropical sprue. 

Malignant diseases and mortality rate. Scand J 

Gastroenterol 20: 13-18 

Not T, Horvath K, Hill ID, Partanen J, Hammed A, 

Magazzu G, Fasano A (1998) Celiac disease risk in the 

USA: high prevalence of antiendomysium antibodies in 

healthy blood donors. Scand J Gastroenterol 33: 494-498 

Nuti R, Martini G, Valenti R, Giovani S, Salvadori S, 

Avanzati A (2001) Prevalence of undiagnosed coeliac 

syndrome in osteoporotic women. J Intern Med 250: 361-

366 

Oxentenko AS, Grisolano SW, Murray JA, Burgart LJ, 

Dierkhising RA, Alexander JA (2002) The insensitivity of 

endoscopic markers in celiac disease. Am J Gastroenterol 

97: 933-938 

Pacht A, Sinai N, Hornstein L, Kumar V, Ish-Shalom N, 

Lerner A (1995) The diagnostic reliability of antiendomysial antibody in celiac disease: the north Israel 

experience. Isr J Med Sci 31: 218-220 

Page SR, Lloyd CA, Hill PG, Peacock I, Holmes GK 

(1994) The prevalence of coeliac disease in adult diabetes 

mellitus. Q J Med 87: 631-637 

Picarelli A, Sabbatella L, Di Tola M, Gabrielli F, Greco R, 

Di Cello T, Mastracchio A, Anania MC (2000) Celiac 

disease diagnosis in misdiagnosed children. Pediatric 

Research 48: 590-592 

Pittschieler K, Gentili L, Niederhofer H (2003) Onset of 

coeliac disease: A prospective longitudinal study. Acta 

Paediatr Int J Paediatr 92: 1149-1152 

Pittschieler K, Ladinser B (1996) Coeliac disease: screened 

by a new strategy. Acta Paediatr 412: 42-45 

Poddar U, Thapa BR, Nain CK, Prasad A, ingh K (2002) 

Celiac disease in India: are they true cases of celiac 

disease? J Pediatr Gastroenterol Nutr 35: 508-512 

Polvi A, Eland C, Koskimies S, Maki M, Partanen J (1996) 

HLA DQ and DP in Finnish families with celiac disease. 

Eur J Immunogenet 23: 221-234 

Ransford Rupert AJ, Hayes M, Palmer M, Hall MJ (2002) 

A controlled, prospective screening study of celiac disease 

presenting as iron deficiency anemia. J Clin Gastroenterol 

35: 228-233 

Rea F, Polito C, Marotta A, Di Toro A, Iovene A, Collini 

R, Rea L, Sessa G (1996) Restoration of body composition 

in celiac children after one year of gluten-free diet. J 

Pediatr Gastroenterol Nutr 23: 408-412 

Rensch MJ, Merenich JA, Lieberman M, Long BD, Davis 

DR, McNally PR (1996) Gluten-sensitive enteropathy in 

patients with insulin-dependent diabetes mellitus. Ann 

Intern Med 124: 564-567 
A-295

Rich EJ, Christie DL (1990) Anti-gliadin antibody panel 

and xylose absorption test in screening for celiac disease. 

Journal of Pediatric Gastroenterology and Nutrition 10: 

174-178 

Riestra S, Fernandez E, Rodrigo L, Garcia S, Ocio G 

(2000) Prevalence of Coeliac disease in the general 

population of northern Spain. Strategies of serologic 

screening. Scand J Gastroenterol 35: 398-402 

Robinson DC, Watson AJ, Wyatt EH, Marks JM, Roberts 

DF (1971) Incidence of small-intestinal mucosal 

abnormalities and of clinical coeliac disease in the relatives 

of children with coeliac disease. Gut 12: 789-793 

Roldan MB, Barrio R, Roy G, Parra C, Alonso M, 

Yturriaga R, Camarero C (1998) Diagnostic value of 

serological markers for celiac disease in diabetic children 

and adolescents. J Pediatr Endocrinol Metab 11: 751-756 

Rolles CJ, Myint TO, Sin WK, Anderson M (1974) 

Proceedings: Family study of coeliac disease. Gut 15: 827 

Rossi TM, Albini CH, Kumar V (1993) Incidence of celiac 

disease identified by the presence of serum endomysial 

antibodies in children with chronic diarrhea, short stature, 

or insulin-dependent diabetes mellitus. J Pediatr 123: 262-

264 

Rostami K, Mulder CJ, van Overbeek FM, Kerckhaert J, 

Meijer JW, von Blomberg MB, Heymans HS (2000) 

Should relatives of coeliacs with mild clinical complaints 

undergo a small-bowel biopsy despite negative serology? 

Eur J Gastroenterol Hepatol 12: 51-55 

Rostami K, Mulder CJ, Werre JM, van Beukelen FR, 

Kerchhaert J, Crusius JB, Pena AS, Willekens FL, Meijer 

JW (1999) High prevalence of celiac disease in apparently 

healthy blood donors suggests a high prevalence of 

undiagnosed celiac disease in the Dutch population. Scand 

J Gastroenterol 34: 276-279 

Russo PA, Chartrand LJ, Seidman E (1999) Comparative 

analysis of serologic screening tests for the initial diagnosis 

of celiac disease. Pediatrics 104: 75-78 

Rutz R, Ritzler E, Fierz W, Herzog D (2002) Prevalence of 

asymptomatic celiac disease in adolescents of eastern 

Switzerland. Swiss Med Wkly 132: 43-47 

Sacchetti L, Calcagno G, Ferrajolo A, Sarrantonio C, 

Troncone R, Micillo M, Auricchio S, Salvatore F (1998) 

Discrimination between celiac and other gastrointestinal 

disorders in childhood by rapid human lymphocyte antigen 

typing. Clinical Chemistry 44: 1755-1757 

Salmaso C, Ocmant A, Pesce G, Altrinetti V, Montagna P, 

Descalzi D, Martino S, Bagnasco M, Mascart F (2001) 

Comparison of ELISA for tissue transglutaminase 

autoantibodies with antiendomysium antibodies in pediatric 

and adult patients with celiac disease. Allergy 56: 544-547 

Sanders DS, Patel D, Stephenson TJ, Ward AM, 

McCloskey EV, Hadjivassiliou M, Lobo AJ (2003) A 

primary care cross-sectional study of undiagnosed adult 

coeliac disease. Eur J Gastroenterol Hepatol 15: 407-413 

Sategna-Guidetti C, Grosso S (1994) Changing pattern in 

adult coeliac disease: A 24-year survey. Eur J Gastroenterol 

Hepatol 6: 15-19 

Sategna-Guidetti C, Grosso S, Bruno M, Grosso SB (1995) 

Comparison of serum anti-gliadin, anti-endomysium, and 

anti-jejunum antibodies in adult celiac sprue. Journal of 

Clinical Gastroenterology 20: 17-21 

Sategna-Guidetti C, Grosso S, Bruno M, Grosso SB (1996) 

Reliability of immunologic markers of celiac sprue in the 

assessment of mucosal recovery after gluten withdrawal. J 

Clin Gastroenterol 23: 101-104 

Sategna-Guidetti C, Volta U, Ciacci C, Usai P, Carlino A, 

De Franceschi L, Camera A, Pelli A, Brossa C (2001) 

Prevalence of thyroid disorders in untreated adult celiac 

disease patients and effect of gluten withdrawal: an Italian 

multicenter study. Am J Gastroenterol 96: 751-757 

Saukkonen T, Savilahti E, Reijonen H, Ilonen J, 

Tuomilehto-Wolf E, Akerblom HK (1996) Coeliac disease: 

frequent occurrence after clinical onset of insulindependent diabetes mellitus. Childhood Diabetes in Finland 

Study Group. Diabet Med 13: 464-470 

Saukkonen T, Vaisanen S, Akerblom HK, Savilahti E 

(2002) Coeliac disease in children and adolescents with 

type 1 diabetes: a study of growth, glycaemic control, and 

experiences of families. Acta Paediatr 91: 297-302 

Sblattero D, Berti I, Trevisiol C, Marzari R, Tommasini A, 

Bradbury A, Fasano A, Ventura A, Not T (2000) Human 

recombinant tissue transglutaminase ELISA: an innovative 

diagnostic assay for celiac disease. American Journal of 

Gastroenterology 95: 1253-1257 

Scalici C, Manzoni D, Licastro G, Varia F, Di Prima L, 

Vitali R (2003) Reliability of EMA assay in the evaluation 

of gluten-free diet compliance in celiac patients during 

follow-up. Acta Med Mediterr 19: 67-69 

Schober E, Bittmann B, Granditsch G, Huber WD, Huppe 

A, Jager A, Oberhuber G, Rami B, Reichel G (2000) 

Screening by anti-endomysium antibody for celiac disease 

in diabetic children and adolescents in Austria. J Pediatr 

Gastroenterol Nutr 30: 391-396 
A-296

Selby WS, Gallagher ND (1979) Malignancy in a 19-year 

experience of adult celiac disease. Dig Dis Sci 24: 684-688 

Selby WS, Painter D, Collins A, Faulkner-Hogg KB, 

Loblay RH (1999) Persistent mucosal abnormalities in 

coeliac disease are not related to the ingestion of trace 

amounts of gluten. Scand J Gastroenterol 34: 909-914 

Sigurs N, Johansson C, Elfstrand PO, Viander M, Lanner A 

(1993) Prevalence of coeliac disease in diabetic children 

and adolescents in Sweden. Acta Paediatr 82: 748-751 

Sjoberg K, Alm R, Ivarsson SA, Lindstrom C, Eriksson S 

(1994) Prevalence and clinical significance of gliadin 

antibodies in healthy children and adults. Scand J 

Gastroenterol 29: 248-254 

Sjoberg K, Eriksson KF, Bredberg A, Wassmuth R, 

Eriksson S (1998) Screening for coeliac disease in adult 

insulin-dependent diabetes mellitus. J Intern Med 243: 133-

140 

Sjoberg K, Eriksson S (1999) Regional differences in 

coeliac disease prevalence in Scandinavia? Scand J 

Gastroenterol 34: 41-45 

Smecuol E, Gonzalez D, Mautalen C, Siccardi A, Cataldi 

M, Niveloni S, Mazure R, Vazquez H, Pedreira S, Soifer G, 

Boerr LA, Maurino E, Bai JC (1997) Longitudinal study on 

the effect of treatment on body composition and 

anthropometry of celiac disease patients. Am J 

Gastroenterol 92: 639-643 

Spiekerkoetter U, Seissler J, Wendel U (2002) General 

screening for celiac disease is advisable in children with 

type 1 diabetes. Horm Metab Res 34: 192-195 

Stokes PL, Ferguson R, Holmes GK, Cooke WT (1976) 

Familial aspects of coeliac disease. Quarterly Journal of 

Medicine 45: 567-582 

Sulkanen S, Collin P, Laurila K, Maki M (1998) IgA- and 

IgG-class antihuman umbilical cord antibody tests in adult 

coeliac disease. Scandinavian Journal of Gastroenterology 

33: 251-254 

Sulkanen S, Halttunen T, Laurila K, Kolho KL, KorponaySzabo IR, Sarnesto A, Savilahti E, Collin P, Maki M (1998) 

Tissue transglutaminase autoantibody enzyme-linked 

immunosorbent assay in detecting celiac disease. 

Gastroenterology 115: 1322-1328 

Talal AH, Murray JA, Goeken JA, Sivitz W, I (1997) 

Celiac disease in an adult population with insulindependent diabetes mellitus: use of endomysial antibody 

testing. Am J Gastroenterol 92: 1280-1284 

Talley NJ, Valdovinos M, Petterson TM, Carpenter HA, 

Melton LJ (1994) Epidemiology of celiac sprue: a 

community-based study. Am J Gastroenterol 89: 843-846 

Tesei N, Sugai E, Vazquez H, Smecuol E, Niveloni S, 

Mazure R, Moreno ML, Gomez JC, Maurino E, Bai JC 

(2003) Antibodies to human recombinant tissue 

transglutaminase may detect coeliac disease patients 

undiagnosed by endomysial antibodies. Alimentary 

Pharmacology & Therapeutics 17: 1415-1423 

Thomas AG, Phillips AD, Walker-Smith JA (1992) The 

value of proximal small intestinal biopsy in the differential 

diagnosis of chronic diarrhoea. Arch Dis Child 67: 741-743 

Thomason K, West J, Logan RFA, Coupland C, Holmes 

GKT (2003) Fracture experience of patients with coeliac 

disease: a population based survey. Gut 52: 518-522 

Trevisiol C, Not T, Berti I, Buratti E, Citta A, Neri E, Torre 

G, Martelossi S, Tommasini A, Alu A, Barillari G, Facchini 

S, Ventura A (1999) Screening for coeliac disease in 

healthy blood donors at two immuno-transfusion centres in 

north-east Italy. Ital J Gastroenterol Hepatol 31: 584-586 

Troncone R, Maurano F, Rossi M, Micillo M, Greco L, 

Auricchio R, Salerno G, Salvatore F, Sacchetti L (1999) 

IgA antibodies to tissue transglutaminase: An effective 

diagnostic test for celiac disease. Journal of Pediatrics 134: 

166-171 

Troncone R, Mayer M, Spagnuolo F, Maiuri L, Greco L 

(1995) Endomysial antibodies as unreliable markers for 

slight dietary transgressions in adolescents with celiac 

disease. J Pediatr Gastroenterol Nutr 21: 69-72 

Tursi A, Brandimarte G, Giorgetti GM, Inchingolo CD 

(2003) Effectiveness of the sorbitol HSUB2 breath test in 

detecting histological damage among relatives of coeliacs. 

Scand J Gastroenterol 38: 727-731 

Unsworth DJ, Lock RJ, Harvey RF (2000) Improving the 

diagnosis of coeliac disease in anaemic women. Br J 

Haematol 111: 898-901 

Vahedi K, Mascart-Lemone F, Mary JY, Laberenne JE, 

Bouhnik Y, Morin MC, Velly C, Colombel JF, 

Matuchansky C (2000) Are Anti-Endomysial (AEM) and 

Anti-Transglutaminase (TTG) Antibodies Reliable Markers 

of Strict Diet Compliance in Adult Celiacs on a Gluten Free 

Diet (GFD)? Gastroenterology 118: AGA 

Valdimarsson T, Franzen L, Grodzinsky E, Skogh T, Strom 

M (1996) Is small bowel biopsy necessary in adults with 

suspected celiac disease and IgA anti-endomysium 

antibodies? 100% positive predictive value for celiac 

disease in adults. Digestive Diseases and Sciences 41: 83-

87 

Valentini RA, Andreani ML, Corazza GR, Gasbarrini G 

(1994) IgA endomysium antibody: a valuable tool in the 

screening of coeliac disease but not its follow-up. Ital J 

Gastroenterol 26: 279-282 
A-297

Valerio G, Maiuri L, Troncone R, Buono P, Lombardi F, 

Palmieri R, Franzese A (2002) Severe clinical onset of 

diabetes and increased prevalence of other autoimmune 

diseases in children with coeliac disease diagnosed before 

diabetes mellitus. Diabetologia 45: 1719-1722 

Valletta EA, Trevisiol D, Mastella G (1990) IgA antigliadin antibodies in the monitoring of gluten challenge in 

celiac disease. J Pediatr Gastroenterol Nutr 10: 169-173 

Van Mook WNKA, Bourass-Bremer IHDN, Bos LP, 

Verhoeven HMJM, Engels LGJB (2001) The outcome of 

esophagogastroduodenoscopy (EGD) in asymptomatic 

outpatients with iron deficiency anemia after a negative 

colonoscopy. Eur J Intern Med 12: 122-126 

Vasquez H, Mazure R, Gonzalez D, Flores D, Pedreira S, 

Niveloni S, Smecuol E, Maurino E, Bai JC (2000) Risk of 

fractures in celiac disease patients: a cross-sectional, casecontrol study. Am J Gastroenterol. 95: 183-189 

Ventura A, Facchini S, Amantidu C, Andreotti MF, 

Andrighetto A, Baggiani A, Benedetti F, Bonati S, 

Buonaterra I, Capozzo M, Ciscato E, Cracco F, Ferrari G, 

Fornale M, Fusco F, Laverda E, Mardiciaro M, Nicolussi E, 

Pasinato L, Pittarello D, Pizio E, Salvadori R, Sambugaro 

D, Sassolino S, Spavanello V, Visan CT, Ziglio G, 

Zuffellato V (2001) Searching for celiac disease in 

pediatric general practice. Clin Pediatr 40: 575-577 

Vestergaard P, Mosekilde L (2002) Fracture risk in patients 

with celiac Disease, Crohn's disease, and ulcerative colitis: 

a nationwide follow-up study of 16,416 patients in 

Denmark. Am J Epidemiol. 156: 1-10 

Vitoria JC, Arrieta A, Astigarraga I, Garcia-Masdevall D, 

Rodriguez-Soriano J (1994) Use of serological markers as a 

screening test in family members of patients with celiac 

disease. J Pediatr Gastroenterol Nutr 19: 304-309 

Vitoria JC, Arrieta A, Ortiz L, Ayesta A (2001) Antibodies 

to human tissue transglutaminase for the diagnosis of celiac 

disease. Journal of Pediatric Gastroenterology and 

Nutrition 33: 349-350 

Vitoria JC, Castano L, Rica I, Bilbao JR, Arrieta A, GarciaMasdevall MD (1998) Association of insulin-dependent 

diabetes mellitus and celiac disease: a study based on 

serologic markers. J Pediatr Gastroenterol Nutr 27: 47-52 

Vogelsang H, Genser D, Wyatt J, Lochs H, Ferenci P, 

Granditsch G, Penner E (1995) Screening for celiac 

disease: a prospective study on the value of noninvasive 

tests. American Journal of Gastroenterology 90: 394-398 

Volta U, Bellentani S, Bianchi FB, Brandi G, De 

Franceschi L, Miglioli L, Granito A, Balli F, Tiribelli C 

(2001) High prevalence of celiac disease in Italian general 

population. Dig Dis Sci 46: 1500-1505 

Volta U, Molinaro N, De Franceschi L, Fratangelo D, 

Bianchi FB (1995) IgA anti-endomysial antibodies on 

human umbilical cord tissue for celiac disease screening. 

Save both money and monkeys. Digestive Diseases and 

Sciences 40: 1902-1905 

Wahab PJ, Meijer Jos WR, Mulder Chris JJ (2002) 

Histologic follow-up of people with celiac disease on a 

gluten-free diet: slow and incomplete recovery. American 

Journal of Clinical Pathology 118: 459-463 

Weile B, Krasilnikoff PA (1993) Extremely low incidence 

rates of celiac disease in the Danish population of children. 

J Clin Epidemiol 46: 661-664 

Weile I, Grodzinsky E, Skogh T, Jordal R, Cavell B, 

Krasilnikoff PA (2001) High prevalence rates of adult 

silent coeliac disease, as seen in Sweden, must be expected 

in Denmark. APMIS 109: 745-750 

West J, Logan RFA, Hill PG, Lloyd A, Lewis S, Hubbard 

R, Reader R, Holmes GKT, Khaw K-T (2003) 

Seroprevalence, correlates, and characteristics of 

undetected coeliac disease in England. Gut 52: 960-965 

West J, Logan Richard FA, Card TR, Smith C, Hubbard R 

(2003) Fracture risk in people with celiac disease: a 

population-based cohort study. Gastroenterology 125: 429-

436 

Westman E, Ambler GR, Royle M, Peat J, Chan A (1999) 

Children with coeliac disease and insulin dependent 

diabetes mellitus--growth, diabetes control and dietary 

intake. J Pediatr Endocrinol Metab 12: 433-442 

Whelan A, Willoughby R, Weir D (1996) Human umbilical 

vein endothelial cells: a new easily available source of 

endomysial antigens. European Journal of Gastroenterology 

& Hepatology 8: 961-966 

Wolters V, Vooijs-Moulaert A, Burger H, Brooimans R, De 

Schryver J, Rijkers G, Houwen R (2002) Human tissue 

transglutaminase enzyme linked immunosorbent assay 

outperforms both the guinea pig based tissue 

transglutaminase assay and anti-endomysium antibodies 

when screening for coeliac disease. European Journal of 

Pediatrics 161: 284-287 
A-298

Appendix J. Quality Assessment Table 1: Celiac 1 diagnostic studies (QUADAS) 

Author 

(Year) 

Item 1: spectrum of 

patients 

Item 2: selection criteria 

Item 3: reference 

standard 

Item 4: time period 

Item 5: sampling 

Item 6: test result 

Item 7: sampling 

independence 

Item 8a: index test 

description 

Item 8b: reference 

standard description 

Item 9a: reference 

standard results(1) 

Item 9b: reference 

standard results (2) 

Item 10: interpretation 

Item 11: uninterpretable/ 

intermediate test result 

p

Altuntas (1998) 

yes yes yes yes yes yes yes yes yes no unclear yes yes y

Artan (1998) 

yes yes yes yes yes yes yes yes yes yes unclear yes yes y

Ascher (1996) 

yes yes yes yes yes yes yes yes yes unclear unclear yes yes y

Ascher (1990) 

yes yes yes yes yes yes yes unclear yes unclear unclear yes yes y

Bahia (2001) ) 

yes yes yes yes yes yes yes yes yes unclear unclear yes no n

Bardella (2001) 

yes yes yes yes yes yes yes unclear yes unclear unclear yes yes y

Berger (1996) 

no yes yes unclear yes yes yes yes yes yes yes yes yes y

Biagi (2001) 

no unclear yes no yes yes yes yes yes no unclear yes yes y

Bode (1993) 

yes yes yes yes yes yes yes yes yes unclear unclear yes yes y

Bonamico (2001) 

no unclear yes no yes yes yes yes unclear no unclear yes yes y
A-299

Table 1: Celiac 1 diagnostic studies (QUADAS) (cont’d)

Author 

(Year) 

Item 1: spectrum of 

patients 

Item 2: selection criteria 

Item 3: reference 

standard 

Item 4: time period 

Item 5: sampling 

Item 6: test result 

Item 7: sampling 

independence 

Item 8a: index test 

description 

Item 8b: reference 

standard description 

Item 9a: reference 

standard results(1) 

Item 9b: reference 

standard results (2) 

Item 10: interpretation 

Item 11: uninterpretable/ 

intermediate test result 

p

Bottaro (1997) 

no no yes no yes yes yes unclear yes yes unclear yes yes y

Carroccio (2002) 

yes yes yes yes yes yes yes yes yes yes unclear yes yes y

Carroccio (1993) 

no yes yes yes yes yes yes yes yes yes unclear yes yes y

Carroccio (2002) 

yes yes yes yes yes yes yes yes yes yes unclear yes yes y

Cataldo (2000) 

no yes yes unclear yes yes yes yes yes no unclear yes yes y

Chan (2001) 

yes yes yes yes yes yes yes yes yes yes unclear yes yes y

Chartrand (1997) 

yes yes yes yes yes yes yes yes yes yes unclear yes yes y

Chirdo (1999) 

yes unclear yes yes yes yes yes yes yes no unclear yes yes y

Chirdo (2000) 

no no yes yes unclear yes yes yes yes unclear unclear yes yes y

Dahele (2001) 

no no yes yes yes yes yes yes yes yes unclear yes yes y

Di Leo (1999) 

no unclear yes unclear yes yes yes yes no no unclear yes yes y

Dickey (2001) 

no unclear yes yes yes yes yes yes yes yes unclear yes yes y
A-300

Table 1: Celiac 1 diagnostic studies (QUADAS) (cont’d)

Author 

(Year) 

Item 1: spectrum of 

patients 

Item 2: selection criteria 

Item 3: reference 

standard 

Item 4: time period 

Item 5: sampling 

Item 6: test result 

Item 7: sampling 

independence 

Item 8a: index test 

description 

Item 8b: reference 

standard description 

Item 9a: reference 

standard results(1) 

Item 9b: reference 

standard results (2) 

Item 10: interpretation 

Item 11: uninterpretable/ 

intermediate test result 

FalthMagnusson (1994) yes yes yes yes yes yes yes yes yes unclear unclear yes yes Gillett (2000) 

no no yes yes yes no yes yes yes unclear unclear yes yes 

Gonczi (1991) 

yes yes yes yes no yes yes yes yes no unclear yes yes 

Hallstrom (1989) 

no no yes unclear yes yes yes yes yes unclear unclear yes yes 

Hansson (2000) 

no no yes yes yes yes yes yes yes unclear unclear yes yes 

Iltanen (1999) 

yes yes yes yes yes yes yes yes yes unclear unclear yes yes 

Kaukinen (2000) 

yes yes yes yes yes yes yes yes yes yes unclear yes yes 

Kolho (1997) 

yes yes yes yes yes yes yes yes yes yes yes yes yes 

Kumar (1989) 

yes yes yes yes unclear yes yes yes yes unclear unclear yes yes 

Ladinser (1994) 

no no yes unclear unclear unclear yes yes yes unclear unclear yes unclear 
A-301

Table 1: Celiac 1 diagnostic studies (QUADAS) (cont’d)

Author 

(Year) 

Item 1: spectrum of 

patients 

Item 2: selection criteria 

Item 3: reference 

standard 

Item 4: time period 

Item 5: sampling 

Item 6: test result 

Item 7: sampling 

independence 

Item 8a: index test 

description 

Item 8b: reference 

standard description 

Item 9a: reference 

standard results(1) 

Item 9b: reference 

standard results (2) 

Item 10: interpretation 

Item 11: uninterpretable/ 

intermediate test result 

Lerner (1994) 

no yes yes yes yes yes yes yes yes yes yes yes yes 

Lindberg (1985) 

yes yes yes yes yes yes yes yes yes unclear unclear yes yes 

Lindquist (1994) 

yes yes yes yes yes yes yes yes yes no unclear yes yes 

Maki (1991) 

yes yes yes yes yes yes yes yes yes yes unclear yes yes 

McMillan (1991) 

yes yes yes yes yes yes yes yes yes yes yes yes yes 

Meini (1996) 

yes yes yes yes yes yes yes yes yes unclear unclear yes yes 

Pacht (1995) 

yes yes yes yes yes yes yes yes yes yes unclear yes yes 

Picarelli (2000) 

yes unclear yes yes yes yes yes yes yes no unclear yes yes 

Poddar (2002) 

yes yes yes yes yes yes yes yes yes yes unclear yes yes 

Rich (1990) 

yes yes yes yes yes yes yes yes yes no unclear yes yes 

Russo (1999) 

yes yes yes yes yes yes yes yes yes yes unclear yes yes 
A-302

Table 1: Celiac 1 diagnostic studies (QUADAS) (cont’d)

Author 

(Year) 

Item 1: spectrum of 

patients 

Item 2: selection criteria 

Item 3: reference 

standard 

Item 4: time period 

Item 5: sampling 

Item 6: test result 

Item 7: sampling 

independence 

Item 8a: index test 

description 

Item 8b: reference 

standard description 

Item 9a: reference 

standard results(1) 

Item 9b: reference 

standard results (2) 

Item 10: interpretation 

Item 11: uninterpretable/ 

intermediate test result 

Salmaso (2001) 

no unclear yes unclear unclear unclear yes yes no unclear unclear yes yes 

SategnaGuidetti (1995) 

no unclear yes unclear yes yes yes yes yes yes yes yes yes 

Sblattero (2000) 

no yes yes no yes no yes yes yes yes unclear yes yes 

Sulkanen (1998) 

no yes yes yes yes yes yes yes yes unclear unclear yes yes 

Tesei (2003) 

yes yes yes yes yes yes yes yes yes yes unclear yes yes 

Troncone (1999) 

yes yes yes yes yes yes yes yes yes unclear unclear yes yes 

Valdimars-son (1996) 

yes yes yes yes yes yes yes yes yes yes unclear yes yes 

Valentini (1994) 

no no yes yes yes yes yes yes yes unclear unclear yes yes 

Vitoria (2001) 

no no yes no yes yes yes yes no no unclear yes yes 

Vogelsang (1995) 

yes yes yes yes yes yes yes yes yes no unclear yes yes 
A-303

Table 1: Celiac 1 diagnostic studies (QUADAS) (cont’d)

Author 

(Year) 

Item 1: spectrum of 

patients 

Item 2: selection criteria 

Item 3: reference 

standard 

Item 4: time period 

Item 5: sampling 

Item 6: test result 

Item 7: sampling 

independence 

Item 8a: index test 

description 

Item 8b: reference 

standard description 

Item 9a: reference 

standard results(1) 

Item 9b: reference 

standard results (2) 

Item 10: interpretation 

Item 11: uninterpretable/ 

intermediate test result 

Volta (1995) 

no unclear yes yes yes yes yes yes yes yes yes yes yes 

Whelan (1996) 

no unclear yes unclear yes yes yes yes unclear unclear unclear yes yes 

Wolters (2002) 

yes no yes unclear yes yes yes yes yes no unclear yes yes 

Item % (+) reported 

59% 64% 100% 75% 91% 93% 100% 95% 91% 41% 11% 100% 96% 

NOTE: (+) reported = postively reported; yes = reported; no = not reported
A-304

Table 2: Celiac 2 prevalence & incidence studies (cross-sectional checklist)

Author (Year) 

Item 1: Source of Information 

Item 2: Inclusion/Exclusion Criteria 

Item 3: Time Period for Identity 

Item 4: Subjects consecutive 

Item 5: Evaluators Masked 

Item 6: Quality Assurance 

Assessments 

Item 7: Patient Exclusions 

assessed/controlled 

Item 8: Confounding 

Item 9: Missing Data 

Item 10: Response Rates 

Acerini (1998) yes no yes no can't tell no no no yes yes Ackerman (1996) can't tell no yes can't tell no no no no no yes Agardh (2001) yes can't tell no can’t tell no no yes no yes can't tell Aktay (2001) yes no yes no no no no no no no Annibale (2001) yes yes yes yes can't tell can't tell yes no no yes Annibale (2003) yes yes yes yes no no yes can't tell no yes Arato (2002) yes yes yes yes no no no can't tell no can't tell Bao (1999) yes no no can’t tell no no no no no can't tell Bardella (1991) yes no no yes can't tell yes no no no yes Bardella (2001) yes no yes yes no no no no no yes Barera (1991) can't tell no yes can’t tell no no no no no yes Barera (2002) no no yes yes no no yes no no can't tell Bode (1996) yes yes yes no can't tell no yes no no yes Bode (1993) yes yes yes yes no yes can't tell yes can't 

tell 

yes 

Book (2003) yes can't tell no no no no can't tell no no no caBorch (2000) yes no no no no no yes can't tell no yes caCalero (1996) yes no yes yes no yes yes yes no no Carlsson (2001) yes yes yes no no no no yes no yes Carroccio (2002) can't tell no yes yes yes no yes yes no yes Catassi (1996) yes no yes can’t tell no yes no yes no yes Catassi (2000) yes yes yes no no no yes yes no yes 
A-305

Table 2: Celiac 2 prevalence & incidence studies (cross-sectional checklist) (cont’d)

Author (Year) 

Item 1: Source of Information 

Item 2: Inclusion/Exclusion Criteria 

Item 3: Time Period for Identity 

Item 4: Subjects consecutive 

Item 5: Evaluators Masked 

Item 6: Quality Assurance 

Assessments 

Item 7: Patient Exclusions 

assessed/controlled 

Item 8: Confounding 

Item 9: Missing Data 

Item 10: Response Rates 

Chan (2001) yes yes yes can’t tell yes no can't tell no no can't tell Chartrand (1997) yes can't tell yes can’t tell no can't tell no no no yes Collin (2002) yes can't tell yes can’t tell no no yes yes no can't tell Collin (1997) yes yes yes no no no no yes no can't tell Corazza (1997) no no no no no no no no no can't tell Corazza (1995) no no no yes no no no no no yes Corazza (1992) no no no can’t tell no no no no no yes Corrao (1996) yes can't tell yes no can't tell yes yes no no yes Cronin (1997) yes no no yes no no no no no yes Csizmadia (1999) yes can't tell yes no can't tell no can't tell no no yes Day (2000) yes yes yes no can't tell no yes no no no De Block (2001) yes no no can’t tell no no no no no can't tell De, Vitis (1996) no no no no no no no no no yes Dickey (1997) no can't tell no can’t tell no no no can't tell no yes Dickey (1992) yes yes no can’t tell no no no no yes no Farre (1999) yes yes yes can’t tell no no no yes no yes Fasano (2003) yes yes yes can’t tell no no no yes no yes Fitzpatrick (2001) yes can't tell no can’t tell no no yes no no yes Fraser-Rey0lds (1998) can't tell can't tell yes no no no no yes no yes Gillett (2001) yes can't tell yes no yes no no yes no yes Gonzalez (2002) can't tell can't tell no yes yes no can't tell yes no yes Green (2000) yes no yes yes yes yes no can't tell no yes Grodzinsky (1996) yes no yes no no yes no no no no 
A-306

Table 2: Celiac 2 prevalence & incidence studies (cross-sectional checklist) (cont’d)

Author (Year) 

Item 1: Source of Information 

Item 2: Inclusion/Exclusion Criteria 

Item 3: Time Period for Identity 

Item 4: Subjects consecutive 

Item 5: Evaluators Masked 

Item 6: Quality Assurance 

Assessments 

Item 7: Patient Exclusions 

assessed/controlled 

Item 8: Confounding 

Item 9: Missing Data 

Item 10: Response Rates 

Hansen (2001) no can't tell no yes no no no no no no Hawkes (2000) yes can't tell yes no no no no no no no Hill (2000) yes no no no no no no yes no yes Hin (1999) yes yes yes yes can't tell yes no can't tell no yes Hoffenberg (2003) yes yes yes can’t tell yes no can't tell yes no yes Hogberg (2003) yes no yes no no no can't tell no no yes Holm (1993) can't tell no no can’t tell no no no can't tell no yes Hovdenak (1999) no no no no no no no no no yes Howard (2002) yes yes yes can’t tell can't tell no yes no no yes Ivarsson (1999) yes can't tell yes yes no no no yes no yes Ivarsson (2003) yes yes yes yes no no no yes no yes Jaeger (2001) no can't tell no no no no no can't tell no yes Jansen Th (1993) yes yes yes no no can't tell no no no yes Johnston (1998) yes can't tell can't 

tell 

can’t tell yes no yes no can't 

tell 

yes 

Kaukinen (1999) can't tell no yes can’t tell no no no no no yes Kepczyk (1995) yes yes yes yes can't tell yes no can't tell no yes Kolho (1998) yes can't tell yes can’t tell no no no no no yes Kordo0uri (2000) no no no no no no yes no no yes Kotze (2001) yes no no no can't tell no no can't tell can't 

tell 

yes 

Lampasona (1999) no no no no no no no no no can't tell Li Voon Chong (2002) no no yes no no no no yes no can't tell Lindh (1992) no no no yes no no no no no yes 
A-307

Table 2: Celiac 2 prevalence & incidence studies (cross-sectional checklist) (cont’d)

Author (Year) 

Item 1: Source of Information 

Item 2: Inclusion/Exclusion Criteria 

Item 3: Time Period for Identity 

Item 4: Subjects consecutive 

Item 5: Evaluators Masked 

Item 6: Quality Assurance 

Assessments 

Item 7: Patient Exclusions 

assessed/controlled 

Item 8: Confounding 

Item 9: Missing Data 

Item 10: Response Rates 

Lopez-Rodriguez (2003) yes can't tell yes yes no yes no no no yes Lorini (1996) no no no no no yes no no no yes Magazzu (1994) yes can't tell yes no can't tell no no no no yes Maki (1988) yes no yes yes can't tell no no no no no Maki (2003) yes can't tell yes can’t tell no no yes yes no yes Mather (2001) no no no yes no no can't tell no yes yes Mazzetti (1992) yes yes no no no no no no no no McIntyre (1993) yes no yes yes no no yes no no yes Mustalahti (2002) no can't tell no can’t tell no yes yes no no yes Ot (1998) can't tell no no no can't tell no no yes no can't tell Ot (2001) yes no yes yes no no no no no yes Nuti (2001) yes yes yes yes can't tell yes can't tell no can't 

tell 

yes 

Oxentenko (2002) yes can't tell yes no no no yes can't tell no yes Page (1994) yes yes yes yes yes no yes yes no no Pittschieler (1996) yes no no no no no no no no no Pittschieler (2003) yes can't tell yes can’t tell no no can't tell can't tell no can't tell Polvi (1996) yes yes no yes no no yes no yes yes Ransford (2002) no no no yes no no yes no no yes Rensch (1996) yes yes yes yes can't tell yes yes no yes yes Riestra (2000) can't tell can't tell yes no no yes no yes no yes Robinson (1971) yes no no yes no no no no no no Roldan (1998) yes no yes no no yes no no no no 
A-308

Table 2: Celiac 2 prevalence & incidence studies (cross-sectional checklist) (cont’d)

Author (Year) 

Item 1: Source of Information 

Item 2: Inclusion/Exclusion Criteria 

Item 3: Time Period for Identity 

Item 4: Subjects consecutive 

Item 5: Evaluators Masked 

Item 6: Quality Assurance 

Assessments 

Item 7: Patient Exclusions 

assessed/controlled 

Item 8: Confounding 

Item 9: Missing Data 

Item 10: Response Rates 

Rolles (1974) yes yes no no no no no no no yes caRossi (1993) yes can't tell yes no no no no no no yes Rostami (2000) no no no no yes no no no no yes Rostami (1999) yes no yes no no no no no no yes Rutz (2002) can't tell no no no no yes no yes no yes Sanders (2003) yes no yes no no no no yes no yes Sategna-Guidetti (1994) yes no no no no no no no no yes Saukkonen (1996) yes no yes yes no yes yes can't tell no yes Schober (2000) yes no no no no no no yes no no Sigurs (1993) yes yes yes no no no yes no no yes Sjoberg (1999) yes can't tell yes yes can't tell no can't tell yes no yes Sjoberg (1994) yes can't tell yes yes no no yes no no yes Sjoberg (1998) yes no yes no no yes yes no no yes Spiekerkoetter (2002) no no yes can’t tell can't tell no no no no yes Stokes (1976) yes no no can’t tell no no can't tell yes no yes Talal (1997) no yes no can’t tell no no yes yes no yes Talley (1994) yes yes yes no no can't tell yes yes no yes Thomas (1992) yes no yes can’t tell can't tell can't tell no no no yes Trevisiol (1999) yes can't tell yes can’t tell no no no no no no Tursi (2003) no no no can’t tell yes no no no no no 
A-309

Table 2: Celiac 2 prevalence & incidence studies (cross-sectional checklist) (cont’d)

Author (Year) 

Item 1: Source of Information 

Item 2: Inclusion/Exclusion Criteria 

Item 3: Time Period for Identity 

Item 4: Subjects consecutive 

Item 5: Evaluators Masked 

Item 6: Quality Assurance 

Assessments 

Item 7: Patient Exclusions 

assessed/controlled 

Item 8: Confounding 

Item 9: Missing Data 

Item 10: Response Rates 

Unsworth (2000) yes can't tell yes can’t tell no no no yes no yes Valerio (2002) yes can't tell yes can’t tell no no no no no yes Van Mook (2001) yes yes no no can't tell no yes no no yes Ventura (2001) can't tell yes can't 

tell 

can’t tell no no yes can't tell no yes 

Vitoria (1994) no can't tell no can’t tell no no can't tell no no can't tell Vitoria (1998) yes no no no no no no no no no Volta (2001) can't tell yes yes no no no no no no yes Weile (1993) yes yes yes no no no no no no yes Weile (2001) yes no no yes no no no yes no yes West (2003) yes can't tell yes no no no yes yes no yes % Items (+) reported: 71% 27% 60% 29% 8% 16% 28% 27% 5% 73% 2
A-310

Table 3. Celiac 3 cohort studies (Ottawa-Newcastle Scale)

Author (Year) 

Item 1: selection of 

exposed 

Item 2: selection of nonexposed 

Item 3: ascertainment of 

exposure 

Item 4: outcome missing 

data at initiation 

Item 5: control factors 

(2*'s) 

Item 6: assessment of 

outcome 

Item 7: adequacy of followup length 

Item 8: accountability for 

follow-up 

Askling (2002) 1 1 1 1 2 1 1 1 9 (*) awarded 

Collin (1996) 1 1 1 1 2 1 1 0 8 (*) awarded 

Corrao (2001) 1 1 1 0 2 1 1 1 8 (*) awarded 

Cottone (1999) 1 1 1 1 2 1 1 1 9 (*) awarded 

Green (2003) 1 1 1 1 2 1 1 0 8 (*) awarded 

Holmes (1989) 1 1 1 1 2 1 1 1 9 (*) awarded 

Logan (1989) 1 1 1 0 2 1 1 1 8 (*) awarded 

Nielsen (1985) 1 1 1 1 2 1 1 0 8 (*) awarded 

Selby (1979) 1 1 1 1 2 1 1 0 8 (*) awarded 

Item % (+) reported 100% 100% 100% 78% 100% 100% 100% 56% 

NOTE: a maximum of 9 stars* may be awarded per study
A-311

Table 4: Celiac 3 case-control study (Ottawa-Newcastle Scale)

Author (Year) 

Item 1: case definition 

Item 2: representativeness 

of cases 

Item 3: selection of 

controls 

Item 4: definition of 

controls 

Item 5: control factors 

Item 6: ascertainment of 

exposure 

Item 7: method of 

ascertainment for cases 

and controls 

Item 8: non-response rate 

 

 

Delco (1999) 1 1 1 1 2 0 1 0 7 (*) awarded 

NOTE: a maximum of 9 stars* may be awarded per study

Table 5. Celiac 4 cohort studies (Ottawa-Newcastle Scale)

Author (Year) 

Item 1: selection of exposed 

Item 2: selection of nonexposed 

Item 3: ascertainment of 

exposure 

Item 4: outcome missing data 

at initiation 

Item 5: control factors (2*'s) 

Item 6: assessment of 

outcome 

Item 7: adequacy of follow-up 

length 

Item 8: accountability for 

follow-up 

 

 

Amin (2002) 1 1 1 0 1 0 1 0 5 (*) awarded 

Greco (1997) 1 1 0 0 1 1 1 0 5 (*) awarded 

Harewood (2001) 1 1 0 0 1 0 1 1 5 (*) awarded 

Holmes (1976) 1 1 1 1 1 0 1 0 6 (*) awarded 

Johnston (1998) 1 1 1 1 2 1 0 1 8 (*) awarded 

Poddar (2002) 1 1 1 1 0 0 1 0 5 (*) awarded 

Item % (+) 

reported 

100% 100% 70% 50% 50% 33% 83% 33% 

 

NOTE: a maximum of 9 stars* may be awarded per 

study 
A-312

Table 6. Celiac 4 case-control study (Ottawa-Newcastle Scale)

Author (Year) 

Item 1: case definition 

Item 2: representativeness 

of cases 

Item 3: selection of controls 

Item 4: definition of 

controls 

Item 5: control factors (2*'s) 

Item 6: ascertainment of 

exposure 

Item 7: method of 

ascertainment for cases 

and controls 

Item 8: non-response rate 

 

 

Ciacci (1996) 1 0 1 1 0 1 1 0 4 (*) awarded 

Fabiani (1996) 1 1 1 1 1 1 1 0 7 (*) awarded 

Thomason (2003) 1 0 1 1 2 0 1 1 6 (*) awarded 

Westman (1999) 1 0 1 1 2 0 1 0 5 (*) awarded 

Item % (+) 

reported 

100% 25% 100% 100% 62.5% 50% 100% 25% 

 

NOTE: a maximum of 9 stars* may be awarded per study 

Table 7: Celiac 4—Quality assessment not applicable to those studies identified as 

'Other' in design 

Author (Year) 

Annibale (2001)

Arato (2002) 

Atkinson (1997) 

Bai (1997) 

Bardella (2000) 

Bardella (1985) 

Barera (2000) 

Boersma (2002) 

Corrao (2001) 

Fabiani (2000) 

Kemppainen (1999) 

Kemppainen(1998) 

Mora (2001) 

Mustalahti (1999) 

Rea (1996) 

Sategna-Guidetti (2000) 

Sategna-Guidetti (2001) 

Saukkonen (2002) 

Valdimarsson (2000) 

Zaccari (1996) 
A-313

Table 8: Celiac 4—Quality assessment pending 

Author (Year) 

Smecuol (1997) 

Valdimarsson (1996) 

Table 9: Celiac 5 case-control studies (Ottawa-Newcastle Scale)

Author (Year) 

Item 1: case definition 

Item 2: representativeness of cases 

Item 3: selection of controls 

Item 4: definition of controls 

Item 5: control factors (2*’s) 

Item 6: ascertainment of exposure 

Item 7: method of ascertainment 

for cases and controls 

Item 8: Non-response rate 

Bardella (2001) 1 1 1 1 1 1 1 1 8 (*) awarded 

Fabiani (2001) 1 1 1 0 1 0 1 1 6 (*) awarded 

Anson (1990) 1 1 1 0 1 0 1 1 6 (*) awarded 

Fabiani (2000) 1 1 1 1 1 0 1 1 7 (*) awarded 

Item % (+) reported 100% 100% 100% 50% 50% 25% 100% 100% 

NOTE: a maximum of 9 stars* may be awarded per study 
A-314

Table 10. Celiac 5 cohort studies (Ottawa-Newcastle Scale)

Author (Year) 

Item 1: Selection of exposed 

Item 2: selection of non-exposed 

Item 3: ascertainment of exposure 

Item 4: outcome missing data at 

initiation 

Item 5: control factors (2*'s) 

Item 6: assessment of outcome 

Item 7: adequacy of follow-up 

length 

Item 8: accountability for follow-up 

 

 

McNicholl (1976) 0 1 1 0 1 1 1 1 6 (*) awarded 

Pacht (1995) 1 1 0 0 1 1 1 1 6 (*) awarded 

Sategna-Guidetti 

(1996) 

1 1 1 1 0 1 1 1 7 (*) awarded 

Troncone (1995) 1 1 1 0 0 1 1 1 6 (*) awarded 

Hogberg (2003) 1 1 1 1 1 1 1 1 8 (*) awarded 

Fabiani (1996) 1 1 1 1 1 0 1 1 7 (*) awarded 

Item % (+) reported 83% 100% 83% 50% 33% 83% 100% 100% 

NOTE: a maximum of 9 stars* may be awarded per study 
A-315

Table 11. Celiac 5 non-comparative case series checklist 

Author (Year) 

Item 1: Intervention 

Item 2: Inclusion/exclusion criteria 

Item 3: follow-up as an inclusion 

Item 4: sample size determination 

Irem 5: sample size calculations 

Item 6: method & 

length/accumulation of cases 

Item 7: sources of participants 

Item 8: method of outcome 

assessments 

Item: 9: blinding 

Item 9: primary and secondary 

measures 

Item 11: timing of outcome 

assessment 

Item 12: follow-up schedule 

Item 13: maintaining follow-up 

Item 14: compliance with follow-up 

Item 15: method of data collection 

Item 16: exclusions 

analysis 

BurginWolff (1991) 

yes yes no can't 

tell 

no no yes yes no yes can't 

tell 

can't tell 

yes yes yes can't 

tell 

yes 

BurginWolff (2002) 

yes yes can'

t tell 

can't tell 

no no yes yes no yes yes yes no no yes no yes 

Dickey (2000) 

yes yes no yes no yes yes yes no yes yes yes can't 

tell 

yes yes yes yes 

Fotoulaki (1999) 

yes yes no yes no yes yes yes no yes yes yes no no yes no yes 

Kaukinen (2002) 

yes yes no yes no no no yes no yes yes yes no no yes no yes 

Lee (2003) 

yes yes no yes no yes yes yes no yes yes yes can't 

tell 

yes yes yes yes 

Martini (2002) 

yes yes no yes no yes yes yes no yes yes yes can't 

tell 

no yes no yes 

Scalici (2003) 

yes yes can'

t tell 

can't tell 

no no can't 

tell 

can't tell 

yes yes yes yes can't 

tell 

can't tell 

yes can't 

tell 

yes 

Selby (1999) 

yes yes no yes no yes yes yes no yes yes yes can't 

tell 

yes yes can't 

tell 

yes 
A-316

Table 11. Celiac 5 non-comparative case Series checklist (cont’d) 

Author (Year) 

Item 1: Intervention 

Item 2: Inclusion/exclusion criteria 

Item 3: follow-up as an inclusion 

Item 4: sample size determination 

Irem 5: sample size calculations 

Item 6: method & 

length/accumulation of cases 

Item 7: sources of participants 

Item 8: method of outcome 

assessments 

Item: 9: blinding 

Item 9: primary and secondary 

measures 

Item 11: timing of outcome 

assessment 

Item 12: follow-up schedule 

Item 13: maintaining follow-up 

Item 14: compliance with follow-up 

Item 15: method of data collection 

Item 16: exclusions 

analysis 

Valentini (1994) 

yes yes no no no no can't 

tell 

yes no yes yes yes no no yes no yes 

Valletta (1990) 

yes yes no no no no no yes no yes yes yes can't 

tell 

no yes no yes 

% of items (+) reported 

100% 100% 0% 55% 0% 45% 64% 91% 9% 100% 91% 91% 9% 36% 100% 18% 10

NOTE: yes = reported; no = not reported
A-317

Table 12: Celiac 5—Quality assessment not 

applicable to the following study designs 

Author (Year) Study type 

Jackson (1985) questionnaire 

Lamontagne (2001) questionnaire 

Ljungman (1993) questionnaire 

Vahedi (2000) abstract 

Table 13: Celiac 5—Quality assessment pending 

Author (Year) 

Baker (1975)

Bartholomeusz (1990)

Ciacci (2002)

Ciacci (2002) 

Fabiani (1996)

Hogberg (2003)

Johnston (1998)

Kotze (2001)

Mayer (1991)

Skerritt (1991)

Vahedi (2003)

Volta (1990)
A-318

Appendix K. Additional Acknowledgements 

The UO-EPC gratefully acknowledges the following individuals who served on our Technical Expert 

Panel (TEP). Acknowledgement does not reflect endorsement of this report.

J Decker Butzner, MD

Associate Professor Faculty of Medicine 

Dept. of Pediatrics Gastrointestinal Research 

Group 

Head, Division of Pediatric Gastroenterology 

and Nutrition 

Alberta Children's Hospital 

Calgary, AB 

Richard J Farrell, MD 

Gastroenterology Division 

Beth Israel Deaconess Medical Center 

Harvard Medical School 

Boston, MA 

Maha Guindi, MD 

Department of Laboratory Medicine and 

Pathobiology 

University of Toronto 

Department of Pathology, Toronto General 

Hospital 

Toronto, ON 

Connie Switzer, MD 

Division of Gastroenterology & 

Department of Medicine 

University of Alberta 

Chair of Professional Advisory Board, CCA 

Edmonton, AB 

Jerry Trier, MD 

Brigham and Women's Hospital 

Department of Medicine Gastroenterology 

Harvard Medical School 

Boston, MA 

Sander JOV van Zanten, MD 

Department of Medicine 

Dalhousie University 

Queen Elizabeth II Health Sciences Center 

Victoria General Site 

Halifax, NS 

*Charles O Elson III, MD 

Department of Medicine 

University of Birmingham 

Birmingham, AL

*Dr. Elson was named to the Technical Expert 

Panel given his position as Panel Chair of the 

NIH Consensus Conference on Celiac Disease
A-319

The UO-EPC gratefully acknowledges the following individuals who reviewed the initial draft of this 

evidence report, and provided constructive feedback. Acknowledgement does not reflect endorsement of 

this report. 

David Atkins, MD, MPH 

Chief Medical Officer 

Center for Outcomes and Evidence 

Agency for Healthcare Research Quality 

Rockville, MD 

Linda S. Book, MD 

Chief Pediatric Gastroenterology 

and Liver Transplantation 

University of Utah 

Primary Children's Medical Center 

Salt Lake City, UT 

William Depew, MD 

Department of Gastroenterology, 

Hotel Dieu Hospital 

Division of Gastroenterology 

Queen’s University 

Kingston, ON 

Richard J Farrell, MD 

Gastroenterology Division 

Beth Israel Deaconess Medical Center 

Harvard Medical School, 

Boston, MA 

Martin R. Howard, MD 

Department of Haematology 

York District Hospital 

York, UK 

Richard A McPherson, MD 

Department of Pathology 

Medical College of Virginia Hospitals 

Richmond, VA 

Grant Thompson 

Faculty of Medicine, Gastroenterology 

University of Ottawa 

Ottawa, ON 
Appendix L. Listing of Excluded Studies 

Objective 1 – Sensitivity and Specificity of Tests for CD 

Abdulkarim A S, Murray J A. Review article: The 

diagnosis of coeliac disease. Alimentary Pharmacology & 

Therapeutics 2003;17(8):987-995. Not sensitivity or 

specificity of an identified test

Abdulkarim Ahmad S, Burgart Lawrence J, See Jacalyn et

al. Etiology of nonresponsive celiac disease: results of a 

systematic approach. American Journal of

Gastroenterology 2002;97(8):2016-2021. Not sensitivity or 

specificity of an identified test

Abdullah A M. Aetiology of chronic diarrhoea in children: 

Experience at King Khalid University Hospital, Riyadh,

Saudi Arabia. Ann Trop Paediatr 1994;14(2):111-117. Not 

sensitivity or specificity of an identified test 

Abdullah A M, Elrab M G, Al Herbish A et al. Serum 

antigliadin antibody as a marker of coeliac disease in

children with chronic diarrhoea in Saudi Arabia. Med Sci 

Res 1994;22(3):229Not sensitivity or specificity of an 

identified test 

Abe K K, Michinaga I, Hiratsuka T et al. Association of 

DQB1(*)0302 alloantigens in Japanese pediatric patients 

with steroid-sensitive nephrotic syndrome. Nephron 

1995;70(1):28-34. Not sensitivity or specificity of an 

identified test 

Abele M, Burk K, Schols L et al. The aetiology of sporadic

adult-onset ataxia. Brain 2002;125(Pt 5):961-968. Not 

sensitivity or specificity of an identified test 

Abele M, Schols L, Schwartz S et al. Prevalence of 

antigliadin antibodies in ataxia patients. Neurology

2003;60(10):1674-1675. Not sensitivity or specificity of an 

identified test 

Abenoza P, Lillemoe T. CD34 and factor XIIIa in the 

differential diagnosis of dermatofibroma and

dermatofibrosarcoma protuberans. American Journal of

Dermatopathology 1993;15(5):429-434. Not sensitivity or

specificity of an identified test

Ablin R J, Whyard T C. Identification and possible 

biological relevance of spermatozoal transglutaminase.

Experientia 1991;47(3):277-279. Not sensitivity or 

specificity of an identified test

Acerini C L, Ahmed M L, Ross K M et al. Coeliac disease

in children and adolescents with IDDM: clinical

characteristics and response to gluten-free diet. Diabetic 

Medicine - a Journal of the British Diabetic Association 

1998;15(1):38-44. Not sensitivity or specificity of an 

identified test 

Achyuthan K E, Goodell R J, Kennedye J R et al. 

Immunochemical analyses of human plasma fibronectincytosolic transglutaminase interactions. Journal of

Immunological Methods 1995;180(1):69-79. Not 

sensitivity or specificity of an identified test 

Achyuthan K E, Slaughter T F, Santiago M A et al. Factor

XIIIa-derived peptides inhibit transglutaminase activity. 

Localization of substrate recognition sites. Journal of 

Biological Chemistry 1993;268(28):21284-21292. Not 

sensitivity or specificity of an identified test 

Ackerman Z, Eliakim R, Stalnikowicz R et al. Role of 

small bowel biopsy in the endoscopic evaluation of adults 

with iron deficiency anemia. American Journal of

Gastroenterology 1996;91(10):2099-2102. Not sensitivity

or specificity of an identified test

Adam Gregory C, Sorensen Erik J, Cravatt Benjamin F.

Trifunctional chemical probes for the consolidated 

detection and identification of enzyme activities from

complex proteomes. Molecular & Cellular Proteomics - 

Mcp 2002;1(10):828-835. Not sensitivity or specificity of

an identified test

Adams E, Basten A, Rodda S et al. Human T-cell clones to

the 70-kilodalton heat shock protein of Mycobacterium 

leprae define mycobacterium-specific epitopes rather than 

shared epitopes. Infect Immun 1997;65(3):1061-1070. Not 

sensitivity or specificity of an identified test 

Adany R, Glukhova M A, Kabakov A Y et al. 

Characterisation of connective tissue cells containing factor

XIII subunit a. Journal of Clinical Pathology

1988;41(1):49-56. Not sensitivity or specificity of an 

identified test 

Adini A, Krugliak M, Ginsburg H et al. Transglutaminase 

in Plasmodium parasites: Activity and putative role in

oocysts and blood stages. Mol Biochem Parasitol 

2001;117(2):161-168. Not sensitivity or specificity of an

identified test 

Adleff V, Racz K, Szende B et al. Coexpression of p53 and

tissue transglutaminase genes in human normal and 

pathologic adrenal tissues. Journal of Steroid Biochemistry

and Molecular Biology 1998;66(1-2):27-33. Not sensitivity

or specificity of an identified test

Aeschlimann D, Thomazy V. Protein crosslinking in 

assembly and remodelling of extracellular matrices: the 

role of transglutaminases. Connective Tissue Research

2000;41(1):1-27. Not sensitivity or specificity of an 

identified test 

Aeschlimann D, Koeller M K, Allen-Hoffmann B L et al. 

A-321
Isolation of a cDNA encoding a novel member of the 

transglutaminase gene family from human keratinocytes. 

Detection and identification of transglutaminase gene 

products based on reverse transcription-polymerase chain 

reaction with degenerate primers. Journal of Biological 

Chemistry 1998;273(6):3452-3460. Not sensitivity or 

specificity of an identified test

Aeschlimann D, Mosher D, Paulsson M. Tissue 

transglutaminase and factor XIII in cartilage and bone 

remodeling. Semin Thromb Hemost 1996;22(5):437-443. 

Not sensitivity or specificity of an identified test

Aeschlimann D, Wetterwald A, Fleisch H et al. Expression 

of tissue transglutaminase in skeletal tissues correlates with

events of terminal differentiation of chondrocytes. J Cell 

Biol 1993;120(6):1461-1470. Not sensitivity or specificity

of an identified test 

Agardh D, Agardh E, Landin-Olsson M et al. Inverse 

relationship between GAD65 antibody levels and severe 

retinopathy in younger type 1 diabetic patients. Diabetes 

Res Clin Pract 1998;40(1):9-14. Not sensitivity or

specificity of an identified test

Agardh D, Gaur L K, Agardh E et al. HLADQB1*0201/0302 is associated with severe retinopathy in 

patients with IDDM. Diabetologia 1996;39(11):1313-1317. 

Not sensitivity or specificity of an identified test

Agardh D, Nilsson A, Carlsson A et al. Tissue 

transglutaminase autoantibodies and human leucocyte 

antigen in Down Syndrome patients with coeliac disease.

Acta Paediatrica (Oslo, Norway - 1992) 2002;91(1):34-38. 

Improper control group 

Agardh D, Nilsson A, Tuomi T et al. Prediction of silent

celiac disease at diagnosis of childhood type 1 diabetes by

tissue transglutaminase autoantibodies and HLA. Pediatr

Diabetes 2001;2(2):58-65. Not sensitivity or specificity of 

an identified test

Agardh Daniel, Borulf Stefan, Lernmark Ake et al. Tissue

transglutaminase immunoglobulin isotypes in children with

untreated and treated celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 2003;36(1):77-82. 

Improper control group 

Agrawal S, Gupta A, Yachha S K et al. Association of 

human leucocyte-DR and DQ antigens in coeliac disease: a 

family study. Journal of Gastroenterology and Hepatology

2000;15(7):771-774. Improper control group 

Agreus L, Svardsudd K, Tibblin G et al. Endomysium 

antibodies are superior to gliadin antibodies in screening

for coeliac disease in patients presenting supposed 

functional gastrointestinal symptoms. Scandinavian Journal 

of Primary Health Care 2000;18(2):105-110. Improper 

control group 

Aguirre J M, Rodriguez R, Oribe D et al. Dental enamel 

defects in celiac patients. Oral Surgery, Oral Medicine, 

Oral Pathology, Oral Radiology, and Endodontics

1997;84(6):646-650. Not sensitivity or specificity of an 

identified test 

Ahmed A R, Mohimen A, Yunis E J et al. Linkage of 

pemphigus vulgaris antibody to the major

histocompatibility complex in healthy relatives of patients.

J Exp Med 1993;177(2):419-424. Not sensitivity or 

specificity of an identified test

Ahmed A R, Yunis J J, Marcus-Bagley D et al. Major 

histocompatibility complex susceptibility genes for 

dermatitis herpetiformis compared with those for glutensensitive enteropathy. Journal of Experimental Medicine 

1993;178(6):2067-2075. Not sensitivity or specificity of an 

identified test 

Aho H J, Ping W, Soderstrom K O et al. Acid cysteine 

proteinase inhibitor in cutaneous lymphocytic infiltrates. 

American Journal of Dermatopathology 1995;17(2):115-

125. Not sensitivity or specificity of an identified test 

Ahvazi Bijan, Kim Hee, Chul Kee et al. Three-dimensional 

structure of the human transglutaminase 3 enzyme: binding 

of calcium ions changes structure for activation. Embo 

Journal 2002;21(9):2055-2067. Not sensitivity or 

specificity of an identified test

Aiba S, Tabata N, Ohtani H et al. CD34+ spindle-shaped 

cells selectively disappear from the skin lesion of

scleroderma. Archives of Dermatology 1994;130(5):593-

597. Not sensitivity or specificity of an identified test 

Aine L. Coeliac-type permanent-tooth enamel defects. Ann 

Med 1996;28(1):9-12. Not sensitivity or specificity of an

identified test 

Aine L, Maki M, Reunala T. Coeliac-type dental enamel 

defects in patients with dermatitis herpetiformis. Acta 

Dermato-Venereologica 1992;72(1):25-27. Not sensitivity

or specificity of an identified test

Akagi Atsushi, Tajima Shingo, Ishibashi Akira et al. Type 

XVI collagen is expressed in factor XIIIa+ monocytederived dermal dendrocytes and constitutes a potential

substrate for factor XIIIa. Journal of Investigative 

Dermatology 2002;118(2):267-274. Not sensitivity or 

specificity of an identified test

Akimov S S, Belkin A M. Cell surface tissue

transglutaminase is involved in adhesion and migration of 

monocytic cells on fibronectin. Blood 2001;98(5):1567-

1576. Not sensitivity or specificity of an identified test 

Akimov S S, Belkin A M. Cell-surface transglutaminase 

promotes fibronectin assembly via interaction with the 

gelatin-binding domain of fibronectin: A role in TGF-betadependent matrix deposition. Journal of Cell Science 

2001;114(16):2989-3000. Not sensitivity or specificity of

an identified test

Akimov S S, Krylov D, Fleischman L F et al. Tissue 

A-322
transglutaminase is an integrin-binding adhesion coreceptor 

for fibronectin. Journal of Cell Biology 2000;148(4):825-

838. Not sensitivity or specificity of an identified test 

Akiyama H, Kondo H, Ikeda K et al. Immunohistochemical 

detection of coagulation factor XIIIa in postmortem human 

brain tissue. Neuroscience Letters 1995;202(1-2):29-32. 

Not sensitivity or specificity of an identified test

Akiyama M, Matsuo I, Shimizu H. Formation of cornified 

cell envelope in human hair follicle development. British 

Journal of Dermatology 2002;146(6):968-976. Not 

sensitivity or specificity of an identified test 

Akiyama M, Smith L T, Yoneda K et al. Transglutaminase

and major cornified cell envelope precursor proteins, 

loricrin, small proline-rich proteins 1 and 2, and involucrin

are coordinately expressed in the sites defined to form hair 

canal in developing human hair follicle. Exp Dermatol 

1999;8(4):313-314. Not sensitivity or specificity of an 

identified test 

Aktay A N, Lee P C, Kumar V et al. The prevalence and 

clinical characteristics of celiac disease in juvenile diabetes

in Wisconsin. Journal of Pediatric Gastroenterology and 

Nutrition 2001;33(4):462-465. Not sensitivity or specificity

of an identified test 

Al Ashwal A A, Shabib S M, Sakati N A et al. Prevalence

and characteristics of celiac disease in type I diabetes

mellitus in Saudi Arabia. Saudi Med J 2003;24(10):1113-

1115. Not sensitivity or specificity of an identified test 

Al Attas R A. How common is celiac disease in Eastern

Saudi Arabia?. Ann Saudi Med 2002;22(5-6):315-319. Not 

sensitivity or specificity of an identified test 

Al Bayatti S M. Etiology of chronic diarrhea. Saudi Med J

2002;23(6):675-679. Not sensitivity or specificity of an 

identified test 

al Bayaty H F, Aldred M J, Walker D M et al. Salivary and 

serum antibodies to gliadin in the diagnosis of celiac 

disease. Journal of Oral Pathology & Medicine - Official 

Publication of the International Association of Oral 

Pathologists and the American Academy of Oral Pathology 

1989;18(10):578-581. Serology <1990 

al Dawoud A, Nakshabendi I, Foulis A et al. 

Immunohistochemical analysis of mucosal gammainterferon production in coeliac disease. Gut 

1992;33(11):1482-1486. Not sensitivity or specificity of an 

identified test 

Al Harbi S, Fouad F, Kaaba S A. The first HLA 

anthropological study in the Kuwaiti population. Eur J

Immunogenet 1994;21(5):295-300. Not sensitivity or 

specificity of an identified test

Al Mofleh I A, Jessen K, Al-Rashed Al-Hmaid et al. 

Pediatric esophagogastroduodenoscopy in Saudi Arabia. 

Ann Saudi Med 1989;9(1):32-35. Not sensitivity or 

specificity of an identified test

al Tawaty A I, Elbargathy S M. Coeliac disease in northeastern Libya. Annals of Tropical Paediatrics 

1998;18(1):27-30. Not sensitivity or specificity of an 

identified test 

Albert E D, Harms K, Wank R et al. Segregation analysis

of HL-A antigens and haplotypes in 50 families of patients

with coeliac disease. Transplantation Proceedings 

1973;5(4):1785-1789. Not sensitivity or specificity of an

identified test 

Aldener-Cannava A, Olerup O. HLA-DOB1 "lowresolution' typing by PCR amplification with sequencespecific primers (PCR-SSP). European Journal of

Immunogenetics - Official Journal of the British Society for 

Histocompatibility and Immunogenetics 1994;21(6):447-

455. Not sensitivity or specificity of an identified test 

Aldersley M A, Hamlin P J, Jones P F et al. No 

polymorphism in the tissue transglutaminase gene detected

in coeliac disease patients. Scandinavian Journal of 

Gastroenterology 2000;35(1):61-63. Not sensitivity or 

specificity of an identified test

Aleanzi M, Demonte A M, Esper C et al. Celiac disease:

antibody recognition against native and selectively 

deamidated gliadin peptides. Clinical Chemistry 

2001;47(11):2023-2028. Not sensitivity or specificity of an 

identified test 

Alfonso P, Soto C, Albar J P et al. Beta structure motif

recognition by anti-gliadin antibodies in coeliac disease. 

Febs Letters 1998;427(1):36-40. Not sensitivity or

specificity of an identified test

Alfos S, Boucheron C, Pallet V et al. A retinoic acid

receptor antagonist suppresses brain retinoic acid receptor 

overexpression and reverses a working memory deficit

induced by chronic ethanol consumption in mice. Alcohol 

Clin Exp Res 2001;25(10):1506-1514. Not sensitivity or

specificity of an identified test

Alfos S, Higueret P, Pallet V et al. Chronic ethanol 

consumption increases the amount of mRNA for retinoic 

acid and triiodothyronine receptors in mouse brain. 

Neurosci Lett 1996;206(2-3):73-76. Not sensitivity or 

specificity of an identified test

Alkushi A, Irving J, Hsu F et al. Immunoprofile of cervical 

and endometrial adenocarcinomas using a tissue 

microarray. Virchows Arch 2003;442(3):271-277. Not 

sensitivity or specificity of an identified test 

Alper C A, Fleischnick E, Awdeh Z et al. Extended major

histocompatibility complex haplotypes in patients with 

gluten-sensitive enteropathy. Journal of Clinical 

Investigation 1987;79(1):251-256. Not sensitivity or 

specificity of an identified test

Alpers D H. Another piece to the celiac puzzle. Journal of

A-323
Pediatric Gastroenterology and Nutrition 1987;6(1):5-7. 

Not sensitivity or specificity of an identified test

Alsaigh N, Odze R, Goldman H et al. Gastric and 

esophageal intraepithelial lymphocytes in pediatric celiac 

disease. American Journal of Surgical Pathology 

1996;20(7):865-870. Not sensitivity or specificity of an 

identified test 

Altmann D M. HLA-DQ associations with autoimmune 

disease. Autoimmunity 1992;14(1):79-83. Not sensitivity 

or specificity of an identified test

Altmann D M, Sansom D, Marsh S G. What is the basis for 

HLA-DQ associations with autoimmune disease?. 

Immunology Today 1991;12(8):267-270. Not sensitivity or 

specificity of an identified test

Altuntas B, Kansu A, Girgin N. Hepatic damage in gluten 

sensitive enteropathy. Acta Paediatrica Japonica 

1998;Overseas Edition; 40(6):597-599. Not sensitivity or

specificity of an identified test

Altuntas cedil, Filik B, Ensari A et al. Can zinc deficiency

be used as a marker for the diagnosis of celiac disease in 

Turkish children with short stature?. Pediatr Int 

2000;42(6):682-684. Not sensitivity or specificity of an 

identified test 

Alvarez D, Vazquez H, Bai J C et al. Superior mesenteric 

artery blood flow in celiac disease. Digestive Diseases and

Sciences 1993;38(7):1175-1182. Not sensitivity or

specificity of an identified test

Amann E, Abel K J, Grundmann U et al. Synthesis of 

human factor XIIIa in bacterial cells. Behring Institute

Mitteilungen 1988;(82):35-42. Not sensitivity or specificity

of an identified test 

Amanzadeh A, Shokrgozar M-A, Samadi-Bahrami Z et al. 

Frequency analysis of HLA antigens in Iranian patients

with common variable immunodeficiency. Arch Iran Med 

2003;6(1):16-22. Not sensitivity or specificity of an 

identified test 

Amara W, Husebekk A. Improved method for serological 

testing in celiac disease--IgA anti-endomysium antibody

test: a comparison between monkey oesophagus and human 

umbilical cord as substrate in indirect immunofluorescence 

test. Scandinavian Journal of Clinical and Laboratory

Investigation 1998;58(7):547-554. Not sensitivity or 

specificity of an identified test

Ambrus A, Fesus L. Polyethylene glycol enhanced 

refolding of the recombinant human tissue 

transglutaminase. Preparative Biochemistry & 

Biotechnology 2001;31(1):59-70. Not sensitivity or 

specificity of an identified test

Ambrus A, Banyai I, Weiss M S et al. Calcium binding of 

transglutaminases: a 43Ca NMR study combined with 

surface polarity analysis. Journal of Biomolecular Structure 

& Dynamics 2001;19(1):59-74. Not sensitivity or

specificity of an identified test

Amendola A, Gougeon M L, Poccia F et al. Induction of 

"tissue" transglutaminase in HIV pathogenesis: evidence

for high rate of apoptosis of CD4+ T lymphocytes and 

accessory cells in lymphoid tissues. Proceedings of the 

National Academy of Sciences of the United States of 

America 1996;93(20):11057-11062. Not sensitivity or 

specificity of an identified test

Amendola A, Lombardi G, Oliverio S et al. HIV-1 gp120-

dependent induction of apoptosis in antigen-specific human

T cell clones is characterized by 'tissue' transglutaminase 

expression and prevented by cyclosporin A. Febs Lett 

1994;339(3):258-264. Not sensitivity or specificity of an

identified test 

Amendola A, Rodolfo C, Di Caro A et al. "Tissue" 

transglutaminase expression in HIV-infected cells: an

enzyme with an antiviral effect?. Annals of the New York 

Academy of Sciences 2001;946108-120. Not sensitivity or

specificity of an identified test

Amendola Alessandra, Fesus Laszlo, Piacentini Mauro et 

al. "Tissue" transglutaminase in AIDS. Journal of

Immunological Methods 2002;265(1-2):145-159. Not 

sensitivity or specificity of an identified test 

Ament M E. Diagnosis and treatment of giardiasis. Journal 

of Pediatrics 1972;80(4):633-637. Not sensitivity or 

specificity of an identified test

Ament M E, Ochs H D. Gastrointestinal manifestations of

chronic granulomatous disease. New England Journal of

Medicine 1973;288(8):382-387. Not sensitivity or

specificity of an identified test

Ament M E, Perera D R, Esther L J. Sucrase-isomaltase

deficiency-a frequently misdiagnosed disease. Journal of

Pediatrics 1973;83(5):721-727. Not sensitivity or

specificity of an identified test

Amin M, Eckhardt T, Kapitza S et al. Correlation between

tissue transglutaminase antibodies and endomysium 

antibodies as diagnostic markers of coeliac disease. Clinica 

Chimica Acta 1999;International Journal of Clinical 

Chemistry; 282(1-2):219-225. Not sensitivity or specificity

of an identified test 

Amoah J, Williams C, Long R G. Calmodulin content and

activity in normal and coeliac duodenum. Gut 

1992;33(3):303-306. Not sensitivity or specificity of an 

identified test 

Amoroso A, Mazzola G, Canale L et al. HLA in juvenile

dermatitis herpetiformis: clinical heterogeneity correlated

with DNA and serological polymorphism. J Immunogenet 

1990;17(3):195-206. Not sensitivity or specificity of an 

identified test 

Anand B S, Piris J, Truelove S C. The role of various 

A-324
cereals in coeliac disease. Quarterly Journal of Medicine 

1978;47(185):101-110. Not sensitivity or specificity of an

identified test 

Anand B S, Piris J, Jerrome D W et al. The timing of 

histological damage following a single challenge with 

gluten in treated coeliac disease. Quarterly Journal of 

Medicine 1981;50(197):83-94. Not sensitivity or specificity

of an identified test 

Anantharaman V, Koonin E V, Aravind L. Peptide-Nglycanases and DNA repair proteins, Xp-C/Rad4, are, 

respectively, active and inactivated enzymes sharing a 

common transglutaminase fold. Human Molecular Genetics 

2001;10(16):1627-1630. Not sensitivity or specificity of an 

identified test 

Andersen K J, Schjonsby H, Skagen D W. Jejunal mucosal 

enzymes in untreated and treated coeliac disease.

Scandinavian Journal of Gastroenterology 1983;18(2):251-

256. Not sensitivity or specificity of an identified test 

Andersen K J, Schjonsby H, Skagen D W et al. Enzyme 

activities in jejunal biopsy samples from patients with adult 

coeliac disease with and without steatorrhoea. 

Scandinavian Journal of Gastroenterology 1983;18(3):365-

368. Not sensitivity or specificity of an identified test 

Anderson R P, Degano P, Godkin A J et al. In vivo antigen

challenge in celiac disease identifies a single 

transglutaminase-modified peptide as the dominant Agliadin T-cell epitope. Nature Medicine 2000;6(3):337-342. 

Not sensitivity or specificity of an identified test

Andersson H, Bjorkman A C, Gillberg R et al. Influence of

the amount of dietary gluten on gastrointestinal 

morphology and function in dermatitis herpetiformis. 

Human Nutrition.Clinical Nutrition 1984;38(4):279-285. 

Not sensitivity or specificity of an identified test

Ando M, Tatematsu T, Kunii S et al. Blockade effect of 

nerve growth factor on GM1 ganglioside-induced

activation of transglutaminase in superior cervical 

sympathetic ganglia excised from adult rat. Neurosci Res 

1994;19(4):373-378. Not sensitivity or specificity of an 

identified test 

Ando Y, Imamura S, Owada M K et al. Calcium-induced

intracellular cross-linking of lipocortin I by tissue

transglutaminase in A431 cells. Augmentation by

membrane phospholipids. Journal of Biological Chemistry

1991;266(2):1101-1108. Not sensitivity or specificity of an 

identified test 

Ando Y, Imamura S, Owada M K et al. Cross-linking of 

lipocortin I and enhancement of its Ca2+ sensitivity by

tissue transglutaminase. Biochemical and Biophysical 

Research Communications 1989;163(2):944-951. Not 

sensitivity or specificity of an identified test 

Andria G, Cucchiara S, De Vizia B. Brush border and 

cytosol peptidase activities of human small intestine in 

normal subjects and celiac patients. Pediatric Research

1980;14(6):812-818. Not sensitivity or specificity of an 

identified test 

Annibale B, Capurso G, Chistolini A et al. Gastrointestinal

causes of refractory iron deficiency anemia in patients

without gastrointestinal symptoms. Am J Med 

2001;111(6):439-445. Not sensitivity or specificity of an

identified test 

Annibale B, Lahner E, Chistolini A et al. Endoscopic 

evaluation of the upper gastrointestinal tract is worthwhile 

in premenopausal women with iron-deficiency anaemia 

irrespective of menstrual flow. Scandinavian Journal of

Gastroenterology 2003;38(3):239-245. Not sensitivity or 

specificity of an identified test

Annibale B, Severi C, Chistolini A et al. Efficacy of glutenfree diet alone on recovery from iron deficiency anemia in

adult celiac patients. American Journal of Gastroenterology

2001;96(1):132-137. Not sensitivity or specificity of an 

identified test 

Annicchiarico-Petruzzelli M, Bernassola F, Lovat P E et al. 

Apoptosis in neuroblastomas induced by interferon-gamma 

involves the CD95/CD95L pathway. Medical and Pediatric 

Oncology 2001;36(1):115-117. Not sensitivity or

specificity of an identified test

Anonymous. Collagenous sprue. Lancet 

1971;1(7701):692Not sensitivity or specificity of an 

identified test 

Anonymous. Collagenous sprue. British Medical Journal 

1971;2(753):65-66. Not sensitivity or specificity of an 

identified test 

Anonymous. Giardia lamblia and coeliac disease. Lancet 

1973;2(7821):138Not sensitivity or specificity of an 

identified test 

Anonymous. The gut and dermatitis herpetiformis. British 

Medical Journal 1971;4(778):5Not sensitivity or specificity

of an identified test 

Anonymous. Medical grand rounds from the University of

Alabama Medical Center. Southern Medical Journal 

1969;62(1):65-70. Not sensitivity or specificity of an 

identified test 

Anonymous. Dermatitis herpetiformis--the thin veneer?.

Lancet 1978;2(8087):458-459. Not sensitivity or specificity

of an identified test 

Anonymous. Bird fancier's lung and jejunal villous atrophy.

Med J Aust 1976;1(22):813-814. Not sensitivity or 

specificity of an identified test

Anonymous. A guide for patients. Pract Gastroenterol 

2002;26(11):58-61. Not sensitivity or specificity of an 

identified test 

A-325
Anonymous. Highly inheritable coeliac disease. Med 

Today 2002;3(7):15Not sensitivity or specificity of an 

identified test 

Anonymous. Latent coeliac disease. Arch Dis Child 

1990;65(10):1192Not sensitivity or specificity of an 

identified test 

Anonymous. A new type intestinal lymphoma. J Clin

Pathol Mol Pathol 2002;55(5):314Not sensitivity or 

specificity of an identified test

Anonymous. Oats safe for coeliac disease patients. Pharm J

2002;268(7185):200Not sensitivity or specificity of an 

identified test 

Anonymous. On the pathogenesis of gluten sensitive 

enteropathy. Nutr Rev 1974;32(9):267-270. Not sensitivity

or specificity of an identified test

Anonymous. PIR quiz. Pediatr Rev 2003;24(6):205-206. 

Not sensitivity or specificity of an identified test

Anstey A, Cerio R, Ramnarain N et al. Desmoplastic

malignant melanoma. An immunocytochemical study of 25

cases. American Journal of Dermatopathology

1994;16(1):14-22. Not sensitivity or specificity of an 

identified test 

Anstey A, Wilkinson J D, Walshe M M. Dermatitis 

herpetiformis in monozygous twins--concordance for 

dermatitis herpetiformis and gluten-sensitive enteropathy.

Clinical and Experimental Dermatology 1991;16(1):51-52. 

Not sensitivity or specificity of an identified test

Antonioli D A. Celiac disease: A progress report. Mod 

Pathol 2003;16(4):342-346. Not sensitivity or specificity of 

an identified test

Antonowicz I, Shwachman H, Sotoo I. Beta-galactosidase 

and beta-glucuronidase activities in intestinal mucosa of 

infants and children. Pediatrics 1971;47(4):737-744. Not 

sensitivity or specificity of an identified test 

Antonyak M A, Singh U S, Lee D A et al. Effects of tissue 

transglutaminase on retinoic acid-induced cellular

differentiation and protection against apoptosis. Journal of

Biological Chemistry 2001;276(36):33582-33587. Not 

sensitivity or specificity of an identified test 

Antonyak Marc A, Boehm Jason E, Cerione Richard A.

Phosphoinositide 3-kinase activity is required for retinoic 

acid-induced expression and activation of the tissue 

transglutaminase. Journal of Biological Chemistry

2002;277(17):14712-14716. Not sensitivity or specificity of 

an identified test

Aoun J P, Moukarbel N, Aftimos G. Value of duodenal 

endoscopic markers of villous atrophy. Le Journal Medical 

Libanais.The Lebanese Medical Journal 2001;49(6):319-

324. Not sensitivity or specificity of an identified test 

Appelt D M, Balin B J. The association of tissue 

transglutaminase with human recombinant tau results in the

formation of insoluble filamentous structures. Brain 

Research 1997;745(1-2):21-31. Not sensitivity or

specificity of an identified test

Appelt D M, Kopen G C, Boyne L J et al. Localization of 

transglutaminase in hippocampal neurons: implications for 

Alzheimer's disease. Journal of Histochemistry and 

Cytochemistry - Official Journal of the Histochemistry

Society 1996;44(12):1421-1427. Not sensitivity or

specificity of an identified test

Applegate D, Steben L S, Hertzberg K M et al. The 

alpha(E)C domain of human fibrinogen-420 is a stable and

early plasmin cleavage product. Blood 2000;95(7):2297-

2303. Not sensitivity or specificity of an identified test 

Arai T, Michalski J P, McCombs C C et al. T cell receptor 

gamma gene polymorphisms and class II human

lymphocyte antigen genotypes in patients with celiac 

disease from the west of Ireland. American Journal of the 

Medical Sciences 1995;309(3):171-178. Not sensitivity or

specificity of an identified test

Arany I, Evans T, Tyring S K. Tissue specific HPV 

expression and downregulation of local immune responses 

in condylomas from HIV seropositive individuals. Sexually

Transmitted Infections 1998;74(5):349-353. Not sensitivity

or specificity of an identified test

Arato A, Hacsek G, Savilahti E. Immunohistochemical 

findings in the jejunal mucosa of patients with coeliac 

disease. Scandinavian Journal of 

Gastroenterology.Supplement 1998;2283-10. Not 

sensitivity or specificity of an identified test 

Arato A, Savilahti E, Tainio V M et al. HLA-DR 

expression, natural killer cells and IgE containing cells in

the jejunal mucosa of coeliac children. Gut 1987;28(8):988-

994. Not sensitivity or specificity of an identified test 

Arato Andras, Korner Anna, Veres Gabor et al. Frequency

of coeliac disease in Hungarian children with type 1 

diabetes mellitus. European Journal of Pediatrics 

2002;162(1):1-5. Not sensitivity or specificity of an 

identified test 

Araya M, Henderson-Smart D. Letter: Coeliac disease: an

undiagnosed disorder with important implications. Medical 

Journal of Australia 1974;1(14):549Not sensitivity or 

specificity of an identified test

Araya M, Walker-Smith J A. Specificity of ultrastructural 

changes of small intestinal epithelium in early childhood. 

Archives of Disease in Childhood 1975;50(11):844-855. 

Not sensitivity or specificity of an identified test

Araya M, Mondragon A, Perez-Bravo F et al. Celiac 

disease in a Chilean population carrying Amerindian traits. 

Journal of Pediatric Gastroenterology and Nutrition 

2000;31(4):381-386. Not sensitivity or specificity of an 

A-326
identified test 

Arellanes-Garcia L, Bautista N, Mora P et al. HLA-DR is 

strongly associated with Vogt-Koyanagi-Harada disease in 

Mexican Mestizo patients. Ocul Immunol Inflamm 

1998;6(2):93-100. Not sensitivity or specificity of an 

identified test 

Arentz-Hansen E H, McAdam S N, Molberg O et al. 

Production of a panel of recombinant gliadins for the 

characterisation of T cell reactivity in coeliac disease. Gut

2000;46(1):46-51. Not sensitivity or specificity of an 

identified test 

Arentz-Hansen H, Korner R, Molberg O et al. The 

intestinal T cell response to alpha-gliadin in adult celiac 

disease is focused on a single deamidated glutamine 

targeted by tissue transglutaminase. Journal of

Experimental Medicine 2000;191(4):603-612. Not 

sensitivity or specificity of an identified test 

Arentz-Hansen Helene, McAdam Stephen N, Molberg 

Oyvind et al. Celiac lesion T cells recognize epitopes that 

cluster in regions of gliadins rich in proline residues. 

Gastroenterology 2002;123(3):803-809. Not sensitivity or

specificity of an identified test

Argenyi Z B, Santa Cruz D, Bromley C. Comparative lightmicroscopic and immunohistochemical study of traumatic 

and palisaded encapsulated neuromas of the skin. American 

Journal of Dermatopathology 1992;14(6):504-510. Not 

sensitivity or specificity of an identified test 

Arilla E, Hernandez M, Polanco I et al. Modification of 

somatostatin content and binding in jejunum from celiac 

children. Journal of Pediatric Gastroenterology and 

Nutrition 1987;6(2):228-233. Not sensitivity or specificity

of an identified test 

Armes J, Gee D C, Macrae F A et al. Collagenous colitis:

jejunal and colorectal pathology. Journal of Clinical 

Pathology 1992;45(9):784-787. Not sensitivity or

specificity of an identified test

Arnaiz-Villena A, Benmamar D, Alvarez M et al. HLA 

allele and haplotype frequencies in Algerians: Relatedness 

to Spaniards and Basques. Hum Immunol 1995;43(4):259-

268. Not sensitivity or specificity of an identified test 

Arnaiz-Villena A, Martinez-Laso J, Corell A et al. 

Frequencies of HLA-A24 and HLA-DR4-DQ8 are 

increased and that of HLA-B blank is decreased in chronic 

toxic oil syndrome. Eur J Immunogenet 1996;23(3):211-

219. Not sensitivity or specificity of an identified test 

Arnason A, Skaftadottir I, Sigmundsson J et al. The 

association between coeliac disease, dermatitis

herpetiformis and certain HLA-antigens in Icelanders. 

European Journal of Immunogenetics - Official Journal of

the British Society for Histocompatibility and

Immunogenetics 1994;21(6):457-460. Improper control 

group 

Arnason J A, Gudjonsson H, Freysdottir J et al. Do adults 

with high gliadin antibody concentrations have subclinical 

gluten intolerance?. Gut 1992;33(2):194-197. Not 

sensitivity or specificity of an identified test 

Arnaud-Battandier F, Cerf-Bensussan N, Amsellem R et al. 

Increased HLA-DR expression by enterocytes in children 

with celiac disease. Gastroenterology 1986;91(5):1206-

1212. Not sensitivity or specificity of an identified test 

Arnaud-Battandier F, Schmitz J, Muller J Y et al. HLA and 

gluten cytotoxicity in vitro. Gastroenterology

1983;84(1):201Not sensitivity or specificity of an identified 

test 

Arnett F C, Reveille J D, Moutsopoulos H M et al. 

Ribosomal P autoantibodies in systemic lupus 

erythematosus: Frequencies in different ethnic groups and 

clinical and immunogenetic associations. Arthritis Rheum 

1996;39(11):1833-1839. Not sensitivity or specificity of an 

identified test 

Arnett F C, Targoff I N, Mimori T et al. Interrelationship of 

major histocompatibility complex class II alleles and 

autoantibodies in four ethnic groups with various forms of 

myositis. Arthritis Rheum 1996;39(9):1507-1518. Not 

sensitivity or specificity of an identified test 

Arnett F C, Thiagarajan P, Ahn C et al. Associations of 

anti-betainf 2-glycoprotein I autoantibodies with HLA class 

II alleles in three ethnic groups. Arthritis Rheum

1999;42(2):268-274. Not sensitivity or specificity of an 

identified test 

Arranz E, Ferguson A. Intestinal antibody pattern of celiac

disease: occurrence in patients with normal jejunal biopsy 

histology. Gastroenterology 1993;104(5):1263-1272. Not 

sensitivity or specificity of an identified test 

Arranz E, Ferguson A. Jejunal fluid antibodies and mucosal 

gamma/delta IEL in latent and potential coeliac disease.

Adv Exp Med Biol 1995;371(B):1345-1348. Not sensitivity

or specificity of an identified test

Arranz E, Bode J, Kingstone K et al. Intestinal antibody 

pattern of coeliac disease: association with gamma/delta T

cell receptor expression by intraepithelial lymphocytes, and

other indices of potential coeliac disease. Gut

1994;35(4):476-482. Not sensitivity or specificity of an 

identified test 

Arranz E, Telleria J J, Sanz A et al. HLA-DQA1*0501 and 

DQB1*02 homozygosity and disease susceptibility in 

Spanish coeliac patients. Experimental and Clinical

Immunogenetics 1997;14(4):286-290. Improper control 

group 

Arrese Estrada J, Pierard G E. Dendrocytes in verruga 

peruana and bacillary angiomatosis. Dermatology (Basel,

Switzerland) 1992;184(1):22-25. Not sensitivity or 

specificity of an identified test

A-327
Arroyo H A, De Rosa S, Ruggieri V et al. Epilepsy, 

occipital calcifications, and oligosymptomatic celiac

disease in childhood. J Child Neurol 2002;17(11):800-806. 

Not sensitivity or specificity of an identified test

Arthur A B, Clayton B E, Cottom D G et al. Importance of

disaccharide intolerance in the treatment of coeliac disease.

Lancet 1966;1(7430):172-174. Not sensitivity or specificity

of an identified test 

Artuc Metin, Steckelings U, Muscha Grutzkau et al. A 

long-term coculture model for the study of mast cellkeratinocyte interactions. Journal of Investigative 

Dermatology 2002;119(2):411-415. Not sensitivity or 

specificity of an identified test

Arvola Taina, Mustalahti Kirsi, Saha Marja et al. Celiac 

disease, thyrotoxicosis, and autoimmune hepatitis in a 

child. Journal of Pediatric Gastroenterology and Nutrition

2002;35(1):90-92. Not sensitivity or specificity of an 

identified test 

Ascher H, Holm K, Kristiansson B et al. Different features 

of coeliac disease in two neighbouring countries. Archives 

of Disease in Childhood 1993;69(3):375-380. Not 

sensitivity or specificity of an identified test 

Ascher H, Krantz I, Kristiansson B. Increasing incidence of

coeliac disease in Sweden. Arch Dis Child 1991;66(5):608-

611. Not sensitivity or specificity of an identified test 

Ascher H, Kristiansson B, Krasilnikoff Collin et al. The 

highest incidence of celiac disease in Europe: The Swedish 

experience. Journal of Pediatric Gastroenterology and 

Nutrition 1997;24(5):S3-S6. Not sensitivity or specificity

of an identified test 

Ashabani A, Errabtea H, Shapan A et al. Serologic markers

of untreated celiac disease in Libyan children: antigliadin,

antitransglutaminase, antiendomysial, and anticalreticulin

antibodies. Journal of Pediatric Gastroenterology and 

Nutrition 2001;33(3):276-282. Improper control group 

Ashabani Abdelhakim, Abushofa Umaima, Abusrewill 

Suliman et al. The prevalence of coeliac disease in Libyan

children with type 1 diabetes mellitus.

Diabetes/Metabolism Research and Reviews

2003;19(1):69-75. Not sensitivity or specificity of an 

identified test 

Ashkenazi A, Berrebi A, Levi R et al. Frequency of HLAB8 in Israeli children with celiac disease. Israel Journal of

Medical Sciences 1979;15(10):826-828. Not sensitivity or

specificity of an identified test

Asquith P. Adult coeliac disease and malignancy. Ir Med J 

1974;67(15):417-420. Not sensitivity or specificity of an

identified test 

Asquith P, Johnson A G, Cooke W T. Scanning electron 

microscopy of normal and celiac jejunal mucosa. American 

Journal of Digestive Diseases 1970;15(6):511-521. Unable 

to extract data

Asselineau D, Bernard B A, Bailly C et al. Retinoic acid 

improves epidermal morphogenesis. Developmental 

Biology 1989;133(2):322-335. Not sensitivity or specificity

of an identified test 

Assi A, Declich P, Iacobellis M et al. Secretory 

meningioma, a rare meningioma subtype with characteristic 

glandular differentation: an histological and

immunohistochemical study of 9 cases. Advances in 

Clinical Pathology - the Official Journal of Adriatic Society 

of Pathology 1999;3(3):47-53. Not sensitivity or specificity

of an identified test 

Astill T P, Ellis R J, Arif S et al. Promiscuous binding of 

proinsulin peptides to Type 1 diabetes-permissive and -

protective HLA class II molecules. Diabetologia 

2003;46(4):496-503. Not sensitivity or specificity of an 

identified test 

Atherton D J. Diagnosis and management of skin disorders 

caused by food allergy. Annals of Allergy 1984;53(6 Pt 

2):623-628. Not sensitivity or specificity of an identified

test 

Atkinson K, Tokmakajian S, Watson W et al. Evaluation of 

the endomysial antibody for celiac disease: operating 

properties and associated cost implications in clinical

practice. Canadian Journal of Gastroenterology = Journal 

Canadien De Gastroenterologie 1997;11(8):673-677. 

Improper control group 

Auld G C, Ritchie H, Robbie L A et al. Thrombin 

upregulates tissue transglutaminase in endothelial cells: a 

potential role for tissue transglutaminase in stability of 

atherosclerotic plaque. Arteriosclerosis, Thrombosis, and

Vascular Biology 2001;21(10):1689-1694. Not sensitivity

or specificity of an identified test

Auricchio S. Gluten-sensitive enteropathy and infant 

nutrition. Journal of Pediatric Gastroenterology and 

Nutrition 1983;2 Suppl 1s304-s309. Not sensitivity or 

specificity of an identified test

Auricchio S, Troncone R. Effects of small amounts of 

gluten in the diet of coeliac patients. Panminerva Medica 

1991;33(2):83-85. Not sensitivity or specificity of an 

identified test 

Auricchio S, Greco L, Troncone R. Gluten-sensitive 

enteropathy in childhood. Pediatric Clinics of North 

America 1988;35(1):157-187. Not sensitivity or specificity

of an identified test 

Auricchio S, Mazzacca G, Tosi R et al. Coeliac disease as a

familial condition: Identification of asymptomatic coeliac 

patients within family groups. Gastroenterol Int 

1988;1(1):25-31. Not sensitivity or specificity of an 

identified test 

A-328
Auricchio S, Troncone R, Maurano F. Coeliac disease in 

the year 2000. Italian Journal of Gastroenterology and 

Hepatology 1999;31(8):773-780. Not sensitivity or 

specificity of an identified test

Autuori F, Farrace M G, Oliverio S et al. "Tissue"

transglutaminase and apoptosis. Advances in Biochemical 

Engineering/Biotechnology 1998;62129-136. Not 

sensitivity or specificity of an identified test 

Avigad S, Manuel P, Bampoe V. Small-intestinal mucosal 

antibodies against antigens of non-pathogenic luminal or 

mucosal bacteria in young children with and without 

diarrhoea. Lancet 1978;1(8074):1130-1132. Not sensitivity

or specificity of an identified test

Avila-Portillo L M, Vargas-Alarcon G, Andrade F et al.

Linkage disequilibrium of HLA-DR3 and HLA-DR4 with 

HLA-B alleles in Mexican patients with rheumatoid 

arthritis. Clin Exp Rheumatol 1994;12(5):497-502. Not 

sensitivity or specificity of an identified test 

Azurdia R M, Luzzi G A, Byren I et al. Lichen sclerosus in 

adult men: A study of HLA associations and susceptibility 

to autoimmune disease. Br J Dermatol 1999;140(1):79-83. 

Not sensitivity or specificity of an identified test

Baden H P. Common transglutaminase substrates shared by

hair, epidermis and nail and their function. Journal of 

Dermatological Science 1994;7 Suppls20-s26. Not 

sensitivity or specificity of an identified test 

Baden H P, Kubilus J K, Phillips S B. Characterization of

monoclonal antibodies generated to the cornified envelope

of human cultured keratinocytes. Journal of Investigative 

Dermatology 1987;89(5):454-459. Not sensitivity or 

specificity of an identified test

Baden H P, Kubilus J, Phillips S B et al. A new class of 

soluble basic protein precursors of the cornified envelope 

of mammalian epidermis. Biochimica Et Biophysica Acta

1987;925(1):63-73. Not sensitivity or specificity of an 

identified test 

Badenhoop K, Donner H, Pani M et al. Genetic 

susceptibility to type 1 diabetes: clinical and molecular 

heterogeneity of IDDM1 and IDDM12 in a german 

population. Experimental and Clinical Endocrinology & 

Diabetes - Official Journal, German Society of 

Endocrinology and German Diabetes Association 1999;107 

Suppl 3s89-s92. Not sensitivity or specificity of an 

identified test 

Bagdi E, Diss T C, Munson P et al. Mucosal intra-epithelial 

lymphocytes in enteropathy-associated T-cell lymphoma, 

ulcerative jejunitis, and refractory celiac disease constitute

a neoplastic population. Blood 1999;94(1):260-264. Not 

sensitivity or specificity of an identified test 

Bagnasco M, Montagna P, De Alessandri A et al. IgA 

antiendomysium antibodies in human umbilical cord 

sections as a screening test in relatives of patients with 

celiac disease. Allergy 1997;52(10):1017-1021. Improper 

control group 

Bahna S L, Tateno K, Heiner D C. Elevated IgD antibodies 

to wheat in celiac disease. Annals of Allergy 

1980;44(3):146-151. Not sensitivity or specificity of an 

identified test 

Bai J C. Malabsorption syndromes. Digestion 

1998;59(5):530-546. Not sensitivity or specificity of an 

identified test 

Bai J C, Sambuelli A, Sugai E et al. Gluten challenge in

patients with celiac disease: evaluation of alpha 1-

antitrypsin clearance. American Journal of 

Gastroenterology 1991;86(3):312-316. Not sensitivity or 

specificity of an identified test

Bai J, Moran C, Martinez C et al. Celiac sprue after surgery

of the upper gastrointestinal tract. Report of 10 patients 

with special attention to diagnosis, clinical behavior, and

follow-up. Journal of Clinical Gastroenterology

1991;13(5):521-524. Not sensitivity or specificity of an 

identified test 

Bailey D S, Freedman A R, Price S C et al. Early

biochemical responses of the small intestine of coeliac 

patients to wheat gluten. Gut 1989;30(1):78-85. Not 

sensitivity or specificity of an identified test 

Baker P G, Read A E. Oats and barley toxicity in coeliac

patients. Postgrad Med J 1976;52(607):264-268. Not 

sensitivity or specificity of an identified test 

Baker P G, Barry R E, Read A E. Detection of continuing 

gluten ingestion in treated coeliac patients. British Medical

Journal 1975;1(5956):486-488. Not sensitivity or 

specificity of an identified test

Baklien K, Brandtzaeg P, Fausa O. Immunoglobulins in

jejunal mucosa and serum from patients with adult coeliac

disease. Scandinavian Journal of Gastroenterology

1977;12(2):149-159. Not sensitivity or specificity of an 

identified test 

Baklien K, Fausa O, Brandtzaeg P. Malabsorption, villous 

atrophy, and excessive serum IgA in a patient with unusual 

intestinal immunocyte infiltration. Scandinavian Journal of

Gastroenterology 1977;12(4):421-432. Not sensitivity or 

specificity of an identified test

Balaji Madhuri, Shtauvere-Brameus A, Balaji V et al. 

Women diagnosed with gestational diabetes mellitus do not 

carry antibodies against minor islet cell antigens. Annals of 

the New York Academy of Sciences 2002;958281-284. Not 

sensitivity or specificity of an identified test 

Balas A, Garcia-Novo M D, Martinez J et al. Intestinal 

alphabeta T cells of symptomatic celiac disease patients

show oligoclonal TCRBV repertoire but polyclonal 

rearrangement patterns. Human Immunology

2000;61(3):247-254. Not sensitivity or specificity of an 

A-329
identified test 

Balas A, Santos S, Aviles M J et al. Elongation of the 

cytoplasmic domain, due to a point deletion at exon 7, 

results in an HLA-C null allele, Cw*0409 N. Tissue 

Antigens 2002;59(2):95-100. Not sensitivity or specificity

of an identified test 

Balas A, Vicario J L, Zambrano A et al. Absolute linkage 

of celiac disease and dermatitis herpetiformis to HLA-DQ. 

Tissue Antigens 1997;50(1):52-56. Improper control group 

Baldas V, Tommasini A, Trevisiol C et al. Development of 

a novel rapid non-invasive screening test for coeliac 

disease. Gut 2000;47(5):628-631. Improper control group 

Balducci-Silano P L, Layrisse Z E. HLA-DP and 

susceptibility to insulin-dependent diabetes mellitus in an 

ethnically mixed population. Associations with other HLAalleles. J Autoimmun 1995;8(3):425-437. Not sensitivity or

specificity of an identified test

Baldwin J A. Schizophrenia and physical disease. 

Psychological Medicine 1979;9(4):611-618. Not sensitivity

or specificity of an identified test

Ball D J, Mayhew S, Vernon D I et al. Decreased efficiency

of trypsinization of cells following photodynamic therapy:

evaluation of a role for tissue transglutaminase.

Photochemistry and Photobiology 2001;73(1):47-53. Not 

sensitivity or specificity of an identified test 

Balster Douglas A, O'Dorisio M, Sue Albers et al. 

Suppression of tumorigenicity in neuroblastoma cells by

upregulation of human vasoactive intestinal peptide 

receptor type 1. Regulatory Peptides 2002;109(1-3):155-

165. Not sensitivity or specificity of an identified test 

Bansal A S, Bruce J, Thomson A et al. Serum levels of 

sCD23, interleukin-10 and interferon-gamma in patients 

with coeliac disease. J Gastroenterol Hepatol 1997;12(9-

10):685-689. Not sensitivity or specificity of an identified 

test 

Banwell J G, Gorbach S L, Mitra R et al. Tropical sprue 

and malnutrition in West Bengal. II. Fluid and electrolyte 

transport in the small intestine. American Journal of 

Clinical Nutrition 1970;23(12):1559-1568. Not sensitivity

or specificity of an identified test

Bao F, Yu L, Babu S et al. One third of HLA DQ2 

homozygous patients with type 1 diabetes express celiac 

disease-associated transglutaminase autoantibodies. Journal 

of Autoimmunity 1999;13(1):143-148. Improper control 

group 

Bar H, Schlote W. Malignant melanoma in the CNS, 

subtyping and immunocytochemistry. Clinical 

Neuropathology 1997;16(6):337-345. Not sensitivity or

specificity of an identified test

Barakat M H, Ali S M, Badawi A R et al. Peroral

endoscopic duodenal biopsy in infants and children. Acta 

Paediatrica Scandinavica 1983;72(4):563-569. Not 

sensitivity or specificity of an identified test 

Barbato M, Miglietta M R, Viola F et al. Impact of

modification of diagnostic techniques and criteria on the 

presentation of celiac disease in the last 16 years.

Observation in Rome. Minerva Pediatrica 1996;48(9):359-

363. Not sensitivity or specificity of an identified test 

Barbato M, Miglietta M R, Viola F et al. Value of

antigliadin antibodies (AGA) in latent coeliac disease (CD).

Minerva Pediatrica 2000;52(11):617-621. Test-specific 

exclusion 

Barbeau W E, Novascone M A, Elgert K D. Is celiac 

disease due to molecular mimicry between gliadin peptideHLA class II molecule-T cell interactions and those of 

some unidentified superantigen?. Molecular Immunology

1997;34(7):535-541. Not sensitivity or specificity of an 

identified test 

Barbera C, Fusco P, Ansaldi N et al. HLA and antigluten 

antibodies in children with celiac disease. Diagn Clin 

Immunol 1987;5(3):158-161. Not sensitivity or specificity

of an identified test 

Bardare M, Villani R, Giunta A. Anti reticulin antibodies in 

malabsorption syndromes. Helv Paediatr Acta 

1974;29(3):203-211. Not sensitivity or specificity of an 

identified test 

Bardella M T, Fredella C, Prampolini L et al. Gluten 

sensitivity in monozygous twins: A long-term follow-up of 

five pairs. American Journal of Gastroenterology

2000;95(6):1503-1505. Not sensitivity or specificity of an

identified test 

Bardella M T, Minoli G, Radaelli F et al. Reevaluation of 

duodenal endoscopic markers in the diagnosis of celiac 

disease. Gastrointestinal Endoscopy 2000;51(6):714-716. 

Not sensitivity or specificity of an identified test

Bardella M T, Minoli G, Ravizza D et al. Increased 

prevalence of celiac disease in patients with dyspepsia. 

Archives of Internal Medicine 2000;160(10):1489-1491. 

Not sensitivity or specificity of an identified test

Bardella M T, Molteni N, Cesana B et al. IgA antigliadin

antibodies, cellobiose/mannitol sugar test, and carotenemia 

in the diagnosis of and screening for celiac disease. 

American Journal of Gastroenterology 1991;86(3):309-311. 

Improper control group 

Bardella M T, Molteni N, Quatrini M et al. Clinical, 

biochemical and histological abnormalities in adult celiac 

patients on gluten-free diet. Gastroenterologie Clinique Et 

Biologique 1985;9(11):787-789. Not sensitivity or

specificity of an identified test

Bardella M T, Quatrini M, Zuin M et al. Screening patients

with celiac disease for primary biliary cirrhosis and vice 

A-330
versa. American Journal of Gastroenterology

1997;92(9):1524-1526. Not sensitivity or specificity of an

identified test 

Bardella M T, Vecchi M, Conte D et al. Chronic 

unexplained hypertransaminasemia may be caused by

occult celiac disease. Hepatology (Baltimore, Md.) 

1999;29(3):654-657. Not sensitivity or specificity of an 

identified test 

Bardos H, Juhasz A, Repassy G et al. Fibrin deposition in

squamous cell carcinomas of the larynx and hypopharynx. 

Thrombosis and Haemostasis 1998;80(5):767-772. Not 

sensitivity or specificity of an identified test 

Barera G, Bianchi C, Calisti L et al. Screening of diabetic

children for coeliac disease with antigliadin antibodies and

HLA typing. Archives of Disease in Childhood

1991;66(4):491-494. Not sensitivity or specificity of an 

identified test 

Barera Graziano, Bonfanti Riccardo, Viscardi Matteo et al. 

Occurrence of celiac disease after onset of type 1 diabetes: 

a 6-year prospective longitudinal study. Pediatrics 

2002;109(5):833-838. Not sensitivity or specificity of an

identified test 

Barlow J M, Johnson C D, Stephens D H. Celiac disease: 

how common is jejunoileal fold pattern reversal found at 

small-bowel follow-through?. Ajr.American Journal of

Roentgenology 1996;166(3):575-577. Not sensitivity or

specificity of an identified test

Barna M, Pinter E. Anti-gliadin and anti-endomysium 

antibodies in children with celiac disease consuming a 

gluten free diet. Zeitschrift Fur Ernahrungswissenschaft 

1998;37 Suppl 1103-105. Not sensitivity or specificity of

an identified test

Barnes G L. Duodenal biopsy in 75 New Zealand children. 

New Zealand Medical Journal 1976;83(564):349-351. Not 

sensitivity or specificity of an identified test 

Barnes R M, Lewis-Jones M S. Isotype distribution and 

serial levels of antibodies reactive with dietary protein

antigens in dermatitis herpetiformis. Journal of Clinical & 

Laboratory Immunology 1989;30(2):87-91. Not sensitivity

or specificity of an identified test

Barnes R M, Harvey M M, Blears J et al. IgG subclass of 

human serum antibodies reactive with dietary proteins. 

International Archives of Allergy and Applied Immunology

1986;81(2):141-147. Not sensitivity or specificity of an 

identified test 

Barr G D, Grehan M J. Coeliac disease. Med J Aust

1998;169(2):109-114. Not sensitivity or specificity of an

identified test 

Barr G, Cameron D, King S et al. Current status and 

management of coeliac disease. Med Today 2003;4(6):30-

39. Not sensitivity or specificity of an identified test 

Barresi G, Tuccari G, Magazzu G. Neutral mucins in 

coeliac disease. Basic and Applied Histochemistry

1983;27(1):55-60. Not sensitivity or specificity of an 

identified test 

Barresi G, Tuccari G, Magazzu G et al. Acid mucins in

duodeno-jejunal biopsies from infants with coeliac disease. 

Applied Pathology 1983;1(1):34-40. Not sensitivity or 

specificity of an identified test

Barry E L, Mosher D F. Binding and degradation of blood 

coagulation factor XIII by cultured fibroblasts. Journal of

Biological Chemistry 1990;265(16):9302-9307. Not 

sensitivity or specificity of an identified test 

Barry R E. 'Coeliac disease and malignancy'. Tgastro-Ent

1973;16(1):23-34. Not sensitivity or specificity of an 

identified test 

Barry R E, Read A E. Coeliac disease and malignancy.

Quarterly Journal of Medicine 1973;42(168):665-675. Not 

sensitivity or specificity of an identified test 

Barshack I, Goldberg I, Chowers Y et al. 

Immunohistochemical analysis of candidate gene product 

expression in the duodenal epithelium of children with 

coeliac sprue. Journal of Clinical Pathology

2001;54(9):684-688. Not sensitivity or specificity of an 

identified test 

Barsoum R, Nabil M, Saady G et al. Immunoglobulin-A 

and the pathogenesis of schistosomal glomerulopathy. 

Kidney International 1996;50(3):920-928. Not sensitivity

or specificity of an identified test

Barta L, Kosnai I, Molnar M et al. Simultaneous

occurrence of diabetes mellitus and coeliac disease. Acta

Paediatrica Hungarica 1985;26(4):303-306. Not sensitivity

or specificity of an identified test

Barta Z, Csipo tilde, Szabo G G et al. Seroreactvity against 

Saccharomyces cerevisiae in patients with Crohn's disease 

and celiac disease. World J Gastroenterol 2003;9(10):2308-

2312. Not sensitivity or specificity of an identified test 

Bartholomeusz R C, Labrooy J T, Davidson G P et al. 

Polymeric IgA antibody to gliadin in the serum of patients 

with coeliac disease. Journal of Gastroenterology and 

Hepatology 1990;5(6):675-681. Not sensitivity or

specificity of an identified test

Batar P, Dale G L. Simultaneous engagement of thrombin 

and Fc gamma RIIA receptors results in platelets 

expressing high levels of procoagulant proteins. Journal of 

Laboratory and Clinical Medicine 2001;138(6):393-402. 

Not sensitivity or specificity of an identified test

Bateson M C, Hopwood D, MacGillivray J B. Jejunal 

morphology in multiple sclerosis. Lancet 

1979;1(8126):1108-1110. Not sensitivity or specificity of

an identified test

A-331
Batt R M, Carter M W, McLean L. Morphological and

biochemical studies of a naturally occurring enteropathy in 

the Irish setter dog: a comparison with coeliac disease in

man. Research in Veterinary Science 1984;37(3):339-346. 

Not sensitivity or specificity of an identified test

Battelli M G, Musiani S, Tazzari P L et al. Oxidative stress 

to human lymphocytes by xanthine oxidoreductase activity.

Free Radical Research 2001;35(6):665-679. Not sensitivity

or specificity of an identified test

Baur X, Rihs H-P, Altmeyer P et al. Systemic sclerosis in 

German uranium miners under special consideration of 

autoantibody subsets and HLA class II alleles. Respiration 

1996;63(6):368-375. Not sensitivity or specificity of an 

identified test 

Bayless T M, Wheby M S, Swanson V L. Tropical sprue in 

Puerto Rico. American Journal of Clinical Nutrition 

1968;21(9):1030-1041. Not sensitivity or specificity of an

identified test 

Bazinet P, Marin G A. Malabsorption in systemic lupus 

erythematosus. American Journal of Digestive Diseases

1971;16(5):460-466. Not sensitivity or specificity of an 

identified test 

Bazzigaluppi E, Lampasona V, Barera G et al. Comparison 

of tissue transglutaminase-specific antibody assays with

established antibody measurements for coeliac disease.

Journal of Autoimmunity 1999;12(1):51-56. Improper 

control group 

Beard R L, Chandraratna R A, Colon D F et al. Synthesis

and structure-activity relationships of stilbene retinoid 

analogs substituted with heteroaromatic carboxylic acids.

Journal of Medicinal Chemistry 1995;38(15):2820-2829. 

Not sensitivity or specificity of an identified test

Beaumont D M, Mian M S. Coeliac disease in old age: 'A 

catch in the rye'. Age Ageing 1998;27(4):535-538. Not 

sensitivity or specificity of an identified test 

Beck I T, Da Costa L R, Beck M. Sugar absorption by

small bowel biopsy samples from patients with primary 

lactase deficiency and with adult celiac disease. American 

Journal of Digestive Diseases 1976;21(11):946-952. Not 

sensitivity or specificity of an identified test 

Beckett C G, Ciclitira P J. Celiac disase. Curr Opin 

Gastroenterol 1997;13(2):107-111. Not sensitivity or 

specificity of an identified test

Beckett C G, Dell'Olio D, Ellis H J et al. The detection and

localization of inducible nitric oxide synthase production in 

the small intestine of patients with coeliac disease. 

European Journal of Gastroenterology & Hepatology

1998;10(8):641-647. Not sensitivity or specificity of an 

identified test 

Beckett C G, Dell'Olio D, Kontakou M et al. Analysis of

interleukin-4 and interleukin-10 and their association with

the lymphocytic infiltrate in the small intestine of patients 

with coeliac disease. Gut 1996;39(96):818-823. Not 

sensitivity or specificity of an identified test 

Beckett C G, Dell'Olio D, Schidrawi R G et al. Gluteninduced nitric oxide and pro-inflammatory cytokine release 

by cultured coeliac small intestinal biopsies. European 

Journal of Gastroenterology & Hepatology 1999;11(5):529-

535. Not sensitivity or specificity of an identified test 

Bedrossian C W, Bonsib S, Moran C. Differential diagnosis 

between mesothelioma and adenocarcinoma: a multimodal

approach based on ultrastructure and 

immunocytochemistry. Seminars in Diagnostic Pathology

1992;9(2):124-140. Not sensitivity or specificity of an 

identified test 

Behr W, Barnert J. Adult celiac disease and primary biliary 

cirrhosis. American Journal of Gastroenterology

1986;81(9):796-799. Not sensitivity or specificity of an 

identified test 

Behrendt N, Ronne E, Dano K. A novel, specific prourokinase complex on monocyte-like cells, detected by

transglutaminase-catalyzed cross-linking. Febs Letters

1993;336(3):394-396. Not sensitivity or specificity of an

identified test 

Belkin A M, Akimov S S, Zaritskaya L S et al. Matrixdependent proteolysis of surface transglutaminase by

membrane-type metalloproteinase regulates cancer cell 

adhesion and locomotion. Journal of Biological Chemistry

2001;276(21):18415-18422. Not sensitivity or specificity of 

an identified test

Bell J I. The major histocompatibility complex and disease.

Current Opinion in Immunology 1989;2(1):114-116. Not 

sensitivity or specificity of an identified test 

Bell J, Rassenti L, Smoot S et al. HLA-DQ beta-chain 

polymorphism linked to myasthenia gravis. Lancet 

1986;1(8489):1058-1060. Not sensitivity or specificity of

an identified test

Bell S, Green P H R, Kagnoff M F. American 

gastroenterological association medical position statement:

Celiac sprue. Gastroenterology 2001;120(6):1522-1525. 

Not sensitivity or specificity of an identified test

Bellanti J A, Zeligs B J, Malka-Rais J et al. Abnormalities

of ThSUB1 function in non-IgE food allergy, celiac 

disease, and ileal lymphonodular hyperplasia: A new 

relationship?. Annals of Allergy, Asthma & Immunology - 

Official Publication of the American College of Allergy,

Asthma, & Immunology 2003;90(Suppl):84-89. Not 

sensitivity or specificity of an identified test 

Belloni Cesare, Avanzini Maria A, De Silvestri et al. No 

evidence of autoimmunity in 6-year-old children

immunized at birth with recombinant hepatitis B vaccine.

Pediatrics 2002;110(1 Pt 1):E4Not sensitivity or specificity

A-332
of an identified test 

Beltrami C A, Barbatelli G, Criante P et al. An

immunohistochemical study in thyroid cancer. Applied

Pathology 1987;5(4):229-245. Not sensitivity or specificity

of an identified test 

Bender S W, Posselt H G, Staps M et al. Biochemical 

quantification of crypt hyperplastic villous atrophy by

aldolase activity assay. Journal of Pediatric 

Gastroenterology and Nutrition 1984;3(4):506-509. Not

sensitivity or specificity of an identified test 

Bendixen E, Harpel P C, Sottrup-Jensen L. Location of the 

major epsilon-(gamma-glutamyl)lysyl cross-linking site in

transglutaminase-modified human plasminogen. Journal of

Biological Chemistry 1995;270(30):17929-17933. Not 

sensitivity or specificity of an identified test 

Bendl B J, Williams P B. Histopathological changes in the 

jejunal mucosa in dermatitis herpetiformis. Canadian 

Medical Association Journal 1968;98(12):575-577. Not 

sensitivity or specificity of an identified test 

Beninati S, Senger D R, Cordella-Miele E et al. 

Osteopontin: Its transglutaminase-catalyzed 

posttranslational modifications and cross-linking to 

fibronectin. J Biochem 1994;115(4):675-682. Not 

sensitivity or specificity of an identified test 

Bennett R A, Whitelock T, Kelley J L. Eosinophilic 

gastroenteritis, gluten enteropathy, and dermatitis

herpetiformis. American Journal of Digestive Diseases

1974;19(12):1154-1161. Not sensitivity or specificity of an 

identified test 

Benzinger T L, Gregory D M, Burkoth T S et al. 

Propagating structure of Alzheimer's beta-amyloid(10-35) 

is parallel beta-sheet with residues in exact register. 

Proceedings of the National Academy of Sciences of the

United States of America 1998;95(23):13407-13412. Not 

sensitivity or specificity of an identified test 

Berdoz J, Tiercy J-M, Rollini P et al. Remarkable sequence

conservation of the HLA-DQB2 locus (DXbeta) within the 

highly polymorphic DQ subregion of the human MHC. 

Immunogenetics 1989;29(4):241-248. Not sensitivity or

specificity of an identified test

Berg A, Eriksson M, Barany F. Hydrogen concentration in

expired air analyzed with a new hydrogen sensor, plasma 

glucose rise, and symptoms of lactose intolerance after oral 

administration of 100 gram lactose. Scandinavian Journal 

of Gastroenterology 1985;20(7):814-822. Not sensitivity or 

specificity of an identified test

Berg L, Ronnelid J, Sanjeevi C B et al. Interferon-gamma

production in response to in vitro stimulation with collagen 

type II in rheumatoid arthritis is associated with HLADRB1*0401 and HLA-DQ8. Arthritis Res 2000;2(1):75-

84. Not sensitivity or specificity of an identified test 

Berg N O, Lindberg T. Incidence of coeliac disease and

transient gluten intolerance in children in a Swedish urban 

community. Acta Paediatr Scand 1979;68(3):397-400. Not 

sensitivity or specificity of an identified test 

Berg N O, Dahlqvist A, Lindberg T et al. Correlation 

between morphological alterations and enzyme activities in 

the mucosa of the small intestine. Scandinavian Journal of

Gastroenterology 1973;8(8):703-712. Not sensitivity or

specificity of an identified test

Bergamini A, Capozzi M, Piacentini M. Macrophagecolony stimulating factor (M-CSF) stimulation induces cell

death in HIV-infected human monocytes. Immunology

Letters 1994;42(1-2):35-40. Not sensitivity or specificity of 

an identified test

Bergamini C M, Signorini M. Studies on tissue 

transglutaminases: interaction of erythrocyte type-2 

transglutaminase with GTP. Biochemical Journal 

1993;291(Pt 1):37-39. Not sensitivity or specificity of an

identified test 

Bergamini C M, Signorini M, Barbato R et al. 

Transglutaminase-catalyzed polymerization of troponin in

vitro. Biochemical and Biophysical Research 

Communications 1995;206(1):201-206. Not sensitivity or

specificity of an identified test

Bernard B A, Asselineau D, Schaffar-Deshayes L et al. 

Abnormal sequence of expression of differentiation 

markers in psoriatic epidermis: inversion of two steps in the 

differentiation program?. Journal of Investigative 

Dermatology 1988;90(6):801-805. Not sensitivity or 

specificity of an identified test

Bernard B A, Reano A, Darmon Y M et al. Precocious 

appearance of involucrin and epidermal transglutaminase

during differentiation of psoriatic skin. British Journal of

Dermatology 1986;114(3):279-283. Not sensitivity or 

specificity of an identified test

Bernardini S, Melino G, Cortese C et al. Modulation of 

glutathione transferase P1-1 activity by retinoic acid in

neuroblastoma cells. Journal of Cellular Biochemistry

1999;75(3):375-381. Not sensitivity or specificity of an 

identified test 

Bernassola F, Rossi A, Melino G. Regulation of 

transglutaminases by nitric oxide. Annals of the New York 

Academy of Sciences 1999;88783-91. Not sensitivity or

specificity of an identified test

Bernassola F, Scheuerpflug C, Herr I et al. Induction of 

apoptosis by IFNgamma in human neuroblastoma cell lines 

through the CD95/CD95L autocrine circuit. Cell Death and 

Differentiation 1999;6(7):652-660. Not sensitivity or 

specificity of an identified test

Bernstein Charles N, Leslie William D, Leboff Meryl S. 

AGA technical review on osteoporosis in gastrointestinal 

diseases. Gastroenterology 2003;124(3):795-841. Not 

A-333
sensitivity or specificity of an identified test 

Berrill W T, van Rood J J. HLA-DW6 and avian 

hypersensitivity. Lancet 1977;2(8031):248-249. Not 

sensitivity or specificity of an identified test 

Berrill W T, Eade O E, Fitzpatrick P F. Bird Fancier's lung

and jejunal villous atrophy. Lancet 1975;2(7943):1006-

1008. Not sensitivity or specificity of an identified test 

Berrutti L, Silverman J S. Cardiac myxoma is rich in factor 

XIIIa positive dendrophages: immunohistochemical study

of four cases. Histopathology 1996;28(6):529-535. Not 

sensitivity or specificity of an identified test 

Berstad A E, Brandtzaeg P. Expression of cell membrane 

complement regulatory glycoproteins along the normal and

diseased human gastrointestinal tract. Gut 1998;42(4):522-

529. Not sensitivity or specificity of an identified test 

Bertele R M, Burgin-Wolff A, Berger R et al. The 

fluorescent immunosorbent test for IgG gliadin antibodies

and the leucocyte migration inhibition test in coeliac 

disease; comparison of diagnostic value. European Journal 

of Pediatrics 1985;144(1):58-62. Not sensitivity or

specificity of an identified test

Berthon P, Pancino G, de Cremoux P et al. Characterization

of normal breast epithelial cells in primary cultures: 

differentiation and growth factor receptors studies. In Vitro 

Cellular & Developmental Biology - Journal of the Tissue 

Culture Association 1992;28a(11-12):716-724. Not 

sensitivity or specificity of an identified test 

Berti I, Trevisiol C, Tommasini A et al. Usefulness of 

screening program for celiac disease in autoimmune 

thyroiditis. Digestive Diseases and Sciences

2000;45(2):403-406. Not sensitivity or specificity of an 

identified test 

Berzina L, Ludvigsson J, Sadauskaite-Kuehne V et al. DR3 

is associated with type 1 diabetes and blood group ABO 

incompatibility. Annals of the New York Academy of 

Sciences 2002;958345-348. Not sensitivity or specificity of 

an identified test

Berzina L, Shtauvere-Brameus A, Ludvigsson J et al. 

Newborn screening for high-risk human leukocyte antigen

markers associated with insulin-dependent diabetes

mellitus: the ABIS study. Annals of the New York 

Academy of Sciences 2002;958312-316. Not sensitivity or

specificity of an identified test

Besterman H S, Cook G C, Sarson D L. Gut hormones in 

tropical malabsorption. Br Med J 1979;2(6200):1252-1255. 

Not sensitivity or specificity of an identified test

Bettinotti M P, Hartung K, Deicher H et al. Polymorphism

of the tumor necrosis factor beta gene in systemic lupus 

erythematosus: TNFB-MHC haplotypes. Immunogenetics 

1993;37(6):449-454. Not sensitivity or specificity of an 

identified test 

Betuel H, Gebuhrer L, Descos L et al. Adult celiac disease 

associated with HLA-DRw3 and -DRw7. Tissue Antigens

1980;15(3):231-238. Not sensitivity or specificity of an 

identified test 

Beutner E H, Chorzelski T P, Kumar V et al. Sensitivity 

and specificity of IgA-class antiendomysial antibodies for 

dermatitis herpetiformis and findings relevant to their 

pathogenic significance. Journal of the American Academy

of Dermatology 1986;15(3):464-473. Not sensitivity or

specificity of an identified test

Beutner E H, Kumar V, Chorzelski T P et al. IgG 

endomysial antibodies in IgA-deficient patient with coeliac 

disease. Lancet 1989;1(8649):1261-1262. Not sensitivity or 

specificity of an identified test

Bevan S, Popat S, Houlston R S. Relative power of linkage 

and transmission disequilibrium test strategies to detect 

non-HLA linked coeliac disease susceptibility genes. Gut 

1999;45(5):668-671. Not sensitivity or specificity of an 

identified test 

Bevan S, Popat S, Braegger C P et al. Contribution of the 

MHC region to the familial risk of coeliac disease. Journal 

of Medical Genetics 1999;36(9):687-690. Not sensitivity or 

specificity of an identified test

Bhatnagar S, Bhan M K. Serological diagnosis of celiac 

disease. Indian Journal of Pediatrics 1999;66(1 Suppl):S26-

S31. Review article 

Biagi F, Corazza G R. Tissue transglutaminase antibodies: 

is sensitivity more important than specificity?. Digestive

and Liver Disease - Official Journal of the Italian Society 

of Gastroenterology and the Italian Association for the

Study of the Liver 2001;33(5):401-402. Review article 

Biagi F, Corazza G R. Contribution of molecular genetics 

to gastroenterology: the case of coeliac disease. Italian 

Journal of Gastroenterology and Hepatology

1999;31(3):202-204. Not sensitivity or specificity of an 

identified test 

Biagi F, Corazza G R. Gene and gliadin/gut and kidney.

American Journal of Gastroenterology 2002;97(10):2486-

2488. Not sensitivity or specificity of an identified test 

Biagi F, Corazza G R. Clinical features of coeliac disease.

Digestive and Liver Disease - Official Journal of the Italian

Society of Gastroenterology and the Italian Association for

the Study of the Liver 2002;34(3):225-228. Not sensitivity

or specificity of an identified test

Biagi F, Corazza G R. Defining gluten refractory 

enteropathy. European Journal of Gastroenterology & 

Hepatology 2001;13(5):561-565. Not sensitivity or 

specificity of an identified test

Biagi F, Bassi E, Ardigo M et al. In patients with dermatitis 

herpetiformis distribution of transglutaminase in cutaneous 

A-334
tissue does not differ from controls. Digestive and Liver 

Disease - Official Journal of the Italian Society of 

Gastroenterology and the Italian Association for the Study

of the Liver 2003;35(1):41-45. Not sensitivity or specificity

of an identified test 

Biagi F, Ellis H J, Parnell N D et al. A non-toxic analogue 

of a coeliac-activating gliadin peptide: a basis for

immunomodulation?. Alimentary Pharmacology & 

Therapeutics 1999;13(7):945-950. Not sensitivity or 

specificity of an identified test

Biagi F, Ellis H J, Yiannakou J Y et al. Tissue 

transglutaminase antibodies in celiac disease. American

Journal of Gastroenterology 1999;94(8):2187-2192. 

Improper control group 

Biagi F, Lorenzini P, Corazza G R. Literature review on the

clinical relationship between ulcerative jejunoileitis, coeliac 

disease, and enteropathy-associated T-cell lymphoma. 

Scandinavian Journal of Gastroenterology 2000;35(8):785-

790. Not sensitivity or specificity of an identified test 

Biagi F, Parnell N D, Ellis H J et al. Endomysial antibody

production is not related to histological damage after in 

vitro gluten challenge. European Journal of 

Gastroenterology & Hepatology 2000;12(1):57-60. Not 

sensitivity or specificity of an identified test 

Biagi F, Parnell N D, Thomas P D et al. A new model for 

the pathogenesis of celiac disease. Gastroenterology

1999;116(5):1277-1278. Not sensitivity or specificity of an 

identified test 

Biagi F, Zimmer K P, Thomas P D et al. Is gliadin 

mispresented to the immune system in coeliac disease? A 

hypothesis. Qjm - Monthly Journal of the Association of

Physicians 1999;92(2):119-122. Not sensitivity or

specificity of an identified test

Bianchi L, Farrace M G, Nini G et al. Abnormal Bcl-2 and 

"tissue" transglutaminase expression in psoriatic skin. 

Journal of Investigative Dermatology 1994;103(6):829-

833. Not sensitivity or specificity of an identified test 

Bieda K, Pani M A, van der et al. A retroviral long terminal

repeat adjacent to the HLA DQB1 gene (DQ-LTR13) 

modifies Type I diabetes susceptibility on high risk DQ 

haplotypes. Diabetologia 2002;45(3):443-447. Not 

sensitivity or specificity of an identified test 

Biempica L, Toccalino H, O'Donnell J C. Cytochemical

and ultrastructural studies of the intestinal mucosa of 

children with celiac disease. American Journal of 

Pathology 1968;52(4):795-823. Unable to extract data 

Bilbao J R, Martin-Pagola A, Calvo B et al. Contribution of

MIC-A polymorphism to type 1 diabetes mellitus in 

Basques. Ann New York Acad Sci 2002;958(-):321-324. 

Not sensitivity or specificity of an identified test

Bilbao J R, Martin-Pagola A, Vitoria J C et al. HLA-DRB1 

and MHC class 1 chain-related A haplotypes in Basque 

families with celiac disease. Tissue Antigens 

2002;60(1):71-76. Not sensitivity or specificity of an 

identified test 

Bilbao J, Ramon Vitoria, Juan C et al. Immunoglobulin G 

autoantibodies against tissue-transglutaminase. A sensitive, 

cost-effective assay for the screening of celiac disease.

Autoimmunity 2002;35(4):255-259. Improper control 

group 

Binder G, Ranke M B, Martin D D. Auxology Is a Valuable 

Instrument for the Clinical Diagnosis of SHOX 

Haploinsufficiency in School-Age Children with 

Unexplained Short Stature. J Clin Endocrinol Metab 

2003;88(10):4891-4896. Not sensitivity or specificity of an 

identified test 

Binder H J. Cediac sprue--"unmasking" after vagotomy and 

hiatal-hernia repair. New England Journal of Medicine

1970;283(10):520-521. Not sensitivity or specificity of an

identified test 

Bini E J. Helicobacter pylori and iron deficiency anemia:

Guilty as charged?. Am J Med 2001;111(6):495-497. Not 

sensitivity or specificity of an identified test 

Birckbichler P J, Patterson M K. Transglutaminase and 

epsilon-(gamma-glutamyl) lysine isopeptide bonds in 

eukaryotic cells. Progress in Clinical and Biological 

Research 1980;41845-855. Not sensitivity or specificity of 

an identified test

Birckbichler P J, Bonner R B, Hurst R E et al. Loss of 

tissue transglutaminase as a biomarker for prostate 

adenocarcinoma. Cancer 2000;89(2):412-423. Not 

sensitivity or specificity of an identified test 

Birckbichler P J, Orr G R, Patterson M K et al. Enhanced

transglutaminase activity in transformed human lung 

fibroblast cells after exposure to sodium butyrate. 

Biochimica Et Biophysica Acta 1983;763(1):27-34. Not 

sensitivity or specificity of an identified test 

Birckbichler P J, Upchurch H F, Patterson M K et al.

Detection of cellular transglutaminase using monoclonal 

antibody. Fed Proc 1984;43(6):No 2082Not sensitivity or

specificity of an identified test

Birckbichler P J, Upchurch H F, Patterson M K et al. A 

monoclonal antibody to cellular transglutaminase. 

Hybridoma 1985;4(2):179-186. Not sensitivity or 

specificity of an identified test

Birinci A, Birinci H, Abidinoglu R et al. Diabetic 

retinopathy and HLA antigens in type 2 diabetes mellitus.

Eur J Ophthalmol 2002;12(2):89-93. Not sensitivity or

specificity of an identified test

Birol Ahu, Anadolu Rana, Yavuzer Tutkak et al. HLAclass 1 and class 2 antigens in Turkish patients with 

pemphigus. International Journal of Dermatology

A-335
2002;41(2):79-83. Not sensitivity or specificity of an 

identified test 

Bischoff S C, Mayer J, Wedemeyer J et al. Colonoscopic 

allergen provocation (COLAP): a new diagnostic approach

for gastrointestinal food allergy. Gut 1997;40(6):745-753. 

Not sensitivity or specificity of an identified test

Bishara A, Brautbar C, Nagler A. HLA and graft-versushost disease: A population-based study of HLA phenotypes 

of Jewish and Arabic bone marrow transplanted patients in

Israel. Leuk Res 1997;21(2):111-118. Not sensitivity or

specificity of an identified test

Bittinger M, Barnert J, Schmidbaur W et al. D-xylose 

hydrogen-breath test as a noninvasive screening test for 

Coeliac disease. What is the optimum xylose dose?. Rom J

Gastroenterol 1997;6(4):235-238. Not sensitivity or 

specificity of an identified test

Bittolo M, Not T, Perticarari S et al. A dot immunobinding 

assay to detect anti-alpha-gliadin antibodies in celiac 

disease. Journal of Pediatric Gastroenterology and

Nutrition 1990;11(3):337-341. Not sensitivity or specificity

of an identified test 

Bizzaro N, Villalta D, Tonutti E et al. Association of celiac 

disease with connective tissue diseases and autoimmune 

diseases of the digestive tract. Autoimmun Rev 

2003;2(6):358-363. Not sensitivity or specificity of an 

identified test 

Bjarnason I, Batt R, Catt S et al. Evaluation of differential

disaccharide excretion in urine for non-invasive

investigation of altered intestinal disaccharidase activity

caused by alpha-glucosidase inhibition, primary

hypolactasia, and coeliac disease. Gut 1996;39(3):374-381. 

Not sensitivity or specificity of an identified test

Bjarnason I, Goolamali S K, Levi A J et al. Intestinal

permeability in patients with atopic eczema. British Journal 

of Dermatology 1985;112(3):291-297. Not sensitivity or

specificity of an identified test

Bjarnason I, Marsh M N, Price A et al. Intestinal 

permeability in patients with coeliac disease and dermatitis

herpetiformis. Gut 1985;26(11):1214-1219. Not sensitivity

or specificity of an identified test

Bjarnason I, Peters T J, Veall N. A persistent defect in 

intestinal permeability in coeliac disease demonstrated by a 

51Cr-labelled EDTA absorption test. Lancet

1983;1(8320):323-325. Not sensitivity or specificity of an

identified test 

Bjerrum O J, Heegaard N H H. Has immunoblotting 

replaced electroimmunoprecipitation? Examples from the 

analysis of autoantigens and transglutaminase-induced 

polymers of the human erythrocyte membrane. J 

Chromatogr 1989;470(2):351-367. Not sensitivity or 

specificity of an identified test

Bjorksten F, Backman A, Jarvinen K A et al. 

Immunoglobulin E specific to wheat and rye flour proteins. 

Clinical Allergy 1977;7(5):473-483. Not sensitivity or 

specificity of an identified test

Bjorneklett A, Fausa O, Refsum S B. Jejunal villous 

atrophy and granulomatous inflammation responding to a 

gluten free diet. Gut 1977;18(10):814-816. Not sensitivity

or specificity of an identified test

Black Kay E, Murray Joseph A, David Chella S. HLA-DQ 

determines the response to exogenous wheat proteins: a 

model of gluten sensitivity in transgenic knockout mice. 

Journal of Immunology (Baltimore, Md.- 1950)

2002;169(10):5595-5600. Not sensitivity or specificity of

an identified test

Blackwell P J, Hill P G, Holmes G K T. Autoantibodies to

human tissue transglutaminase: superior predictors of 

coeliac disease. Scandinavian Journal of Gastroenterology

2002;37(11):1282-1285. Improper control group

Blanco A, Alonso M, Cilleruelo M L et al. Increased serum

beta2-microglobulin levels in active celiac disease. Journal 

of Pediatric Gastroenterology and Nutrition 1985;4(3):388-

392. Not sensitivity or specificity of an identified test 

Blanco A, Arranz E, Alonso M et al. IgA1, IgA2 or 

secretory piece containing antigliadin antibodies in the sera 

of coeliac patients. Allergologia Et Immunopathologia 

1989;17(2):77-80. Not sensitivity or specificity of an 

identified test 

Blanco A, Garrote J A, Alonso M et al. Soluble CD4 

antigen is increased in active coeliac disease. Advances in 

Experimental Medicine and Biology 1995;371b1355-1358. 

Not sensitivity or specificity of an identified test

Blanco A, Garrote J A, Arranz E et al. Increased serum IL2R levels in coeliac disease are related to CD4 but not CD8 

antigens. Journal of Pediatric Gastroenterology and 

Nutrition 1992;15(4):413-417. Not sensitivity or specificity

of an identified test 

Blazer S, Naveh Y, Berant M et al. Serum IgG antibodies 

to gliadin in children with celiac disease as measured by an 

immunofluorescence method. Journal of Pediatric 

Gastroenterology and Nutrition 1984;3(2):205-209. 

Serology <1990

Bloch R, Menge H, Lingelbach B et al. The relationship 

between structure and function of small intestine in patients 

with a sprue syndrome and in healthy controls. Klinische

Wochenschrift 1973;51(23):1151-1158. Not sensitivity or 

specificity of an identified test

Blomme B, Gerlo E, Hauser B et al. Disaccharidase 

activities in Belgian children: Reference intervals and 

comparison with non-Belgian Caucasian children. Acta 

Paediatr Int J Paediatr 2003;92(7):806-810. Not sensitivity

or specificity of an identified test

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Boberg K M, Spurkland A, Rocca G et al. The HLADR3,DQ2 heterozygous genotype is associated with an 

accelerated progression of primary sclerosing cholangitis. 

Scandinavian Journal of Gastroenterology 2001;36(8):886-

890. Not sensitivity or specificity of an identified test 

Bock S A. Food sensitivity: a critical review and practical 

approach. American Journal of Diseases of Children (1960)

1980;134(10):973-982. Not sensitivity or specificity of an

identified test 

Boda M, Nemeth I, Boda D. The caffeine metabolic ratio as 

an index of xanthine oxidase activity in clinically active 

and silent celiac patients. Journal of Pediatric 

Gastroenterology and Nutrition 1999;29(5):546-550. Not

sensitivity or specificity of an identified test 

Bodanszky H, Horvath K, Horn G. The D-xylose test in

coeliac disease. Acta Paediatrica Hungarica 1983;24(1):17-

22. Not sensitivity or specificity of an identified test 

Bodanszky H, Horvath K, Bata A et al. Hydrogen breath 

test in small intestinal malabsorption. Acta Paediatrica 

Hungarica 1987;28(1):45-49. Not sensitivity or specificity

of an identified test 

Bode S, Gudmand-Hoyer E. Symptoms and haematologic 

features in consecutive adult coeliac patients. Scandinavian 

Journal of Gastroenterology 1996;31(1):54-60. Not 

sensitivity or specificity of an identified test 

Bode S, Gudmand-Hoyer E. Incidence and clinical 

significance of lactose malabsorption in adult coeliac 

disease. Scandinavian Journal of Gastroenterology

1988;23(4):484-488. Not sensitivity or specificity of an 

identified test 

Bodmer W F. The HLA system and disease. The Oliver

Sharpey Lecture 1979. Journal of the Royal College of 

Physicians of London 1980;14(1):43-50. Not sensitivity or

specificity of an identified test

Boehm Jason E, Singh Ugra, Combs Carolyn et al. Tissue 

transglutaminase protects against apoptosis by modifying 

the tumor suppressor protein p110 Rb. Journal of

Biological Chemistry 2002;277(23):20127-20130. Not 

sensitivity or specificity of an identified test 

Boersma E R. Serum immunoglobulins IgG, IgM, and IgA 

in maternal cord blood pairs from infants of normal and 

low birthweights in Tanzania. Archives of Disease in

Childhood 1981;56(1):31-35. Not sensitivity or specificity

of an identified test 

Bognetti E, Riva M C, Bonfanti R et al. Growth changes in 

children and adolescents with short-term diabetes. Diabetes

Care 1998;21(8):1226-1229. Not sensitivity or specificity

of an identified test 

Bolme P, Eriksson M, Stintzing G. The gastrointestinal

absorption of penicillin V in children with suspected 

coeliac disease. Acta Paediatrica Scandinavica

1977;66(5):573-578. Not sensitivity or specificity of an 

identified test 

Bolognesi E, Karell K, Percopo S et al. Additional factor in

some HLA DR3/DQ2 haplotypes confers a fourfold 

increased genetic risk of celiac disease. Tissue Antigens

2003;61(4):308-316. Not sensitivity or specificity of an 

identified test 

Bolsover W J, Hall M A, Vaughan R W et al. A family

study confirms that the HLA-DP associations with celiac 

disease are the result of an extended HLA-DR3 haplotype.

Human Immunology 1991;31(2):100-108. Not sensitivity

or specificity of an identified test

Bonamico M, Ballati G, Mariani P et al. Screening for 

coeliac disease: the meaning of low titers of anti-gliadin

antibodies (AGA) in non-coeliac children. European 

Journal of Epidemiology 1997;13(1):55-59. Not sensitivity

or specificity of an identified test

Bonamico M, Bottaro G, Pasquino A M et al. Celiac 

disease and turner syndrome. Journal of Pediatric 

Gastroenterology and Nutrition 1998;26(5):496-499. Not

sensitivity or specificity of an identified test 

Bonamico M, Culasso F, Pitzalis G et al. Beta 2-

microglobulin levels in celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 1990;11(3):330-336. Not

sensitivity or specificity of an identified test 

Bonamico M, Mariani P, Danesi H M et al. Prevalence and 

clinical picture of celiac disease in italian down syndrome 

patients: a multicenter study. Journal of Pediatric 

Gastroenterology and Nutrition 2001;33(2):139-143. Not

sensitivity or specificity of an identified test 

Bonamico M, Mariani P, Mazzilli M C et al. Frequency and 

clinical pattern of celiac disease among siblings of celiac 

children. Journal of Pediatric Gastroenterology and 

Nutrition 1996;23(2):159-163. Not sensitivity or specificity

of an identified test 

Bonamico M, Mazzilli M C, Morellini M et al. Expression 

of class II MHC antigens in the intestinal epithelium of 

pediatric celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 1989;9(3):269-275. Not

sensitivity or specificity of an identified test 

Bonamico M, Morellini M, Mariani P et al. HLA antigens 

and antigliadin antibodies in coeliac disease. Disease 

Markers 1991;9(6):313-317. Improper control group 

Bonamico M, Rasore-Quartino A, Mariani P et al. Down 

syndrome and coeliac disease: Usefulness of antigliadin

and antiendomysium antibodies. Acta Paediatr Int J 

Paediatr 1996;85(12):1503-1505. Not sensitivity or

specificity of an identified test

Bonamico M, Scire G, Mariani P et al. Short stature as the

primary manifestation of monosymptomatic celiac disease. 

Journal of Pediatric Gastroenterology and Nutrition 

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1992;14(1):12-16. Not sensitivity or specificity of an 

identified test 

Bonamico Margherita, Pasquino Anna M, Mariani Paolo et 

al. Prevalence and clinical picture of celiac disease in 

Turner syndrome. Journal of Clinical Endocrinology and 

Metabolism 2002;87(12):5495-5498. Not sensitivity or

specificity of an identified test

Bonelli Raphael M, Aschoff Andreas, Jirikowski Gustaf. 

Cerebrospinal fluid tissue transglutaminase in vascular

dementia. Journal of the Neurological Sciences 2002;203-

204207-209. Not sensitivity or specificity of an identified 

test 

Bonelli Raphael M, Aschoff Andreas, Niederwieser Gerald 

et al. Cerebrospinal fluid tissue transglutaminase as a 

biochemical marker for Alzheimer's disease. Neurobiology

of Disease 2002;11(1):106-110. Not sensitivity or

specificity of an identified test

Bonini S, Ruffilli A. Genetics of food allergy. Environ 

Toxicol Pharmacol 1997;4(1-2):71-78. Not sensitivity or 

specificity of an identified test

Boniotto M, Braida L, Ventura A et al. Promoter 

polymorphisms of the CD14 gene in Italian patients with 

coeliac disease. Journal of Medical Genetics 

2003;40(9):E108Not sensitivity or specificity of an 

identified test 

Boniotto Michele, Braida Laura, Spano Andrea et al. 

Variant mannose-binding lectin alleles are associated with 

celiac disease. Immunogenetics 2002;54(8):596-598. Not 

sensitivity or specificity of an identified test 

Bontems P, Deprettere A, Cadranel S et al. The coeliac 

iceberg: A consensus in paediatrics. Acta Gastro-Enterol

Belg 2000;63(2):157-162. Not sensitivity or specificity of

an identified test

Bonvicini F, Zoli G, Maltarello M C et al. Clinical 

applications of scanning electron microscopy in 

gastrointestinal diseases. Scanning Electron Microscopy

1985;(Pt 3):1279-1294. Not sensitivity or specificity of an

identified test 

Book L, Hart A, Black J et al. Prevalence and clinical 

characteristics of celiac disease in Downs syndrome in a 

US study. American Journal of Medical Genetics 

2001;98(1):70-74. Improper control group 

Book Linda S. Diagnosing celiac disease in 2002: who, 

why, and how?. Pediatrics 2002;109(5):952-954. Not 

sensitivity or specificity of an identified test 

Book Linda, Zone John J, Neuhausen Susan L. Prevalence 

of celiac disease among relatives of sib pairs with celiac 

disease in U.S. families. American Journal of 

Gastroenterology 2003;98(2):377-381. Not sensitivity or 

specificity of an identified test

Booth I W. The nutritional consequences of gastrointestinal

disease in adolescence. Acta Paediatr Scand Suppl 

1991;80(373):91-102. Not sensitivity or specificity of an

identified test 

Borch K, Grodzinsky E, Petersson F et al. Prevalence of

coeliac disease and relations to Helicobacter pylori

infection and duodenitis in a Swedish adult population

sample: A histomorphological and serological survey. 

Inflammopharmacology 2000;8(4):341-350. Not sensitivity

or specificity of an identified test

Borg M, Phillips A D, Smith M W et al. Enteric disease in 

early childhood inhibits microvillus expression by potential 

stem cells. Clinical Science (London, England - 1979) 

1993;84(4):377-379. Not sensitivity or specificity of an 

identified test 

Borner H, Osman A A, Meergans T et al. Isolation of 

antigens recognized by coeliac disease autoantibodies and

their use in enzyme immunoassay of endomysium and 

reticulin antibody-positive human sera. Clinical and 

Experimental Immunology 1996;106(2):344-350. Not 

sensitivity or specificity of an identified test 

Borth W, Chang V, Bishop P et al. Lipoprotein (a) is a 

substrate for factor XIIIa and tissue transglutaminase. J

Biol Chem 1991;266(27):18149-18153. Not sensitivity or 

specificity of an identified test

Bossart R, Henry K, Booth C C et al. Subepithelial 

collagen in intestinal malabsorption. Gut 1975;16(1):18-22. 

Not sensitivity or specificity of an identified test

Bossart R, Henry K, Doe W F et al. Proceedings:

Collagenous basement membrane thickening in jejunal 

biopsies from patients with adult coeliac disease. Gut 

1974;15(4):338Not sensitivity or specificity of an identified 

test 

Bottaro G, Failla P, Rotolo N et al. Changes in coeliac 

disease behaviour over the years. Acta Paediatrica (Oslo, 

Norway - 1992) 1993;82(6-7):566-568. Not sensitivity or 

specificity of an identified test

Boudraa G, Hachelaf W, Benbouabdellah M et al. 

Prevalence of coeliac disease in diabetic children and their

first- degree relatives in west Algeria: screening with 

serological markers. Acta Paediatrica (Oslo, Norway - 

1992).Supplement 1996;41258-60. Improper control group 

Bouguerra F, Babron M C, Eliaou J F et al. Synergistic 

effect of two HLA heterodimers in the susceptibility to

celiac disease in Tunisia. Genetic Epidemiology

1997;14(4):413-422. Improper control group 

Bouguerra F, Dugoujon J M, Babron M C et al. 

Susceptibility to coeliac disease in Tunisian children and

GM immunoglobulin allotypes. European Journal of 

Immunogenetics - Official Journal of the British Society for 

Histocompatibility and Immunogenetics 1999;26(4):293-

297. Not sensitivity or specificity of an identified test 

A-338
Bouissou F, Meissner I, Konrad M et al. Clinical

implications from studies of HLA antigens in idiopathic

nephrotic syndrome in children. Clin Nephrol

1995;44(5):279-283. Not sensitivity or specificity of an 

identified test 

Bourgain C, Genin E, Holopainen P et al. Use of closely

related affected individuals for the genetic study of

complex diseases in founder populations. American Journal 

of Human Genetics 2001;68(1):154-159. Not sensitivity or

specificity of an identified test

Bourke M, O'Donovan M, Stevens F M et al. Alpha 1-

antitrypsin phenotypes in coeliac patients and a control 

population in the west of Ireland. Irish Journal of Medical 

Science 1993;162(5):171-172. Not sensitivity or specificity

of an identified test 

Bourne J T, Kumar P, Huskisson E C. Arthritis and coeliac

disease. Ann Rheum Dis 1985;44(9):592-598. Not 

sensitivity or specificity of an identified test 

Bowness J M, Tarr A H. Lipoprotein binding of crosslinked 

type III collagen aminopropeptide and fractions of its 

antigen in blood. Biochemical and Biophysical Research

Communications 1990;170(2):519-525. Not sensitivity or

specificity of an identified test

Bowness J M, Tarr A H, Wiebe R I. Transglutaminasecatalysed cross-linking: a potential mechanism for the

interaction of fibrinogen, low density lipoprotein and 

arterial type III procollagen. Thromb Res 1989;54(4):357-

367. Not sensitivity or specificity of an identified test 

Bowron A, Moorghen M, Morgan J E et al. Cost-effective 

strategy for the serological investigation of coeliac disease.

Ann Clin Biochem 2000;37(4):467-470. Improper control 

group 

Boy M F, La Nasa G, Balestrieri A et al. Distribution of 

HLA-DPB1, -DQB1 -DQA1 alleles among Sardinian celiac 

patients. Disease Markers 1995;12(3):199-204. Improper 

control group 

Boyce S, Michel S, Reichert U et al. Reconstructed skin 

from cultured human keratinocytes and fibroblasts on a 

collagen-glycosaminoglycan biopolymer substrate. Skin 

Pharmacology - the Official Journal of the Skin 

Pharmacology Society 1990;3(2):136-143. Not sensitivity

or specificity of an identified test

Boyd S, Collins B J, Bell P M et al. Clinical presentation of 

coeliac disease in adult gastroenterological practice. Ulster

Medical Journal 1985;54(2):140-147. Not sensitivity or

specificity of an identified test

Boyton R J, Lohmann T, Londei M et al. Glutamic acid

decarboxylase T lymphocyte responses associated with 

susceptibility or resistance to type I diabetes: Analysis in 

disease discordant human twins, non-obese diabetic mice 

and HLA-DQ transgenic mice. Int Immunol 

1998;10(12):1765-1776. Not sensitivity or specificity of an 

identified test 

Brack M, Schroeder C, Fooke M et al. IgM/IgA 

nephropathy in callitrichids: Antigen studies. Nephron 

1999;82(3):221-231. Not sensitivity or specificity of an 

identified test 

Brackin M N, Lewis R E, Brackin B T et al. Progression of 

HIV infection is asssciated with HLA-DQ antigens in 

Caucasians and African Americans. Pathobiology 

1995;63(1):22-41. Not sensitivity or specificity of an 

identified test 

Bradgate M G, Redman C W, Rollason T P et al. Binding

of anti-EMA, AGF 4:48 and the lectin UEA-1 to human 

ovarian carcinomas: histological and clinical correlations. 

British Journal of Obstetrics and Gynaecology

1989;96(7):854-860. Not sensitivity or specificity of an 

identified test 

Bradway S D, Bergey E J, Scannapieco F A et al.

Formation of salivary-mucosal pellicle: The role of 

transglutaminase. Biochem J 1992;284(2):557-564. Not 

sensitivity or specificity of an identified test 

Braegger C P, MacDonald T T. The immunologic basis for 

celiac disease and related disorders. Seminars in

Gastrointestinal Disease 1996;7(3):124-133. Not sensitivity

or specificity of an identified test

Bramble M G, Watson A J, Scott J et al. Clinical, 

biochemical and morphological responses of patients with

villous atrophy to oral betamethasone valerate and 

clobetasone butyrate. Digestion 1981;22(6):281-288. Not 

sensitivity or specificity of an identified test 

Bramble M G, Zucoloto S, Wright N A et al. Acute gluten

challenge in treated adult coeliac disease: a morphometric 

and enzymatic study. Gut 1985;26(2):169-174. Not 

sensitivity or specificity of an identified test 

Brandborg L L. Histologic diagnosis of diseases of 

malabsorption. American Journal of Medicine 

1979;67(6):999-1006. Not sensitivity or specificity of an

identified test 

Brandborg L L, Goldberg S B, Breidenbach W C. Human 

coccidiosis--a possible cause of malabsorption. New 

England Journal of Medicine 1970;283(24):1306-1313. Not 

sensitivity or specificity of an identified test 

Brandt L J, Locke G R, Olden K et al. An evidence-based 

approach to the management of irritable bowel syndrome in 

North America. American Journal of Gastroenterology

2002;97(11 SUPPL.):S1-S26. Not sensitivity or specificity

of an identified test 

Brandtzaeg P. Immunologic basis for celiac disease, 

inflammatory bowel disease, and type B chronic gastritis. 

Curr Opin Gastroenterol 1991;7(3):450-462. Not sensitivity

or specificity of an identified test

A-339
Brandtzaeg P, Valnes K, Scott H et al. The human

gastrointestinal secretory immune system in health and 

disease. Scandinavian Journal of 

Gastroenterology.Supplement 1985;11417-38. Not 

sensitivity or specificity of an identified test 

Branski D, Troncone R. Celiac disease: A reappraisal.

Journal of Pediatrics 1998;133(2):181-187. Not sensitivity

or specificity of an identified test

Branski D, Faber J, Shiner M. A comparison of smallintestinal mucosal biopsies in children obtained by blind

suction capsule with those obtained by endoscopy. Journal 

of Pediatric Gastroenterology and Nutrition 

1996;22(2):194-196. Not sensitivity or specificity of an 

identified test 

Branski D, Faber J, Freier S et al. Histologic evaluation of 

endoscopic versus suction biopsies of small intestinal 

mucosae in children with and without celiac disease. 

Journal of Pediatric Gastroenterology and Nutrition 

1998;27(1):6-11. Not sensitivity or specificity of an 

identified test 

Brautbar C, Freier S, Ashkenazi A et al. Histocompatibility

determinants in Israeli Jewish patients with coeliac disease:

population and family study. Tissue Antigens 

1981;17(3):313-322. Not sensitivity or specificity of an 

identified test 

Brautbar C, Zlotogora J, Laufer N et al. Do identical HLADR3 genes convey susceptibility to celiac disease and 

insulin dependent diabetes mellitus?. Tissue Antigens 

1984;23(1):58-60. Not sensitivity or specificity of an 

identified test 

Breen E G, Coughlan G, Connolly C E et al. Coeliac 

proctitis. Scandinavian Journal of Gastroenterology

1987;22(4):471-477. Not sensitivity or specificity of an 

identified test 

Brett P M, Yiannakou J Y, Morris M A et al. A pedigreebased linkage study of coeliac disease: failure to replicate 

previous positive findings. Annals of Human Genetics 

1998;62(Pt 1):25-32. Not sensitivity or specificity of an 

identified test 

Brett P M, Yiannakou J Y, Morris M A et al. Common 

HLA alleles, rather than rare mutants, confer susceptibility

to coeliac disease. Annals of Human Genetics 1999;63(Pt 

3):217-225. Unable to extract data 

Brewster D, Pakorny C S. Investigating the child with 

malnutrition. Med Today 2001;2(7):88-93. Not sensitivity

or specificity of an identified test

Brocchi E, Corazza G R, Caletti G et al. Endoscopic 

demonstration of loss of duodenal folds in the diagnosis of 

celiac diasease. New Engl J Med 1988;319(12):741-744. 

Not sensitivity or specificity of an identified test

Brocchi E, Tomassetti P, Misitano B et al. Endoscopic 

markers in adult coeliac disease. Digestive and Liver 

Disease - Official Journal of the Italian Society of 

Gastroenterology and the Italian Association for the Study

of the Liver 2002;34(3):177-182. Not sensitivity or 

specificity of an identified test

Broekaert D, Leigh I M, Lane E B et al. An

immunohistochemical and histochemical study of

cytokeratin, involucrin and transglutaminase in seborrhoeic

keratosis. Archives of Dermatological Research

1993;285(8):482-490. Not sensitivity or specificity of an

identified test 

Broekaert D, Pattin C, Coucke P et al. Keratinization of 

middle ear cholesteatomas. I. A histochemical study of 

epidermal transglutaminase. European Archives of OtoRhino-Laryngology - Official Journal of the European 

Federation of Oto-Rhino-Laryngological Societies (Eufos) 

- Affiliated With the German Society for Oto-RhinoLaryngolog 1990;247(5):312-317. Not sensitivity or 

specificity of an identified test

Brooks A P, Harrington C I. Acquired ichthyosis and toxic 

epidermal necrolysis and mesenteric reticulum cell sarcoma

and malabsorption. Br Med J 1977;2(6089):739-740. Not 

sensitivity or specificity of an identified test 

Brooks F P, Powell K C, Cerda J J. Variable clinical course 

of adult celiac disease. Archives of Internal Medicine

1966;117(6):789-794. Not sensitivity or specificity of an

identified test 

Brow J R, Parker F, Weinstein W M et al. The small 

intestinal mucosa in dermatitis herpetiformis. I. Severity

and distribution of the small intestinal lesion and associated 

malabsorption. Gastroenterology 1971;60(3):355-361. Not 

sensitivity or specificity of an identified test 

Brown M R, Lillibridge C B. When to think of celiac 

disease: the classical features of gluten sensitive 

enteropathy are absent. Clinical Pediatrics 1975;14(1):76-

82. Not sensitivity or specificity of an identified test 

Brucato A, Franceschini F, Gasparini M et al. Isolated 

congenital complete heart block: Longterm outcome of 

mothers, maternal antibody specificity and immunogenetic 

background. J Rheumatol 1995;22(3):533-540. Not 

sensitivity or specificity of an identified test 

Bruce G, Woodley J F, Swan C H J. Breakdown of gliadin 

peptides by intestinal brush borders from coeliac patients. 

Gut 1984;25(9):919-924. Not sensitivity or specificity of an 

identified test 

Bruce S E, Bjarnason I, Peters T J. Human jejunal 

transglutaminase: demonstration of activity, enzyme 

kinetics and substrate specificity with special relation to

gliadin and coeliac disease. Clinical Science (London, 

England - 1979) 1985;68(5):573-579. Not sensitivity or

specificity of an identified test

A-340
Bruges-Armas J, Martinez-Laso J, Martins B et al. HLA in 

the Azores Archipelago: Possible presence of Mongoloid 

genes. Tissue Antigens 1999;54(4):349-359. Not sensitivity

or specificity of an identified test

Bruno C J, Batts K P, Ahlquist D A. Evidence against flat 

dysplasia as a regional field defect in small bowel 

adenocarcinoma associated with celiac sprue. Mayo Clinic

Proceedings 1997;72(4):320-322. Not sensitivity or 

specificity of an identified test

Brusco G, Di Stefano M, Corazza G R. Increased red cell 

distribution width and coeliac disease. Digestive and Liver 

Disease - Official Journal of the Italian Society of 

Gastroenterology and the Italian Association for the Study

of the Liver 2000;32(2):128-130. Not sensitivity or 

specificity of an identified test

Brusco G, Izzi L, Corazza G R. Tissue transglutaminase

antibodies for coeliac disease screening. Italian Journal of

Gastroenterology and Hepatology 1998;30(5):496-497. 

Improper control group 

Brusco G, Muzi P, Ciccocioppo R et al. Transglutaminase 

and coeliac disease: endomysial reactivity and small bowel 

expression. Clinical and Experimental Immunology

1999;118(3):371-375. Not sensitivity or specificity of an

identified test 

Bryant D A, Mintz E D, Puhr N D et al. Colonic epithelial 

lymphocytosis associated with an epidemic of chronic 

diarrhea. American Journal of Surgical Pathology 

1996;20(9):1102-1109. Not sensitivity or specificity of an

identified test 

Brzechwa-Ajdukiewicz A, McCarthy C F, Austad W et al. 

Carcinoma, villous atrophy, and steatorrhoea. Gut

1966;7(6):572-577. Not sensitivity or specificity of an 

identified test 

Buchan A M, Grant S, Brown J C et al. A quantitative 

study of enteric endocrine cells in celiac sprue. Journal of

Pediatric Gastroenterology and Nutrition 1984;3(5):665-

671. Not sensitivity or specificity of an identified test 

Bucht A, Soderstrom K, Esin S et al. Analysis of gamma 

delta V region usage in normal and diseased human 

intestinal biopsies and peripheral blood by polymerase 

chain reaction (PCR) and flow cytometry. Clinical and 

Experimental Immunology 1995;99(1):57-64. Not 

sensitivity or specificity of an identified test 

Buckley D B, English J, Molloy W et al. Dermatitis 

herpetiformis: a review of 119 cases. Clinical and

Experimental Dermatology 1983;8(5):477-487. Not 

sensitivity or specificity of an identified test 

Budzynski A Z. Fibrinogen and fibrin: biochemistry and 

pathophysiology. Critical Reviews in 

Oncology/Hematology 1986;6(2):97-146. Not sensitivity or 

specificity of an identified test

Bugawan T L, Angelini G, Larrick J et al. A combination

of a particular HLA-DP beta allele and an HLA-DQ 

heterodimer confers susceptibility to coeliac disease. 

Nature 1989;339(6224):470-473. Not sensitivity or

specificity of an identified test

Bugawan T L, Horn G T, Long C M et al. Analysis of 

HLA-DP allelic sequence polymorphism using the in vitro

enzymatic DNA amplification of DP-alpha and DP-beta 

loci. J Immunol 1988;141(11):4024-4030. Not sensitivity

or specificity of an identified test

Bullen A W, Hall R, Gowland G et al. Hyposplenism, adult 

coeliac disease, and autoimmunity. Gut 1981;22(1):28-33. 

Not sensitivity or specificity of an identified test

Bunce M, Taylor C J, Welsh K I. Rapid HLA-DQB typing

by eight polymerase chain reaction amplifications with 

sequence-specific primers (PCR-SSP). Human 

Immunology 1993;37(4):201-206. Not sensitivity or 

specificity of an identified test

Buommino E, Morelli F, Metafora S et al. Porin from 

Pseudomonas aeruginosa induces apoptosis in an epithelial 

cell line derived from rat seminal vesicles. Infection and 

Immunity 1999;67(9):4794-4800. Not sensitivity or 

specificity of an identified test

Burgin-Wolff A, Berger R, Gaze H et al. IgG, IgA and IgE 

gliadin antibody determinations as screening test for 

untreated coeliac disease in children, a multicentre study. 

European Journal of Pediatrics 1989;148(6):496-502. 

Improper control group 

Burgin-Wolff A, Bertele R M, Berger R et al. A reliable 

screening test for childhood celiac disease: fluorescent 

immunosorbent test for gliadin antibodies. A prospective 

multicenter study. Journal of Pediatrics 1983;102(5):655-

660. Serology <1990 

Burgin-Wolff A, Dahlbom I, Hadziselimovic F et al.

Antibodies against human tissue transglutaminase and 

endomysium in diagnosing and monitoring coeliac disease. 

Scandinavian Journal of Gastroenterology 2002;37(6):685-

691. Improper control group 

Burgin-Wolff A, Gaze H, Hadziselimovic F et al. 

Antigliadin and antiendomysium antibody determination

for coeliac disease. Archives of Disease in Childhood 

1991;66(8):941-947. Improper control group 

Burgin-Wolff A, Hernandez R, Just M et al. 

Immunofluorescent antibodies against gliadin: a screening 

test for coeliac disease. Helvetica Paediatrica Acta

1976;31(4-5):375-380. Serology <1990 

Burhol P G, Myren J. Dehydrogenase activity and mucosal 

measurements in jejunal biopsies from patients with 

gastrointestinal diseases. Scandinavian Journal of

Gastroenterology 1966;1(2):142-148. Not sensitivity or

specificity of an identified test

A-341
Burk K, Bosch S, Muller C A et al. Sporadic cerebellar 

ataxia associated with gluten sensitivity. Brain 2001;A 

Journal of Neurology; 124(Pt 5):1013-1019. Not sensitivity

or specificity of an identified test

Burke V, Colebatch J H, Anderson C M et al. Association 

of pancreatic insufficiency and chronic neutropenia in 

childhood. Archives of Disease in Childhood

1967;42(222):147-157. Not sensitivity or specificity of an

identified test 

Burnie J. A possible immunological mechanism for the 

pathogenesis of dermatitis herpetiformis with reference to

coeliac disease. Clinical and Experimental Dermatology 

1980;5(4):451-463. Not sensitivity or specificity of an 

identified test 

Burrows R, Leiva L, Burgueno M et al. Bone mineral

density (BMD) in children with celiac disease (CD): Its

relation to puberty and calcium intake. Nutr Res 

1999;19(4):493-499. Not sensitivity or specificity of an 

identified test 

Busch H J, Jirikowski G F, Aschoff A P et al. Actin in 

semithin sections of myocardial biopsies as a tool to

visualize myofibrillary degradation in humans. Cellular and 

Molecular Biology (Noisy-Le-Grand, France) 2001;47 

Online Pubol89-ol94. Not sensitivity or specificity of an

identified test 

Bushara K O, Goebel S U, Shill H et al. Gluten sensitivity

in sporadic and hereditary cerebellar ataxia. Annals of 

Neurology 2001;49(4):540-543. Not sensitivity or

specificity of an identified test

Buts J P, Morin C L, Roy C C et al. One-hour blood xylose 

test: a reliable index of small bowel function. Journal of

Pediatrics 1978;92(5):729-733. Not sensitivity or

specificity of an identified test

Butterworth Jeffrey R, Cooper Brian T, Rosenberg William

M C et al. The role of hemochromatosis susceptibility gene

mutations in protecting against iron deficiency in celiac

disease. Gastroenterology 2002;123(2):444-449. Not 

sensitivity or specificity of an identified test 

Buxman M M. The role of enzymatic coupling of drugs to 

proteins in induction of drug specific antibodies. J Invest 

Dermatol 1979;73(3):256-258. Not sensitivity or specificity

of an identified test 

Buxman M M, Wuepper K D. Keratin cross-linking and

epidermal transglutaminase. A review with observations on

the histochemical and immunochemical localization of the 

enzyme. Journal of Investigative Dermatology

1975;65(1):107-112. Not sensitivity or specificity of an 

identified test 

Buyse I, Sandkuyl L A, Zamani Ghabanbasani M et al. 

Association of particular HLA class II alleles, haplotypes 

and genotypes with susceptibility to IDDM in the Belgian

population. Diabetologia 1994;37(8):808-817. Not 

sensitivity or specificity of an identified test 

Cacciamani Tiziana, Virgili Samantha, Centurelli Matteo et 

al. Specific methylation of the CpG-rich domains in the

promoter of the human tissue transglutaminase gene. Gene 

2002;297(1-2):103-112. Not sensitivity or specificity of an 

identified test 

Cacciari E, Salardi S, Lazzari R et al. Short stature and

celiac disease: a relationship to consider even in patients

with no gastrointestinal tract symptoms. Journal of

Pediatrics 1983;103(5):708-711. Not sensitivity or

specificity of an identified test

Cacciari E, Salardi S, Volta U et al. Antigliadin antibodies

in coeliac children with short stature. Lancet 1985;2(8469-

8470):1434Not sensitivity or specificity of an identified test 

Cacciari E, Salardi S, Volta U et al. Can antigliadin 

antibody detect symptomless coeliac disease in children 

with short stature?. Lancet 1985;1(8444):1469-1471. 

Serology <1990

Caffarelli C, Romanini E, Caruana P et al. Clinical food

hypersensitivity: the relevance of duodenal 

immunoglobulin E-positive cells. Pediatric Research 

1998;44(4):485-490. Not sensitivity or specificity of an 

identified test 

Caffrey C, Hitman G A, Niven M J et al. HLA-DP and 

coeliac disease: family and population studies. Gut 

1990;31(6):663-667. Not sensitivity or specificity of an 

identified test 

Calabuig M, Torregosa R, Polo P et al. Serological markers

and celiac disease: a new diagnostic approach?. Journal of

Pediatric Gastroenterology and Nutrition 1990;10(4):435-

442. Improper control group 

Calam J, Ellis A, Dockray G J. Identification and 

measurement of molecular variants of cholecystokinin in

duodenal mucosa and plasma. Diminished concentrations

in patients with celiac disease. Journal of Clinical

Investigation 1982;69(1):218-225. Not sensitivity or 

specificity of an identified test

Calero P, Ribes-Koninckx C, Albiach V et al. IgA 

antigliadin antibodies as a screening method for nonovert 

celiac disease in children with insulin-dependent diabetes

mellitus. Journal of Pediatric Gastroenterology and 

Nutrition 1996;23(1):29-33. Not sensitivity or specificity of 

an identified test

Camarero C, Eiras P, Asensio A et al. Intraepithelial

lymphocytes and coeliac disease: permanent changes in 

CD3-/CD7+ and T cell receptor gammadelta subsets 

studied by flow cytometry. Acta Paediatrica (Oslo, Norway

- 1992) 2000;89(3):285-290. Not sensitivity or specificity

of an identified test 

Cameron E A, Stewart J A, West K P et al. Coeliac disease

presenting with intraperitoneal haemorrhage. European 

A-342
Journal of Gastroenterology & Hepatology 1998;10(7):619-

620. Not sensitivity or specificity of an identified test 

Cameron P U, Mallal S A, French M A H et al. Major 

histocompatibility complex genes influence the outcome of

HIV infection: Ancestral haplotypes with C4 null alleles 

explain diverse HLA associations. Hum Immunol

1990;29(4):282-295. Not sensitivity or specificity of an 

identified test 

Campbell C B, Roberts R K, Cowen A E. The changing 

clinical presentation of coeliac disease in adults. Medical 

Journal of Australia 1977;1(4):89-93. Not sensitivity or

specificity of an identified test

Campbell R D, Dodds A W, Porter R R. The binding of 

human complement component C4 to antibody-antigen

aggregates. Biochemical Journal 1980;189(1):67-80. Not 

sensitivity or specificity of an identified test 

Candi E, Paradisi A, Terrinoni A et al. Role of

transglutaminase 5 in epidermis. Minerva Biotecnol 

2002;14(2):155-158. Not sensitivity or specificity of an 

identified test 

Candi Eleonora, Oddi Sergio, Paradisi Andrea et al. 

Expression of transglutaminase 5 in normal and pathologic 

human epidermis. Journal of Investigative Dermatology

2002;119(3):670-677. Not sensitivity or specificity of an

identified test 

Caraglia M, Marra M, Giuberti G et al. The role of

eukaryotic initiation factor 5A in the control of cell 

proliferation and apoptosis. Amino Acids 2001;20(2):91-

104. Not sensitivity or specificity of an identified test 

Caraglia Michele, Marra Monica, Giuberti Gaia et al. 

Theophylline-induced apoptosis is paralleled by protein

kinase A-dependent tissue transglutaminase activation in

cancer cells. Journal of Biochemistry 2002;132(1):45-52. 

Not sensitivity or specificity of an identified test

Carbonara A O, DeMarchi M, van Loghem E et al. Gm 

markers in celiac disease. Human Immunology

1983;6(2):91-95. Not sensitivity or specificity of an 

identified test 

Carbonnel F, D'Almagne H, Lavergne A et al. The 

clinicopathological features of extensive small intestinal

CD4 T cell infiltration. Gut 1999;45(5):662-667. Not 

sensitivity or specificity of an identified test 

Carbonnel F, Grollet-Bioul L, Brouet J C et al. Are 

complicated forms of celiac disease cryptic T-cell

lymphomas?. Blood 1998;92(10):3879-3886. Not 

sensitivity or specificity of an identified test 

Carcassi C, Cottoni F, Floris L et al. HLA haplotypes and 

class II molecular alleles in Sardinian and Italian patients

with pemphigus vulgaris. Tissue Antigens 1996;48(6):662-

667. Not sensitivity or specificity of an identified test 

Cardaba B, Cortegano I, Flondo F et al. Genetic restrictions 

in olive pollen allergy. J Allergy Clin Immunol 2000;105(2 

I):292-298. Not sensitivity or specificity of an identified

test 

Cardaba B, de Pablo R, Vilches C et al. Allergy to olive 

pollen: T-cell response from olive allergic patients is 

restricted by DR7-DQ2 antigens. Clin Exp Allergy 

1996;26(3):316-322. Not sensitivity or specificity of an 

identified test 

Cardaba B, Ezendam J, Gallardo S et al. DR2 antigens are

associated with severity of disease in toxic oil syndrome

(TOS). Tissue Antigens 2000;55(2):110-117. Not 

sensitivity or specificity of an identified test 

Cardaba B, Vilches C, Martin E et al. DR7 and DQ2 are 

positively associated with immunoglobulin-E response to 

the main antigen of olive pollen (Ole e I) in allergic 

patients. Hum Immunol 1993;38(4):293-299. Not 

sensitivity or specificity of an identified test 

Cariello L, Velasco P T, Wilson J et al. Probing the 

transglutaminase-mediated, posttranslational modification 

of proteins during development. Biochemistry

1990;29(21):5103-5108. Not sensitivity or specificity of an 

identified test 

Carlsson A K, Axelsson I E, Borulf S K et al. Serological 

screening for celiac disease in healthy 2.5-year-old children

in Sweden. Pediatrics 2001;107(1):42-45. Not sensitivity or 

specificity of an identified test

Carlsson A K, Axelsson I E, Borulf S K et al. Prevalence of 

IgA-antiendomysium and IgA-antigliadin autoantibodies at 

diagnosis of insulin-dependent diabetes mellitus in Swedish 

children and adolescents. Pediatrics 1999;103(6 Pt 1):1248-

1252. Not sensitivity or specificity of an identified test 

Carlsson A, Axelsson I, Borulf S et al. Prevalence of IgAantigliadin antibodies and IgA-antiendomysium antibodies 

related to celiac disease in children with Down syndrome. 

Pediatrics 1998;101(2):272-275. Not sensitivity or

specificity of an identified test

Carlsson Annelie K, Lindberg Bengt A, Bredberg Anders C 

A et al. Enterovirus infection during pregnancy is not a risk 

factor for celiac disease in the offspring. Journal of

Pediatric Gastroenterology and Nutrition 2002;35(5):649-

652. Not sensitivity or specificity of an identified test 

Carnicer J, Farre C, Varea V et al. Prevalence of coeliac 

disease in Down Syndrome. European Journal of

Gastroenterology & Hepatology 2001;13(3):263-267. Not 

sensitivity or specificity of an identified test 

Carpenter C B. Autoimmunity and HLA. Journal of 

Clinical Immunology 1982;2(3):157-165. Not sensitivity or

specificity of an identified test

Carpino F, Ceccamea A, Magliocca F M et al. Scanning 

electron microscopy of jejunal biopsies in patients with 

A-343
untreated and treated coeliac disease. Acta Paediatrica 

Scandinavica 1985;74(5):775-781. Unable to extract data 

Carr K E, Toner P G. Surface studies of acute radiation

injury in the mouse intestine. Virchows Archiv.B- Cell

Pathology 1972;11(3):201-210. Not sensitivity or

specificity of an identified test

Carroccio A, Cavataio F, Iacono G et al. IgA 

antiendomysial antibodies on the umbilical cord in

diagnosing celiac disease. Sensitivity, specificity, and 

comparative evaluation with the traditional kit.

Scandinavian Journal of Gastroenterology 1996;31(8):759-

763. Improper control group 

Carroccio A, Custro N, Montalto G et al. Evidence of 

transient IgA anti-endomysial antibody positivity in a 

patient with Graves' disease. Digestion 1999;60(1):86-88. 

Not sensitivity or specificity of an identified test

Carroccio A, Giannitrapani L, Soresi M et al. Guinea pig

transglutaminase immunolinked assay does not predict 

coeliac disease in patients with chronic liver disease. Gut

2001;49(4):506-511. Not sensitivity or specificity of an 

identified test 

Carroccio A, Iacono G, Montalto G et al. Pancreatic 

insufficiency in celiac disease is not dependent on

nutritional status. Digestive Diseases and Sciences

1994;39(10):2235-2242. Not sensitivity or specificity of an 

identified test 

Carroccio A, Iannitto E, Cavataio F et al. Sideropenic 

anemia and celiac disease: one study, two points of view. 

Digestive Diseases and Sciences 1998;43(3):673-678. Not 

sensitivity or specificity of an identified test 

Carroccio A, Iovanna J L, Iacono G et al. Pancreatitisassociated protein in patients with celiac disease: serum

levels and immunocytochemical localization in small 

intestine. Digestion 1997;58(2):98-103. Not sensitivity or 

specificity of an identified test

Carroccio Antonio, Iannitto Emilio, Di Prima et al. 

Screening for celiac disease in non-Hodgkin's lymphoma 

patients: a serum anti-transglutaminase-based approach.

Digestive Diseases and Sciences 2003;48(8):1530-1536. 

Not sensitivity or specificity of an identified test

Carswell F, Ferguson A. Food antibodies in serum--a 

screening test for coeliac disease. Archives of Disease in 

Childhood 1972;47(254):594-596. Not sensitivity or 

specificity of an identified test

Carswell F, Ferguson A. Plasma food antibodies during 

withdrawal and reintroduction of dietary gluten in coeliac

disease. Arch Dis Child 1973;48(8):583-586. Not 

sensitivity or specificity of an identified test 

Carswell F, Gibson A A, McAllister T A. Giardiasis and 

coeliac disease. Archives of Disease in Childhood

1973;48(6):414-418. Not sensitivity or specificity of an 

identified test 

Carter M J, Willcocks M M, Mitchison H C et al. Is a 

persistent adenovirus infection involved in coeliac disease?. 

Gut 1989;30(11):1563-1567. Not sensitivity or specificity

of an identified test 

Caruso C, Candore G, Modica M A et al. Immunoglobulin

heavy chain allotypes in a sample of Sicilian patients with

celiac disease. Experimental and Clinical Immunogenetics 

1991;8(1):1-5. Not sensitivity or specificity of an identified

test 

Casadio R, Polverini E, Mariani P et al. The structural basis

for the regulation of tissue transglutaminase by calcium

ions. European Journal of Biochemistry / Febs 

1999;262(3):672-679. Not sensitivity or specificity of an

identified test 

Case April, Stein Ross L. Kinetic analysis of the action of

tissue transglutaminase on peptide and protein substrates. 

Biochemistry 2003;42(31):9466-9481. Not sensitivity or

specificity of an identified test

Casellas F, de Torres I, Malagelada J R. Improved 

screening for intestinal villous atrophy by D-xylose breath 

test. Digestive Diseases and Sciences 2000;45(1):18-22. 

Not sensitivity or specificity of an identified test

Casellas F, de Torres I, Malagelada J-R. Follow-up of 

celiac disease with D-xylose breath test. Digestive Diseases

and Sciences 1996;41(10):2106-2111. Not sensitivity or

specificity of an identified test

Casellas F, Sardi J, de Torres I et al. Hydrogen breath test

with D-xylose for celiac disease screening is as useful in 

the elderly as in other age groups. Digestive Diseases and

Sciences 2001;46(10):2201-2205. Not sensitivity or 

specificity of an identified test

Caspary W F, Winckler K, Lankisch P G et al. Influence of

exocrine and endocrine pancreatic function on intestinal

brush border enaymatic activities. Gut 1975;16(2):89-92. 

Not sensitivity or specificity of an identified test

Cassiman J J, van der, Schueren B et al. Qualitative and

quantitative differences in spreading of human fibroblasts 

on various protein coats. Modulation by treatment of the 

cells with amines. Journal of Cell Science 1982;5479-95. 

Not sensitivity or specificity of an identified test

Castellino F, Scaglione N, Grosso S B et al. A novel 

method for detecting IgA endomysial antibodies by using 

human umbilical vein endothelial cells. European Journal 

of Gastroenterology & Hepatology 2000;12(1):45-49. 

Improper control group 

Castro M, Crino A, Papadatou B et al. Down Syndrome 

and celiac disease: the prevalence of high IgA-antigliadin

antibodies and HLA-DR and DQ antigens in trisomy 21. 

Journal of Pediatric Gastroenterology and Nutrition 

1993;16(3):265-268. Improper control group 

A-344
Cataldo F, Lio D, Marino V et al. Cytokine genotyping

(TNF and IL-10) in patients with celiac disease and 

selective IgA deficiency. American Journal of 

Gastroenterology 2003;98(4):850-856. Not sensitivity or 

specificity of an identified test

Cataldo F, Marino V, Bottaro G et al. Celiac disease and

selective immunoglobulin A deficiency. Journal of

Pediatrics 1997;131(2):306-308. Not sensitivity or

specificity of an identified test

Cataldo F, Marino V, Ventura A et al. Prevalence and

clinical features of selective immunoglobulin A deficiency

in coeliac disease: an Italian multicentre study. Italian

Society of Paediatric Gastroenterology and Hepatology

(SIGEP) and "Club del Tenue" Working Groups on Coeliac 

Disease. Gut 1998;42(3):362-365. Not sensitivity or 

specificity of an identified test

Cataldo F, Ventura A, Lazzari R et al. Antiendomysium 

antibodies and coeliac disease: solved and unsolved 

questions. An Italian multicentre study. Acta Paediatrica

(Oslo, Norway - 1992) 1995;84(10):1125-1131. Improper 

control group 

Cataldo Francesco, Marino Vincenzo. Increased prevalence

of autoimmune diseases in first-degree relatives of patients

with celiac disease. Journal of Pediatric Gastroenterology

and Nutrition 2003;36(4):470-473. Not sensitivity or 

specificity of an identified test

Catassi C. Intestinal permeability tests: Research or

diagnosis?. Pediatr Rev Commun 1993;7(3):202-205. Not 

sensitivity or specificity of an identified test 

Catassi C, Fabiani E. The spectrum of coeliac disease in

children. Bailliere's Clinical Gastroenterology

1997;11(3):485-507. Not sensitivity or specificity of an 

identified test 

Catassi C, Doloretta Macis M, Ratsch I M et al. The

distribution of DQ genes in the Saharawi population 

provides only a partial explanation for the high celiac 

disease prevalence. Tissue Antigens 2001;58(6):402-406. 

Improper control group 

Catassi C, Fabiani E, Gasparin M et al. Quantitative

antigliadin antibody measurement in clinical practice: an

Italian multicentre study. SIGEP Working Group on 

Quantitative AGA Standardization. Italian Journal of 

Gastroenterology and Hepatology 1999;31(5):366-370. 

Improper control group 

Catassi C, Fabiani E, Ratsch I M et al. Celiac disease in the 

general population: Should we treat asymptomatic cases?. 

Journal of Pediatric Gastroenterology and Nutrition 

1997;24(5):S10-S13. Not sensitivity or specificity of an

identified test 

Catassi C, Fabiani E, Ratsch I M et al. The coeliac iceberg 

in Italy. A multicentre antigliadin antibodies screening for

coeliac disease in school-age subjects. Acta Paediatrica 

(Oslo, Norway - 1992).Supplement 1996;41229-35. Not 

sensitivity or specificity of an identified test 

Catassi C, Fanciulli G, D'Appello A R et al. 

Antiendomysium versus antigliadin antibodies in screening 

the general population for coeliac disease. Scandinavian

Journal of Gastroenterology 2000;35(7):732-736. Improper 

control group 

Catassi C, Fornaroli F, Fasano A. Celiac disease: From 

basic immunology to bedside practice. Clin Appl Immunol 

Rev 2002;3(1-2):61-71. Not sensitivity or specificity of an 

identified test 

Catassi C, Guerrieri A, Bartolotta E. Antigliadin antibodies

at onset of diabetes in children. Lancet 

1987;2(8551):158Not sensitivity or specificity of an 

identified test 

Catassi C, Ratsch I M, Fabiani E et al. High prevalence of 

undiagnosed coeliac disease in 5280 Italian students 

screened by antigliadin antibodies. Acta Paediatrica (Oslo,

Norway - 1992) 1995;84(6):672-676. Not sensitivity or

specificity of an identified test

Catassi C, Ratsch I M, Fabiani E et al. Coeliac disease in

the year 2000: exploring the iceberg. Lancet 

1994;343(8891):200-203. Not sensitivity or specificity of

an identified test

Catassi C, Ratsch I-M, Gandolfi L et al. Why is coeliac 

disease endemic in the people of the Sahara?. Lancet

1999;354(9179):647-648. Not sensitivity or specificity of

an identified test

Catassi C, Rossini M, Ratsch I M et al. Dose dependent 

effects of protracted ingestion of small amounts of gliadin 

in coeliac disease children: a clinical and jejunal 

morphometric study. Gut 1993;34(11):1515-1519. Not 

sensitivity or specificity of an identified test 

Catassi Carlo, Fabiani Elisabetta, Corrao Giovanni et al.

Risk of non-Hodgkin lymphoma in celiac disease. Jama - 

the Journal of the American Medical Association 

2002;287(11):1413-1419. Not sensitivity or specificity of

an identified test

Catino M, Tumini S, Mezzetti A et al. Coeliac disease and 

diabetes mellitus in children: A non casual association.

Diabetes Nutr Metab Clin Exp 1998;11(5):296-302. Not 

sensitivity or specificity of an identified test 

Cavataio F, Iacono G, Carroccio A et al. Diagnostic 

accuracy of a new stick micromethod with which to 

measure antigliadin antibodies. Journal of Pediatric 

Gastroenterology and Nutrition 1994;19(4):401-402. Not

sensitivity or specificity of an identified test 

Cellier C, Cervoni J P, Patey N et al. Gluten-free diet

induces regression of T-cell activation in the rectal mucosa

of patients with celiac disease. American Journal of 

A-345
Gastroenterology 1998;93(9):1527-1530. Not sensitivity or 

specificity of an identified test

Cellier C, Cuillerier E, Patey-Mariaud de et al. Push 

enteroscopy in celiac sprue and refractory sprue.

Gastrointestinal Endoscopy 1999;50(5):613-617. Not 

sensitivity or specificity of an identified test 

Cellier C, Delabesse E, Helmer C et al. Refractory sprue,

coeliac disease, and enteropathy-associated T-cell

lymphoma. French Coeliac Disease Study Group. Lancet 

2000;356(9225):203-208. Not sensitivity or specificity of

an identified test

Cellier C, Patey N, Mauvieux L et al. Abnormal intestinal 

intraepithelial lymphocytes in refractory sprue. 

Gastroenterology 1998;114(3):471-481. Not sensitivity or

specificity of an identified test

Cerio R, Griffiths C E, Cooper K D et al. Characterization

of factor XIIIa positive dermal dendritic cells in normal and

inflamed skin. British Journal of Dermatology 

1989;121(4):421-431. Not sensitivity or specificity of an

identified test 

Cerio R, Rao B K, Spaull J et al. An immunohistochemical 

study of fibrous papule of the nose: 25 cases. Journal of

Cutaneous Pathology 1989;16(4):194-198. Not sensitivity

or specificity of an identified test

Cerio R, Spaull J, Jones E W. Histiocytoma cutis: a tumour 

of dermal dendrocytes (dermal dendrocytoma). British 

Journal of Dermatology 1989;120(2):197-206. Not 

sensitivity or specificity of an identified test 

Cerio R, Spaull J, Oliver G F et al. A study of factor XIIIa 

and MAC 387 immunolabeling in normal and pathological 

skin. American Journal of Dermatopathology

1990;12(3):221-233. Not sensitivity or specificity of an 

identified test 

Cervetto J L, Ramonet M, Nahmod L H et al. Giardiasis. 

Functional, immunological and histological study of the 

small bowel. Therapeutic trial with a single dose of 

tinidazole. Arquivos De Gastroenterologia 1987;24(2):102-

112. Not sensitivity or specificity of an identified test 

Cetinkaya H, Altintas B, Palabiyikoglu M et al. Diagnostic 

value of antigliadin antibodies in gluten sensitive 

enteropathy. Turk J Gastroenterol 1997;8(1):89-93. 

Improper control group 

Chakrabarti S, Kobayashi K S, Flavell R A et al. Impaired 

membrane resealing and autoimmune myositis in

synaptotagmin VII-deficient mice. J Cell Biol 

2003;162(4):543-549. Not sensitivity or specificity of an

identified test 

Challacombe D N. Screening tests for coeliac disease.

Archives of Disease in Childhood 1995;73(1):3-4. Not 

sensitivity or specificity of an identified test 

Challacombe D N, Dawkins P D. Increased tissue 

concentrations of histamine in the duodenal mucosa of 

children with coeliac disease. Journal of Clinical Pathology 

1982;35(6):596-598. Not sensitivity or specificity of an 

identified test 

Challacombe D N, McDonald D T, Wheeler E E. A 

quantitative assessment of jejunal villous damage in coeliac 

disease, using the mucosal index. Hepato-Gastroenterology

1983;30(3):113-115. Unable to extract data 

Challacombe D N, Mecrow I K, Elliott K et al. Changing 

infant feeding practices and declining incidence of coeliac 

disease in West Somerset. Arch Dis Child 1997;77(3):206-

209. Not sensitivity or specificity of an identified test 

Challacombe D N, Sandler M, Southgate J. Decreased 

duodenal monoamine oxidase activity in coeliac disease. 

Archives of Disease in Childhood 1971;46(246):213-215. 

Not sensitivity or specificity of an identified test

Champliaud M F, Burgeson R E, Jin W et al. cDNA 

cloning and characterization of sciellin, a LIM domain 

protein of the keratinocyte cornified envelope. Journal of

Biological Chemistry 1998;273(47):31547-31554. Not 

sensitivity or specificity of an identified test 

Chan K N, Philips A D, Walker-Smith J A et al. Serum

interleukin-2 receptor in infants and young children. Acta 

Paediatr Int J Paediatr 1995;84(2):151-155. Not sensitivity

or specificity of an identified test

Chan K N, Phillips A D, Mirakian R et al. Endomysial 

antibody screening in children. Journal of Pediatric 

Gastroenterology and Nutrition 1994;18(3):316-320. 

Improper control group 

Chandra R K, Sahni S. Immunological aspects of gluten

intolerance. Nutrition Reviews 1981;39(3):117-120. Not 

sensitivity or specificity of an identified test 

Chapman B L, Henry K, Paice F et al. A new technique for 

examining intestinal biopsies. Gut 1972;13(10):846Not 

sensitivity or specificity of an identified test 

Chapman B L, Henry K, Paice F et al. A new technique for 

examining intestinal biopsies. Gut 1973;14(11):905-909. 

Not sensitivity or specificity of an identified test

Chapoval S P, Iijima K, Marietta E V et al. Allergic 

inflammatory response to short ragweed allergenic extract 

in HLA-DQ transgenic mice lacking CD4 gene. J Immunol 

2002;168(2):890-899. Not sensitivity or specificity of an

identified test 

Charron D. HLA class II disease associations: Molecular 

basis. J Autoimmun 1992;5(Suppl A):45-53. Not sensitivity

or specificity of an identified test

Chartrand L J, Russo P A, Duhaime A G et al. Wheat

starch intolerance in patients with celiac disease. Journal of 

the American Dietetic Association 1997;97(6):612-618. 

A-346
Not sensitivity or specificity of an identified test

Chatzicostas Costantinos, Roussomoustakaki Maria, 

Drygiannakis Dimitrios et al. Primary biliary cirrhosis and 

autoimmune cholangitis are not associated with coeliac 

disease in Crete. Bmc Gastroenterology Electronic 

Resource 2002;2(1):5Not sensitivity or specificity of an 

identified test 

Chauhan B, Santiago L, Hutcheson P S et al. Evidence for 

the involvement of two different MHC class II regions in 

susceptibility or protection in allergic bronchopulmonary

aspergillosis. J Allergy Clin Immunol 2000;106(4):723-

729. Not sensitivity or specificity of an identified test 

Cheli R, Giacosa A. Inflammatory cell count and

identification in specific duodenitis. (Celiac disease, 

Whipple's disease and Crohn's disease). Comparison with 

jejunal findings. Endoscopy 1977;9(3):147-151. Unable to

extract data

Cheli R, Giacosa A. Does malabsorption occur in atrophic 

duodenitis?. Hepato-Gastroenterology 1984;31(6):272-273. 

Not sensitivity or specificity of an identified test

Chen D, Ueda R, Harding F et al. Characterization of HLA 

DR3/DQ2 transgenic mice: A potential humanized animal

model for autoimmune disease studies. Eur J Immunol 

2003;33(1):172-182. Not sensitivity or specificity of an 

identified test 

Chen J S, Mehta K. Tissue transglutaminase: an enzyme 

with a split personality. International Journal of

Biochemistry & Cell Biology 1999;31(8):817-836. Not 

sensitivity or specificity of an identified test 

Chen S, Lin F, Iismaa S et al. Alpha1-adrenergic receptor 

signaling via Gh is subtype specific and independent of its

transglutaminase activity. Journal of Biological Chemistry

1996;271(50):32385-32391. Not sensitivity or specificity of 

an identified test

Chen Z, Dudek N, Wijburg O et al. A 320-kilobase 

artificial chromosome encoding the human HLA DR3-DQ2 

MHC haplotype confers HLA restriction in transgenic 

mice. J Immunol 2002;168(6):3050-3056. Not sensitivity or 

specificity of an identified test

Cheng Hong, Wang Jun, Zhang Chuan et al. 

Clinicopathologic study of mucosa-associated lymphoid 

tissue lymphoma in gastroscopic biopsy. World Journal of

Gastroenterology - Wjg 2003;9(6):1270-1272. Not 

sensitivity or specificity of an identified test 

Cheong K Y, Allcock R J N, Eerligh P et al. Localization

of central MHC genes influencing type I diabetes. Hum 

Immunol 2001;62(12):1363-1370. Not sensitivity or 

specificity of an identified test

Chernavsky Alejandra C, Rubio Andrea E, Vanzulli Silvia

et al. Evidences of the involvement of Bak, a member of 

the Bcl-2 family of proteins, in active coeliac disease. 

Autoimmunity 2002;35(1):29-37. Not sensitivity or 

specificity of an identified test

Chhaya S U, Shankarkumar U. HLA antigen distribution in

Jain population from Mumbai, Maharashtra, India. Indian J 

Med Res 2001;113(July):25-29. Not sensitivity or

specificity of an identified test

Chiantore M V, Giandomenico V, De Luca L M.

Carcinoma cell lines resistant for growth inhibition and 

apoptosis to retinoic acid are responsive to 4-hydroxyphenyl-retinamide: correlation with tissue 

transglutaminase. Biochemical and Biophysical Research

Communications 1999;254(3):636-641. Not sensitivity or

specificity of an identified test

Chicz R M, Lane W S, Robinson R A et al. Self-peptides 

bound to the type I diabetes associated class II MHC 

molecules HLA-DQ1 and HLA-DQ8. Int Immunol 

1994;6(11):1639-1649. Not sensitivity or specificity of an

identified test 

Chimenti C, Pieroni M, Frustaci A. Celiac disease in

idiopathic dilated cardiomyopathy. Ital Heart J 

2001;2(9):658-659. Not sensitivity or specificity of an 

identified test 

Chin R L, Sander H W, Brannagan T H et al. Celiac 

neuropathy. Neurology 2003;60(10):1581-1585. Not 

sensitivity or specificity of an identified test 

Chirdo F G, Rumbo M, Anon M C et al. Presence of high 

levels of non-degraded gliadin in breast milk from healthy

mothers. Scandinavian Journal of Gastroenterology

1998;33(11):1186-1192. Not sensitivity or specificity of an 

identified test 

Chirdo F G, Zwirner N W, Rumbo M et al. In vitro 

presentation of gliadin-derived peptides by different cell 

lines. Clin Chim Acta 2002;317(1-2):151-158. Not 

sensitivity or specificity of an identified test 

Choate K A, Khavari P A. Sustainability of keratinocyte 

gene transfer and cell survival in vivo. Human Gene 

Therapy 1997;8(8):895-901. Not sensitivity or specificity

of an identified test 

Chorzelski T P, Beutner E H, Sulej J et al. IgA antiendomysium antibody. A new immunological marker of

dermatitis herpetiformis and coeliac disease. British Journal 

of Dermatology 1984;111(4):395-402. Serology <1990 

Chorzelski T P, Jablonska S, Chadzynska M et al. IgA 

endomysium antibody in children with dermatitis

herpetiformis treated with gluten-free diet. Pediatric 

Dermatology 1986;3(4):291-294. Not sensitivity or 

specificity of an identified test

Chorzelski T P, Sulej J, Tchorzewska H et al. IgA class

endomysium antibodies in dermatitis herpetiformis and 

coeliac disease. Annals of the New York Academy of 

Sciences 1983;420325-334. Not sensitivity or specificity of 

A-347
an identified test

Chou K-Y, Chan M, Bias W B. Differential expression of 

the down-regulatory function of CD8 cells in trichosanthininduced immunosuppression and its genetic control in

humans. Eur J Immunogenet 1996;23(1):29-40. Not 

sensitivity or specificity of an identified test 

Chou S M, Taniguchi A, Wang H S et al. Serpin=serine 

protease-like complexes within neurofilament 

conglomerates of motoneurons in amyotrophic lateral 

sclerosis. Journal of the Neurological Sciences 1998;160 

Suppl 1s73-s79. Not sensitivity or specificity of an 

identified test 

Chowdhury Z A, Barsigian C, Chalupowicz G D et al. 

Colocalization of tissue transglutaminase and stress fibers 

in human vascular smooth muscle cells and human 

umbilical vein endothelial cells. Experimental Cell 

Research 1997;231(1):38-49. Not sensitivity or specificity

of an identified test 

Christenson M J, LaRosa T, Jung M et al. Hypomorphic 

C4B*15 variant of the fourth component of complement. 

Febs Lett 1990;260(2):183-186. Not sensitivity or

specificity of an identified test

Christiansen O B. The possible role of classical human 

leukocyte antigens in recurrent miscarriage. Am J Reprod 

Immunol 1999;42(2):110-115. Not sensitivity or specificity

of an identified test 

Christou H, Connors J M, Ziotopoulou M et al. Cord blood 

leptin and insulin-like growth factor levels are independent

predictors of fetal growth. Journal of Clinical 

Endocrinology and Metabolism 2001;86(2):935-938. Not 

sensitivity or specificity of an identified test 

Chrysomali E, Papanicolaou S I, Dekker N P et al. Benign 

neural tumors of the oral cavity: a comparative 

immunohistochemical study. Oral Surgery, Oral Medicine, 

Oral Pathology, Oral Radiology, and Endodontics

1997;84(4):381-390. Not sensitivity or specificity of an 

identified test 

Chuang C K, Shen Y C, Wu J H et al. Immunobiologic, 

cytogenetic and drug response features of a newly

established cell line (SCRC-1) from renal small cell 

carcinoma. Journal of Urology 2000;163(3):1016-1021. 

Not sensitivity or specificity of an identified test

Chumpitazi B F, Boussaid A, Pelloux H et al. Diagnosis of 

congenital toxoplasmosis by immunoblotting and

relationship with other methods. Journal of Clinical 

Microbiology 1995;33(6):1479-1485. Not sensitivity or

specificity of an identified test

Chun W, Lesort M, Tucholski J et al. Tissue 

transglutaminase selectively modifies proteins associated 

with truncated mutant huntingtin in intact cells. 

Neurobiology of Disease 2001;8(3):391-404. Not 

sensitivity or specificity of an identified test 

Chun W, Lesort M, Tucholski J et al. Tissue 

transglutaminase does not contribute to the formation of 

mutant huntingtin aggregates. Journal of Cell Biology

2001;153(1):25-34. Not sensitivity or specificity of an 

identified test 

Chung M H. Analysis of small bowel biopsies. A clinical 

and histopathological correlation. Yonsei Medical Journal 

1968;9(2):105-115. Unable to extract data 

Chung Wu, Mathews K P. Generation of drug metabolite 

antigenicity in the intestinal mucosa. 

Immunopharmacology 1986;12(1):53-58. Not sensitivity or 

specificity of an identified test

Chuttani H K, Jain K, Misra R C. Small bowel in typhoid 

fever. Gut 1971;12(9):709-712. Not sensitivity or

specificity of an identified test

Chuttani H K, Kasthuri D, Misra R C. Course and

prognosis of tropical sprue. Journal of Tropical Medicine

and Hygiene 1968;71(4):96-99. Not sensitivity or

specificity of an identified test

Ciacci C, Cirillo M, Giorgetti G et al. Low plasma

cholesterol: a correlate of nondiagnosed celiac disease in

adults with hypochromic anemia. American Journal of

Gastroenterology 1999;94(7):1888-1891. Not sensitivity or 

specificity of an identified test

Ciacci C, Di Vizio D, Seth R et al. Selective reduction of 

intestinal trefoil factor in untreated coeliac disease. Clinical

and Experimental Immunology 2002;130(3):526-531. Not 

sensitivity or specificity of an identified test 

Ciacci C, Iavarone A, Mazzacca G et al. Depressive 

symptoms in adult coeliac disease. Scandinavian Journal of

Gastroenterology 1998;33(3):247-250. Not sensitivity or 

specificity of an identified test

Ciacci C, Squillante A, Rendina D et al. Helicobacter pylori

infection and peptic disease in coeliac disease. European 

Journal of Gastroenterology & Hepatology

2000;12(12):1283-1287. Not sensitivity or specificity of an 

identified test 

Ciacci Carolina, Cirillo Massimo, Cavallaro Raimondo et

al. Long-term follow-up of celiac adults on gluten-free diet: 

prevalence and correlates of intestinal damage. Digestion 

2002;66(3):178-185. Not sensitivity or specificity of an 

identified test 

Ciampolini M, Bini S. Serum lipids in celiac children. 

Journal of Pediatric Gastroenterology and Nutrition 

1991;12(4):459-460. Not sensitivity or specificity of an 

identified test 

Ciampolini M, Bini S, Orsi A. Microflora persistence on

duodenojejunal flat or normal mucosa in time after a meal 

in children. Physiol Behav 1996;60(6):1551-1556. Not 

sensitivity or specificity of an identified test 

A-348
Ciccocioppo R, D'Alo S, Di Sabatino A et al. Mechanisms 

of villous atrophy in autoimmune enteropathy and coeliac 

disease. Clinical and Experimental Immunology

2002;128(1):88-93. Not sensitivity or specificity of an 

identified test 

Ciccocioppo R, Di Sabatino A, Parroni R et al. Cytolytic 

mechanisms of intraepithelial lymphocytes in coeliac 

disease (CoD). Clinical and Experimental Immunology

2000;120(2):235-240. Not sensitivity or specificity of an

identified test 

Ciccocioppo R, Di Sabatino A, Parroni R et al. Increased

enterocyte apoptosis and Fas-Fas ligand system in celiac 

disease. American Journal of Clinical Pathology

2001;115(4):494-503. Not sensitivity or specificity of an

identified test 

Ciclitira P J. Recent advances in coeliac disease. Clin Med

2003;3(2):166-169. Not sensitivity or specificity of an 

identified test 

Ciclitira P J, Ellis H J. In vivo gluten ingestion in coeliac 

disease. Digestive Diseases (Basel, Switzerland) 

1998;16(6):337-340. Not sensitivity or specificity of an 

identified test 

Ciclitira P J, Hall M A. Coeliac disease. Baillieres Clin

Gastroenterol 1990;4(1):43-59. Not sensitivity or 

specificity of an identified test

Ciclitira P J, Sturgess R. Clinicopathologic mechanisms in 

celiac disease. Curr Opin Gastroenterol 1992;8(2):262-267. 

Not sensitivity or specificity of an identified test

Ciclitira P J, Cerio R, Ellis H J. Evaluation of a gliadincontaining gluten-free product in coeliac patients. Hum 

Nutr Clin Nutr 1985;39(4):303-308. Not sensitivity or 

specificity of an identified test

Ciclitira P J, Ellis H J, Evans D J. A solid-phase

radioimmunoassay for measurement of circulating antibody

titres to wheat gliadin and its subfractions in patients with 

adult coeliac disease. Journal of Immunological Methods 

1983;62(2):231-239. Not sensitivity or specificity of an 

identified test 

Ciclitira P J, Ellis H J, Venning V A. Circulating antibodies 

to gliadin subfractions in dermatitis herpetiformis and 

linear IgA dermatosis of adults and children. Clin Exp 

Dermatol 1986;11(5):502-509. Not sensitivity or specificity

of an identified test 

Ciclitira P J, Ellis H J, Evans D J et al. A 

radioimmunoassay for wheat gliadin to assess the 

suitability of gluten free foods for patients with coeliac 

disease. Clinical and Experimental Immunology

1985;59(3):703-708. Not sensitivity or specificity of an 

identified test 

Ciclitira P J, Ellis H J, Wood G M et al. Secretion of 

gliadin antibody by coeliac jejunal mucosal biopsies 

cultured in vitro. Clinical and Experimental Immunology

1986;64(1):119-124. Not sensitivity or specificity of an 

identified test 

Ciclitira P J, Evans D J, Fagg N L et al. Clinical testing of

gliadin fractions in coeliac patients. Clinical Science 

(London, England - 1979) 1984;66(3):357-364. Not 

sensitivity or specificity of an identified test 

Ciclitira P J, Hooper L B, Ellis H J et al. Gliadin antibody

production by small intestinal lymphocytes from patients 

with coeliac disease. International Archives of Allergy and

Applied Immunology 1989;89(2-3):246-249. Not 

sensitivity or specificity of an identified test 

Ciclitira P J, King A L, Fraser J S. AGA technical review 

on Celiac Sprue. American Gastroenterological

Association. Gastroenterology 2001;120(6):1526-1540. Not 

sensitivity or specificity of an identified test 

Ciclitira P J, Nelufer J M, Ellis H J et al. The effect of 

gluten on HLA-DR in the small intestinal epithelium of 

patients with coeliac disease. Clinical and Experimental 

Immunology 1986;63(1):101-104. Not sensitivity or 

specificity of an identified test

Ciclitira P J, Stewart J, Evan G et al. Expression of c-myc 

oncogene in coeliac disease. Journal of Clinical Pathology

1987;40(3):307-311. Not sensitivity or specificity of an 

identified test 

Ciclitira Paul J, Moodie Simon J. Transition of care 

between paediatric and adult gastroenterology. Coeliac 

disease. Best Practice & Research.Clinical

Gastroenterology 2003;17(2):181-195. Not sensitivity or 

specificity of an identified test

Cinek O, Dr caron, umnik Z et al. NEUROD polymorphism 

Ala45Thr is associated with Type 1 diabetes mellitus in 

Czech children. Diabetes Res Clin Pract 2003;60(1):49-56. 

Not sensitivity or specificity of an identified test

Cipolli M, Valletta E A, Zampieri C et al. Increased serum

levels of antigliadin antibodies in cystic fibrosis. Acta 

Paediatrica (Oslo, Norway - 1992) 1993;82(1):95-97. Not 

sensitivity or specificity of an identified test 

Citron B A, Gregory E J, Steigerwalt D S et al. Regulation 

of the dual function tissue transglutaminase/Galpha(h) 

during murine neuromuscular development: Gene and 

enzyme isoform expression. Neurochem Int 

2000;37(4):337-349. Not sensitivity or specificity of an 

identified test 

Citron B A, SantaCruz K S, Davies P J et al. Intron-exon 

swapping of transglutaminase mRNA and neuronal Tau

aggregation in Alzheimer's disease. Journal of Biological 

Chemistry 2001;276(5):3295-3301. Not sensitivity or 

specificity of an identified test

Citron Bruce A, Suo Zhiming, SantaCruz Karen et al. 

A-349
Protein crosslinking, tissue transglutaminase, alternative 

splicing and neurodegeneration. Neurochemistry

International 2002;40(1):69-78. Not sensitivity or

specificity of an identified test

Clark M L, Senior J R. Small gut mucosal activites of 

pyrimidine precursor enzymes in celiac disease.

Gastroenterology 1969;56(5):887-894. Not sensitivity or 

specificity of an identified test

Clegg D O, Pincus S H, Zone J J et al. Circulating HLADR bearing T cells: correlation with genetic rather than

clinical variables. Journal of Rheumatology

1986;13(5):870-874. Not sensitivity or specificity of an 

identified test 

Clemente M G, Congia M, De Virgiliis S. The laboratory in 

autoimmune diseases. Ital J Pediat 2002;28(1):12-18. Not 

sensitivity or specificity of an identified test 

Clemente M G, Musu M P, Frau F et al. Immune reaction 

against the cytoskeleton in coeliac disease. Gut 

2000;47(4):520-526. Not sensitivity or specificity of an 

identified test 

Clemente Maria, Grazia Musu, Maria Paola et al. 

Antitissue transglutaminase antibodies outside celiac

disease. Journal of Pediatric Gastroenterology and

Nutrition 2002;34(1):31-34. Test-specific exclusion 

Clerget-Darpoux F, Bouguerra F, Kastally R et al. High 

risk genotypes for celiac disease. Comptes Rendus De 

L'academie Des Sciences.Serie Iii, Sciences De La Vie

1994;317(10):931-936. Improper control group 

Clerici N, Fernandez M, Saiz I et al. Human leukocyte 

antigen alleles and haplotypes associated with selective 

immunoglobulin A deficiency in Spanish pediatric patients. 

Journal of Pediatric Gastroenterology and Nutrition 

1993;16(4):381-386. Not sensitivity or specificity of an 

identified test 

Clot F, Babron M C. Genetics of celiac disease. Molecular 

Genetics and Metabolism 2000;71(1-2):76-80. Review 

article 

Clot F, Babron M C, Percopo S et al. Study of two 

ectopeptidases in the susceptibility to celiac disease: two 

newly identified polymorphisms of dipeptidylpeptidase IV. 

Journal of Pediatric Gastroenterology and Nutrition 

2000;30(4):464-466. Not sensitivity or specificity of an 

identified test 

Clot F, Fulchignoni-Lataud M C, Renoux C et al. Linkage

and association study of the CTLA-4 region in coeliac 

disease for Italian and Tunisian populations. Tissue 

Antigens 1999;54(5):527-530. Not sensitivity or specificity

of an identified test 

Clot F, Gianfrani C, Babron M C et al. HLA-DR53 

molecules are associated with susceptibility to celiac 

disease and selectively bind gliadin-derived peptides. 

Immunogenetics 1999;49(9):800-807. Improper control 

group 

Clot F, Gianfrani C, Babron M-C et al. Response. 

Immunogenetics 2000;51(3):251Not sensitivity or

specificity of an identified test

Cluysenaer O J J, Van Tongeren J H M. The natural history

of coeliac sprue, and factors which may influence it. Neth J 

Med 1978;21(1):35-43. Not sensitivity or specificity of an

identified test 

Cluysenaer O J, Schillings P H, van Tongeren J H. Mucosal

lesions and malabsorption in celiac sprue. Journal of 

Clinical Gastroenterology 1982;4(5):425-429. Unable to

extract data

Cobain T J, Stuckey M S, McCluskey J. The coexistence of

IgA deficiency and 21-hydroxylase deficiency marked by

specific MHC supratypes. Ann New York Acad Sci 

1985;458(-):76-84. Not sensitivity or specificity of an 

identified test 

Cogulu O, Ozkinay F, Gunduz C et al. Celiac disease in

children with down syndrome: Importance of follow-up 

and serologic screening. Pediatr Int 2003;45(4):395-399. 

Not sensitivity or specificity of an identified test

Cohen I, Anderson B. Immunochemical characterization of

the transglutaminase-catalyzed polymer of activated 

platelets. Thrombosis Research 1987;47(4):409-416. Not 

sensitivity or specificity of an identified test 

Cole S G, Kagnoff M F. Celiac disease. Annual Review of

Nutrition 1985;5241-266. Not sensitivity or specificity of

an identified test

Collier P M, Wojnarowska F, Welsh K et al. Adult linear

IgA disease and chronic bullous disease of childhood: The 

association with human lymphocyte antigens Cw7, B8, 

DR3 and tumour necrosis factor influences disease 

expression. Br J Dermatol 1999;141(5):867-875. Not 

sensitivity or specificity of an identified test 

Collighan R, Cortez J, Griffin M. The biotechnological 

applications of transglutaminases. Minerva Biotecnol 

2002;14(2):143-148. Not sensitivity or specificity of an 

identified test 

Collin P. New diagnostic findings in coeliac disease. 

Annals of Medicine 1999;31(6):399-405. Not sensitivity or

specificity of an identified test

Collin P. Serologic screening for coeliac disease--time for

tissue transglutaminase test?. Italian Journal of

Gastroenterology and Hepatology 1998;30(5):498-499. Not 

sensitivity or specificity of an identified test 

Collin P, Maki M. Celiac disease--even a neurological 

disorder. Journal of Pediatric Gastroenterology and 

Nutrition 1997;24(1):116-117. Not sensitivity or specificity

of an identified test 

A-350
Collin P, Hallstrom O, Maki M et al. Atypical coeliac 

disease found with serologic screening. Scandinavian 

Journal of Gastroenterology 1990;25(3):245-250. Not 

sensitivity or specificity of an identified test 

Collin P, Helin H, Maki M et al. Follow-up of patients

positive in reticulin and gliadin antibody tests with normal 

small-bowel biopsy findings. Scandinavian Journal of

Gastroenterology 1993;28(7):595-598. Not sensitivity or 

specificity of an identified test

Collin P, Kaukinen K, Maki M. Clinical features of celiac

disease today. Digestive Diseases (Basel, Switzerland) 

1999;17(2):100-106. Not sensitivity or specificity of an 

identified test 

Collin P, Korpela M, Hallstrom O et al. Rheumatic 

complaints as a presenting symptom in patients with 

coeliac disease. Scandinavian Journal of Rheumatology

1992;21(1):20-23. Not sensitivity or specificity of an 

identified test 

Collin P, Pirttila T, Nurmikko T et al. Celiac disease, brain 

atrophy, and dementia. Neurology 1991;41(3):372-375. Not 

sensitivity or specificity of an identified test 

Collin P, Rasmussen M, Kyronpalo S et al. The hunt for 

coeliac disease in primary care. Qjm - Monthly Journal of

the Association of Physicians 2002;95(2):75-77. Not 

sensitivity or specificity of an identified test 

Collin P, Reunala T, Rasmussen M et al. High incidence 

and prevalence of adult coeliac disease. Augmented 

diagnostic approach. Scandinavian Journal of

Gastroenterology 1997;32(11):1129-1133. Not sensitivity

or specificity of an identified test

Collin P, Salmi J, Hallstrom O et al. High frequency of 

coeliac disease in adult patients with Type-I diabetes.

Scandinavian Journal of Gastroenterology 1989;24(1):81-

84. Not sensitivity or specificity of an identified test 

Collin P, Salmi J, Hallstrom O et al. Autoimmune thyroid 

disorders and coeliac disease. European Journal of

Endocrinology / European Federation of Endocrine 

Societies 1994;130(2):137-140. Not sensitivity or

specificity of an identified test

Collin P, Vilska S, Heinonen P K et al. Infertility and 

coeliac disease. Gut 1996;39(3):382-384. Not sensitivity or 

specificity of an identified test

Collin Pekka, Reunala Timo. Recognition and management 

of the cutaneous manifestations of celiac disease: a guide

for dermatologists. American Journal of Clinical 

Dermatology 2003;4(1):13-20. Not sensitivity or specificity

of an identified test 

Collin Pekka, Kaukinen Katri, Valimaki Matti et al.

Endocrinological disorders and celiac disease. Endocrine 

Reviews 2002;23(4):464-483. Not sensitivity or specificity

of an identified test 

Collin Pekka, Syrjanen Jaana, Partanen Jukka et al. Celiac 

disease and HLA DQ in patients with IgA nephropathy.

American Journal of Gastroenterology 2002;97(10):2572-

2576. Improper control group 

Collins A L, Brookfield D S, Hyde I et al. Small bowel 

biopsy. Archives of Disease in Childhood 

1985;60(11):1082-1085. Not sensitivity or specificity of an 

identified test 

Collins B J, Bell P M, Thomson J M et al. Dietary history 

and nutritional state in treated coeliac patients. Journal of

the Royal Society of Medicine 1986;79(4):206-209. Not 

sensitivity or specificity of an identified test 

Colombel J F, Mascart-Lemone F, Nemeth J et al. Jejunal 

immunoglobulin and antigliadin antibody secretion in adult 

coeliac disease. Gut 1990;31(12):1345-1349. Not 

sensitivity or specificity of an identified test 

Colombel J F, Torpier G, Janin A et al. Activated

eosinophils in adult coeliac disease: evidence for a local 

release of major basic protein. Gut 1992;33(9):1190-1194. 

Not sensitivity or specificity of an identified test

Colombo Gualtiero, Buffa Roberto, Bardella Maria et al. 

Anti-inflammatory effects of alpha-melanocyte-stimulating 

hormone in celiac intestinal mucosa. 

Neuroimmunomodulation 2003;10(4):208-216. Not 

sensitivity or specificity of an identified test 

Colonna M, Mantovani W, Corazza G R et al. 

Reassessment of HLA association with celiac disease in 

special reference to the DP association. Human 

Immunology 1990;29(4):263-274. Improper control group 

Colston K W, Mackay A G, Finlayson C et al. Localisation

of vitamin D receptor in normal human duodenum and in

patients with coeliac disease. Gut 1994;35(9):1219-1225. 

Not sensitivity or specificity of an identified test

Combarros O, Infante J, Lopez-Hoyos M et al. Celiac 

disease and idiopathic cerebellar ataxia. Neurology

2000;54(12):2346Not sensitivity or specificity of an 

identified test 

Commo S, Bernard B A. Immunohistochemical analysis of 

tissue remodelling during the anagen-catagen transition of

the human hair follicle. British Journal of Dermatology 

1997;137(1):31-38. Not sensitivity or specificity of an 

identified test 

Commo S, Bernard B A. Immunohistochemical analysis of 

tissue remodelling during the anagen-catagen transition of

the human hair follicle. G Ital Dermatol Venereol

2002;137(2 SUPPL. 1):3-11. Not sensitivity or specificity

of an identified test 

Congdon P J, Fiddler G I, Littlewood J M et al. Coeliac 

disease associated with congenital heart disease. Archives 

A-351
of Disease in Childhood 1982;57(1):78-79. Not sensitivity

or specificity of an identified test

Congdon P, Mason M K, Smith S et al. Small-bowel 

mucosa in asymptomatic children with celiac disease.

Mucosal changes with gluten-free diets. American Journal 

of Diseases of Children (1960) 1981;135(2):118-121. 

Unable to extract data 

Congia M, Cucca F, Frau F et al. A gene dosage effect of

the DQA1*0501/DQB1*0201 allelic combination

influences the clinical heterogeneity of celiac disease.

Human Immunology 1994;40(2):138-142. Improper control 

group 

Congia M, Frau F, Lampis R et al. A high frequency of the 

A30, B18, DR3, DRw52, DQw2 extended haplotype in 

Sardinian celiac disease patients: further evidence that

disease susceptibility is conferred by DQ A1*0501, 

B1*0201. Tissue Antigens 1992;39(2):78-83. Improper 

control group 

Conkling P R, Achyuthan K E, Greenberg C S et al. Human 

mononuclear phagocyte transglutaminase activity crosslinks fibrin. Thrombosis Research 1989;55(1):57-68. Not 

sensitivity or specificity of an identified test 

Connon J J, McFarland J, Kelly A. Acute abdominal 

complications of coeliac disease. Scandinavian Journal of

Gastroenterology 1975;10(8):843-846. Not sensitivity or 

specificity of an identified test

Conrad Karsten, Schmechta Helmut, Klafki Agnes et al.

Serological differentiation of inflammatory bowel diseases.

European Journal of Gastroenterology & Hepatology

2002;14(2):129-135. Not sensitivity or specificity of an 

identified test 

Contini D, Torti A, Monti M et al. A freeze-fracture study 

of the enteropathy associated with dermatitis herpetiformis: 

a comparative investigation with coeliac disease. Journal of 

Cutaneous Pathology 1986;13(4):293-300. Not sensitivity

or specificity of an identified test

Cook D M, Evans N, Lloyd A et al. Coeliac disease. 

Reappraisal of clinical diagnosis. Archives of Disease in

Childhood 1971;46(249):705-708. Not sensitivity or 

specificity of an identified test

Cook H B, Burt M J, Collett J A et al. Adult coeliac 

disease: prevalence and clinical significance. Journal of

Gastroenterology and Hepatology 2000;15(9):1032-1036. 

Not sensitivity or specificity of an identified test

Cooke W T, Asquith P. Introduction and definition. Clin 

Gastroenterol 1974;3(1):3-10. Not sensitivity or specificity

of an identified test 

Coombs R R, Kieffer M, Fraser D R et al. Naturally 

developing antibodies to wheat gliadin fractions and to 

other cereal antigens in rabbits, rats and guinea pigs on 

normal laboratory diets. International Archives of Allergy

and Applied Immunology 1983;70(3):200-204. Not 

sensitivity or specificity of an identified test 

Cooper Arthur J L, Jeitner Thomas M, Gentile Vittorio et 

al. Cross linking of polyglutamine domains catalyzed by

tissue transglutaminase is greatly favored with

pathological-length repeats: does transglutaminase activity 

play a role in (CAG)(n)/Q(n)-expansion diseases?.

Neurochemistry International 2002;40(1):53-67. Not 

sensitivity or specificity of an identified test 

Cooper A J L, Sheu K-F, Burke J R et al. Inhibition of 

alpha-ketoglutarate-and pyruvate dehydrogenase 

complexes in E. coli by a glutathione S-transferase 

containing a pathological length poly- Q domain: A 

possible role of energy deficit in neurological diseases 

associated with poly-Q expansions?. Age 1998;21(1):25-

30. Not sensitivity or specificity of an identified test 

Cooper A J L, Sheu K-F, Burke J R et al. 

Transglutaminase-catalyzed inactivation of glyceraldehyde

3-phosphate dehydrogenase and alpha-ketoglutarate 

dehydrogenase complex by polyglutamine domains of 

pathological length. Proc Natl Acad Sci U S A

1997;94(23):12604-12609. Not sensitivity or specificity of 

an identified test

Cooper A J, Sheu K F, Burke J R et al. Pathogenesis of 

inclusion bodies in (CAG)n/Qn-expansion diseases with 

special reference to the role of tissue transglutaminase and

to selective vulnerability. Journal of Neurochemistry

1999;72(3):889-899. Not sensitivity or specificity of an 

identified test 

Cooper A J, Wang J, Pasternack R et al. Lysine-rich 

histone (H1) is a lysyl substrate of tissue transglutaminase: 

possible involvement of transglutaminase in the formation 

of nuclear aggregates in (CAG)(n)/Q(n) expansion 

diseases. Developmental Neuroscience 2000;22(5-6):404-

417. Not sensitivity or specificity of an identified test 

Cooper B T, Holmes G K T, Ferguson R. Celiac disease 

and malignancy. Medicine 1980;59(4):249-261. Not 

sensitivity or specificity of an identified test 

Cooper B T, Holmes G K, Ferguson R et al. Glutensensitive diarrhea without evidence of celiac disease. 

Gastroenterology 1980;79(5 Pt 1):801-806. Not sensitivity

or specificity of an identified test

Cooper D L, Doria R, Salloum E. Primary gastrointestinal 

lymphomas. Gastroenterologist 1996;4(1):54-64. Not 

sensitivity or specificity of an identified test 

Coppo R. The pathogenetic potential of environmental 

antigens in IgA nephropathy. American Journal of Kidney

Diseases - the Official Journal of the National Kidney 

Foundation 1988;12(5):420-424. Not sensitivity or

specificity of an identified test

Coppo R, Amore A, Roccatello D. Dietary antigens and 

primary immunoglobulin A nephropathy. Journal of the 

A-352
American Society of Nephrology - Jasn 1992;2(10 

Suppl):S173-S180. Not sensitivity or specificity of an 

identified test 

Coppo R, Mazzucco G, Martina G et al. Gluten-induced 

experimental IgA glomerulopathy. Lab Invest 

1989;60(4):499-506. Not sensitivity or specificity of an 

identified test 

Corazza G R, Gasbarrini G. Coeliac disease in adults. 

Bailliere's Clinical Gastroenterology 1995;9(2):329-350. 

Not sensitivity or specificity of an identified test

Corazza G R, Andreani M L, Biagi F et al. The smaller size

of the 'coeliac iceberg' in adults. Scandinavian Journal of

Gastroenterology 1997;32(9):917-919. Not sensitivity or 

specificity of an identified test

Corazza G R, Biagi F, Volta U et al. Autoimmune 

enteropathy and villous atrophy in adults. Lancet 

1997;350(9071):106-109. Not sensitivity or specificity of

an identified test

Corazza G R, Brusco G, Andreani M L et al. Previous

misdiagnosis and diagnostic delay in adult celiac sprue. 

Journal of Clinical Gastroenterology 1996;22(4):324-325. 

Not sensitivity or specificity of an identified test

Corazza G R, Caletti G C, Lazzari R et al. Scalloped 

duodenal folds in childhood celiac disease. Gastrointestinal 

Endoscopy 1993;39(4):543-545. Not sensitivity or

specificity of an identified test

Corazza G R, Falasca A, Strocchi A et al. Decreased 

plasma postheparin diamine oxidase levels in celiac 

disease. Digestive Diseases and Sciences 1988;33(8):956-

961. Not sensitivity or specificity of an identified test 

Corazza G R, Frazzoni M, Gasbarrini G. Jejunal

intraepithelial lymphocytes in coeliac disease: are they

increased or decreased?. Gut 1984;25(2):158-162. Not 

sensitivity or specificity of an identified test 

Corazza G R, Frazzoni M, Dixon M F et al. Quantitative

assessment of the mucosal architecture of jejunal biopsy

specimens: a comparison between linear measurement, 

stereology, and computer aided microscopy. Journal of

Clinical Pathology 1985;38(7):765-770. Unable to extract 

data 

Corazza G R, Frisoni M, Mantovani W et al. Dermatitis 

herpetiformis, severity of jejunal lesions and HLA DR7. 

European Journal of Gastroenterology & Hepatology

1990;2(5):357-360. Not sensitivity or specificity of an 

identified test 

Corazza G R, Frisoni M, Treggiari E A et al. Subclinical

celiac sprue. Increasing occurrence and clues to its

diagnosis. Journal of Clinical Gastroenterology

1993;16(1):16-21. Not sensitivity or specificity of an 

identified test 

Corazza G R, Ginaldi L, Falasca A et al. Diamine oxidase

plasma activities after treatment with heparin and jejunal

morphometry in untreated coeliac disease. Journal of 

Clinical Pathology 1989;42(11):1136-1139. Not sensitivity

or specificity of an identified test

Corazza G R, Tabacchi P, Frisoni M et al. T-lymphocyte

subsets in adult coeliac disease. Clinical Science (London, 

England - 1979) 1983;65(1):89-90. Not sensitivity or 

specificity of an identified test

Corazza G R, Tabacchi P, Frisoni M et al. DR and non-DR 

Ia allotypes are associated with susceptibility to coeliac 

disease. Gut 1985;26(11):1210-1213. Not sensitivity or

specificity of an identified test

Corazza G R, Valentini R A, Andreani M L et al.

Subclinical coeliac disease is a frequent cause of irondeficiency anaemia. Scandinavian Journal of 

Gastroenterology 1995;30(2):153-156. Not sensitivity or 

specificity of an identified test

Corazza G, Valentini R A, Frisoni M et al. Gliadin immune 

reactivity is associated with overt and latent enteropathy in 

relatives of celiac patients. Gastroenterology

1992;103(5):1517-1522. Not sensitivity or specificity of an 

identified test 

Cordella-Miele E, Miele L, Mukherjee A B. A novel 

transglutaminase-mediated post-translational modification

of phospholipase A2 dramatically increases its catalytic 

activity. Journal of Biological Chemistry 

1990;265(28):17180-17188. Not sensitivity or specificity of 

an identified test

Cornell H J. Amino acid composition of peptides remaining 

after in vitro digestion of a gliadin sub-fraction with 

duodenal mucosa from patients with coeliac disease. Clin

Chim Acta 1988;176(3):279-290. Not sensitivity or 

specificity of an identified test

Cornell H J, Townley R R. The effect of gliadin peptides 

on rat-liver lysosomes in relation to the pathogenesis of 

coeliac disease. Clinica Chimica Acta 1973;International 

Journal of Clinical Chemistry; 49(2):181-188. Not 

sensitivity or specificity of an identified test 

Corrado F, Magazzu G, Sferlazzas C. Diagnosis of celiac 

disease in pregnancy and puerperium: Think about it. Acta

Obstet Gynecol Scand 2002;81(2):180-181. Not sensitivity

or specificity of an identified test

Corrao G, Corazza G R, Andreani M L et al. Serological 

screening of coeliac disease: choosing the optimal

procedure according to various prevalence values. Gut 

1994;35(6):771-775. Improper control group 

Costantini V, Zacharski L R, Memoli V A et al. Fibrinogen

deposition without thrombin generation in primary human 

breast cancer tissue. Cancer Research 1991;51(1):349-353. 

Not sensitivity or specificity of an identified test

A-353
Cottone M, Marrone C, Casa A et al. Familial occurrence

of inflammatory bowel disease in celiac disease.

Inflammatory Bowel Dis 2003;9(5):321-323. Not 

sensitivity or specificity of an identified test 

Cottone M, Termini A, Oliva L et al. Mortality and causes

of death in celiac disease in a Mediterranean area. 

Digestive Diseases and Sciences 1999;44(12):2538-2547. 

Not sensitivity or specificity of an identified test

Coutinho H B, Robalinho T I, Coutinho V B et al. 

Immunocytochemistry of mucosal changes in patients 

infected with the intestinal nematode Strongyloides 

stercoralis. Journal of Clinical Pathology 1996;49(9):717-

720. Not sensitivity or specificity of an identified test 

Cox A D, Devine D V. Factor XIIIa binding to activated 

platelets is mediated through activation of glycoprotein IIbIIIa. Blood 1994;83(4):1006-1016. Not sensitivity or 

specificity of an identified test

Cox M A, Lewis K O, Cooper B T. Sucrosemia in

untreated celiac disease: a potential screening test. 

Digestive Diseases and Sciences 1998;43(5):1096-1101. 

Not sensitivity or specificity of an identified test

Crabtree J E, Heatley R V, Trejdosiewicz L K et al. T

lymphocyte stimulation of human small intestinal 

glycoprotein biosynthesis: effects of anti-CD3 antibody on

normal and coeliac mucosa. International Archives of 

Allergy and Applied Immunology 1990;93(1):35-40. Not 

sensitivity or specificity of an identified test 

Cremata J A, Sorell L, Montesino R et al.

Hypogalactosylation of serum IgG in patients with coeliac 

disease. Clinical and Experimental Immunology

2003;133(3):422-429. Not sensitivity or specificity of an

identified test 

Crenn Pascal, Vahedi Kouroche, Lavergne-Slove Anne et 

al. Plasma citrulline: A marker of enterocyte mass in

villous atrophy-associated small bowel disease.

Gastroenterology 2003;124(5):1210-1219. Not sensitivity

or specificity of an identified test

Cristallo M, Braga M, Agape D et al. Nutritional status,

function of the small intestine and jejunal morphology after

total gastrectomy for carcinoma of the stomach. Surgery,

Gynecology & Obstetrics 1986;163(3):225-230. Not 

sensitivity or specificity of an identified test 

Crofton R W, Gvozdanovic S, Gvozdanovic D. Abnormal 

oral zinc tolerance but normal true absorption of zinc in

coeliac disease?. Nutr Res 1985;5(Suppl 1):S-410. Not 

sensitivity or specificity of an identified test 

Cronin C, Shanahan F. A significant step in the celiac 

puzzle. Gastroenterology 1998;114(6):1339-1341. Not 

sensitivity or specificity of an identified test 

Cronin C C, Feighery A, Ferriss J B et al. High prevalence

of celiac disease among patients with insulin-dependent 

(type I) diabetes mellitus. American Journal of 

Gastroenterology 1997;92(12):2210-2212. Not sensitivity

or specificity of an identified test

Cronin C C, Jackson L M, Feighery C et al. Coeliac disease

and epilepsy. Qjm - Monthly Journal of the Association of 

Physicians 1998;91(4):303-308. Not sensitivity or

specificity of an identified test

Cronin Cornelius C, Shanahan Fergus. Exploring the 

iceberg--the spectrum of celiac disease. American Journal 

of Gastroenterology 2003;98(3):518-520. Not sensitivity or 

specificity of an identified test

Cryan E M, Stevens F M, Skehill R et al. Immunoglobulins 

in healthy controls: HLA-B8 and sex differences. Tissue 

Antigens 1985;26(4):254-258. Not sensitivity or specificity

of an identified test 

Csizmadia C G D S, Mearin M L, Von Blomberg B M E et 

al. An iceberg of childhood coeliac disease in the 

Netherlands. Lancet 1999;353(9155):813-814. Not 

sensitivity or specificity of an identified test 

Csizmadia C G, Mearin M L, Oren A et al. Accuracy and 

cost-effectiveness of a new strategy to screen for celiac

disease in children with Down syndrome. Journal of 

Pediatrics 2000;137(6):756-761. Improper control group 

Cuillerier E, Landi B, Cellier C. Is push enteroscopy useful 

in patients with malabsorption of unclear origin?. American 

Journal of Gastroenterology 2001;96(7):2103-2106. Not 

sensitivity or specificity of an identified test 

Cummins A G, Thompson F M, Butler R N et al. 

Improvement in intestinal permeability precedes

morphometric recovery of the small intestine in coeliac 

disease. Clinical Science (London, England - 1979) 

2001;100(4):379-386. Not sensitivity or specificity of an

identified test 

Cunningham-Rundles S, Cunningham-Rundles C, Pollack

M S. Response to wheat antigen in in vitro lymphocyte 

transformation among HLA-B8-positive normal donors. 

Transplant Proc 1978;10(4):977-979. Not sensitivity or

specificity of an identified test

Cuoco L, Cammarota G, Jorizzo R A et al. Link between

Helicobacter pylori infection and iron-deficiency anaemia

in patients with coeliac disease. Scandinavian Journal of

Gastroenterology 2001;36(12):1284-1288. Not sensitivity

or specificity of an identified test

Cuoco L, Cammarota G, Tursi A et al. Disappearance of

gastric mucosa-associated lymphoid tissue in coeliac

patients after gluten withdrawal. Scandinavian Journal of

Gastroenterology 1998;33(4):401-405. Not sensitivity or 

specificity of an identified test

Cuoco L, Certo M, Jorizzo R A et al. Prevalence and early

diagnosis of coeliac disease in autoimmune thyroid 

disorders. Italian Journal of Gastroenterology and 

A-354
Hepatology 1999;31(4):283-287. Not sensitivity or 

specificity of an identified test

Cuomo A, Romano M, Rocco A et al. Reflux oesophagitis

in adult coeliac disease: Beneficial effect of a gluten free

diet. Gut 2003;52(4):514-517. Not sensitivity or specificity

of an identified test 

Cuzzi-Maya T, Sidbury R, Epstein W L et al. 

Thrombomodulin expression on dermal cells in normal and

psoriatic skin. Archives of Dermatological Research 

1998;290(5):233-239. Not sensitivity or specificity of an

identified test 

Czaja A J. Autoimmune liver disease. Curr Opin

Gastroenterol 1999;15(3):240-248. Not sensitivity or 

specificity of an identified test

Czaja A J, Norman G L. Autoantibodies in the diagnosis 

and management of liver disease. Journal of Clinical 

Gastroenterology 2003;37(4):315-329. Not sensitivity or 

specificity of an identified test

Czaja A J, Santrach P J, Moore S B. HLA-DQ associations

in type 1 autoimmune hepatitis. Mayo Clin Proc 

1995;70(12):1154-1160. Not sensitivity or specificity of an 

identified test 

D'Agostino L, Ciacci C, Daniele B et al. Postheparin 

plasma diamine oxidase in subjects with small bowel 

mucosal atrophy. Digestive Diseases and Sciences

1987;32(3):313-317. Not sensitivity or specificity of an 

identified test 

D'Agostino L, Daniele B, Pignata S et al. Postheparin 

plasma diamine oxidase increases in patients with coeliac 

disease during gluten free diet. Gut 1987;28 Suppl131-134. 

Not sensitivity or specificity of an identified test

D'Agostino L, Daniele B, Pignata S et al. Postheparin 

plasma diamine oxidase in subjects with small bowel 

disease. Diagnostic efficiency of a simplified test. 

Digestion 1988;41(1):46-54. Not sensitivity or specificity

of an identified test 

D'Argenio G, Biancone L, Cosenza V et al.

Transglutaminases in Crohn's disease. Gut 1995;37(5):690-

695. Not sensitivity or specificity of an identified test 

D'Argenio G, Grossman A, Cosenza V et al. Recombinant 

factor XIII improves established experimental colitis in

rats. Digestive Diseases and Sciences 2000;45(5):987-997. 

Not sensitivity or specificity of an identified test

D'Argenio G, Sorrentini I, Ciacci C et al. Human serum

transglutaminase and coeliac disease: correlation between

serum and mucosal activity in an experimental model of rat 

small bowel enteropathy. Gut 1989;30(7):950-954. Not 

sensitivity or specificity of an identified test 

Dadabay C Y, Pike L J. Purification and characterization of

a cytosolic transglutaminase from a cultured human 

tumour-cell line. Biochemical Journal 1989;264(3):679-

685. Not sensitivity or specificity of an identified test 

Dahan S, Slater P E, Cooper M et al. Coeliac disease in the 

Rehovot-Ashdod region of Israel: incidence and ethnic 

distribution. Journal of Epidemiology and Community

Health 1984;38(1):58-60. Not sensitivity or specificity of

an identified test

Dahele A, Ghosh S. Vitamin B12 deficiency in untreated 

celiac disease. American Journal of Gastroenterology

2001;96(3):745-750. Not sensitivity or specificity of an 

identified test 

Dahele Anna, Aldhous Marian C, Kingstone Kathleen et al. 

Gut mucosal immunity to tissue transglutaminase in 

untreated celiac disease and other gastrointestinal disorders.

Digestive Diseases and Sciences 2002;47(10):2325-2335. 

Improper control group 

Dahlqvist A, Lindberg T, Meeuwisse G et al. Intestinal

dipeptidases and disaccharidases in children with

malabsorption. Acta Paediatrica Scandinavica 

1970;59(6):621-630. Not sensitivity or specificity of an 

identified test 

Dahlqvist G. Celiac disease and insulin-dependent diabetes

mellitus--no proof for a causal association. Acta Paediatr 

1995;84(12):1337-1338. Not sensitivity or specificity of an 

identified test 

Dallabrida S M, Falls L A, Farrell D H. Factor XIIIa 

supports microvascular endothelial cell adhesion and 

inhibits capillary tube formation in fibrin. Blood 

2000;95(8):2586-2592. Not sensitivity or specificity of an

identified test 

Damoiseaux Jan G M C, Bouten Bas, Linders Annick M L 

W et al. Diagnostic value of anti-Saccharomyces cerevisiae

and antineutrophil cytoplasmic antibodies for inflammatory

bowel disease: high prevalence in patients with celiac 

disease. Journal of Clinical Immunology 2002;22(5):281-

288. Not sensitivity or specificity of an identified test 

Damoiseaux J G M C, Tervaert J W C. Celiac disease: the

role of (auto)antibody detection in diagnosis and follow-up. 

Netherlands Journal of Medicine 2002;60(7):303-304. Not 

sensitivity or specificity of an identified test 

Dandalides S M, Carey W D, Petras R et al. Endoscopic 

small bowel mucosal biopsy: a controlled trial evaluating 

forceps size and biopsy location in the diagnosis of normal 

and abnormal mucosal architecture. Gastrointestinal 

Endoscopy 1989;35(3):197-200. Not sensitivity or

specificity of an identified test

Danielsson L, Stenhammar L, Astrom E. Is gluten

challenge necessary for the diagnosis of coeliac disease in

young children?. Scandinavian Journal of Gastroenterology

1990;25(9):957-960. Not sensitivity or specificity of an 

identified test 

A-355
Dardik R, Shenkman B, Tamarin I et al. Factor XIII 

mediates adhesion of platelets to endothelial cells through 

alpha(v)beta(3) and glycoprotein IIb/IIIa integrins. 

Thrombosis Research 2002;105(4):317-323. Not sensitivity

or specificity of an identified test

Darke C, Winkler S, Guttridge M G et al. Molecular,

serological and population studies of the alleles and 

products of HLA-B*41. Exp Clin Immunogenet 

1999;16(3):139-149. Not sensitivity or specificity of an 

identified test 

Datta M, Shtauvere-Brameus A, Gupta V et al. 

Autoimmune diabetes in 26 villages outside Madras. Ann 

New York Acad Sci 2002;958(-):285-288. Not sensitivity

or specificity of an identified test

Daum S, Bauer U, Foss H D et al. Increased expression of 

mRNA for matrix metalloproteinases-1 and -3 and tissue 

inhibitor of metalloproteinases-1 in intestinal biopsy

specimens from patients with coeliac disease. Gut

1999;44(1):17-25. Not sensitivity or specificity of an 

identified test 

Daum S, Bauer U, Foss H D et al. Expression of matrix 

metalloprotease-1 and collagen I mRNA in biopsies from 

patients with celiac disease. Annals of the New York 

Academy of Sciences 1998;859254-257. Not sensitivity or

specificity of an identified test

Daum S, Weiss D, Hummel M et al. Frequency of clonal 

intraepithelial T lymphocyte proliferations in enteropathytype intestinal T cell lymphoma, coeliac disease, and 

refractory sprue. Gut 2001;49(6):804-812. Not sensitivity

or specificity of an identified test

Dausset J. Biologic role of the HLA system. HLA complex 

in human biology in the light of associations with disease. 

Transplantation Proceedings 1977;9(1):523-529. Not 

sensitivity or specificity of an identified test 

Dausset J, Hors J. Some contributions of the HL-A

complex to the genetics of human diseases. Transplantation

Reviews 1975;2244-74. Not sensitivity or specificity of an 

identified test 

David T J, Ajdukiewicz A B. A family study of coeliac 

disease. J Med Genet 1975;12(1):79-82. Not sensitivity or 

specificity of an identified test

Davidson A G, Hassall E G. Screening for celiac disease.

Cmaj - Canadian Medical Association Journal = Journal De 

L'association Medicale Canadienne 1997;157(5):547-548. 

Not sensitivity or specificity of an identified test

Davies M L, Taylor E J, Gordon C et al. Candidate T cell 

epitopes of the human La/SSB autoantigen. Arthritis 

Rheum 2002;46(1):209-214. Not sensitivity or specificity

of an identified test 

Davies P J A, Cornwell M M, Johnson J D. Studies on the 

effects of dansylcadaverine and related compounds on 

receptor-mediated endocytosis in cultured cells. Diabetes 

Care 1984;7(Suppl 1):35-41. Not sensitivity or specificity

of an identified test 

Davies P J, Chiocca E A, Stein J P. Retinoid--regulated 

expression of tissue transglutaminase in normal and 

leukemic myeloid cells. Advances in Experimental

Medicine and Biology 1988;23163-71. Not sensitivity or

specificity of an identified test

Davies P J, Murtaugh M P, Moore W T et al. Retinoic acidinduced expression of tissue transglutaminase in human 

promyelocytic leukemia (HL-60) cells. Journal of

Biological Chemistry 1985;260(8):5166-5174. Not 

sensitivity or specificity of an identified test 

Dawood F H, Jabbar A A, Al Mudaris A F et al. 

Association of HLA antigens with coeliac disease among 

Iraqi children. Tissue Antigens 1981;18(1):35-39. Not 

sensitivity or specificity of an identified test 

Dawson D J, Lobley R W, Burrows P C. Lactose digestion

by human jejunal biopsies: The relationship between 

hydrolysis and absorption. Gut 1986;27(5):521-527. Not 

sensitivity or specificity of an identified test 

Dawson D J, Lobley R W, Burrows P C et al. Changes in

jejunal permeability and passive permeation of sugars in 

intestinal biopsies in coeliac disease and Crohn's disease. 

Clinical Science (London, England - 1979)

1988;74(4):427-431. Not sensitivity or specificity of an 

identified test 

Dawson J, Bryant M G, Bloom S R et al. Gastrointestinal

regulatory peptide storage granule abnormalities in jejunal 

mucosal diseases. Gut 1984;25(6):636-643. Not sensitivity

or specificity of an identified test

Day A S, Cook H B, Whitehead M et al. Anti-endomysial 

and anti-gliadin antibodies in screening for coeliac disease 

in children at greater risk of developing coeliac disease. 

New Zealand Medical Journal 2000;113(1119):412-413. 

Improper control group 

De Block C E, De Leeuw I, Vertommen J J et al. Beta-cell,

thyroid, gastric, adrenal and coeliac autoimmunity and 

HLA-DQ types in type 1 diabetes. Clinical and

Experimental Immunology 2001;126(2):236-241. Not 

sensitivity or specificity of an identified test 

De Giacomo C, Gianatti A, Negrini R et al. Lymphocytic

gastritis: a positive relationship with celiac disease. Journal

of Pediatrics 1994;124(1):57-62. Not sensitivity or

specificity of an identified test

de la, Concha E G, Fernandez-Arquero M et al. Celiac 

disease and TNF promoter polymorphisms. Human 

Immunology 2000;61(5):513-517. Not sensitivity or 

specificity of an identified test

de la, Paz Bettinotti M, Kolek A et al. Polymorphism of the

5' flanking region of the HLA-DQA1 gene in coeliac 

A-356
disease. European Journal of Immunogenetics - Official 

Journal of the British Society for Histocompatibility and

Immunogenetics 1993;20(5):399-407. Not sensitivity or

specificity of an identified test

de Launey W E. Letter: Dermatitis herpetiformis and the 

enteropathy of celiac disease. Archives of Dermatology 

1974;110(2):301Not sensitivity or specificity of an 

identified test 

de Lecea A, Ribes-Koninckx C, Polanco I et al. Serological 

screening (antigliadin and antiendomysium antibodies) for

non-overt coeliac disease in children of short stature. Acta 

Paediatrica (Oslo, Norway - 1992).Supplement 

1996;41254-55. Improper control group 

De Libero G, Rocci M P, Casorati G et al. T cell receptor 

heterogeneity in gammadelta T cell clones from intestinal

biopsies of patients with celiac disease. Eur J Immunol 

1993;23(2):499-504. Not sensitivity or specificity of an 

identified test 

De Martelaere D, Cassiman J J, van Leuven F. Human 

osteosarcoma derived clonal variants: Stable differences in 

cell surface composition. Cell Biol Int Rep 1982;6(5):489-

494. Not sensitivity or specificity of an identified test 

de Pablo R, Vilches C, Moreno M E et al. Distribution of

HLA antigens in Spanish Gypsies: a comparative study.

Tissue Antigens 1992;40(4):187-196. Not sensitivity or

specificity of an identified test

de Ritis G, Auricchio S, Jones H W et al. In vitro (organ

culture) studies of the toxicity of specific A-gliadin 

peptides in celiac disease. Gastroenterology 1988;94(1):41-

49. Not sensitivity or specificity of an identified test 

de Sousa J S, Duarte J P. Letter: Fingerprints in childhood 

coeliac disease. Archives of Disease in Childhood

1974;49(1):80Not sensitivity or specificity of an identified

test 

De Vizia B, Poggi V, Conenna R et al. Iron absorption and 

iron deficiency in infants and children with gastrointestinal

diseases. Journal of Pediatric Gastroenterology and 

Nutrition 1992;14(1):21-26. Not sensitivity or specificity of 

an identified test

De Vos M. Articular diseases and the gut: evidence for a 

strong relationship between spondylarthropathy and 

inflammation of the gut in man. Acta Clinica Belgica

1990;45(1):20-24. Not sensitivity or specificity of an 

identified test 

De Vries N, Van Elderen C, Tijssen H et al. No support for 

HLA-DQ encoded susceptibility in rheumatoid arthritis.

Arthritis Rheum 1999;42(8):1621-1627. Not sensitivity or 

specificity of an identified test

de Freitas I, Sipahi Aytan, Miranda Damiao et al. Celiac 

disease in Brazilian adults. Journal of Clinical 

Gastroenterology 2002;34(4):430-434. Not sensitivity or 

specificity of an identified test

De Laurenzi V, Melino G. Gene disruption of tissue 

transglutaminase. Mol Cell Biol 2001;21(1):148-155. Not 

sensitivity or specificity of an identified test 

De Vitis I, Ghirlanda G, Gasbarrini G. Prevalence of 

coeliac disease in type I diabetes: a multicentre study. Acta

Paediatrica (Oslo, Norway - 1992).Supplement 

1996;41256-57. Not sensitivity or specificity of an 

identified test 

Dedeoglu Alpaslan, Kubilus James K, Jeitner Thomas M et

al. Therapeutic effects of cystamine in a murine model of

Huntington's disease. Journal of Neuroscience - the Official

Journal of the Society for Neuroscience 2002;22(20):8942-

8950. Not sensitivity or specificity of an identified test 

Defacque H, Commes T, Contet V et al. Differentiation of

U937 myelomonocytic cell line by all-trans retinoic acid

and 1,25-dihydroxyvitamin D3: synergistic effects on tissue 

transglutaminase. Leukemia - Official Journal of the 

Leukemia Society of America, Leukemia Research Fund, 

U.k 1995;9(10):1762-1767. Not sensitivity or specificity of 

an identified test

deFranchis R, Primignani M, Cipolla M et al. Small-bowel

involvement in dermatitis herpetiformis and in linear-IgA 

bullous dermatosis. Journal of Clinical Gastroenterology

1983;5(5):429-436. Not sensitivity or specificity of an 

identified test 

Degli-Esposti M A, Abraham L J, McCann V et al. 

Ancestral haplotypes reveal the role of the central MHC in 

the immunogenetics of IDDM. Immunogenetics 

1992;36(6):345-356. Not sensitivity or specificity of an 

identified test 

Deininger M H, Grote E, Wickboldt J et al. Distinct 

radiochemotherapy protocols differentially influence 

cellular proliferation and expression of p53 and Bcl-2 in 

glioblastoma multiforme relapses in vivo. J Neuro-Oncol 

2000;48(2):121-129. Not sensitivity or specificity of an 

identified test 

Dejmek A, Hjerpe A. Reactivity of six antibodies in 

effusions of mesothelioma, adenocarcinoma and

mesotheliosis: stepwise logistic regression analysis. 

Cytopathology - Official Journal of the British Society for

Clinical Cytology 2000;11(1):8-17. Not sensitivity or 

specificity of an identified test

Del Rosario M A, Fitzgerald J F, Chong S K et al. Further 

studies of anti-endomysium and anti-gliadin antibodies in

patients with suspected celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 1998;27(2):191-195. 

Improper control group 

Deller D J, Murrell T G, Blowes R. Jejunal biopsy in 

malignant disease. Australasian Annals of Medicine 

1967;16(3):236-241. Not sensitivity or specificity of an 

identified test 

A-357
Delprato G R, Petit-Phar M, Maadi A B et al. IgA 

antigliadin antibodies as a possible marker for IgA 

mesangial glomerulonephritis in adults with primary 

glomerulonephritis. New Engl J Med 1989;320(19):1283-

1284. Not sensitivity or specificity of an identified test 

DeMarchi M, Borelli I, Olivetti E et al. Two HLA-D and 

DR alleles are associated with coeliac disease. Tissue 

Antigens 1979;14(4):309-316. Not sensitivity or specificity

of an identified test 

DeMarchi M, Carbonara A, Ansaldi N et al. HLA-DR3 and 

DR7 in coeliac disease: immunogenetic and clinical 

aspects. Gut 1983;24(8):706-712. Not sensitivity or 

specificity of an identified test

Demediuk B. Investigating a patient with a positive test for 

antigliadin antibodies. Med Today 2001;2(9):87Not 

sensitivity or specificity of an identified test 

Demir H, Yuce A, Kocak N et al. Celiac disease in Turkish 

children: presentation of 104 cases. Pediatrics International 

- Official Journal of the Japan Pediatric Society 

2000;42(5):483-487. Improper control group 

Dempfle C E, Harenberg J, Hochreuter K et al. Microtiter

assay for measurement of factor XIII activity in plasma. 

Journal of Laboratory and Clinical Medicine

1992;119(5):522-528. Not sensitivity or specificity of an

identified test 

Deng Lei, Shipley Gregory L, Loose-Mitchell David S et 

al. Coordinate regulation of the production and signaling of 

retinoic acid by estrogen in the human endometrium. 

Journal of Clinical Endocrinology and Metabolism 

2003;88(5):2157-2163. Not sensitivity or specificity of an

identified test 

Dennis N R, Stokes C R. Risk of coeliac disease in children

of patients and effect of HLA genotype. Journal of Medical 

Genetics 1978;15(1):20-22. Not sensitivity or specificity of 

an identified test

Deprez Pierre H, Sempoux Christine, De Saeger et al. 

Expression of cholecystokinin in the duodenum of patients 

with coeliac disease: respective role of atrophy and 

lymphocytic infiltration. Clinical Science (London, 

England - 1979) 2002;103(2):171-177. Not sensitivity or

specificity of an identified test

DerSimonian H, Sugita M, Glass D N et al. Clonal 

Valpha12.1sup + T cell expansions in the peripheral blood

of rheumatoid arthritis patients. J Exp Med

1993;177(6):1623-1631. Not sensitivity or specificity of an 

identified test 

Desai H G, Chitre A V, Jeejeebhoy K N. Lactose loading.

A simple test for detecting intestinal lactase. Evaluation of 

different methods. Gastroenterologia 1967;108(4):177-188. 

Not sensitivity or specificity of an identified test

Desjeux J F, Sandler L, Sassier P et al. Acquired and 

congenital disorders of intestinal transport of D. glucose in 

children. Revue Europeenne D'etudes Cliniques Et 

Biologiques.European Journal of Clinical and Biological 

Research 1971;16(4):364-366. Not sensitivity or specificity

of an identified test 

Desombere I, Van der, Wielen M et al. Immune response of 

HLA DQ2 positive subjects, vaccinated with HBsAg/AS04, 

a hepatitis B vaccine with a novel adjuvant. Vaccine 

2002;20(19-20):2597-2602. Not sensitivity or specificity of 

an identified test

Devery J M, La Brooy J T, Krillis S et al. Anti-gliadin 

antibody specificity for gluten-derived peptides toxic to 

coeliac patients. Clinical and Experimental Immunology

1989;76(3):384-390. Not sensitivity or specificity of an 

identified test 

Devi Rampertab S, Fleischauer A, Neugut A I et al. Risk of 

duodenal adenoma in celiac disease. Scandinavian Journal 

of Gastroenterology 2003;38(8):831-833. Not sensitivity or 

specificity of an identified test

Devine D V. Novel markers for the detection of platelet

activation. Transfusion Medicine Reviews 1990;4(2):115-

120. Not sensitivity or specificity of an identified test 

Devine P L, Birrell G W, Golder J P et al. Screening and 

monitoring coeliac disease: multicentre trial of a new serum

antibody test kit. Disease Markers 1994;12(1):71-80. 

Improper control group 

Dewar D, Pereira S P, Ciclitira P J. The pathogenesis of 

coeliac disease. Int J Biochem Cell Biol 2004;36(1):17-24. 

Not sensitivity or specificity of an identified test

Dezi R, Niveloni S, Sugai E et al. Gluten sensitivity in the

rectal mucosa of first-degree relatives of celiac disease 

patients. American Journal of Gastroenterology

1997;92(8):1326-1330. Not sensitivity or specificity of an

identified test 

Dhar A, Goenka M K. Endomysial antibody and celiac 

disease. Indian Journal of Gastroenterology - Official 

Journal of the Indian Society of Gastroenterology

1993;12(4):157-158. Not sensitivity or specificity of an 

identified test 

Dhesi I, Marsh M N, Kelly C et al. Morphometric analysis 

of small intestinal mucosa. II. Determination of lamina 

propria volumes; plasma cell and neutrophil populations 

within control and coeliac disease mucosae. Virchows

Archiv.A, Pathological Anatomy and Histopathology

1984;403(2):173-180. Not sensitivity or specificity of an

identified test 

Di Mario U, Anastasi E, Mariani P et al. Diabetes-related

autoantibodies do appear in children with coeliac disease. 

Acta Paediatrica (Oslo, Norway - 1992) 1992;81(8):593-

597. Not sensitivity or specificity of an identified test 

A-358
Di Sabatino A, Bertrandi E, Casadei Maldini M et al. 

Phenotyping of peripheral blood lymphocytes in adult 

coeliac disease. Immunology 1998;95(4):572-576. Not 

sensitivity or specificity of an identified test 

Di Sabatino A, Ciccocioppo R, D'Alo S et al. Intraepithelial 

and lamina propria lymphocytes show distinct patterns of 

apoptosis whereas both populations are active in Fas based 

cytotoxicity in coeliac disease. Gut 2001;49(3):380-386. 

Not sensitivity or specificity of an identified test

Di Stefano M, Jorizzo R A, Veneto G et al. Bone mass and 

metabolism in dermatitis herpetiformis. Digestive Diseases

and Sciences 1999;44(10):2139-2143. Not sensitivity or

specificity of an identified test

Diamanti A, Maino C, Niveloni S et al. Characterization of

gastric mucosal lesions in patients with celiac disease: a

prospective controlled study. American Journal of

Gastroenterology 1999;94(5):1313-1319. Not sensitivity or 

specificity of an identified test

Dias J, Unsworth D J, Walker-Smith J A. Antigliadin and 

antireticulin antibodies in screening for coeliac disease. 

Lancet 1987;2(8551):157-158. Not sensitivity or specificity

of an identified test 

Dickey W. Diagnosis of coeliac disease at open-access

endoscopy. Scandinavian Journal of Gastroenterology

1998;33(6):612-615. Not sensitivity or specificity of an 

identified test 

Dickey W. Endoscopy, serology and histology in the 

diagnosis of coeliac disease. Digestive and Liver Disease -

Official Journal of the Italian Society of Gastroenterology

and the Italian Association for the Study of the Liver 

2002;34(3):172-174. Not sensitivity or specificity of an 

identified test 

Dickey W. Epilepsy, cerebral calcifications, and coeliac 

disease. Lancet 1994;344(8937):1585-1586. Not sensitivity

or specificity of an identified test

Dickey W, Hughes D. Disappointing sensitivity of

endoscopic markers for villous atrophy in a high-risk 

population: implications for celiac disease diagnosis during 

routine endoscopy. American Journal of Gastroenterology

2001;96(7):2126-2128. Not sensitivity or specificity of an

identified test 

Dickey W, Hughes D. Prevalence of celiac disease and its 

endoscopic markers among patients having routine upper

gastrointestinal endoscopy. American Journal of 

Gastroenterology 1999;94(8):2182-2186. Not sensitivity or 

specificity of an identified test

Dickey W, McConnell J B. How many hospital visits does 

it take before celiac sprue is diagnosed?. Journal of Clinical 

Gastroenterology 1996;23(1):21-23. Not sensitivity or 

specificity of an identified test

Dickey W, Hughes D F, McMillan S A. Disappearance of 

endomysial antibodies in treated celiac disease does not 

indicate histological recovery. American Journal of 

Gastroenterology 2000;95(3):712-714. Not sensitivity or 

specificity of an identified test

Dickey W, Hughes D F, McMillan S A. Reliance on serum 

endomysial antibody testing underestimates the true 

prevalence of coeliac disease by one fifth. Scandinavian

Journal of Gastroenterology 2000;35(2):181-183. Unable to

extract data

Dickey W, Kenny B D, McMillan S A et al. Gastric as well 

as duodenal biopsies may be useful in the investigation of 

iron deficiency anaemia. Scandinavian Journal of 

Gastroenterology 1997;32(5):469-472. Not sensitivity or 

specificity of an identified test

Dickey W, McMillan S A, Callender M E. High prevalence

of celiac sprue among patients with primary biliary

cirrhosis. Journal of Clinical Gastroenterology

1997;25(1):328-329. Not sensitivity or specificity of an 

identified test 

Dickey W, McMillan S A, Hughes D F. Identification of 

coeliac disease in primary care. Scandinavian Journal of

Gastroenterology 1998;33(5):491-493. Not sensitivity or 

specificity of an identified test

Dickey W, McMillan S A, Bharucha C et al. Antigliadin

antibodies in blood donors in Northern Ireland. European 

Journal of Gastroenterology & Hepatology 1992;4(9):739-

741. Not sensitivity or specificity of an identified test 

Dickey W, McMillan S A, McCrum E E et al. Association

between serum levels of total IgA and IgA class 

endomysial and antigliadin antibodies: implications for 

coeliac disease screening. European Journal of

Gastroenterology & Hepatology 1997;9(6):559-562. 

Improper control group 

Dickey W, Stewart F, Nelson J et al. Screening for coeliac 

disease as a possible maternal risk factor for neural tube 

defect. Clinical Genetics 1996;49(2):107-108. Not 

sensitivity or specificity of an identified test 

Dickey William. Low serum vitamin B12 is common in

coeliac disease and is not due to autoimmune gastritis.

European Journal of Gastroenterology & Hepatology

2002;14(4):425-427. Not sensitivity or specificity of an 

identified test 

Dieterich W, Ehnis T, Bauer M et al. Identification of 

tissue transglutaminase as the autoantigen of celiac disease.

Nature Medicine 1997;3(7):797-801. Not sensitivity or 

specificity of an identified test

Dieterich W, Esslinger B, Schuppan D. Pathomechanisms 

in celiac disease. Int Arch Allergy Immunol 

2003;132(2):98-108. Not sensitivity or specificity of an 

identified test 

Dieterich W, Laag E, Bruckner-Tuderman L et al. 

A-359
Antibodies to tissue transglutaminase as serologic markers 

in patients with dermatitis herpetiformis. Journal of 

Investigative Dermatology 1999;113(1):133-136. Not 

sensitivity or specificity of an identified test 

Dieterich W, Laag E, Schopper H et al. Autoantibodies to

tissue transglutaminase as predictors of celiac disease.

Gastroenterology 1998;115(6):1317-1321. Improper 

control group 

Dieterich W, Storch W B, Schuppan D. Serum antibodies

in celiac disease. Clinical Laboratory 2000;46(7-8):361-

364. Review article 

Dieterich W, Trapp D, Esslinger B et al. Autoantibodies of 

patients with coeliac disease are insufficient to block tissue 

transglutaminase activity. Gut 2003;52(11):1562-1566. Not 

sensitivity or specificity of an identified test 

Dieye A, Diaw M L, Rogier C et al. HLA-A, -B, -C, -DR, -

DQ typing in a population group of Senegal: Distribution 

of HLA antigens and HLA-DRB 1(*)13 and DRB 1(*)11 

subtyping by PCR using sequence-specific primers (PCRSSP). Tissue Antigens 1996;47(3):194-199. Not sensitivity

or specificity of an identified test

Dinari G, Rosenbach Y, Marcus H et al. IgA antigliadin

antibodies in childhood celiac disease. Israel Journal of

Medical Sciences 1988;24(6):286-290. Serology <1990 

Dinari G, Zahavi I, Marcus H et al. Placental ferritin in

coeliac disease: relation to clinical stage, origin, and 

possible role in the pathogenesis of malignancy. Gut 

1991;32(9):999-1003. Not sensitivity or specificity of an

identified test 

Dissanayake A S, Truelove S C, Whitehead R. Jejunal 

mucosal recovery in coeliac disease in relation to the

degree of adherence to a gluten-free diet. Quarterly Journal 

of Medicine 1974;43(170):161-185. Not sensitivity or 

specificity of an identified test

Dissanayake A S, Truelove S C, Whitehead R. Lack of

harmful effect of oats on small-intestinal mucosa in coeliac 

disease. British Medical Journal 1974;4(5938):189-191. 

Not sensitivity or specificity of an identified test

Djilali-Saiah I, Benini V, Schmitz J et al. Absence of 

primary association between DM gene polymorphism and 

insulin-dependent diabetes mellitus or celiac disease. 

Human Immunology 1996;49(1):22-27. Not sensitivity or 

specificity of an identified test

Djilali-Saiah I, Caillat-Zucman S, Schmitz J et al. 

Polymorphism of antigen processing (TAP, LMP) and 

HLA class II genes in celiac disease. Human Immunology

1994;40(1):8-16. Improper control group 

Djilali-Saiah I, Schmitz J, Harfouch-Hammoud E et al. 

CTLA-4 gene polymorphism is associated with

predisposition to coeliac disease. Gut 1998;43(2):187-189. 

Improper control group 

Djoulah S, Khalil I, Beressi J P et al. The HLADRB1*0405 haplotype is most strongly associated with 

IDDM in Algerians. European Journal of Immunogenetics -

Official Journal of the British Society for

Histocompatibility and Immunogenetics 1992;19(6):381-

389. Not sensitivity or specificity of an identified test 

Dobbins W O, Tomasini J T, Rollins E L. Electron and 

light microscopic identification of the mast cell of the

gastrointestinal tract. Gastroenterology 1969;56(2):268-

279. Not sensitivity or specificity of an identified test 

Dobru D, Pascu O, Tant cedil et al. The prevalence of

coeliac disease at endoscopy units in Romania: Routine 

biopsies during gastroscopy are mandatory (A multicentre 

study). Rom J Gastroenterol 2003;12(2):97-100. Not 

sensitivity or specificity of an identified test 

Dohan F C. Schizophrenia, celiac disease, gluten

antibodies, and the importance of beta. Biological 

Psychiatry 1981;16(11):1115-1117. Not sensitivity or 

specificity of an identified test

Doherty M, Barry R E. Gluten-induced mucosal changes in

subjects without overt small-bowel disease. Lancet 

1981;1(8219):517-520. Not sensitivity or specificity of an

identified test 

Dollberg L, Gurevitz M, Freier S. Gastrointestinal mast 

cells in health, and in coeliac disease and other conditions. 

Arch Dis Child 1980;55(9):702-705. Not sensitivity or

specificity of an identified test

Dolly J O, Fottrell P F. Multiple forms of dipeptidases in 

normal human intestinal mucosa and in mucosa from 

children with coeliac disease. Clinica Chimica Acta 

1969;International Journal of Clinical Chemistry;

26(3):555-558. Not sensitivity or specificity of an identified 

test 

Dolly J O, Dillon A, Duffy M J et al. Further studies on 

multiple forms of peptidases in mammalian tissues 

including intestinal mucosa from children with treated and 

untreated coeliac disease. Clinica Chimica Acta

1971;International Journal of Clinical Chemistry; 31(1):55-

62. Not sensitivity or specificity of an identified test 

Dolynchuk K N, Pettigrew N M. Transglutaminase levels

in Dupuytren's disease. Journal of Hand Surgery

1991;16(5):787-790. Not sensitivity or specificity of an 

identified test 

Dolynchuk K N, Ziesmann M, Serletti J M. Topical

putrescine (Fibrostat) in treatment of hypertrophic scars:

phase II study. Plastic and Reconstructive Surgery 

1996;97(1):117-123. Not sensitivity or specificity of an 

identified test 

Domenico Sebastiani G, Minisola G, Galeazzi M. HLA 

class II alleles and genetic predisposition to the

antiphospholipid syndrome. Autoimmun Rev 

A-360
2003;2(6):387-394. Not sensitivity or specificity of an 

identified test 

Domschke S, Bloom S R, Adrian T E et al. Abundance of 

VIP in duodenal mucosa of coeliacs and duodenal ulcer

patients. Peptides 1984;5(2):411-413. Not sensitivity or

specificity of an identified test

Domschke S, Bloom S R, Adrian T E et al. Coeliac sprue:

abnormalities of the hormone profile of gastroduodenal 

mucosa. Scandinavian Journal of 

Gastroenterology.Supplement 1989;16786-89. Not 

sensitivity or specificity of an identified test 

Doniach S. The impact of intestinal biopsy on 

gastroenterology. Gastroenterology 1968;54(4):SupplNot 

sensitivity or specificity of an identified test 

Donner H, Seidl C, Braun J et al. CTLA4 gene haplotypes 

cannot protect from IDDM in the presence of high-risk 

HLA DQ8 or DQ2 alleles in German families. Diabetes 

1998;47(7):1158-1160. Not sensitivity or specificity of an

identified test 

Donohoue P A, Guethlein L, Collins M M et al. The HLAA3,Cw6,B47,DR7 extended haplotypes in salt losing 21-

hydroxylase deficiency and in the Old Order Amish: 

Identical class I antigens and class II alleles with at least

two crossover sites in the class III region. Tissue Antigens 

1995;46(3 I):163-172. Not sensitivity or specificity of an

identified test 

Douglas A P, Crabbe P A, Hobbs J R. Immunochemical 

studies on the serum, intestinal secretions and intestinal

mucosa in patients with adult celiac disease and other 

forms of the celiac syndrome. Gastroenterology

1970;59(3):414-425. Not sensitivity or specificity of an 

identified test 

Douthwaite J A, Johnson T S, Haylor J L et al. Effects of

transforming growth factor-beta1 on renal extracellular

matrix components and their regulating proteins. Journal of 

the American Society of Nephrology - Jasn 

1999;10(10):2109-2119. Not sensitivity or specificity of an 

identified test 

Douvin C, Simon D, Charles M-A et al. Hepatitis B 

vaccination in diabetic patients: Randomized trial 

comparing recombinant vaccines containing and not 

containing pre-S2 antigen. Diabetes Care 1997;20(2):148-

151. Not sensitivity or specificity of an identified test 

Drago S, Di Pierro M, Catassi C et al. Recent developments

in the pathogenesis, diagnosis and treatment of celiac 

disease. Expert Opin Ther Pat 2002;12(1):45-51. Not 

sensitivity or specificity of an identified test 

Drossman D A. Irritable bowel syndrome: how far do you

go in the workup?. Gastroenterology 2001;121(6):1512-

1515. Not sensitivity or specificity of an identified test 

Drover S, Karr R W, Fu X T et al. Analysis of monoclonal 

antibodies specific for unique and shared determinants on 

HLA-DR4 molecules. Human Immunology 1994;40(1):51-

60. Not sensitivity or specificity of an identified test 

Drukker A, Goldstein R, Maeir D M et al. Disaccharidase 

activity in the rectal mucosa. Israel Journal of Medical 

Sciences 1972;8(4):502-507. Not sensitivity or specificity

of an identified test 

Drut R, Rua E C. The histopathology of pediatric celiac 

disease: order must prevail out of chaos. International 

Journal of Surgical Pathology 2001;9(4):261-264. Not 

sensitivity or specificity of an identified test 

Duggan J M. Recent developments in our understanding of

adult coeliac disease. Medical Journal of Australia

1997;166(6):312-315. Not sensitivity or specificity of an

identified test 

Dugoujon J M, Cambon-Thomsen A. Immunoglobulin 

allotypes (GM and KM) and their interactions with HLA 

antigens in autoimmune diseases: a review. Autoimmunity 

1995;22(4):245-260. Not sensitivity or specificity of an 

identified test 

Dumic M, Mardesic D, Plavsic V et al. Coincidence of

pseudohypoaldosteronism with gluten-enteropathy. Journal 

of Endocrinological Investigation 1984;7(4):395-398. Not 

sensitivity or specificity of an identified test 

Duncan A, Park R P, Lee F D et al. A retrospective 

assessment of the clinical value of jejunal disaccharidase

analysis. Scandinavian Journal of Gastroenterology

1994;29(12):1111-1116. Not sensitivity or specificity of an 

identified test 

Dutz W, Asvadi S, Sadri S et al. Intestinal lymphoma and 

sprue: a systematic approach. Gut 1971;12(10):804-810. 

Not sensitivity or specificity of an identified test

Duvic M, Nelson D C, Annarella M et al. Keratinocyte

transglutaminase expression varies in squamous cell 

carcinomas. Journal of Investigative Dermatology

1994;102(4):462-469. Not sensitivity or specificity of an

identified test 

Dvorcakova M, Macejova D, Pallet V et al. 

Transglutamines and endocrine system (minireview). 

Endocrine Regulations 2002;36(1):31-36. Not sensitivity or 

specificity of an identified test

Dwinell M B, Kagnoff M F. Mucosal immunity. Curr Opin 

Gastroenterol 1999;15(1):33-38. Not sensitivity or

specificity of an identified test

Dyduch A, Karczewska K, Grzybek H et al. Transmission 

electron microscopy of microvilli of intestinal epithelial

cells in celiac disease in remission and transient gluten

enteropathy in children after a gluten-free diet. Journal of

Pediatric Gastroenterology and Nutrition 1993;16(3):269-

272. Not sensitivity or specificity of an identified test 

A-361
Eade O E, Lloyd R S, Lang C et al. IgA and IgG reticulin

antibodies in coeliac and non-coeliac patients. Gut 

1977;18(12):991-993. Not sensitivity or specificity of an

identified test 

Eckert R L, Welter J F. Epidermal keratinocytes - genes

and their regulation. Cell Death Differ 1996;3(4):373-383. 

Not sensitivity or specificity of an identified test

Ectors N. Infectious disorders of the duodenum: 

MALADIES INFECTIEUSES DU DUODENUM. Acta 

Endosc 2002;32(2):133-156. Not sensitivity or specificity

of an identified test 

Egan C A, O'Loughlin S, Gormally S et al. Dermatitis

Herpetiformis: a review of fifty-four patients. Irish Journal 

of Medical Science 1997;166(4):241-244. Not sensitivity or 

specificity of an identified test

Egyud L G, Lipinski B. Significance of fibrin formation 

and dissolution in the pathogenesis and treatment of cancer. 

Medical Hypotheses 1991;36(4):336-340. Not sensitivity or 

specificity of an identified test

Ehrmann Jiri, Kolek Antonin, Kod'ousek Rostislav et al. 

Immunohistochemical study of the apoptotic mechanisms 

in the intestinal mucosa during children's coeliac disease.

Virchows Archiv - an International Journal of Pathology

2003;442(5):453-461. Not sensitivity or specificity of an

identified test 

Eichler I, Frisch H, Granditsch G. Growth failure and 

insulin-like growth factor (IGF-I) in childhood celiac 

disease. Klinische Wochenschrift 1991;69(18):825-829. 

Not sensitivity or specificity of an identified test

Eiermann T H, Vejbaesya S, Prestel H et al. Association 

and linkage of human leukocyte antigens with psoriasis - 

Revisited. Infusther Transfusionsmed 2002;29(6):326-330. 

Not sensitivity or specificity of an identified test

Eiras P, Roldan E, Camarero C et al. Flow cytometry

description of a novel CD3-/CD7+ intraepithelial 

lymphocyte subset in human duodenal biopsies: potential 

diagnostic value in coeliac disease. Cytometry - the Journal 

of the Society for Analytical Cytology 1998;34(2):95-102. 

Not sensitivity or specificity of an identified test

Ejderhamn J, Samuelson K, Strandvik B. Serum primary

bile acids in the course of celiac disease in children. Journal 

of Pediatric Gastroenterology and Nutrition 

1992;14(4):443-449. Not sensitivity or specificity of an 

identified test 

Ek J, Albrechtsen D, Solheim B G et al. Strong association

between the HLA-Dw3-related B cell alloantigen -DRw3 

and coeliac disease. Scandinavian Journal of

Gastroenterology 1978;13(2):229-233. Not sensitivity or 

specificity of an identified test

el Alaoui S, Legastelois S, Roch A M et al. 

Transglutaminase activity and N epsilon (gamma glutamyl) 

lysine isopeptide levels during cell growth: an enzymic and

immunological study. International Journal of

Cancer.Journal International Du Cancer 1991;48(2):221-

226. Not sensitivity or specificity of an identified test 

El Gabalawy H S, Goldbach-Mansky R, Smith D et al.

Association of HLA alleles and clinical features in patients

with synovitis of recent onset. Arthritis Rheum

1999;42(8):1696-1705. Not sensitivity or specificity of an

identified test 

el Salhy M. The nature and implication of intestinal 

endocrine cell changes in coeliac disease. Histology and 

Histopathology 1998;13(4):1069-1075. Not sensitivity or 

specificity of an identified test

Elewaut A, Dacremont G, Robberecht E et al. IgA 

isotyping of antigliadin antibodies. A possible clue for a 

less invasive diagnosis of coeliac disease. Clinica Chimica 

Acta 1989;International Journal of Clinical Chemistry;

183(3):285-294. Serology <1990

Elia C, Carneiro A J, Carvalho A T P et al. Small intestinal

morphology in dermatitis herpetiformis: Experience of the 

Federal University Hospital of Rio de Janeiro, Brazil. An 

Bras Dermatol 1998;73(2):87-90. Not sensitivity or 

specificity of an identified test

Eliakim R, Heyman S, Kornberg A. Celiac disease and

keratoconjunctivitis. Occurrence with thrombocytopenic

purpura. Archives of Internal Medicine 

1982;142(5):1037Not sensitivity or specificity of an 

identified test 

Ellis A. The genetic epidemiology of coeliac disease. 

Genetic Epidemiology.Supplement 1986;1267-269. Not 

sensitivity or specificity of an identified test 

Ellis A, Taylor C J, Dillon-Remmy M et al. HLA-DR 

typing in coeliac disease: evidence for genetic

heterogeneity. British Medical Journal (Clinical Research

Ed.) 1984;289(6458):1571-1573. Not sensitivity or 

specificity of an identified test

Ellis H J, Ciclitira P J. In vivo gluten challenge in celiac

disease. Canadian Journal of Gastroenterology = Journal 

Canadien De Gastroenterologie 2001;15(4):243-247. Not 

sensitivity or specificity of an identified test 

Ellis H J, Pollock E L, Engel W et al. Investigation of the 

putative immunodominant T cell epitopes in coeliac 

disease. Gut 2003;52(2):212-217. Not sensitivity or 

specificity of an identified test

Elmes M E, Jones J G, Stanton M R. Changes in the Paneth 

cell population of human small intestine assessed by image 

analysis of the secretory granule area. Journal of Clinical 

Pathology 1983;36(8):867-872. Not sensitivity or

specificity of an identified test

Elms M J, Bunce I H, Bundesen P G et al. Rapid detection

of cross-linked fibrin degradation products in plasma using 

A-362
monoclonal antibody-coated latex particles. American

Journal of Clinical Pathology 1986;85(3):360-364. Not 

sensitivity or specificity of an identified test 

Elsasser H P, MacDonald R, Dienst M et al. 

Characterization of a transglutaminase expressed in human 

pancreatic adenocarcinoma cells. European Journal of Cell 

Biology 1993;61(2):321-328. Not sensitivity or specificity

of an identified test 

Enderlin V, Alfos S, Pallet V et al. Aging decreases the 

abundance of retinoic acid (RAR) and triiodothyronine 

(TR) nuclear receptor mRNA in rat brain: Effect of the 

administration of retinoids. Febs Lett 1997;412(3):629-632. 

Not sensitivity or specificity of an identified test

Enderlin V, Pallet V, Alfos S et al. Age-related decreases in

mRNA for brain nuclear receptors and target genes are

reversed by retinoic acid treatment. Neurosci Lett

1997;229(2):125-129. Not sensitivity or specificity of an

identified test 

Engstrom J, Hellstrom K. Microflora of the small intestine

and the incidence of liver disease, steatorrhoea, and 

indicanuria in patients subjected to partial gastrectomy.

Acta Chirurgica Scandinavica 1973;139(6):539-545. Not 

sensitivity or specificity of an identified test 

Engstrom J, Hellstrom K, Lundh G et al. Microflora of

small intestine, incidence of steatorrhoea and indicanuria 

before and after conversion of billroth II to billroth I type

of gastric resection. Acta Chirurgica Scandinavica 

1973;139(6):546-550. Not sensitivity or specificity of an

identified test 

Engstrom P E, Sundin U, Lavo B et al. Class and subclassassociated specificity differences of anti-gliadin antibodies

from mucosa and serum. Immunology 1992;77(4):604-608. 

Not sensitivity or specificity of an identified test

Ensari A, Marsh M N, Loft D E et al. Morphometric 

analysis of intestinal mucosa. V. Quantitative histological 

and immunocytochemical studies of rectal mucosae in 

gluten sensitivity. Gut 1993;34(9):1225-1229. Not 

sensitivity or specificity of an identified test 

Ensari A, Marsh M N, Morgan S et al. Diagnosing coeliac 

disease by rectal gluten challenge: a prospective study

based on immunopathology, computerized image analysis 

and logistic regression analysis. Clinical Science (London, 

England - 1979) 2001;101(2):199-207. Not sensitivity or

specificity of an identified test

Eriksson M-O, Hagforsen E, Lundin I P et al. Palmoplantar

pustulosis: A clinical and immunohistological study. Br J 

Dermatol 1998;138(3):390-398. Not sensitivity or

specificity of an identified test

Erkan T, Kutlu T, Yilmaz E et al. Human leukocyte 

antigens in Turkish pediatric celiac patients. Turkish 

Journal of Pediatrics 1999;41(2):181-188. Improper control 

group 

Ermacora E, Prampolini L, Tribbia G. Long-term follow-up 

of dermatitis herpetiformis in children. J Am Acad 

Dermatol 1986;15(1):24-30. Not sensitivity or specificity

of an identified test 

Ertem D, Tuney D, Baloglu H et al. Superior mesenteric 

artery blood flow in children with celiac disease. Journal of 

Pediatric Gastroenterology and Nutrition 1998;26(2):140-

145. Not sensitivity or specificity of an identified test 

Esposito C, Lombardi M L, Ruocco V et al. Implication of

tissue transglutaminase and desmoplakin in cell adhesion 

mechanism in human epidermis. Molecular and Cellular 

Biochemistry 2000;206(1-2):57-65. Not sensitivity or 

specificity of an identified test

Esposito C, Paparo F, Caputo I et al. Anti-tissue 

transglutaminase antibodies from coeliac patients inhibit 

transglutaminase activity both in vitro and in situ. Gut 

2002;51(2):177-181. Not sensitivity or specificity of an 

identified test 

Esposito Carla, Marra Monica, Giuberti Gaia et al. 

Ubiquitination of tissue transglutaminase is modulated by

interferon alpha in human lung cancer cells. Biochemical

Journal 2003;370(Pt 1):205-212. Not sensitivity or 

specificity of an identified test

Esposito Carla, Paparo Francesco, Caputo Ivana et al. 

Expression and enzymatic activity of small intestinal tissue 

transglutaminase in celiac disease. American Journal of

Gastroenterology 2003;98(8):1813-1820. Not sensitivity or 

specificity of an identified test

Esterre P, Risteli L, Ricard-Blum S. Immunohistochemical 

study of type I collagen turn-over and of matrix

metalloproteinases in chromoblastomycosis before and

after treatment by terbinafine. Pathology, Research and 

Practice 1998;194(12):847-853. Not sensitivity or

specificity of an identified test

Eterman K P, Nefkens M J J, Van Der et al. Failure to 

detect specific gluten antigens associated with the immune 

aggregates in the skin in dermatitis herpetiformis. Arch 

Dermatol Res 1977;260(3):247-252. Not sensitivity or 

specificity of an identified test

Euler A R, Ament M E. Celiac sprue and Crohn's disease:

an association causing severe growth retardation. 

Gastroenterology 1977;72(4 $U1):729-731. Not sensitivity

or specificity of an identified test

Evans D J, Patey A L. Chemistry of wheat proteins and the 

nature of the damaging substances. Clinics in 

Gastroenterology 1974;3(1):199-211. Not sensitivity or

specificity of an identified test

Evans Mark J, Harris Heather A, Miller Chris P et al. 

Estrogen receptors alpha and beta have similar activities in

multiple endothelial cell pathways. Endocrinology

2002;143(10):3785-3795. Not sensitivity or specificity of

A-363
an identified test

Evans P C, Smith S, Hirschfield G et al. Recipient HLADR3, tumour necrosis factor-alpha promoter allele-2 

(tumour necrosis factor-2) and cytomegalovirus infection 

are interrelated risk factors for chronic rejection of liver 

grafts. J Hepatol 2001;34(5):711-715. Not sensitivity or

specificity of an identified test

Fabbi M, Marimpietri D, Martini S et al. Tissue 

transglutaminase is a caspase substrate during apoptosis. 

Cleavage causes loss of transamidating function and is a

biochemical marker of caspase 3 activation. Cell Death and 

Differentiation 1999;6(10):992-1001. Not sensitivity or

specificity of an identified test

Fabiani E, Catassi C. The serum IgA class anti-tissue 

transglutaminase antibodies in the diagnosis and follow up 

of coeliac disease. Results of an international multi-centre

study. International Working Group on Eu-tTG. European

Journal of Gastroenterology & Hepatology 2001;13(6):659-

665. Improper control group 

Fabiani E, Catassi C, De Rosa S et al. The serum IgA class

anti-tissue transglutaminase antibodies in the diagnosis and 

follow up of coeliac disease. Results of an international

multi-centre study. Pediatrika 2001;21(10):13-21. Improper 

control group 

Fabiani E, Catassi C, Villari A et al. Dietary compliance in 

screening-detected coeliac disease adolescents. Acta

Paediatrica (Oslo, Norway - 1992).Supplement 

1996;41265-67. Not sensitivity or specificity of an 

identified test 

Fabiani E, Taccari L M, Ratsch I M et al. Compliance with 

gluten-free diet in adolescents with screening-detected 

celiac disease: a 5-year follow-up study. Journal of

Pediatrics 2000;136(6):841-843. Not sensitivity or

specificity of an identified test

Fabris L, Strazzabosco M, Crosby H A et al. 

Characterization and isolation of ductular cells 

coexpressing neural cell adhesion molecule and Bcl-2 from 

primary cholangiopathies and ductal plate malformations. 

American Journal of Pathology 2000;156(5):1599-1612. 

Not sensitivity or specificity of an identified test

Failla P, Ruberto C, Pagano M C et al. Celiac disease in

Down Syndrome with HLA serological and molecular

studies. Journal of Pediatric Gastroenterology and Nutrition 

1996;23(3):303-306. Improper control group 

Fairman M J, Scott B B, Toothill C et al. Jejunal mucosal 

gamma glutamyl transferase activity in coeliac disease. Gut 

1977;18(6):484-487. Not sensitivity or specificity of an 

identified test 

Fais S, Maiuri L, Pallone F et al. Gliadin induced changes 

in the expression of MHC-class II antigens by human small 

intestinal epithelium. Organ culture studies with coeliac 

disease mucosa. Gut 1992;33(4):472-475. Not sensitivity or 

specificity of an identified test

Falchuk K R, Falchuk Z M. Selective immunoglobulin a 

deficiency, ulcerative colitis, and gluten-sensitive

enteropathy--a unique association. Gastroenterology

1975;69(2):503-506. Not sensitivity or specificity of an 

identified test 

Falchuk Z M. Update on gluten-sensitive enteropathy.

American Journal of Medicine 1979;67(6):1085-1096. Not 

sensitivity or specificity of an identified test 

Falchuk Z M. Gluten-sensitive enteropathy. Clin

Gastroenterol 1983;12(2):475-494. Not sensitivity or 

specificity of an identified test

Falchuk Z M, Strober W. Gluten-sensitive enteropathy:

synthesis of antigliadin antibody in vitro. Gut 

1974;15(12):947-952. Not sensitivity or specificity of an

identified test 

Falchuk Z M, Gebhard R L, Sessoms C et al. An in vitro

model of gluten-sensitive enteropathy. Effect of gliadin on 

intestinal epithelial cells of patients with gluten-sensitive

enteropathy in organ culture. Journal of Clinical 

Investigation 1974;53(2):487-500. Not sensitivity or 

specificity of an identified test

Falchuk Z M, Katz A J, Shwachman H et al. Glutensensitive enteropathy: genetic analysis and organ culture

study in 35 families. Scandinavian Journal of

Gastroenterology 1978;13(7):839-843. Not sensitivity or 

specificity of an identified test

Falchuk Z M, Nelson D L, Katz A J et al. Gluten-sensitive 

enteropathy. Influence of histocompatibility type on gluten 

sensitivity in vitro. Journal of Clinical Investigation 

1980;66(2):227-233. Not sensitivity or specificity of an 

identified test 

Falk M C, NG G, Zhang G Y et al. Predominance of T cell 

receptor V delta 3 in small bowel biopsies from coeliac 

disease patients. Clinical and Experimental Immunology

1994;98(1):78-82. Not sensitivity or specificity of an 

identified test 

Fallstrom S P, Kristiansson B, Ryd W. Histological studies

of small-intestinal biopsies from infants with low rate of 

weight gain. Acta Pathol Microbiol Scand Sect A Pathol 

1981;89(6):431-438. Not sensitivity or specificity of an 

identified test 

Falorni A, Laureti S. Adrenal autoimmunity and correlation 

with adrenal dysfunction. Endocrinologist 2000;10(3):145-

154. Not sensitivity or specificity of an identified test 

Falorni A, Kockum I, Sanjeevi C B et al. Pathogenesis of 

insulin-dependent diabetes mellitus. Bailliere's Clin 

Endocrinol Metab 1995;9(1):25-46. Not sensitivity or 

specificity of an identified test

Falth-Magnusson K, Jansson G, Stenhammar L et al. 

A-364
Intestinal permeability assessed with different-sized 

polyethylene glycols in children undergoing smallintestinal biopsy for suspected celiac disease. Scandinavian 

Journal of Gastroenterology 1989;24(1):40-46. Not 

sensitivity or specificity of an identified test 

Farkas G, Buday L, Csermely P et al. Lipocortin I is not 

accessible for protein kinase C bound to the cytoplasmic 

surface of the plasma membrane in streptolysin-Opermeabilized pig granulocytes. Biochimica Et Biophysica 

Acta 1994;1220(3):315-322. Not sensitivity or specificity

of an identified test 

Farre C, Esteve M, Curcoy A et al. Hypertransaminasemia 

in pediatric celiac disease patients and its prevalence as a

diagnostic clue. American Journal of Gastroenterology

2002;97(12):3176-3181. Not sensitivity or specificity of an 

identified test 

Farre C, Humbert P, Vilar P et al. Serological markers and

HLA-DQ2 haplotype among first-degree relatives of celiac 

patients. Catalonian Coeliac Disease Study Group. 

Digestive Diseases and Sciences 1999;44(11):2344-2349. 

Improper control group 

Farrell R J, Kelly C P. Diagnosis of celiac sprue. American 

Journal of Gastroenterology 2001;96(12):3237-3246. 

Review article 

Farrell Richard J, Kelly Ciaran P. Celiac sprue. New 

England Journal of Medicine 2002;346(3):180-188. Not 

sensitivity or specificity of an identified test 

Farstad I N, Johansen F-E, Vlatkovic L et al. Heterogeneity

of intraepithelial lymphocytes in refractory sprue: Potential

implications of CD30 expression. Gut 2002;51(3):372-378. 

Not sensitivity or specificity of an identified test

Farthing M J, Rees L H, Dawson A M. Male gonadal 

function in coeliac disease: III. Pituitary regulation. 

Clinical Endocrinology 1983;19(6):661-671. Not 

sensitivity or specificity of an identified test 

Fasano A. Tissue transglutaminase: the Holy Grail for the 

diagnosis of celiac disease, at last?. Journal of Pediatrics 

1999;134(2):134-135. Review article 

Fasano A. Where have all the American celiacs gone?.

Acta paediatrica (Oslo, Norway : 1992).Supplement. 

1996;41220-24. Not sensitivity or specificity of an 

identified test 

Fasano A, Catassi C. Current approaches to diagnosis and 

treatment of celiac disease: an evolving spectrum.

Gastroenterology 2001;120(3):636-651. Not sensitivity or

specificity of an identified test

Fasano Alessio. Celiac disease--how to handle a clinical 

chameleon. New England Journal of Medicine

2003;348(25):2568-2570. Not sensitivity or specificity of

an identified test

Fasano Alessio, Berti Irene, Gerarduzzi Tania et al.

Prevalence of celiac disease in at-risk and not-at-risk 

groups in the United States: a large multicenter study.

Archives of Internal Medicine 2003;163(3):286-292. Not 

sensitivity or specificity of an identified test 

Faulkner-Hogg K B, Selby W S, Loblay R H. Dietary

analysis in symptomatic patients with coeliac disease on a 

gluten-free diet: the role of trace amounts of gluten and 

non-gluten food intolerances. Scandinavian Journal of

Gastroenterology 1999;34(8):784-789. Not sensitivity or 

specificity of an identified test

Fausa D, Thune P. Gastrointestinal dysfunction in

dermatitis herpetiformis. Scandinavian Journal of 

Gastroenterology 1974;9(27 sup.):No 27Not sensitivity or

specificity of an identified test

Fausa O, Eeg Larsen T, Husby G et al. Gastrointestinal

investigations in dermatitis herpetiformis. Acta DermVenereol 1975;55(3):203-206. Not sensitivity or specificity

of an identified test 

Favatier F, Bornman L, Hightower L E et al. Variation in 

hsp gene expression and Hsp polymorphism: Do they

contribute to differential disease susceptibility and stress

tolerance?. Cell Stress Chaperones 1997;2(3):141-155. Not 

sensitivity or specificity of an identified test 

Fedrick J A, Pandey J P, Verkasalo M et al. 

Immunoglobulin allotypes and the immune response to 

wheat gliadin in a Finnish population with celiac disease. 

Experimental and Clinical Immunogenetics 1985;2(4):185-

190. Not sensitivity or specificity of an identified test 

Feeley K M, Heneghan M A, Stevens F M et al. 

Lymphocytic gastritis and coeliac disease: evidence of a 

positive association. Journal of Clinical Pathology 

1998;51(3):207-210. Not sensitivity or specificity of an 

identified test 

Feighery C. Coeliac disease. Br Med J 

1999;319(7204):236-239. Not sensitivity or specificity of

an identified test

Feighery C. Coeliac disease, auto-immunity and thyroid

disease. Ital J Gastroenterol Hepatol 1999;31(4):288-289. 

Not sensitivity or specificity of an identified test

Feighery C F. Coeliac disease: How much of what is toxic

to whom?. Gut 1998;43(2):164-165. Not sensitivity or 

specificity of an identified test

Feighery C, Abuzakouk M, Liddy C et al. Endomysial 

antibody detection using human umbilical cord tissue as

substrate: reactivity of cells in Wharton's jelly. British 

Journal of Biomedical Science 1998;55(2):107-110. 

Improper control group 

Feighery C, Weir DG, Whelan A et al. Diagnosis of glutensensitive enteropathy: is exclusive reliance on histology 

A-365
appropriate? Eur J Gastroenterol Hepatol 1998; 10(11):919-

925. Unable to obtain full article 

Feighery C, Whelan A, Weir D G. Endomysium:

Autoantigen in coeliac disease. European Journal of 

Gastroenterology & Hepatology 1997;9(7):655-656. Not 

sensitivity or specificity of an identified test 

Feighery L, Collins C, Feighery C et al. Antitransglutaminase antibodies and the serological diagnosis 

of coeliac disease. British Journal of Biomedical Science 

2003;60(1):14-18. Not sensitivity or specificity of an 

identified test 

Feighery L, Lynch S, Kilmartin C et al. Flow-cytometric 

detection of lactase expression in normal and coeliac 

intestinal epithelium. European Journal of Gastroenterology

& Hepatology 2001;13(8):897-902. Not sensitivity or 

specificity of an identified test

Feng J F, Rhee S G, Im M J. Evidence that phospholipase 

delta1 is the effector in the Gh (transglutaminase II)-

mediated signaling. Journal of Biological Chemistry

1996;271(28):16451-16454. Not sensitivity or specificity of 

an identified test

Fennessy M, Metcalfe K, Hitman G A et al. A gene in the 

HLA class I region contributes to susceptibility to IDDM in 

the Finnish population. Childhood Diabetes in Finland 

(DiMe) Study Group. Diabetologia 1994;37(9):937-944. 

Not sensitivity or specificity of an identified test

Ferfoglia G, Pulitano R, Sategna-Guidetti C. Do dietary

antibodies still play a role in the diagnosis and follow-up of 

coeliac disease? A comparison among different serological 

tests. Panminerva Medica 1995;37(2):55-59. Improper 

control group 

Ferguson A. Celiac disease, an eminently treatable 

condition, may be underdiagnosed in the United States. 

American Journal of Gastroenterology 1997;92(8):1252-

1254. Not sensitivity or specificity of an identified test 

Ferguson A. Coeliac disease. Prescr J 1997;37(4):206-212. 

Not sensitivity or specificity of an identified test

Ferguson A. Coeliac disease research and clinical practice:

Maintaining momentum into the twenty-first century. 

Bailliere's Clin Gastroenterol 1995;9(2):395-412. Not 

sensitivity or specificity of an identified test 

Ferguson A. The immune system and mucosal

transformation - Historical perspective. Digestion

1990;46(Suppl 2):255-261. Not sensitivity or specificity of 

an identified test

Ferguson A. Intraepithelial lymphocytes of the small 

intestine. Part I: Morphology and experimental 

immunology of intraepithelial lymphocytes. Gut 

1977;18(11):921-937. Not sensitivity or specificity of an

identified test 

Ferguson A, Kingstone K. Coeliac disease and 

malignancies. Acta Paediatrica (Oslo, Norway -

1992).Supplement 1996;41278-81. Not sensitivity or 

specificity of an identified test

Ferguson A, Murray D. Quantitation of intraepithelial 

lymphocytes in human jejunum. Gut 1971;12(12):988-994. 

Not sensitivity or specificity of an identified test

Ferguson A, Ziegler K. Intraepithelial lymphocyte mitosis 

in a jejunal biopsy correlates with intraepithelial

lymphocyte count, irrespective of diagnosis. Gut 

1986;27(6):675-679. Not sensitivity or specificity of an 

identified test 

Ferguson A, Arranz E, O'Mahony S. Spectrum of

expression of intestinal cellular immunity: proposal for a 

change in diagnostic criteria of celiac disease. Annals of 

Allergy 1993;71(1):29-32. Not sensitivity or specificity of 

an identified test

Ferguson A, Arranz E, O'Mahony S. Clinical and

pathological spectrum of coeliac disease - active, silent, 

latent, potential. Gut 1993;34(2):150-151. Not sensitivity or 

specificity of an identified test

Ferguson A, Blackwell J N, Barnetson R S. Effects of 

additional dietary gluten on the small-intestinal mucosa of

volunteers and of patients with dermatitis herpetiformis. 

Scandinavian Journal of Gastroenterology 1987;22(5):543-

549. Not sensitivity or specificity of an identified test 

Ferguson A, Gillett H, Humphreys K et al. Heterogeneity

of celiac disease: clinical, pathological, immunological, and 

genetic. Annals of the New York Academy of Sciences 

1998;859112-120. Not sensitivity or specificity of an 

identified test 

Ferguson A, MacDonald T T, McClure J P et al. Cellmediated immunity to gliadin within the small-intestinal

mucosa in coeliac disease. Lancet 1975;1(7912):895-897. 

Not sensitivity or specificity of an identified test

Ferguson A, McClure J P, Townley R R. Intraepithelial 

lymphocyte counts in small intestinal biopsies from 

children with diarrhoea. Acta Paediatrica Scandinavica

1976;65(5):541-546. Unable to extract data 

Ferguson A, Mowat A M, Strobel S et al. T-cell mediated

immunity in food allergy. Annals of Allergy 1983;51(2 Pt 

2):246-248. Not sensitivity or specificity of an identified

test 

Ferguson A, Ziegler K, Strobel S. Gluten intolerance 

(coeliac disease). Annals of Allergy 1984;53(6 Pt 2):637-

642. Not sensitivity or specificity of an identified test 

Ferguson M M, Wray D, Carmichael H A. Coeliac disease 

associated with recurrent aphthae. Gut 1980;21(3):223-226. 

Not sensitivity or specificity of an identified test

Ferguson R, Asquith P, Cooke W T. The cellular infiltrate 

A-366
of the jejunum in coeliac patients with complicating 

lymphoma. Gut 1974;15(4):338-339. Not sensitivity or

specificity of an identified test

Ferguson R, Asquith P, Cooke W T. The jejunal cellular 

infiltrate in coeliac disease complicated by lymphoma. Gut 

1974;15(6):458-461. Not sensitivity or specificity of an 

identified test 

Ferguson R, Basu M K, Asquith P et al. Jejunal mucosal 

abnormalities in patients with recurrent aphthous 

ulceration. British Medical Journal 1976;1(6000):11-13. 

Not sensitivity or specificity of an identified test

Fernandez L, Fernandez-Arquero M, Gual L et al. Triplet 

repeat polymorphism in the transmembrane region of the 

MICA gene in celiac disease. Tissue Antigens

2002;59(3):219-222. Not sensitivity or specificity of an 

identified test 

Fernandez N, Hitman G A, Festenstein H et al. Novel HLA 

class II-associated structural patterns in coeliac disease and 

type I diabetes. Clinical and Experimental Immunology

1988;72(3):362-366. Not sensitivity or specificity of an 

identified test 

Fernandez-Arquero M, Caldes T, Casado E et al. 

Polymorphism within the HLA-DQB1*02 promoter 

associated with susceptibility to coeliac disease. European 

Journal of Immunogenetics - Official Journal of the British 

Society for Histocompatibility and Immunogenetics 

1998;25(1):1-3. Not sensitivity or specificity of an 

identified test 

Fernandez-Arquero M, Figueredo M A, Maluenda C et al. 

HLA-linked genes acting as additive susceptibility factors 

in celiac disease. Human Immunology 1995;42(4):295-300. 

Improper control group 

Fernandez-Arquero M, Polanco I, Escobar H et al. HLADQ alleles and susceptibility to celiac disease in Spanish 

children. Tissue Antigens 1995;45(2):145-147. Improper 

control group 

Fernandez-Calle P, Codoceo R, Polanco I et al. Is an 

intestinal permeability test a valid marker for slight dietary 

transgressions in adolescents with coeliac disease?. Gut

1993;34(6):774-777. Not sensitivity or specificity of an 

identified test 

Ferrante P, Petronzelli F, Mariani P et al. Oligotyping of 

Italian celiac patients with the 11th International 

Histocompatibility Workshop reagents. Tissue Antigens 

1992;39(1):38-39. Improper control group 

Ferreira M, Davies S L, Butler M et al. Endomysial 

antibody: is it the best screening test for coeliac disease?.

Gut 1992;33(12):1633-1637. Improper control group 

Festenstein H, Nyulassy S. Workshop on HLA and disease. 

Transplantation Proceedings 1979;11(1):1183-1185. Not

sensitivity or specificity of an identified test 

Festoff B W, Suo Z, Citron B A. Plasticity and stabilization

of neuromuscular and CNS synapses: interactions between

thrombin protease signaling pathways and tissue 

transglutaminase. International Review of Cytology

2001;211153-177. Not sensitivity or specificity of an 

identified test 

Festoff B W, Suo Z, Citron B A. Prospects for the 

pharmacotherapy of amyotrophic lateral sclerosis: Old 

strategies and new paradigms for the third millennium. Cns 

Drugs 2003;17(10):699-717. Not sensitivity or specificity

of an identified test 

Fesus L. Transglutaminase-catalyzed protein cross-linking

in the molecular program of apoptosis and its relationship 

to neuronal processes. Cellular and Molecular

Neurobiology 1998;18(6):683-694. Not sensitivity or 

specificity of an identified test

Fesus L, Arato G. Quantitation of tissue transglutaminase 

by a sandwich ELISA system. Journal of Immunological 

Methods 1986;94(1-2):131-136. Not sensitivity or

specificity of an identified test

Fesus L, Thomazy V. Searching for the function of tissue 

transglutaminase: its possible involvement in the 

biochemical pathway of programmed cell death. Advances 

in Experimental Medicine and Biology 1988;231119-134. 

Not sensitivity or specificity of an identified test

Fesus L, Erdei A, Sandor M et al. The influence of tissue 

transglutaminase on the function of Fc receptors. Molecular 

Immunology 1982;19(1):39-43. Not sensitivity or

specificity of an identified test

Fesus L, Falus A, Erdei A et al. Human beta 2-

microglobulin is a substrate of tissue transglutaminase: 

polymerization in solution and on the cell surface. Journal

of Cell Biology 1981;89(3):706-710. Not sensitivity or

specificity of an identified test

Fesus L, Metsis M L, Muszbek L et al. Transglutaminasesensitive glutamine residues of human plasma fibronectin 

revealed by studying its proteolytic fragments. European 

Journal of Biochemistry / Febs 1986;154(2):371-374. Not 

sensitivity or specificity of an identified test 

Fesus L, Nagy L, Basilion J P et al. Retinoic acid receptor 

transcripts in human umbilical vein endothelial cells. 

Biochemical and Biophysical Research Communications

1991;179(1):32-38. Not sensitivity or specificity of an 

identified test 

Fesus L, Tarcsa E, Kedei N et al. Degradation of cells

dying by apoptosis leads to accumulation of

epsilon(gamma-glutamyl)lysine isodipeptide in culture

fluid and blood. Febs Lett 1991;284(1):109-112. Not 

sensitivity or specificity of an identified test 

Fesus Laszlo, Piacentini Mauro. Transglutaminase 2: an

enigmatic enzyme with diverse functions. Trends in 

A-367
Biochemical Sciences 2002;27(10):534-539. Not sensitivity

or specificity of an identified test

Feurle G E. Pathophysiology of diarrhea in patients with 

familial amyloid neuropathy. Digestion 1987;36(1):13-17. 

Not sensitivity or specificity of an identified test

Fielding J F, Doyle G D. Coeliac disease amongst 

adolescents previously labelled as coeliacs on clinical

grounds. J Ir Coll Phys Surg 1978;7(3):89-91. Not 

sensitivity or specificity of an identified test 

Fine K D. The prevalence of occult gastrointestinal 

bleeding in celiac sprue. New England Journal of Medicine

1996;334(18):1163-1167. Not sensitivity or specificity of

an identified test

Fine K D, Do K, Schulte K et al. High prevalence of celiac

sprue-like HLA-DQ genes and enteropathy in patients with 

the microscopic colitis syndrome. American Journal of

Gastroenterology 2000;95(8):1974-1982. Improper control 

group 

Fine K D, Lee E L, Meyer R L. Colonic histopathology in

untreated celiac sprue or refractory sprue: is it lymphocytic 

colitis or colonic lymphocytosis?. Human Pathology

1998;29(12):1433-1440. Not sensitivity or specificity of an 

identified test 

Fine K D, Meyer R L, Lee E L. The prevalence and causes

of chronic diarrhea in patients with celiac sprue treated

with a gluten-free diet. Gastroenterology

1997;112(6):1830-1838. Not sensitivity or specificity of an 

identified test 

Fine K D, Ogunji F, Saloum Y et al. Celiac sprue: another 

autoimmune syndrome associated with hepatitis C. 

American Journal of Gastroenterology 2001;96(1):138-145. 

Not sensitivity or specificity of an identified test

Finney S, Seale L, Sawyer R T et al. Tridegin, a new 

peptidic inhibitor of factor XIIIa, from the blood-sucking 

leech Haementeria ghilianii. Biochemical Journal 

1997;324(Pt 3):797-805. Not sensitivity or specificity of an 

identified test 

Fischer G F, Mayr W R. Molecular genetics of the HLA 

complex. Wiener Klinische Wochenschrift 2001;113(20-

21):814-824. Not sensitivity or specificity of an identified 

test 

Fitzpatrick K P, Sherman P M, Ipp M et al. Screening for 

celiac disease in children with recurrent abdominal pain. 

Journal of Pediatric Gastroenterology and Nutrition 

2001;33(3):250-252. Not sensitivity or specificity of an 

identified test 

Fivenson D P, Douglass M C, Nickoloff B J. Cutaneous 

expression of Thy-1 in mycosis fungoides. American 

Journal of Pathology 1992;141(6):1373-1380. Not 

sensitivity or specificity of an identified test 

Fladby T, Kampman M T, Loseth S et al. Human leukocyte

antigen class I in polymyositis: Leukocyte infiltrates, 

regeneration, and impulse block. Muscle Nerve 

1997;20(12):1534-1540. Not sensitivity or specificity of an 

identified test 

Fleckenstein Burkhard, Molberg Oyvind, Qiao Shuo et al. 

Gliadin T cell epitope selection by tissue transglutaminase 

in celiac disease. Role of enzyme specificity and pH 

influence on the transamidation versus deamidation 

process. Journal of Biological Chemistry 

2002;277(37):34109-34116. Not sensitivity or specificity of 

an identified test

Fleming S C, Duncan A, Russell R I et al. Measurement of

sugar probes in serum: an alternative to urine measurement 

in intestinal permeability testing. Clinical Chemistry 

1996;42(3):445-448. Not sensitivity or specificity of an 

identified test 

Flint A, McCoy J P, Schade W J et al. Cervical carcinoma 

antigen: distribution in neoplastic lesions of the uterine

cervix and comparison to other tumor markers.

Gynecologic Oncology 1988;30(1):63-70. Not sensitivity

or specificity of an identified test

Floreani A, Betterle C, Baragiotta A et al. Prevalence of 

coeliac disease in primary biliary cirrhosis and of

antimitochondrial antibodies in adult coeliac disease 

patients in Italy. Digestive and Liver Disease - Official 

Journal of the Italian Society of Gastroenterology and the 

Italian Association for the Study of the Liver 

2002;34(4):258-261. Not sensitivity or specificity of an 

identified test 

Floreani A, Chiaramonte M, Venturini R et al. Antigliadin

antibody classes in chronic liver disease. Italian Journal of

Gastroenterology 1992;24(8):457-460. Not sensitivity or 

specificity of an identified test

Floren C H, Alm P. Defective synthesis of apolipoprotein

A-I in jejunal mucosa in coeliac disease. Scandinavian

Journal of Gastroenterology 1988;23(7):856-860. Not 

sensitivity or specificity of an identified test 

Fluge G, Aksnes L. Autoradiographic localization of a 

gluten peptide during organ culture of human duodenal 

mucosa. Journal of Pediatric Gastroenterology and

Nutrition 1983;2(3):452-458. Not sensitivity or specificity

of an identified test 

Fluge G, Aksnes L. Influence of cow's milk proteins and 

gluten on human duodenal mucosa in organ culture. Journal 

of Pediatric Gastroenterology and Nutrition 

1990;11(4):481-488. Not sensitivity or specificity of an 

identified test 

Fluge G, Aksnes L. Labelling indices after 3H-thymidine 

incorporation during organ culture of duodenal mucosa in

coeliac disease. Scandinavian Journal of Gastroenterology

1981;16(7):921-928. Not sensitivity or specificity of an 

identified test 

A-368
Fluge G, Aksnes L. Mitotic rate and mitotic time in coeliac 

and non-coeliac duodenal biopsies maintained in organ 

culture. Virchows Archiv.B, Cell Pathology Including 

Molecular Pathology 1981;38(2):159-167. Not sensitivity

or specificity of an identified test

Fluge G, Aksnes L. Morphological and morphometric 

assessment of human duodenal biopsies maintained in 

organ culture. In vitro influences of gluten in coeliac 

disease. Scandinavian Journal of Gastroenterology

1981;16(4):555-567. Not sensitivity or specificity of an 

identified test 

Fluge G, Aksnes L. Quantification of immunoglobulins 

after organ culture of human duodenal mucosa. Journal of

Pediatric Gastroenterology and Nutrition 1983;2(1):62-70. 

Not sensitivity or specificity of an identified test

Fluge G, Andersen K J, Aksnes L et al. Brush border and

lysosomal marker enzyme profiles in duodenal mucosa 

from coeliac patients before and after organ culture. 

Scandinavian Journal of Gastroenterology 1982;17(4):465-

472. Not sensitivity or specificity of an identified test 

Fluge O, Sletten K, Fluge G et al. In vitro toxicity of 

purified gluten peptides tested by organ culture. Journal of

Pediatric Gastroenterology and Nutrition 1994;18(2):186-

192. Not sensitivity or specificity of an identified test 

Flynn J C, Wan Q, Panos J C et al. Coexpression of 

susceptible and resistant HLA class II transgenes in murine 

experimental autoimmune thyroiditis: DQ8 molecules 

downregulate DR3-mediated thyroiditis. J Autoimmun 

2002;18(3):213-220. Not sensitivity or specificity of an 

identified test 

Fois A, Vascotto M, Di Bartolo R M et al. Celiac disease 

and epilepsy in pediatric patients. Child's Nervous System -

Chns - Official Journal of the International Society for 

Pediatric Neurosurgery 1994;10(7):450-454. Not sensitivity

or specificity of an identified test

Foldes-Papp Zeno, Demel Ulrike, Berry Desiree et al. 

Tissue transglutaminase antibody determination in celiac 

disease. Analysis of diagnostic specificity of anti-human 

IgA-type assays. Journal of Immunoassay & 

Immunochemistry 2002;23(2):211-227. Improper control 

group 

Fontana M, Boldorini R, Zuin G et al. Ultrastructural 

changes in the duodenal mucosa of HIV-infected children. 

Journal of Pediatric Gastroenterology and Nutrition 

1993;17(3):255-259. Not sensitivity or specificity of an 

identified test 

Fonti R, Limite G, Sodano A et al. Sentinel lymph node 

identification in breast cancer patients. La Radiologia 

Medica 2002;103(4):370-377. Not sensitivity or specificity

of an identified test 

Fordtran J S, Rector F C, Locklear T W et al. Water and 

solute movement in the small intestine of patients with 

sprue. Journal of Clinical Investigation 1967;46(3):287-

298. Not sensitivity or specificity of an identified test 

Foreman K E, Bacon P E, Hsi E D et al. In situ polymerase

chain reaction-based localization studies support role of

human herpesvirus-8 as the cause of two AIDS-related

neoplasms: Kaposi's sarcoma and body cavity lymphoma. 

Journal of Clinical Investigation 1997;99(12):2971-2978. 

Not sensitivity or specificity of an identified test

Forget P, Grandfils C, Van Cutsem J L et al. Diamine 

oxidase in serum and small intestinal biopsy tissue in 

childhood celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 1986;5(3):379-383. Not

sensitivity or specificity of an identified test 

Forgeur A, Willems F, Winand J et al. Natriuretic peptide 

receptors of type A in human neuroblastomas.

Neuroendocrinology 1999;70(4):288-294. Not sensitivity

or specificity of an identified test

Fornasieri A, Sinico R A, Maldifassi P et al. IgAantigliadin antibodies in IgA mesangial nephropathy

(Berger's disease). British Medical Journal (Clinical 

Research Ed.) 1987;295(6590):78-80. Not sensitivity or

specificity of an identified test

Forsberg Gote, Hernell Olle, Melgar Silvia et al.

Paradoxical coexpression of proinflammatory and downregulatory cytokines in intestinal T cells in childhood celiac 

disease. Gastroenterology 2002;123(3):667-678. Not 

sensitivity or specificity of an identified test 

Fotherby K J, Wraight E P, Neale G. 51Cr-EDTA/14Cmannitol intestinal permeability test. Clinical use in 

screening for coeliac disease. Scandinavian Journal of

Gastroenterology 1988;23(2):171-177. Not sensitivity or 

specificity of an identified test

Fotoulaki M, Nousia-Arvanitakis S, AugoustidouSavvopoulou P et al. Clinical application of immunological 

markers as monitoring tests in celiac disease. Digestive

Diseases and Sciences 1999;44(10):2133-2138. Not 

sensitivity or specificity of an identified test 

Fottrell P F. Intestinal peptide transport and hydrolysis in 

health and disease. Ir J Med Sci 1979;148(4):123-134. Not 

sensitivity or specificity of an identified test 

Fraga M, Brousset P, Schlaifer D et al. Bone marrow 

involvement in anaplastic large cell lymphoma. 

Immunohistochemical detection of minimal disease and its 

prognostic significance. American Journal of Clinical 

Pathology 1995;103(1):82-89. Not sensitivity or specificity

of an identified test 

Fraij B M. GTP hydrolysis by human tissue 

transglutaminase homologue. Biochemical and Biophysical 

Research Communications 1996;218(1):45-49. Not 

sensitivity or specificity of an identified test 

A-369
Fraij B M, Gonzales R A. Organization and structure of the

human tissue transglutaminase gene. Biochimica Et 

Biophysica Acta 1997;1354(1):65-71. Not sensitivity or

specificity of an identified test

Fraij B M, Gonzales R A. A third human tissue

transglutaminase homologue as a result of alternative gene 

transcripts. Biochimica Et Biophysica Acta

1996;1306(1):63-74. Not sensitivity or specificity of an 

identified test 

Fraij B M, Birckbichler P J, Patterson M K et al. A retinoic

acid-inducible mRNA from human erythroleukemia cells 

encodes a novel tissue transglutaminase homologue. 

Journal of Biological Chemistry 1992;267(31):22616-

22623. Not sensitivity or specificity of an identified test 

Francis James, Carty John E, Scott Brian B. The prevalence 

of coeliac disease in rheumatoid arthritis. European Journal

of Gastroenterology & Hepatology 2002;14(12):1355-

1356. Not sensitivity or specificity of an identified test 

Franklin J L, Asquith P, Rosenberg I H. The occurrence of 

cystic fibrosis and celiac sprue within a single sibship. 

American Journal of Digestive Diseases 1974;19(2):149-

155. Not sensitivity or specificity of an identified test 

Fraser J S, Ciclitira P J. Pathogenesis of coeliac disease: 

implications for treatment. World Journal of

Gastroenterology - Wjg 2001;7(6):772-776. Not sensitivity

or specificity of an identified test

Fraser-Reynolds K A, Butzner J D, Stephure D K et al. Use 

of immunoglobulin A-antiendomysial antibody to screen

for celiac disease in North American children with type 1 

diabetes. Diabetes Care 1998;21(11):1985-1989. Improper 

control group 

Frazzoni M, Lonardo A, Grisendi A et al. Are routine 

duodenal and antral biopsies useful in the management of 

"functional" dyspepsia? A diagnostic and therapeutic study.

Journal of Clinical Gastroenterology 1993;17(2):101-108. 

Not sensitivity or specificity of an identified test

Freedman A R, Macartney J C, Nelufer J M et al. Timing 

of infiltration of T lymphocytes induced by gluten into the 

small intestine in coeliac disease. Journal of Clinical 

Pathology 1987;40(7):741-745. Not sensitivity or

specificity of an identified test

Freeman H J. Failure of added dietary gluten to induce 

small intestinal histopathological changes in patients with

watery diarrhea and lymphocytic colitis. Canadian Journal 

of Gastroenterology = Journal Canadien De 

Gastroenterologie 1996;10(7):436-439. Not sensitivity or 

specificity of an identified test

Freeman H J. Small intestinal mucosal biopsy for 

investigation of diarrhea and malabsorption in adults. 

Gastrointestinal Endoscopy Clinics of North America 

2000;10(4):739-53, Vii. Not sensitivity or specificity of an 

identified test 

Freeman H J. Solid-phase ELISA for tissue

transglutaminase, an endomysial target for possible 

serological diagnosis of celiac disease. Canadian Journal of 

Gastroenterology = Journal Canadien De Gastroenterologie 

1998;12(5):323-324. Not sensitivity or specificity of an 

identified test 

Freeman H J. Biopsy-defined adult celiac disease in AsianCanadians. Canadian Journal of Gastroenterology = Journal 

Canadien De Gastroenterologie 2003;17(7):433-436. Not 

sensitivity or specificity of an identified test 

Freeman H J. Celiac-associated autoimmune thyroid 

disease: A study of 16 patients with overt hypothyroidism: 

MALADIE THYROIDIENNE AUTO-IMMUNE DE 

NATURE COELIAQUE: ETUDE PORTANT SUR 16 

PATIENTS ATTEINTS D'HYPOTHYROIDIE AVEREE. 

Canadian Journal of Gastroenterology = Journal Canadien 

De Gastroenterologie 1995;9(5):242-246. Not sensitivity or 

specificity of an identified test

Freeman H J. Clinical spectrum of biopsy defined celiac 

disease in the elderly. Canadian Journal of 

Gastroenterology = Journal Canadien De Gastroenterologie 

1995;9(1):42-46. Not sensitivity or specificity of an 

identified test 

Freeman H J. Free perforation due to intestinal lymphoma 

in biopsy-defined or suspected celiac disease. Journal of

Clinical Gastroenterology 2003;37(4):299-302. Not 

sensitivity or specificity of an identified test 

Freeman H J. Survey of gastroenterologists on the 

diagnosis and treatment of adult patients with celiac disease 

in British Columbia. Canadian Journal of Gastroenterology

= Journal Canadien De Gastroenterologie 1998;12(2):149-

152. Not sensitivity or specificity of an identified test 

Freeman H J. Topography of lectin binding sites in celiac 

sprue. Canadian Journal of Gastroenterology = Journal 

Canadien De Gastroenterologie 1992;6(5):271-276. Not 

sensitivity or specificity of an identified test 

Freemark M, Levitsky L L. Screening for celiac disease in 

children with type 1 diabetes: Two views of the 

controversy. Diabetes Care 2003;26(6):1932-1939. Not 

sensitivity or specificity of an identified test 

Freier S. Paediatric gastrointestinal allergy. Clin Allergy 

1973;3(Suppl):597-618. Not sensitivity or specificity of an 

identified test 

Frew A J, Bright S, Shewry P R et al. Proliferative response 

of lymphocytes of normal individuals to wheat proteins 

(Gliadins). Int Arch Allergy Appl Immunol 

1980;62(2):162-167. Not sensitivity or specificity of an 

identified test 

Frezal J, Rey J. Genetics of disorders of intestinal digestion 

and absorption. Advances in Human Genetics 1970;1275-

336. Not sensitivity or specificity of an identified test 

A-370
Fric P, Lojda Z, Jodl J. Heterogeneity of enzymes of smallintestinal mucosa in malabsorption syndrome. 

Ceskoslovenska Gastroenterologie a Vyziva

1968;22(4):235-249. Not sensitivity or specificity of an 

identified test 

Fric P, Lojda Z, Jodl J et al. Analysis of peroral jejunal

biopsies in clinically asymptomatic parents of children with

celiac sprue. Digestion 1969;2(1):35-42. Not sensitivity or

specificity of an identified test

Friedrich M, Villena-Heinsen C, He J et al. Correlation

between immunoreactivity for transglutaminase K and for

markers of proliferation and differentiation in normal breast 

tissue and breast carcinomas. European Journal of

Gynaecological Oncology 1998;19(5):444-448. Not 

sensitivity or specificity of an identified test 

Friedrich M, Villena-Heinsen C, He J et al. Expression of 

transglutaminase K in normal cervix tissue and cervix 

carcinomas. Histochem J 1999;31(1):13-18. Not sensitivity

or specificity of an identified test

Friedrichs B, Riedmiller H, Goebel H W et al. 

Immunological characterization and activity of

transglutaminases in human normal and malignant prostate 

and in prostate cancer cell lines. Urological Research 

1995;23(5):301-310. Not sensitivity or specificity of an 

identified test 

Friis B, Karup Pedersen F, Schiodt M. Immunological 

studies in two children with recurrent parotitis. Acta 

Paediatr Scand 1983;72(2):265-268. Not sensitivity or 

specificity of an identified test

Friis S U, Gudmand-Hoyer E. Screening for coeliac disease

in adults by simultaneous determination of IgA and IgG 

gliadin antibodies. Scandinavian Journal of 

Gastroenterology 1986;21(9):1058-1062. Improper control 

group 

Friis S U, Larsen K, Boserup J et al. Gliadin antibody titers 

in coeliac patients during short-term provocations with 

bread made from wheat flour and enzymatic digested wheat

flour. European Journal of Gastroenterology & Hepatology

1990;2(5):361-365. Not sensitivity or specificity of an 

identified test 

Friis S U, Noren O, Sjostrom H et al. Patients with coeliac 

disease have a characteristic gliadin antibody pattern. 

Clinica Chimica Acta 1986;International Journal of Clinical 

Chemistry; 155(2):133-141. Not sensitivity or specificity of 

an identified test

Friis S, Dabelsteen E, Sjostrom H et al. Gliadin uptake in

human enterocytes. Differences between coeliac patients in

remission and control individuals. Gut 1992;33(11):1487-

1492. Not sensitivity or specificity of an identified test 

Frisman D M, McCarthy W F, Schleiff P et al. 

Immunocytochemistry in the differential diagnosis of 

effusions: use of logistic regression to select a panel of

antibodies to distinguish adenocarcinomas from 

mesothelial proliferations. Modern Pathology - an Official

Journal of the United States and Canadian Academy of 

Pathology, Inc 1993;6(2):179-184. Not sensitivity or 

specificity of an identified test

Frisoni G B, Carabellese N, Longhi M et al. Is celiac 

disease associated with Alzheimer's disease?. Acta

Neurologica Scandinavica 1997;95(3):147-151. Not 

sensitivity or specificity of an identified test 

Frisoni M, Volta U, Valentini R A et al. Antigliadin 

antibody levels in symptomless celiac disease. Digestive

Diseases and Sciences 1989;34(10):1639-1640. Review 

article 

Fritz P, Mischlinski A, Multhaupt H et al. Application of a

new electrophoresis technique (2D cryostat section 

electrophoresis) to synovial tissue of RA patients and 

comparison with immunohistochemical staining methods. 

Acta Histochemica.Supplementband 1990;40121-126. Not 

sensitivity or specificity of an identified test 

Fronek Z, Cheung M M, Hanbury A M et al. Molecular

analysis of HLA DP and DQ genes associated with

dermatitis herpetiformis. Journal of Investigative 

Dermatology 1991;97(5):799-802. Not sensitivity or 

specificity of an identified test

Frustaci Andrea, Cuoco Lucio, Chimenti Cristina et al. 

Celiac disease associated with autoimmune myocarditis.

Circulation 2002;105(22):2611-2618. Not sensitivity or

specificity of an identified test

Fry L. Dermatitis herpetiformis. Bailliere's Clinical 

Gastroenterology 1995;9(2):371-393. Not sensitivity or

specificity of an identified test

Fry L. Dermatitis herpetiformis: Problems, progress and 

prospects. Eur J Dermatol 2002;12(6):523-531. Not 

sensitivity or specificity of an identified test 

Fry L, McMinn R M. Morphology and functional cytology

of the small intestinal mucosa in malabsorptive disorders 

and other diseases. Journal of Clinical Pathology

1966;19(3):260-265. Not sensitivity or specificity of an 

identified test 

Fry L, Seah P P, Hoffbrand A V. Dermatitis herpetiformis. 

Clin Gastroenterol 1974;3(1):145-157. Not sensitivity or

specificity of an identified test

Fry L, Seah P P, McMinn R M et al. Lymphocytic 

infiltration of epithelium in diagnosis of gluten-sensitive

enteropathy. British Medical Journal 1972;3(823):371-374. 

Not sensitivity or specificity of an identified test

Frye M, Bargon J, Lembcke B et al. Differential expression 

of human alpha- and beta-defensins mRNA in 

gastrointestinal epithelia. European Journal of Clinical 

Investigation 2000;30(8):695-701. Not sensitivity or 

A-371
specificity of an identified test

Fugger L, Svejgaard A. The HLA-DQ7 and -DQ8 

associations in DR4-positive rheumatoid arthritis patients.

Tissue Antigens 1997;50(5):494-500. Not sensitivity or

specificity of an identified test

Fujimoto M, Kanzaki H, Nakayama H et al. Requirement 

for transglutaminase in progesterone-induced 

decidualization of human endometrial stromal cells. 

Endocrinology 1996;137(3):1096-1101. Not sensitivity or 

specificity of an identified test

Fujimoto N, Tajima S, Ishibashi A. Elastin peptides induce

migration and terminal differentiation of cultured

keratinocytes via 67 kDa elastin receptor in vitro: 67 kDa 

elastin receptor is expressed in the keratinocytes

eliminating elastic materials in elastosis perforans

serpiginosa. Journal of Investigative Dermatology

2000;115(4):633-639. Not sensitivity or specificity of an

identified test 

Fujisaku A, Frank M B, Neas B et al. HLA-DQ gene 

complementation and other histocompatibility relationships 

in man with the anti-Ro/SSA autoantibody response of 

systemic lupus erythematosus. J Clin Invest 

1990;86(2):606-611. Not sensitivity or specificity of an 

identified test 

Fujita K, Naito S, Okabe N et al. Immunological studies in 

Crohn's disease. I. Association with HLA systems in the 

Japanese. J Clin Lab Immunol 1984;14(2):99-102. Not 

sensitivity or specificity of an identified test 

Fukayama M, Koike M. So-called sclerosing hemangioma 

of the lung. An immunohistochemical, histochemical and 

ultrastructural study. Acta Pathologica Japonica 

1988;38(5):627-642. Not sensitivity or specificity of an 

identified test 

Fukuda K. Induction of tissue transglutaminase expression 

by propionate and n-butyrate in colon cancer cell lines. J

Nutr Biochem 1999;10(7):397-404. Not sensitivity or 

specificity of an identified test

Fullen D R, Reed J A, Finnerty B et al. S100A6 expression 

in fibrohistiocytic lesions. Journal of Cutaneous Pathology

2001;28(5):229-234. Not sensitivity or specificity of an 

identified test 

Furuya Y, Lundmo P, Short A D et al. The role of calcium, 

pH, and cell proliferation in the programmed (apoptotic)

death of androgen-independent prostatic cancer cells 

induced by thapsigargin. Cancer Research

1994;54(23):6167-6175. Not sensitivity or specificity of an 

identified test 

Gaboardi F, Perletti L, Cambie M et al. Dermatitis 

herpetiformis and nephrotic syndrome. Clinical Nephrology

1983;20(1):49-51. Not sensitivity or specificity of an 

identified test 

Gabrielli Maurizio, Cremonini Filippo, Fiore Giuseppe et 

al. Association between migraine and Celiac disease: 

results from a preliminary case-control and therapeutic 

study. American Journal of Gastroenterology

2003;98(3):625-629. Not sensitivity or specificity of an 

identified test 

Gale L, Wimalaratna H, Brotodiharjo A et al. Down 

Syndrome is strongly associated with coeliac disease. Gut

1997;40(4):492-496. Not sensitivity or specificity of an 

identified test 

Gallagher R B, Cervi P, Kelly J et al. The subclass profile 

and complement activating potential of anti-alpha-gliadin

antibodies in coeliac disease. Journal of Clinical & 

Laboratory Immunology 1989;28(3):115-121. Not 

sensitivity or specificity of an identified test 

Gallagher R B, Feighery C, Weir D G et al. Studies on the 

interaction between alpha-gliadin and HLA and T cell 

receptor molecules in coeliac disease. Clinical and

Experimental Immunology 1988;74(3):413-418. Not 

sensitivity or specificity of an identified test 

Gallagher R B, Kelly C P, Neville S et al. Complement 

activation within the coeliac small intestine is localised to 

Brunner's glands. Gut 1989;30(11):1568-1573. Not 

sensitivity or specificity of an identified test 

Gambelunghe G, Falorni A, Ghaderi M et al. Microsatellite 

polymorphism of the MHC class I chain-related (MIC-A 

and MIC-B) genes marks the risk for autoimmune

Addison's disease. J Clin Endocrinol Metab 

1999;84(10):3701-3707. Not sensitivity or specificity of an 

identified test 

Gambelunghe G, Forini F, Laureti S et al. Increased risk for 

endocrine autoimmunity in Italian type 2 diabetic patients 

with GAD65 autoantibodies. Clin Endocrinol 

2000;52(5):565-573. Not sensitivity or specificity of an 

identified test 

Gambelunghe G, Ghaderi M, Cosentino A et al. 

Association of MHC Class I chain-related A (MIC-A) gene 

polymorphism with Type I diabetes. Diabetologia

2000;43(4):507-514. Not sensitivity or specificity of an 

identified test 

Gandolfi L, Catassi C, Garcia S et al. Antiendomysial 

antibody test reliability in children with frequent diarrhea

and malnutrition: is it celiac disease?. Journal of Pediatric 

Gastroenterology and Nutrition 2001;33(4):483-487. 

Improper control group 

Gandolfi L, Pratesi R, Cordoba J C et al. Prevalence of

celiac disease among blood donors in Brazil. American 

Journal of Gastroenterology 2000;95(3):689-692. Not 

sensitivity or specificity of an identified test 

Garcia Vilela E, De Lourdes, de Abreu et al. Agreement 

between pathologists concerning assessment of intestinal

biopsies from adult celiac disease patients. Gastroenterol 

A-372
Int 2002;15(1-2):1-8. Improper control group 

Garcia-Buey L, Garcia-Monzon C, Rodriguez S et al. 

Latent autoimmune hepatitis triggered during interferon

therapy in patients with chronic hepatitis C.

Gastroenterology 1995;108(6):1770-1777. Not sensitivity

or specificity of an identified test

Gardas A, Bauer A, Rujner J et al. An enzyme-linked 

immunosorbent assay for the detection of serum antibodies 

to alpha-gliadin. Pol J Immunol 1994;19(1):49-60. Not 

sensitivity or specificity of an identified test 

Gardiner A J, Mutton K J, Walker Smith J A. A family

study of coeliac disease. Aust Paediatr J 1973;9(1):18-24. 

Not sensitivity or specificity of an identified test

Garrote J A, Arranz E, Blanco-Quiros A. The HLA-DRB4 

gene is present in half of the Spanish HLA-DQ2-negative 

celiac patients. Immunogenetics 2000;51(12):1045-1046. 

Not sensitivity or specificity of an identified test

Garrote J A, Sorell L, Alfonso P et al. A novel visual 

immunoassay for coeliac disease screening. European 

Journal of Clinical Investigation 1999;29(8):697-699. Not 

sensitivity or specificity of an identified test 

Garrote Jose A, Arranz Eduardo, Telleria Juan J et al. TNF 

alpha and LT alpha gene polymorphisms as additional 

markers of celiac disease susceptibility in a DQ2-positive

population. Immunogenetics 2002;54(8):551-555. Not 

sensitivity or specificity of an identified test 

Gasbarrini Antonio, Ojetti Veronica, Cuoco Lucio et al.

Lack of endoscopic visualization of intestinal villi with the 

"immersion technique" in overt atrophic celiac disease. 

Gastrointestinal Endoscopy 2003;57(3):348-351. Not 

sensitivity or specificity of an identified test 

Gasbarrini G, Miglio F, Serra M A et al. Immunological 

studies of the jejunal mucosa in normal subjects and adult 

celiac patients. Digestion 1974;10(2):122-128. Not 

sensitivity or specificity of an identified test 

Gasparini M, Brucato A, Riccobono S et al. Congenital 

complete heart block (CCHB), cardiac Purkinje cells 

antibodies (CPCA) and HLA typing: Long term follow-up. 

New Trends Arrhythmias 1991;7(4):969-974. Not 

sensitivity or specificity of an identified test 

Gasset A R, Richman A V, Frias J L. HLA antigens and 

keratoconus. Ann Ophthalmol 1977;9(6):767-768. Not 

sensitivity or specificity of an identified test 

Gaudry C A, Verderio E, Jones R A et al. Tissue 

transglutaminase is an important player at the surface of 

human endothelial cells: evidence for its externalization 

and its colocalization with the beta(1) integrin.

Experimental Cell Research 1999;252(1):104-113. Not 

sensitivity or specificity of an identified test 

Gawkrodger D J, Blackwell J N, Gilmour H M et al. 

Dermatitis herpetiformis: diagnosis, diet and demography. 

Gut 1984;25(2):151-157. Not sensitivity or specificity of an 

identified test 

Gawkrodger D J, McDonald C, O'Mahony S et al. Small 

intestinal function and dietary status in dermatitis 

herpetiformis. Gut 1991;32(4):377-382. Not sensitivity or 

specificity of an identified test

Gawkrodger D J, Sweeting V M, Edwards C R et al. Male 

sex hormone status in dermatitis herpetiformis. British 

Journal of Dermatology 1985;112(1):57-61. Not sensitivity

or specificity of an identified test

Gay G J, Delmotte J-S. Enteroscopy in small intestinal

inflammatory diseases. Gastrointest Endosc Clin North Am 

1999;9(1):115-123. Not sensitivity or specificity of an 

identified test 

Gaze H, Rolles C, Signer E et al. Premedication for jejunal

biopsy in childhood using intravenous diazepam and 

metoclopramide. Archives of Disease in Childhood 

1974;49(4):322-324. Not sensitivity or specificity of an 

identified test 

Gazit E, Avigad S, Zfat Z et al. The association of HL-AB8 and childhood celiac disease in an Israeli population.

Israel Journal of Medical Sciences 1977;13(4):400-404. 

Not sensitivity or specificity of an identified test

Ge J, Hannestad K. A cytotoxic human hybridoma 

monoclonal antibody (TrJ6) defining an epitope expressed 

by HLA-DQ4 and -DQ5. Hum Immunol 1994;39(2):106-

112. Not sensitivity or specificity of an identified test 

Ge J, Bartnes K, Hannestad K. A human monoclonal 

hybridoma antibody (TrJ1) specific for HLA-DQ2. Tissue 

Antigens 1993;41(2):81-85. Not sensitivity or specificity of 

an identified test

Gebhard R L, Katz S I, Marks J. HL-A antigen type and

small intestinal disease in dermatitis herpetiformis. Lancet

1973;2(7832):760-762. Not sensitivity or specificity of an

identified test 

Gebhard R L, Stone B G, Prigge W F. 3-Hydroxy-3-

methylglutaryl coenzyme A reductase activity in the human

gastrointestinal tract. Journal of Lipid Research 

1985;26(1):47-53. Not sensitivity or specificity of an 

identified test 

Geboes K, Ectors N, Desmet V J. Coeliac disease 

"anatomic pathology". Acta Gastro-Enterologica Belgica 

1992;55(2):190-199. Not sensitivity or specificity of an 

identified test 

Geboes K, Ray M B, Rutgeerts P et al. Morphological 

identification of alpha-I-antitrypsin in the human small 

intestine. Histopathology 1982;6(1):55-60. Not sensitivity

or specificity of an identified test

Gebuhrer L, Adami N, Javaux F et al. Sequence of a new 

A-373
HLA-DR4 allele with an unusual residue at position 88 that 

does not seem to affect T-cell allo recognition. Hum

Immunol 1996;51(1):60-62. Not sensitivity or specificity of 

an identified test

Gedde-Dahl I I I, Spurkland A, Eriksen J A et al. Memory

T cells of a patient with follicular thyroid carcinoma 

recognize peptides derived from mutated p21 ras (Gln not 

<= Leu61). Int Immunol 1992;4(11):1331-1337. Not 

sensitivity or specificity of an identified test 

Gelfand M D, Spiro H M, Herskovic T. Small intestine 

glutaminase deficiency in celiac disease. American Journal

of Digestive Diseases 1968;13(7):638-642. Not sensitivity

or specificity of an identified test

Gelmetti C, Bonifazi E, Cavalli R et al. Dermatitis 

herpetiformis. Eur J Pediatr Dermatol 1995;5(2):95-110. 

Not sensitivity or specificity of an identified test

Gentile V, Davies P J, Baldini A. The human tissue 

transglutaminase gene maps on chromosome 20q12 by in

situ fluorescence hybridization. Genomics 1994;20(2):295-

297. Not sensitivity or specificity of an identified test 

Gentile V, Porta R, Chiosi E et al. tTGase/G alpha h protein

expression inhibits adenylate cyclase activity in Balb-C 

3T3 fibroblasts membranes. Biochimica Et Biophysica

Acta 1997;1357(1):115-122. Not sensitivity or specificity

of an identified test 

Gentile V, Saydak M, Chiocca E A et al. Isolation and 

characterization of cDNA clones to mouse macrophage and 

human endothelial cell tissue transglutaminases. J Biol 

Chem 1991;266(1):478-483. Not sensitivity or specificity

of an identified test 

Gentile V, Sepe C, Calvani M et al. Tissue

transglutaminase-catalyzed formation of high-molecularweight aggregates in vitro is favored with long

polyglutamine domains: a possible mechanism contributing

to CAG-triplet diseases. Archives of Biochemistry and 

Biophysics 1998;352(2):314-321. Not sensitivity or 

specificity of an identified test

Gentile Vittorio, Violante Vittorio, D'Amico Bonifacio et

al. Tissue transglutaminase and coeliac disease

pathogenesis: potential molecular mechanisms for other

human diseases. Neurochemistry International 

2002;40(1):79-83. Not sensitivity or specificity of an 

identified test 

George E K, Hertzberger-ten Cate R, Suijlekom-Smit L W

et al. Juvenile chronic arthritis and coeliac disease in The

Netherlands. Clinical and Experimental Rheumatology

1996;14(5):571-575. Not sensitivity or specificity of an 

identified test 

George E K, Jansen T L T A, Mearin M L et al. 

Epidemiology of celiac disease in the Netherlands. Journal 

of Pediatric Gastroenterology and Nutrition 1997;24(5):S7-

S9. Not sensitivity or specificity of an identified test 

George E K, Mearin M L, Bouquet J et al. High frequency

of celiac disease in Down syndrome. Journal of Pediatrics 

1996;128(4):555-557. Not sensitivity or specificity of an

identified test 

George E K, Mearin M L, Bouquet J et al. Screening for 

coeliac disease in Dutch children with associated diseases. 

Acta paediatrica (Oslo, Norway : 1992).Supplement. 

1996;41252-53. Not sensitivity or specificity of an 

identified test 

George E K, Mearin M L, Franken H C et al. Twenty years

of childhood coeliac disease in The Netherlands: a rapidly

increasing incidence?. Gut 1997;40(1):61-66. Not 

sensitivity or specificity of an identified test 

George E K, Mearin M L, van der V et al. Low incidence 

of childhood celiac disease in The Netherlands. Pediatric 

Research 1995;37(2):213-218. Not sensitivity or specificity

of an identified test 

George M D, Vollberg T M, Floyd E E et al. Regulation of 

transglutaminase type II by transforming growth factor-beta 

1 in normal and transformed human epidermal 

keratinocytes. Journal of Biological Chemistry 

1990;265(19):11098-11104. Not sensitivity or specificity of 

an identified test

Gerbase-DeLima M, Gallo C A, Daher S et al. HLA 

antigens in asthmatic children. Pediatr Allergy Immunol 

1997;8(3):150-152. Not sensitivity or specificity of an 

identified test 

Gheorghe C, Gheorghe L, Constantinescu A et al. The 

association between primary sclerosing cholangitis and 

adult celiac disease. Genomics 2000;67(2):43-48. Not 

sensitivity or specificity of an identified test 

Gheorghe L, Gheorghe C, Aposteanu G et al. Clinical 

spectrum of adult celiac disease in a referral center for 

Southern Romania. Associated disorders and short-term 

survival. Rom J Gastroenterol 1996;5(4):223-228. Not 

sensitivity or specificity of an identified test 

Ghezzi A, Zaffaroni M. Neurological manifestations of 

gastrointestinal disorders, with particular reference to the 

differential diagnosis of multiple sclerosis. Neurological 

Sciences - Official Journal of the Italian Neurological 

Society and of the Italian Society of Clinical

Neurophysiology 2001;22(Suppl 2):s117-s122. Not 

sensitivity or specificity of an identified test 

Ghoos Y F, Vantrappen G R, Rutgeerts P J et al. A mixedtriglyceride breath test for intraluminal fat digestive 

activity. Digestion 1981;22(5):239-247. Not sensitivity or

specificity of an identified test

Giachino C, Rocci M P, De Libero G et al. An alternative 

approach to the assessment of gamma delta T-cell clonality

in celiac disease intestinal lesions through cDNA 

heteroduplex analysis of T-cell receptor VJ junctions. 

A-374
Human Immunology 1994;40(4):303-311. Not sensitivity

or specificity of an identified test

Gianfrani Carmen, Troncone Riccardo, Mugione Patrizia et 

al. Celiac disease association with CD8+ T cell responses: 

identification of a novel gliadin-derived HLA-A2-restricted 

epitope. Journal of Immunology (Baltimore, Md.- 1950) 

2003;170(5):2719-2726. Not sensitivity or specificity of an 

identified test 

Giannotti A, Tiberio G, Castro M et al. Coeliac disease in

Williams syndrome. Journal of Medical Genetics

2001;38(11):767-768. Not sensitivity or specificity of an

identified test 

Gibran N S, Heimbach D M, Holbrook K A. 

Immunolocalization of FXIIIa+ dendritic cells in human 

burn wounds. Journal of Surgical Research 

1995;59(3):378-386. Not sensitivity or specificity of an 

identified test 

Gibran N S, Nickoloff B J, Holbrook K A. Ontogeny and

characterization of factor XIIIa+ cells in developing human 

skin. Anatomy and Embryology 1996;193(1):35-41. Not 

sensitivity or specificity of an identified test 

Gilchrist J M, Thompson G C, Medina J E. Markers of 

keratinocyte differentiation in snuff-induced leukoplakia. 

American Journal of Surgery 1992;164(6):563-566. Not 

sensitivity or specificity of an identified test 

Gill S S, Heuman D M, Mihas A A. Small intestinal 

neoplasms. Journal of Clinical Gastroenterology

2001;33(4):267-282. Not sensitivity or specificity of an 

identified test 

Gillberg R, Ahren C. Coeliac disease diagnosed by means 

of duodenoscopy and endoscopic duodenal biopsy.

Scandinavian Journal of Gastroenterology 1977;12(8):911-

916. Not sensitivity or specificity of an identified test 

Gillberg R, Dotevall G, Kastrup W et al. Conventional

malabsorption tests: do they detect the adult patient with

villous atrophy?. Scandinavian Journal of Clinical and 

Laboratory Investigation 1984;44(1):91-98. Not sensitivity

or specificity of an identified test

Gillberg R, Kastrup W, Mobacken H. Endoscopic duodenal 

biopsy compared with biopsy with the Watson capsule 

from the upper jejunum in patients with dermatitis 

herpetiformis. Scandinavian Journal of Gastroenterology

1982;17(2):305-308. Not sensitivity or specificity of an 

identified test 

Gillberg R, Kastrup W, Mobacken H et al. Gastric

morphology and function in dermatitis herpetiformis and in

coeliac disease. Scandinavian Journal of Gastroenterology

1985;20(2):133-140. Not sensitivity or specificity of an 

identified test 

Gillet H, Ferguson A, Frier B. Coeliac disease often coexists with Type 1 diabetes mellitus. Pract Diabetes Int 

1998;15(4):117-120. Not sensitivity or specificity of an 

identified test 

Gillett H R, Freeman H J. Prevalence of celiac disease in

collagenous and lymphocytic colitis. Canadian Journal of

Gastroenterology = Journal Canadien De Gastroenterologie 

2000;14(11):919-921. Not sensitivity or specificity of an

identified test 

Gillett H R, Freeman H J. Serological testing in screening 

for adult celiac disease. Canadian Journal of

Gastroenterology = Journal Canadien De Gastroenterologie 

1999;13(3):265-269. Not sensitivity or specificity of an 

identified test 

Gillett H R, Cauch-Dudek K, Jenny E et al. Prevalence of

IgA antibodies to endomysium and tissue transglutaminase 

in primary biliary cirrhosis. Canadian Journal of

Gastroenterology = Journal Canadien De Gastroenterologie 

2000;14(8):672-675. Not sensitivity or specificity of an 

identified test 

Gillett P M, Israel D M. Tissue transglutaminase: does the

key fit the celiac lock?. Journal of Pediatric 

Gastroenterology and Nutrition 2000;30(2):222-223. Not

sensitivity or specificity of an identified test 

Gillett P M, Gillett H R, Israel D M et al. High prevalence

of celiac disease in patients with type 1 diabetes detected

by antibodies to endomysium and tissue transglutaminase. 

Canadian Journal of Gastroenterology = Journal Canadien 

De Gastroenterologie 2001;15(5):297-301. Not sensitivity

or specificity of an identified test

Gillett P M, Gillett H R, Israel D M et al. Increased 

prevalence of celiac disease in girls with Turner syndrome 

detected using antibodies to endomysium and tissue 

transglutaminase. Canadian Journal of Gastroenterology =

Journal Canadien De Gastroenterologie 2000;14(11):915-

918. Not sensitivity or specificity of an identified test 

Giomi B, Cardinali C, Caproni M et al. Immunological 

markers in dermatitis herpetiformis: Anti-endomysium and

anti-transglutaminase in association with increased

myeloperoxidase and eosinophil cationic protein serum 

levels. Int J Med Biol Environ 2001;29(2):149-153. Not 

sensitivity or specificity of an identified test 

Giordano M, Bolognesi E, D'Alfonso S et al. Linkage 

disequilibrium between intra-locus variants in the

aminopeptidase n gene and test of their association with 

coeliac disease. Annals of Human Genetics 1999;63(Pt 

3):207-215. Not sensitivity or specificity of an identified

test 

Giovannini C, Sanchez M, Straface E et al. Induction of 

apoptosis in caco-2 cells by wheat gliadin peptides. 

Toxicology 2000;145(1):63-71. Not sensitivity or

specificity of an identified test

Girdwood R H, Williams A W, McManus J P et al. Jejunal 

biopsy in patients with malabsorptive disease. Scottish 

A-375
Medical Journal 1966;11(10):343-355. Not sensitivity or

specificity of an identified test

Gjertsen H A, Lundin K E, Sollid L M et al. T cells 

recognize a peptide derived from alpha-gliadin presented

by the celiac disease-associated HLA-DQ (alpha 1*0501, 

beta 1*0201) heterodimer. Human Immunology

1994;39(4):243-252. Not sensitivity or specificity of an 

identified test 

Gjertsen H A, Sollid L M, Ek J et al. T cells from the

peripheral blood of coeliac disease patients recognize 

gluten antigens when presented by HLA-DR, -DQ, or -DP 

molecules. Scandinavian Journal of Immunology

1994;39(6):567-574. Not sensitivity or specificity of an 

identified test 

Gjone E, Oyri A. Protein-losing enteropathy in dermatitis 

herpetiformis. Scandinavian Journal of Gastroenterology

1970;5(1):13-15. Not sensitivity or specificity of an 

identified test 

Glasgow J F, Corkey C W, Molla A. Critical assessment of 

small bowel biopsy in children. Archives of Disease in

Childhood 1979;54(8):604-608. Unable to extract data 

Gobbi G, Ambrosetto P, Zaniboni M G et al. Celiac 

disease, posterior cerebral calcifications and epilepsy. Brain

& Development 1992;14(1):23-29. Not sensitivity or 

specificity of an identified test

Gobbi G, Bouquet F, Greco L et al. Coeliac disease, 

epilepsy, and cerebral calcifications. The Italian Working 

Group on Coeliac Disease and Epilepsy. Lancet 

1992;340(8817):439-443. Not sensitivity or specificity of

an identified test

Godkin A, Jewell D. The pathogenesis of celiac disease. 

Gastroenterology 1998;115(1):206-210. Not sensitivity or

specificity of an identified test

Godkin A J, Davenport M P, Willis A et al. Use of

complete eluted peptide sequence data from HLA-DR and -

DQ molecules to predict T cell epitopes, and the influence 

of the nonbinding terminal regions of ligands in epitope

selection. Journal of Immunology (Baltimore, Md.- 1950) 

1998;161(2):850-858. Not sensitivity or specificity of an

identified test 

Godkin A, Friede T, Davenport M et al. Use of eluted

peptide sequence data to identify the binding characteristics

of peptides to the insulin-dependent diabetes susceptibility 

allele HLA-DQ8 (DQ 3.2). International Immunology

1997;9(6):905-911. Not sensitivity or specificity of an 

identified test 

Godot V, Harraga S, Beurton I et al. 

Resistance/susceptibility to Echinococcus multilocularis 

infection and cytokine profile in humans. II. Influence of 

the HLA B8, DR3, DQ2 haplotype. Clinical and 

Experimental Immunology 2000;121(3):491-498. Not 

sensitivity or specificity of an identified test 

Goggins M, Kelleher D. Celiac disease and other nutrient 

related injuries to the gastrointestinal tract. American

Journal of Gastroenterology 1994;89(8 Suppl):S2-17. Not 

sensitivity or specificity of an identified test 

Goggins M, Whelan A, Kelleher D. The immunology of 

coeliac disease. Annales De Medecine Interne

1996;147(1):40-48. Not sensitivity or specificity of an 

identified test 

Goldblum J R, Tuthill R J. CD34 and factor-XIIIa 

immunoreactivity in dermatofibrosarcoma protuberans and

dermatofibroma. American Journal of Dermatopathology

1997;19(2):147-153. Not sensitivity or specificity of an 

identified test 

Goldsmith L A. Human epidermal transglutaminase. 

Journal of Investigative Dermatology 1983;80(Suppl):39s41s. Not sensitivity or specificity of an identified test 

Goldstein F, Wirts C W, Salen G et al. Diverticulosis of the 

small intestine. Clinical, bacteriologic, and metabolic

observations in a group of seven patients. American Journal 

of Digestive Diseases 1969;14(3):170-181. Not sensitivity

or specificity of an identified test

Goldstein N S, Underhill J. Morphologic features 

suggestive of gluten sensitivity in architecturally normal 

duodenal biopsy specimens. American Journal of Clinical 

Pathology 2001;116(1):63-71. Improper control group 

Goldstein R, Sengar D P S. Comparative studies of the

major histocompatibility complex in French Canadian and 

non-French Canadian Caucasians with systemic lupus 

erythematosus. Arthritis Rheum 1993;36(8):1121-1127. 

Not sensitivity or specificity of an identified test

Goldstein R, Moulds J M, Smith C D et al. MHC studies of 

the primary antiphospholipid antibody syndrome and of 

antiphospholipid antibodies in systemic lupus 

erythematosus. J Rheumatol 1996;23(7):1173-1179. Not 

sensitivity or specificity of an identified test 

Gomez J C, Selvaggio G S, Viola M et al. Prevalence of

celiac disease in Argentina: screening of an adult 

population in the La Plata area. American Journal of 

Gastroenterology 2001;96(9):2700-2704. Not sensitivity or 

specificity of an identified test

Gomez Juan C, Selvaggio Gisella, Pizarro Bibiana et al.

Value of a screening algorithm for celiac disease using 

tissue transglutaminase antibodies as first level in a 

population-based study. American Journal of 

Gastroenterology 2002;97(11):2785-2790. Not sensitivity

or specificity of an identified test

Gonczi J, Skerritt J H, Mitchell J D. Differentiation of 

coeliac disease and other malabsorption diseases using 

specific serum antigliadin IgG subclass profiles and IgA1 

levels. International Archives of Allergy and Immunology

1992;98(4):377-385. Not sensitivity or specificity of an 

A-376
identified test 

Gonzalez D, Sugai E, Gomez J C et al. Is it necessary to

screen for celiac disease in postmenopausal osteoporotic 

women?. Calcified Tissue International 2002;71(2):141-

144. Not sensitivity or specificity of an identified test 

Gonzalez-Crussi F, Reyes-Mugica M. Cellular

hemangiomas ("hemangioendotheliomas") in infants. Light 

microscopic, immunohistochemical, and ultrastructural 

observations. American Journal of Surgical Pathology

1991;15(8):769-778. Not sensitivity or specificity of an 

identified test 

Gonzalez-Trevin tilde, Yamamoto-Furusho J K, Cutin tilde 

et al. HLA study on two Mexican mestizo families with 

autoimmune thyroid disease. Autoimmunity

2002;35(4):265-269. Not sensitivity or specificity of an 

identified test 

Goodchild M C, Nelson R, Anderson C M. Cystic fibrosis 

and coeliac disease: coexistence in two children. Arch Dis

Child 1973;48(9):684-691. Not sensitivity or specificity of 

an identified test

Goossens J F, Manechez D, Pommery N et al. VIP

potentiates retinoic-acid effect on tissue transglutaminase

activity in human neuroblastoma, the SK-N-SH cells.

Neuropeptides 1993;24(2):99-103. Not sensitivity or 

specificity of an identified test

Gorczyca Wojciech, Tsang Patricia, Liu Zach et al. CD30-

positive T-cell lymphomas co-expressing CD15: an 

immunohistochemical analysis. International Journal of

Oncology 2003;22(2):319-324. Not sensitivity or

specificity of an identified test

Gorkun O V, Veklich Y I, Weisel J W et al. The conversion 

of fibrinogen to fibrin: recombinant fibrinogen typifies 

plasma fibrinogen. Blood 1997;89(12):4407-4414. Not 

sensitivity or specificity of an identified test 

Gorski J, Niven M J, Sachs J A et al. HLA-DR alpha, -DX 

alpha, and DR beta III gene association studies in DR3 

individuals. Hum Immunol 1987;20(4):273-278. Not 

sensitivity or specificity of an identified test 

Gorza L, Menabo R, Di Lisa F et al. Troponin T crosslinking in human apoptotic cardiomyocytes. American

Journal of Pathology 1997;150(6):2087-2097. Not 

sensitivity or specificity of an identified test 

Gorza L, Menabo R, Vitadello M et al. Cardiomyocyte

troponin T immunoreactivity is modified by cross- linking

resulting from intracellular calcium overload. Circulation

1996;93(10):1896-1904. Not sensitivity or specificity of an 

identified test 

Gosiewska A, Yi C F, Blanc-Brude O et al. 

Characterization of a macrophage-based system for 

studying the activation of latent TGF-beta. Methods in Cell

Science - an Official Journal of the Society for in Vitro 

Biology 1999;21(1):47-56. Not sensitivity or specificity of 

an identified test

Gottardis M M, Lamph W W, Shalinsky D R et al. The 

efficacy of 9-cis retinoic acid in experimental models of 

cancer. Breast Cancer Research and Treatment

1996;38(1):85-96. Not sensitivity or specificity of an 

identified test 

Gottschalk J, Jautzke G, Schreiner C. Epithelial and 

melanoma antigens in gliosarcoma. An 

immunohistochemical study. Pathology, Research and 

Practice 1992;188(1-2):182-190. Not sensitivity or

specificity of an identified test

Gottschalk J, Jautzke G, Marzheuser-Brands S et al. Factor

XIIIa immunoreactivity in primary and secondary tumours 

of the meninges. Zentralblatt Fur Pathologie 1993;139(4-

5):343-349. Not sensitivity or specificity of an identified

test 

Goulet O, Kedinger M, Brousse N et al. Intractable diarrhea 

of infancy with epithelial and basement membrane

abnormalities. Journal of Pediatrics 1995;127(2):212-219. 

Not sensitivity or specificity of an identified test

Goulston K, Bhanthumnavin K, Harrison D. Investigation

of steatorrhoea. Medical Journal of Australia 

1968;2(11):462-466. Not sensitivity or specificity of an 

identified test 

Grabarek Jerzy, Ardelt Barbara, Kunicki Jan et al. 

Detection of in situ activation of transglutaminase during 

apoptosis: correlation with the cell cycle phase by

multiparameter flow and laser scanning cytometry.

Cytometry - the Journal of the Society for Analytical

Cytology 2002;49(2):83-89. Not sensitivity or specificity of 

an identified test

Graff Ronald D, Picher Maryse, Lee Greta M. Extracellular

nucleotides, cartilage stress, and calcium crystal formation. 

Current Opinion in Rheumatology 2003;15(3):315-320. 

Not sensitivity or specificity of an identified test

Graham J, Kockum I, Sanjeevi C B et al. Negative 

association between type 1 diabetes and HLA DQB1*0602-

DQA1*0102 is attenuated with age at onset. Eur J 

Immunogenet 1999;26(2-3):117-127. Not sensitivity or

specificity of an identified test

Graham Jinko, Hagopian William A, Kockum Ingrid et al. 

Genetic effects on age-dependent onset and islet cell 

autoantibody markers in type 1 diabetes. Diabetes

2002;51(5):1346-1355. Not sensitivity or specificity of an

identified test 

Grainger D J, Frow E K. Thrombospondin 1 does not 

activate transforming growth factor beta1 in a chemically

defined system or in smooth-muscle-cell cultures. Biochem

J 2000;350(1):291-298. Not sensitivity or specificity of an 

identified test 

A-377
Granados J, Vargas-Alarcon G, Drenkard C et al. 

Relationship of anticardiolipin antibodies and 

antiphospholipid syndrome to HLA-DR7 in Mexican 

patients with systemic lupus erythematosus (SLE). Lupus

1997;6(1):57-62. Not sensitivity or specificity of an 

identified test 

Granditsch G, Deutsch J, Tsarmaklis G et al. Exposure to 

X-rays during small bowel biopsies in children. European

Journal of Pediatrics 1981;137(2):165-169. Not sensitivity

or specificity of an identified test

Granditsch G, Ludwig H, Polymenidis Z et al. Letter: 

Coeliac disease and HL-A8. Lancet 1973;2(7834):908-909. 

Not sensitivity or specificity of an identified test

Grando S A, Horton R M, Mauro T M et al. Activation of 

keratinocyte nicotinic cholinergic receptors stimulates

calcium influx and enhances cell differentiation. Journal of 

Investigative Dermatology 1996;107(3):412-418. Not 

sensitivity or specificity of an identified test 

Granot E, Korman S M, Sallon S et al. "Early" vs. "late" 

diagnosis of celiac disease in two ethnic groups living in

the same geographic area. Israel Journal of Medical 

Sciences 1994;30(4):271-275. Not sensitivity or specificity

of an identified test 

Gravinghoff J, Huetter H J. The activities of alanine 

aminopeptidase, leucine aminopeptidase, proline 

dipeptidase and prolyl dipeptidase in the mucosa of the 

small intestine. Investigations on normal children and 

patients with the malabsorption syndrome. European 

Journal of Pediatrics 1977;127(1):57-62. Not sensitivity or

specificity of an identified test

Gray M H, Smoller B R, McNutt N S et al.

Immunohistochemical demonstration of factor XIIIa 

expression in neurofibromas. A practical means of 

differentiating these tumors from neurotized melanocytic

nevi and schwannomas. Archives of Dermatology 

1990;126(4):472-476. Not sensitivity or specificity of an

identified test 

Gray M H, Trimble C L, Zirn J et al. Relationship of factor

XIIIa-positive dermal dendrocytes to Kaposi's sarcoma. 

Archives of Pathology & Laboratory Medicine 

1991;115(8):791-796. Not sensitivity or specificity of an

identified test 

Greco L, Babron M C, Corazza G R et al. Existence of a 

genetic risk factor on chromosome 5q in Italian Coeliac 

disease families. Ann Hum Genet 2001;-(1):35-41. Not 

sensitivity or specificity of an identified test 

Greco L, Corazza G, Babron M C et al. Genome search in 

celiac disease. American Journal of Human Genetics

1998;62(3):669-675. Not sensitivity or specificity of an 

identified test 

Greco L, D'Adamo G, Truscelli A et al. Intestinal

permeability after single dose gluten challenge in coeliac

disease. Archives of Disease in Childhood 1991;66(7):870-

872. Not sensitivity or specificity of an identified test 

Greco L, Percopo S, Clot F et al. Lack of correlation 

between genotype and phenotype in celiac disease. Journal 

of Pediatric Gastroenterology and Nutrition 

1998;26(3):286-290. Not sensitivity or specificity of an 

identified test 

Greco L, Romino R, Coto I et al. The first large population

based twin study of coeliac disease. Gut 2002;50(5):624-

628. Not sensitivity or specificity of an identified test 

Greco L, Troncone R, De Vizia B et al. Discriminant 

analysis for the diagnosis of childhood celiac disease. 

Journal of Pediatric Gastroenterology and Nutrition 

1987;6(4):538-542. Improper control group 

Green Peter H R, Jabri Bana. Coeliac disease. Lancet

2003;362(9381):383-391. Not sensitivity or specificity of

an identified test

Green J R, Chiew M K, Low H C et al. The association 

between HLA antigens and the presence of certain diseases.

Statistics in Medicine 1983;2(1):79-85. Not sensitivity or 

specificity of an identified test

Green J R, Goble H L, Edwards C R et al. Reversible 

insensitivity to androgens in men with untreated gluten

enteropathy. Lancet 1977;1(8006):280-282. Not sensitivity

or specificity of an identified test

Green P H R, Stavropoulos S N, Panagi S G et al. 

Characteristics of adult celiac disease in the USA: results of

a national survey. American Journal of Gastroenterology

2001;96(1):126-131. Not sensitivity or specificity of an 

identified test 

Green P H, Shane E, Rotterdam H et al. Significance of

unsuspected celiac disease detected at endoscopy. 

Gastrointestinal Endoscopy 2000;51(1):60-65. Not 

sensitivity or specificity of an identified test 

Greenberg C S, Achyuthan K E, Borowitz M J et al. The 

transglutaminase in vascular cells and tissues could provide 

an alternate pathway for fibrin stabilization. Blood 

1987;70(3):702-709. Not sensitivity or specificity of an 

identified test 

Greenberg C S, Birckbichler P J, Rice R H. 

Transglutaminases: multifunctional cross-linking enzymes 

that stabilize tissues. Faseb Journal - Official Publication of

the Federation of American Societies for Experimental 

Biology 1991;5(15):3071-3077. Not sensitivity or

specificity of an identified test

Greenberg D A, Lange K L. A maximum likelihood test of 

the two locus model for coeliac disease. American Journal

of Medical Genetics 1982;12(1):75-82. Not sensitivity or 

specificity of an identified test

Greenberg D A, Rotter J I. Two locus models for gluten

A-378
sensitive enteropathy: population genetic considerations. 

American Journal of Medical Genetics 1981;8(2):205-214. 

Not sensitivity or specificity of an identified test

Greenberg D A, Hodge S E, Rotter J I. Evidence for 

recessive and against dominant inheritance at the HLA-

"linked" locus in coeliac disease. American Journal of

Human Genetics 1982;34(2):263-277. Not sensitivity or

specificity of an identified test

Greenhouse J P, Monier-Williams M. Geophysical 

monitoring of ground water contamination around waste 

disposal sites. Ground Water Monit Rev 1985;5(4):63-69. 

Not sensitivity or specificity of an identified test

Greenwald A J, Johnson D S, Oskvig R M et al. Alpha-1-

antitrypsin deficiency, emphysema, cirrhosis, and intestinal

mucosal atrophy. Jama - the Journal of the American 

Medical Association 1975;231(3):273-276. Not sensitivity

or specificity of an identified test

Grefte J M, Bouman J G, Grond J et al. Slow and

incomplete histological and functional recovery in adult 

gluten sensitive enteropathy. Journal of Clinical Pathology 

1988;41(8):886-891. Not sensitivity or specificity of an 

identified test 

Grehn S, Fridell K, Lilliecreutz M et al. Dietary habits of

Swedish adult coeliac patients treated by a gluten-free diet 

for 10 years. Scand J Nutr Naringsforsk 2001;45(4):178-

182. Not sensitivity or specificity of an identified test 

Grenard P, Bates M K, Aeschlimann D. Evolution of 

transglutaminase genes: identification of a transglutaminase 

gene cluster on human chromosome 15q15. Structure of the 

gene encoding transglutaminase X and a novel gene family

member, transglutaminase Z. Journal of Biological 

Chemistry 2001;276(35):33066-33078. Not sensitivity or

specificity of an identified test

Grierson A J, Johnson G V, Miller C C. Three different 

human tau isoforms and rat neurofilament light, middle and

heavy chain proteins are cellular substrates for

transglutaminase. Neuroscience Letters 2001;298(1):9-12. 

Not sensitivity or specificity of an identified test

Griffin Martin, Casadio Rita, Bergamini Carlo M.

Transglutaminases: nature's biological glues. Biochemical 

Journal 2002;368(Pt 2):377-396. Not sensitivity or 

specificity of an identified test

Griffiths C E, Barrison I G, Leonard J N et al. Preferential 

activation of CD4 T lymphocytes in the lamina propria of

gluten-sensitive enteropathy. Clinical and Experimental 

Immunology 1988;72(2):280-283. Not sensitivity or 

specificity of an identified test

Grigoriev M Y, Suspitsin E N, Togo A V et al. Tissue 

transglutaminase expression in breast carcinomas. Journal 

of Experimental & Clinical Cancer Research - Cr

2001;20(2):265-268. Not sensitivity or specificity of an 

identified test 

Grillo R, Petronzelli F, Ferrante P et al. Unusual HLA 

typing in celiac disease. Disease Markers 1996;13(1):61-

64. Not sensitivity or specificity of an identified test 

Grodzinsky E. Screening for coeliac disease in apparently

healthy blood donors. Acta paediatrica (Oslo, Norway : 

1992).Supplement. 1996;41236-38. Improper control group 

Grodzinsky E, Franzen L, Hed J et al. High prevalence of

celiac disease in healthy adults revealed by antigliadin 

antibodies. Annals of Allergy 1992;69(1):66-70. Improper 

control group 

Grodzinsky E, Hed J, Skogh T. IgA antiendomysium 

antibodies have a high positive predictive value for celiac 

disease in asymptomatic patients. Allergy 1994;49(8):593-

597. Improper control group 

Grodzinsky E, Hed J, Lieden G et al. Presence of IgA and 

IgG antigliadin antibodies in healthy adults as measured by

micro-ELISA. Effect of various cutoff levels on specificity

and sensitivity when diagnosing coeliac disease. 

International Archives of Allergy and Applied Immunology

1990;92(2):119-123. Improper control group 

Grodzinsky E, Ivarsson A, Juto P et al. New automated 

immunoassay measuring immunoglobulin A antigliadin

antibodies for prediction of celiac disease in childhood. 

Clinical and Diagnostic Laboratory Immunology

2001;8(3):564-570. Improper control group 

Grodzinsky E, Jansson G, Skogh T et al. Anti-endomysium 

and anti-gliadin antibodies as serological markers for 

coeliac disease in childhood: a clinical study to develop a 

practical routine. Acta Paediatrica (Oslo, Norway - 1992)

1995;84(3):294-298. Improper control group 

Groisman G M, Sabo E, Meir A et al. Enterocyte apoptosis 

and proliferation are increased in microvillous inclusion 

disease (familial microvillous atrophy). Human Pathology

2000;31(11):1404-1410. Not sensitivity or specificity of an 

identified test 

Groisman Gabriel M, Amar Mary, Livne Erella. CD10: a 

valuable tool for the light microscopic diagnosis of 

microvillous inclusion disease (familial microvillous 

atrophy). American Journal of Surgical Pathology

2002;26(7):902-907. Not sensitivity or specificity of an 

identified test 

Groll A. Symposium on diarrhea. 3. Investigation of 

chronic diarrhea. Canadian Medical Association Journal 

1977;116(7):742-744. Not sensitivity or specificity of an

identified test 

Groll A, Candy D C, Preece M A et al. Short stature as the 

primary manifestation of coeliac disease. Lancet 

1980;2(8204):1097-1099. Not sensitivity or specificity of

an identified test

Gross Stephane R, Balklava Zita, Griffin Martin.

A-379
Importance of tissue transglutaminase in repair of

extracellular matrices and cell death of dermal fibroblasts

after exposure to a solarium ultraviolet A source. Journal of 

Investigative Dermatology 2003;121(2):412-423. Not 

sensitivity or specificity of an identified test 

Grunewald J, Olerup O, Persson U et al. T-cell receptor

variable region gene usage by CD4sup + and CD8sup + T 

cells in bronchoalveolar lavage fluid and peripheral blood 

of sarcoidosis patients. Proc Natl Acad Sci U S A 

1994;91(11):4965-4969. Not sensitivity or specificity of an 

identified test 

Grunewald J, Shigematsu M, Nagai S et al. T-cell receptor 

V gene expression in HLA-typed Japanese patients with 

pulmonary sarcoidosis. Am J Respir Crit Care Med 

1995;151(1):151-156. Not sensitivity or specificity of an

identified test 

Gryboski J. False security of a gluten-free diet. American 

Journal of Diseases of Children (1960) 1981;135(2):110-

111. Not sensitivity or specificity of an identified test 

Grzybowski J, Antos M, Sakiel S et al. Antidietary antigen

antibodies in the sera of patients with burns as a potential 

marker of gut mucosa integrity failure. Journal of Burn 

Care & Rehabilitation 1992;13(2 Pt 1):194-197. Not 

sensitivity or specificity of an identified test 

Guadiz G, Sporn L A, Simpson-Haidaris P J. Thrombin 

cleavage-independent deposition of fibrinogen in

extracellular matrices. Blood 1997;90(7):2644-2653. Not 

sensitivity or specificity of an identified test 

Guandalini S. Celiac disease in the new world. Journal of

Pediatric Gastroenterology and Nutrition 2000;31(4):362-

364. Not sensitivity or specificity of an identified test 

Guandalini S, Ventura A, Ansaldi N et al. Diagnosis of 

coeliac disease: time for a change?. Archives of Disease in 

Childhood 1989;64(9):1320-1324. Not sensitivity or 

specificity of an identified test

Guarino A, Spagnuolo M I, Russo S et al. Etiology and risk 

factors of severe and protracted diarrhea. Journal of 

Pediatric Gastroenterology and Nutrition 1995;20(2):173-

178. Not sensitivity or specificity of an identified test 

Guariso G, Messina C, Gazzola M V et al. Transient

erythoblastopenia in coeliac disease. Haematologica 

2001;86(8):E23Not sensitivity or specificity of an 

identified test 

Guglielmino C R, De Silvestri A, Martinetti M. HLA class 

I and II genes in relation to the genetic structure and 

epidemiology of an Italian province. Experimental and 

Clinical Immunogenetics 1997;14(2):149-159. Not 

sensitivity or specificity of an identified test 

Guiraldes E, Gutierrez C, Castillo C. Letter: Coeliac 

disease. Medical Journal of Australia 1975;1(10):322Not 

sensitivity or specificity of an identified test 

Guix M, Skinner J M, Whitehead R. Morphometric 

electron and light microscope analysis of lymphoid cells in

coeliac disease. Scandinavian Journal of Gastroenterology

1979;14(3):261-265. Not sensitivity or specificity of an 

identified test 

Guix M, Skinner J M, Whitehead R. Ultrastructural 

analysis of plasma cells in celiac patients. Gut

1979;20(6):504-508. Not sensitivity or specificity of an 

identified test 

Gumurdulu Derya, Zeren E, Handan Cagle et al. Specificity

of MOC-31 and HBME-1 immunohistochemistry in the 

differential diagnosis of adenocarcinoma and malignant 

mesothelioma: a study on environmental malignant 

mesothelioma cases from Turkish villages. Pathology 

Oncology Research - Por 2003;8(3):188-193. Not 

sensitivity or specificity of an identified test 

Gupta M, Nikitina-Zake L, Landin-Olsson M et al. 

Coxsackie virus B antibodies are increased in HLA DR3-

MICA5.1 positive type 1 diabetes patients in the Linkoping

region of Sweden. Hum Immunol 2003;64(9):874-879. Not 

sensitivity or specificity of an identified test 

Gupta M, Nikitina-Zake L, Zarghami M et al. Association

between the transmembrane region polymorphism of MHC 

class I chain related gene-A and type 1 diabetes mellitus in

Sweden. Hum Immunol 2003;64(5):553-561. Not 

sensitivity or specificity of an identified test 

Gupta M, Tandon N, Shtauvere-Brameus A et al. ICA12 

autoantibodies are associated with Non-DR3/Non-DR4 in 

patients with latent autoimmune diabetes in adults from

Northern India. Ann New York Acad Sci 2002;958(-):329-

332. Not sensitivity or specificity of an identified test 

Gupte S. Changing concepts in celiac disease. Jk Science 

2001;3(3):103-104. Not sensitivity or specificity of an 

identified test 

Guvenc cedil, Kaymakog caron, Gurel N et al. The 

prevalence of manifest and latent celiac disease in type 1 

diabetes mellitus. Turk J Gastroenterol 2002;13(2):103-

107. Not sensitivity or specificity of an identified test 

Guzman J, Bross K J, Wurtemberger G et al. 

Immunocytology in malignant pleural mesothelioma. 

Expression of tumor markers and distribution of

lymphocyte subsets. Chest 1989;95(3):590-595. Not 

sensitivity or specificity of an identified test 

Haas L, Petit-Phar M, Terzidis H et al. IgA subclass 

distribution of IgA anti-gliadin antibodies in feces of 

patients with coeliac disease. Advances in Experimental 

Medicine and Biology 1995;371b1349-1353. Not 

sensitivity or specificity of an identified test 

Habior Andrzej, Lewartowska Aleksandra, Orlowska 

Janina et al. Association of coeliac disease with primary 

biliary cirrhosis in Poland. European Journal of

A-380
Gastroenterology & Hepatology 2003;15(2):159-164. Not 

sensitivity or specificity of an identified test 

Hadjivassiliou M, Boscolo S, Davies-Jones G A B et al. 

The humoral response in the pathogenesis of gluten ataxia. 

Neurology 2002;58(8):1221-1226. Not sensitivity or 

specificity of an identified test

Hadjivassiliou M, Chattopadhyay A K, Davies-Jones G A 

B et al. Neuromuscular disorder as a presenting feature of

coeliac disease. J Neurol Neurosurg Psychiatry

1997;63(6):770-775. Not sensitivity or specificity of an 

identified test 

Hadjivassiliou M, Davies-Jones G A B, Sanders D S et al. 

Dietary treatment of gluten ataxia. Journal of Neurology,

Neurosurgery, and Psychiatry 2003;74(9):1221-1224. Not 

sensitivity or specificity of an identified test 

Hadjivassiliou M, Gibson A, Davies-Jones G A et al. Does 

cryptic gluten sensitivity play a part in neurological 

illness?. Lancet 1996;347(8998):369-371. Not sensitivity or 

specificity of an identified test

Hadjivassiliou M, Grunewald R A, Davies-Jones G A B.

Gluten sensitivity: A many headed hydra. Br Med J 

1999;318(7200):1710-1711. Not sensitivity or specificity of 

an identified test

Hadjivassiliou M, Grunewald R A, Davies-Jones G A B.

Gluten sensitivity as a neurological illness. J Neurol 

Neurosurg Psychiatry 2002;72(5):560-563. Not sensitivity

or specificity of an identified test

Hadjivassiliou M, Grunewald R A, Chattopadhyay A K et

al. Clinical, radiological, neurophysiological, and 

neuropathological characteristics of gluten ataxia. Lancet

1998;352(9140):1582-1585. Not sensitivity or specificity of 

an identified test

Hadjivassiliou Marios, Grunewald Richard, Sharrack Basil

et al. Gluten ataxia in perspective: epidemiology, genetic

susceptibility and clinical characteristics. Brain 2003;A 

Journal of Neurology; 126(Pt 3):685-691. Not sensitivity or 

specificity of an identified test

Hadziselimovic F, Emmons L R, Schaub U et al. 

Occurrence of large granular lymphocytes and natural killer 

cells in the epithelium of the gut distinguishes two different 

coeliac diseases. Gut 1992;33(6):767-772. Not sensitivity

or specificity of an identified test

Hafeez A, Ali S, Hassan M. An audit of pediatric upper 

gastrointestinal endoscopies. J Coll Phys Surg Pak

2000;10(1):13-15. Not sensitivity or specificity of an 

identified test 

Hafstrom I, Ringertz B, Spangberg A et al. A vegan diet 

free of gluten improves the signs and symptoms of

rheumatoid arthritis: The effects on arthritis correlate with a

reduction in antibodies to food antigens. Rheumatology

(Uk) 2001;40(10):1175-1179. Not sensitivity or specificity

of an identified test 

Haga P. Plasma ferritin concentrations in preterm infants in

cord blood and during the early anaemia of prematurity.

Acta Paediatrica Scandinavica 1980;69(5):637-641. Not 

sensitivity or specificity of an identified test 

Hager H, Gliemann J, Hamilton-Dutoit S et al. 

Developmental regulation of tissue transglutaminase during

human placentation and expression in neoplastic 

trophoblast. Journal of Pathology 1997;181(1):106-110. 

Not sensitivity or specificity of an identified test

Hager H, Jensen P H, Hamilton-Dutoit S et al. Expression 

of tissue transglutaminase in human bladder carcinoma. 

Journal of Pathology 1997;183(4):398-403. Not sensitivity

or specificity of an identified test

Hagopian W A, Sanjeevi C B, Kockum I et al. Glutamate 

decarboxylase-, insulin-, and islet cell-antibodies and HLA 

typing to detect diabetes in a general population-based 

study of Swedish children. Journal of Clinical Investigation 

1995;95(4):1505-1511. Not sensitivity or specificity of an

identified test 

Hahn-Zoric M, Hytonen A M, Hanson L A et al. 

Association of -1087 IL10 and -308 TNFA gene 

polymorphisms with serological markers of coeliac disease.

J Clin Immunol 2003;23(4):291-296. Not sensitivity or

specificity of an identified test

Hahnel A C, Eddy E M. Cell surface markers of mouse 

primordial germ cells defined by two monoclonal 

antibodies. Gamete Res 1986;15(1):25-34. Not sensitivity

or specificity of an identified test

Hahnel A C, Eddy E M. The distribution of two cell surface

determinants of mouse embryonal carcinoma and early

embryonic cells. J Reprod Immunol 1987;10(2):89-110. 

Not sensitivity or specificity of an identified test

Hajjar E T, Vincenti F, Salti I S. Gluten induced

enteropathy. Osteomalacia as its principal manifestation.

Arch Intern Med 1974;134(3):565-566. Not sensitivity or 

specificity of an identified test

Hakeem V, Fifield R, al Bayaty H F et al. Salivary IgA 

antigliadin antibody as a marker for coeliac disease. 

Archives of Disease in Childhood 1992;67(6):724-727. 

Test-specific exclusion 

Hall M A, Lanchbury J S, Ciclitira P J. HLA class II region 

genes and susceptibility to dermatitis herpetiformis: DPB1 

and TAP2 associations are secondary to those of the DQ 

subregion. European Journal of Immunogenetics - Official 

Journal of the British Society for Histocompatibility and

Immunogenetics 1996;23(4):285-296. Not sensitivity or

specificity of an identified test

Hall M A, Lanchbury J S, Bolsover W J et al. Celiac 

disease is associated with an extended HLA-DR3 haplotype 

which includes HLA-DPw1. Hum Immunol 

A-381
1990;27(3):220-228. Not sensitivity or specificity of an 

identified test 

Hall M A, Lanchbury J S, Bolsover W J et al. HLA 

association with dermatitis herpetiformis is accounted for

by a cis or transassociated DQ heterodimer. Gut 

1991;32(5):487-490. Not sensitivity or specificity of an 

identified test 

Hall M A, Lanchbury J S, Lee J S et al. HLA-DQ2 seconddomain polymorphisms may explain increased transassociated risk in celiac disease and dermatitis

herpetiformis. Human Immunology 1993;38(4):284-292. 

Improper control group 

Hall M A, Lanchbury J S, Sturgess R P et al. TCR Vbeta 

usage in peripheral blood and small intestinal bipsies of 

treated and untreated coeliac disease patients. Eur J

Immunogenet 1992;19(6):439Not sensitivity or specificity

of an identified test 

Hall P A, d'Ardenne A J, Stansfeld A G. Paraffin section 

immunohistochemistry. I. Non-Hodgkin's lymphoma. 

Histopathology 1988;13(2):149-160. Not sensitivity or

specificity of an identified test

Hall R P. Dermatitis herpetiformis and the mucosal 

immune response. Journal of Autoimmunity 1991;4(1):47-

58. Not sensitivity or specificity of an identified test 

Hall R P. The pathogenesis of dermatitis herpetiformis: 

recent advances. Journal of the American Academy of 

Dermatology 1987;16(6):1129-1144. Not sensitivity or

specificity of an identified test

Hall R P, Waldbauer G V. Characterization of the mucosal 

immune response to dietary antigens in patients with 

dermatitis herpetiformis. Journal of Investigative 

Dermatology 1988;90(5):658-663. Not sensitivity or 

specificity of an identified test

Hall R P, Lawley T J, Katz S I. Dermatitis herpetiformis. 

Springer Seminars in Immunopathology 1981;4(1):33-43. 

Not sensitivity or specificity of an identified test

Hall R P, Owen S, Smith A et al. TCR Vbeta expression in 

the small bowel of patients with dermatitis herpetiformis 

and gluten sensitive enteropathy. Limited expression in 

dermatitis herpetiformis and treated asymptomatic gluten 

sensitive enteropathy. Experimental Dermatology 

2000;9(4):275-282. Not sensitivity or specificity of an 

identified test 

Hall R P, Ward F E, Wenstrup R J. An HLA class II region 

restriction fragment length polymorphism (RFLP) in 

patients with dermatitis herpetiformis: association with 

HLA-DP phenotype. Journal of Investigative Dermatology

1990;95(2):172-177. Not sensitivity or specificity of an 

identified test 

Hallert C, Granno C, Grant C et al. Quality of life of adult 

coeliac patients treated for 10 years. Scandinavian Journal 

of Gastroenterology 1998;33(9):933-938. Not sensitivity or 

specificity of an identified test

Hallert C, Tobiasson P, Walan A. Serum folate

determinations in tracing adult coeliacs. Scandinavian

Journal of Gastroenterology 1981;16(2):263-267. Not 

sensitivity or specificity of an identified test 

Hallgren J, Knutson F, Lavo B et al. Increased mucosal 

synthesis of rheumatoid factor (RF) in coeliac disease.

Clinical and Experimental Immunology 1996;103(1):94-98. 

Not sensitivity or specificity of an identified test

Hallgren R, Colombel J F, Dahl R et al. Neutrophil and 

eosinophil involvement of the small bowel in patients with 

celiac disease and Crohn's disease: studies on the secretion 

rate and immunohistochemical localization of granulocyte 

granule constituents. American Journal of Medicine 

1989;86(1):56-64. Not sensitivity or specificity of an 

identified test 

Halsted C H, Reisenauer A M, Romero J J. Jejunal 

perfusion of simple and conjugated folates in celiac sprue. J

Clin Invest 1977;59(5):933-940. Not sensitivity or

specificity of an identified test

Halstensen T S, Hvatum M, Scott H et al. Association of 

subepithelial deposition of activated complement and 

immunoglobulin G and M response to gluten in celiac 

disease. Gastroenterology 1992;102(3):751-759. Not 

sensitivity or specificity of an identified test 

Halstensen T S, Scott H, Brandtzaeg P. Human CD8+ 

intraepithelial T lymphocytes are mainly CD45RA-RB+ 

and show increased co-expression of CD45R0 in celiac 

disease. European Journal of Immunology

1990;20(8):1825-1830. Not sensitivity or specificity of an

identified test 

Halstensen T S, Scott H, Fausa O et al. Gluten stimulation

of coeliac mucosa in vitro induces activation (CD25) of 

lamina propria CD4+ T cells and macrophages but no 

crypt-cell hyperplasia. Scandinavian Journal of

Immunology 1993;38(6):581-590. Not sensitivity or 

specificity of an identified test

Halter S A, Greene H L, Helinek G. Gluten-sensitive 

enteropathy: sequence of villous regrowth as viewed by

scanning electron microscopy. Human Pathology

1982;13(9):811-818. Not sensitivity or specificity of an 

identified test 

Halter S A, Greene H L, Helinek G. Scanning electron 

microscopy of small intestinal repair following treatment

for gluten sensitive enteropathy. Scanning Electron 

Microscopy 1980;(3):155-161. Not sensitivity or specificity

of an identified test 

Halttunen T, Maki M. Serum immunoglobulin A from

patients with celiac disease inhibits human T84 intestinal

crypt epithelial cell differentiation. Gastroenterology

1999;116(3):566-572. Not sensitivity or specificity of an

A-382
identified test 

Hamilton I, Cobden I, Rothwell J et al. Intestinal 

permeability in coeliac disease: the response to gluten 

withdrawal and single-dose gluten challenge. Gut

1982;23(3):202-210. Not sensitivity or specificity of an 

identified test 

Hamilton I, Fairris G M, Rothwell J et al. Small intestinal

permeability in dermatological disease. Quarterly Journal 

of Medicine 1985;56(221):559-567. Not sensitivity or 

specificity of an identified test

Hamilton I, Hill A, Bose B et al. Small intestinal

permeability in pediatric clinical practice. Journal of 

Pediatric Gastroenterology and Nutrition 1987;6(5):697-

701. Not sensitivity or specificity of an identified test 

Hamilton J D, Chambers R A, Wynn Williams A. Role of 

gluten, prednisone, and azathioprine in non responsive 

coeliac disease. Lancet 1976;1(7971):1213-1216. Not 

sensitivity or specificity of an identified test 

Hamilton J R, McNeill L K. Childhood celiac disease: 

response of treated patients to a small uniform daily dose of

wheat gluten. Journal of Pediatrics 1972;81(5):885-893. 

Not sensitivity or specificity of an identified test

Hamilton J R, Lynch M J, Reilly B J. Active coeliac 

disease in childhood. Clinical and laboratory findings of 

forty-two cases. Quarterly Journal of Medicine 

1969;38(150):135-158. Not sensitivity or specificity of an

identified test 

Hand D, Campoy F J, Clark S et al. Activity and

distribution of tissue transglutaminase in association with 

nerve-muscle synapses. J Neurochem 1993;61(3):1064-

1072. Not sensitivity or specificity of an identified test 

Hansen D, Bennedbaek F N, Hansen L K et al. High 

prevalence of coeliac disease in Danish children with type I

diabetes mellitus. Acta Paediatrica (Oslo, Norway - 1992)

2001;90(11):1238-1243. Not sensitivity or specificity of an 

identified test 

Hansen T, Lundin K E A, Markussen G et al. T cell 

receptor usage by HLA-DQ8 specific T cell clones. Eos

Riv Immunol Immunofarmacol 1993;13(1):70-71. Not 

sensitivity or specificity of an identified test 

Hansson T, Anneren G, Sjoberg O et al. Celiac disease in

relation to immunologic serum markers, trace elements, 

and HLA-DR and DQ antigens in Swedish children with 

Down syndrome. Journal of Pediatric Gastroenterology and

Nutrition 1999;29(3):286-292. Improper control group 

Hansson T, Dannaeus A, Klareskog L. Cytokine-producing 

cells in peripheral blood of children with coeliac disease 

secrete cytokines with a type 1 profile. Clinical and 

Experimental Immunology 1999;116(2):246-250. Not 

sensitivity or specificity of an identified test 

Hansson T, Dannaeus A, Kraaz W et al. Production of 

antibodies to gliadin by peripheral blood lymphocytes in 

children with celiac disease: the use of an enzyme-linked

immunospot technique for screening and follow-up. 

Pediatric Research 1997;41(4 Pt 1):554-559. Improper 

control group 

Hansson T, Ulfgren A-K, Lindroos E et al. Transforming 

growth factor-beta (TGF-beta) and tissue transglutaminase

expression in the small intestine in children with coeliac 

disease. Scandinavian Journal of Immunology

2002;56(5):530-537. Not sensitivity or specificity of an 

identified test 

Hansson Tony, Dahlbom Ingrid, Rogberg Siv et al. 

Recombinant human tissue transglutaminase for diagnosis 

and follow-up of childhood coeliac disease. Pediatric 

Research 2002;51(6):700-705. Improper control group 

Hanukoglu A, Mizrachi A, Dalal I et al. Extrapancreatic 

autoimmune manifestations in type 1 diabetes patients and 

their first-degree relatives: A multicenter study. Diabetes 

Care 2003;26(4):1235-1240. Not sensitivity or specificity

of an identified test 

Harbeck N, Untch M, Pache L et al. Tumour cell detection

in the bone marrow of breast cancer patients at primary 

therapy: results of a 3-year median follow-up. British 

Journal of Cancer 1994;69(3):566-571. Not sensitivity or

specificity of an identified test

Hardman C M, Garioch J J, Leonard J N et al. Absence of

toxicity of oats in patients with dermatitis herpetiformis. 

New England Journal of Medicine 1997;337(26):1884-

1887. Not sensitivity or specificity of an identified test 

Hardoff D, Levanon D, Gitay H et al. Evaluation of 

microville in gluten-sensitive enteropathy by means of 

scanning and transmission electron microscopy. Journal of

Pediatric Gastroenterology and Nutrition 1986;5(4):560-

564. Not sensitivity or specificity of an identified test 

Harewood G C, Murray J A. Diagnostic approach to a 

patient with suspected celiac disease: a cost analysis. 

Digestive Diseases and Sciences 2001;46(11):2510-2514. 

Not sensitivity or specificity of an identified test

Harley J B, Reichlin M, Arnett F C. Gene interaction at 

HLA-DQ enhances autoantibody production in primary

Sjogren's syndrome. Science 1986;232(4754):1145-1147. 

Not sensitivity or specificity of an identified test

Harley J B, Sestak A L, Willis L G et al. A model for 

disease heterogeneity in systemic lupus erythematosus. 

Relationships between histocompatibility antigens,

autoantibodies, and lymphopenia or renal disease. Arthritis 

Rheum 1989;32(7):826-836. Not sensitivity or specificity

of an identified test 

Haroon Z A, Lai T-S, Hettasch J M et al. Tissue 

transglutaminase is expressed as a host response to tumor 

invasion and inhibits tumor growth. Lab Invest 

A-383
1999;79(12):1679-1686. Not sensitivity or specificity of an 

identified test 

Haroon Z A, Wannenburg T, Gupta M et al. Localization of 

tissue transglutaminase in human carotid and coronary

artery atherosclerosis: implications for plaque stability and

progression. Laboratory Investigation 2001;A Journal of

Technical Methods and Pathology; 81(1):83-93. Not 

sensitivity or specificity of an identified test 

Harper G D, Wheeler D C, Wicks A C B. Butterfat 

absorption - a valuable screening test in malabsorption. 

Postgrad Med J 1994;70(819):23-26. Not sensitivity or

specificity of an identified test

Harrison L C, Honeyman M C. Cow's milk and type 1 

diabetes: the real debate is about mucosal immune function.

Diabetes 1999;48(8):1501-1507. Not sensitivity or

specificity of an identified test

Haslam N, Probert C S. An audit of the investigation and

treatment of folic acid deficiency. Journal of the Royal 

Society of Medicine 1998;91(2):72-73. Not sensitivity or 

specificity of an identified test

Haslam N, Lock R J, Unsworth D J. Coeliac disease,

anaemia and pregnancy. Clinical Laboratory 2001;47(9-

10):467-469. Not sensitivity or specificity of an identified 

test 

Hathout E H, Hartwick N, Fagoaga O R et al. Clinical, 

autoimmune, and HLA characteristics of children

diagnosed with type 1 diabetes before 5 years of age. 

Pediatrics 2003;111(4):860-863. Not sensitivity or

specificity of an identified test

Hattevig G, Kjellman B, Fallstrom S P. Congenital 

permanent diabetes mellitus and celiac disease. Journal of

Pediatrics 1982;101(6):955-957. Not sensitivity or

specificity of an identified test

Hauert J, Patston P A, Schapira M. C1 inhibitor crosslinking by tissue transglutaminase. Journal of Biological 

Chemistry 2000;275(19):14558-14562. Not sensitivity or

specificity of an identified test

Hauri H P, Kedinger M, Haffen K et al. Re-evaluation of 

the techique of organ culture for studying gluten toxicity in

coeliac disease. Gut 1978;19(12):1090-1098. Not 

sensitivity or specificity of an identified test 

Hausch Felix, Shan Lu, Santiago Nilda A et al. Intestinal

digestive resistance of immunodominant gliadin peptides. 

American Journal of Physiology.Gastrointestinal and Liver

Physiology 2002;283(4):G996-G1003. Not sensitivity or

specificity of an identified test

Hayat M, Arora D S, Dixon M F et al. Effects of 

Helicobacter pylori eradication on the natural history of 

lymphocytic gastritis. Gut 1999;45(4):495-498. Not 

sensitivity or specificity of an identified test 

Hayat M, Arora D S, Wyatt J I et al. The pattern of

involvement of the gastric mucosa in lymphocytic gastritis 

is predictive of the presence of duodenal pathology. Journal 

of Clinical Pathology 1999;52(11):815-819. Not sensitivity

or specificity of an identified test

Hayat M, Cairns A, Dixon M F et al. Quantitation of 

intraepithelial lymphocytes in human duodenum: what is 

normal?. Journal of Clinical Pathology 2002;55(5):393-

394. Not sensitivity or specificity of an identified test 

Haycock G B. Screening test for coeliac disease. Archives

of Disease in Childhood 1976;51(5):401Not sensitivity or 

specificity of an identified test

Hazama H, Omagari K, Masuda J et al. Serial changes in 

enzyme inhibitory antibody to pyruvate dehydrogenase 

complex during the course of primary biliary cirrhosis. 

Journal of Clinical Laboratory Analysis 2000;14(5):208-

213. Not sensitivity or specificity of an identified test 

Hazama Hiroaki, Omagari Katsuhisa, Masuda Jun et al.

Automated enzymatic mitochondrial antibody assay for the 

diagnosis of primary biliary cirrhosis: applications of a 

routine diagnostic tool for the detection of

antimitochondrial antibodies. Journal of Gastroenterology

and Hepatology 2002;17(3):316-323. Not sensitivity or

specificity of an identified test

Heath D J, Downes S, Verderio E et al. Characterization of

tissue transglutaminase in human osteoblast-like cells.

Journal of Bone and Mineral Research - the Official 

Journal of the American Society for Bone and Mineral 

Research 2001;16(8):1477-1485. Not sensitivity or

specificity of an identified test

Heath Deborah J, Christian Paul, Griffin Martin. 

Involvement of tissue transglutaminase in the stabilisation 

of biomaterial/tissue interfaces important in medical 

devices. Biomaterials 2002;23(6):1519-1526. Not 

sensitivity or specificity of an identified test 

Hed J, Lieden G, Ottosson E. IgA anti-gliadin antibodies 

and jejunal mucosal lesions in healthy blood donors. Lancet 

1986;2(8500):215Not sensitivity or specificity of an 

identified test 

Hedin C A, Gerner L, Larsson A. The retrocuspid papilla 

and factor XIIIa: an epidemiologic and histomorphologic 

study. Scandinavian Journal of Dental Research

1994;102(5):290-294. Not sensitivity or specificity of an

identified test 

Heine R G, Catto-Smith A G. Antibodies in the diagnosis 

and management of coeliac disease. J Paediatr Child Health

1993;29(5):331-334. Not sensitivity or specificity of an 

identified test 

Hekimgil M, Soydan S, Nart D et al. Histopathologic and 

immunophenotypic features of childhood and adult 

anaplastic large-cell lymphomas. Turk J Haematol

2001;18(4):265-274. Not sensitivity or specificity of an 

A-384
identified test 

Hellesen C, Friis T, Larsen E et al. Small intestinal

histology, radiology and absorption in hyperthyroidism. 

Scandinavian Journal of Gastroenterology 1969;4(2):169-

175. Not sensitivity or specificity of an identified test 

Helm K F, Peters M S. Immunodermatology update: the 

immunologically mediated vesiculobullous diseases. Mayo

Clinic Proceedings 1991;66(2):187-202. Not sensitivity or

specificity of an identified test

Hendrick D J, Faux J A, Anand B et al. Is bird fancier's 

lung associated with coeliac disease?. Thorax 

1978;33(4):425-428. Not sensitivity or specificity of an 

identified test 

Hendrix T R. Interpretation of intestinal biopsies. 

Gastroenterology 1968;54(5):976-978. Not sensitivity or 

specificity of an identified test

Heneghan M A, Kearns M, Goulding J et al. Secretor status

and human leucocyte antigens in coeliac disease.

Scandinavian Journal of Gastroenterology

1996;31(10):973-976. Not sensitivity or specificity of an

identified test 

Heneghan M A, McHugh P, Stevens F M et al. Addison's 

disease and selective IgA deficiency in two coeliac 

patients. Scandinavian Journal of Gastroenterology

1997;32(5):509-511. Not sensitivity or specificity of an 

identified test 

Heneghan M A, Stevens F M, Cryan E M et al. Celiac 

sprue and immunodeficiency states: a 25-year review. 

Journal of Clinical Gastroenterology 1997;25(2):421-425. 

Not sensitivity or specificity of an identified test

Henriksson P, Becker S, Lynch G et al. Identification of 

intracellular factor XIII in human monocytes and 

macrophages. Journal of Clinical Investigation 

1985;76(2):528-534. Not sensitivity or specificity of an 

identified test 

Herlinger H, Maglinte D D. Jejunal fold separation in adult

celiac disease: relevance of enteroclysis. Radiology

1986;158(3):605-611. Not sensitivity or specificity of an

identified test 

Herman A E, Tisch R M, Patel S D et al. Determination of 

glutamic acid decarboxylase 65 peptides presented by the 

type I diabetes-associated HLA-DQ8 class II molecule 

identifies an immunogenic peptide motif. J Immunol 

1999;163(11):6275-6282. Not sensitivity or specificity of

an identified test

Hermann R, Soltesz G. Prevalence and HLA association of

GAD65 antibodies in Hungarian schoolchildren. Hum 

Immunol 2003;64(1):152-155. Not sensitivity or specificity

of an identified test 

Hermann R, Mijovic C H, Rayner M et al. HLA alleles and 

IDDM in children in Hungary: a comparison with Finland.

Human Immunology 2001;62(4):391-398. Not sensitivity

or specificity of an identified test

Hernandez J L, Michalski J P, McCombs C C et al. 

Evidence for a dominant gene mechanism underlying

coeliac disease in the west of Ireland. Genetic 

Epidemiology 1991;8(1):13-27. Not sensitivity or

specificity of an identified test

Hernandez M A, Colina G, Ortigosa L. Epilepsy, cerebral

calcifications and clinical or subclinical coeliac disease.

Course and follow up with gluten-free diet. Seizure - the 

Journal of the British Epilepsy Association 1998;7(1):49-

54. Not sensitivity or specificity of an identified test 

Hernandez M, Argente J, Navarro A et al. Growth in 

malnutrition related to gastrointestinal diseases: Coeliac 

disease. Horm Res 1992;38(Suppl 1):79-84. Not sensitivity

or specificity of an identified test

Hernanz A, Polanco I, Codoceo R. Gastrointestinal peptide 

profile in children with celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 1987;6(3):341-345. Not

sensitivity or specificity of an identified test 

Herrera M, Chertkoff L, Palavecino E et al. Restriction

fragment length polymorphism in HLA class II genes of 

Latin-American Caucasian celiac disease patients. Human 

Immunology 1989;26(4):272-280. Not sensitivity or 

specificity of an identified test

Herrera M, Theiler G, Augustovski F et al. Molecular 

characterization of HLA class II genes in celiac disease 

patients of Latin American Caucasian origin. Tissue 

Antigens 1994;43(2):83-87. Improper control group 

Herron M D, Zone J J. Treatment of dermatitis 

herpetiformis and linear IgA bullous dermatosis. Dermatol 

Ther 2002;15(4):374-381. Not sensitivity or specificity of

an identified test

Hertervig E, Wieslander J, Johansson C et al. Antineutrophil cytoplasmic antibodies in chronic inflammatory

bowel disease. Prevalence and diagnostic role. 

Scandinavian Journal of Gastroenterology 1995;30(7):693-

698. Not sensitivity or specificity of an identified test 

Herulf M, Blomquist L, Ljung T et al. Increased rectal 

nitric oxide in coeliac disease after local challenge with 

gluten. Scandinavian Journal of Gastroenterology

2001;36(2):169-173. Not sensitivity or specificity of an 

identified test 

Hervonen K, Karell K, Holopainen P et al. Concordance of 

dermatitis herpetiformis and celiac disease in monozygous

twins. Journal of Investigative Dermatology

2000;115(6):990-993. Not sensitivity or specificity of an

identified test 

Hessels J, Eidhof H H M, Steggink J et al. Assessment of 

hypolactasia and site-specific intestinal permeability of

A-385
differential sugar absorption of raffinose, lactose, sucrose 

and mannitol. Clin Chem Lab Med 2003;41(8):1056-1063. 

Not sensitivity or specificity of an identified test

Hettasch J M, Bandarenko N, Burchette J L et al. Tissue

transglutaminase expression in human breast cancer. 

Laboratory Investigation 1996;75(5):637-645. Not 

sensitivity or specificity of an identified test 

Hettasch J M, Peoples K A, Greenberg C S. Analysis of

factor XIII substrate specificity using recombinant human 

factor XIII and tissue transglutaminase Chimeras. J Biol 

Chem 1997;272(40):25149-25156. Not sensitivity or 

specificity of an identified test

Hetzel P A, Bennett G D, Sheldon A B et al. Genetic 

markers in Australian Caucasian subjects with coeliac 

disease. Tissue Antigens 1987;30(1):18-22. Not sensitivity

or specificity of an identified test

Heurkens A H, Hiemstra P S, Lafeber G J et al. Antiendothelial cell antibodies in patients with rheumatoid

arthritis complicated by vasculitis. Clinical and 

Experimental Immunology 1989;78(1):7-12. Not sensitivity

or specificity of an identified test

Hevessy Z, Patthy A, Karpati L et al. alpha(2)-plasmin 

inhibitor is a substrate for tissue transglutaminase: an in 

vitro study. Thrombosis Research 2000;99(4):399-406. Not 

sensitivity or specificity of an identified test 

Heward J M, Mijovic C H, Kelly M A et al. HLA-DQ and 

DRB1 polymorphism and susceptibility to type 1 diabetes 

in Jamaica. European Journal of Immunogenetics - Official 

Journal of the British Society for Histocompatibility and

Immunogenetics 2002;29(1):47-52. Not sensitivity or 

specificity of an identified test

Hidasi V, Adany R, Muszbek L. Localization of 

transglutaminase in human lenses. Journal of 

Histochemistry and Cytochemistry - Official Journal of the 

Histochemistry Society 1995;43(11):1173-1177. Not 

sensitivity or specificity of an identified test 

Hide D W, Burman D. An infant with both cystic fibrosis 

and coeliac disease. Archives of Disease in Childhood 

1969;44(236):533-535. Not sensitivity or specificity of an

identified test 

Higounenc I, Demarchez M, Regnier M et al. Improvement 

of epidermal differentiation and barrier function in

reconstructed human skin after grafting onto athymic nude 

mice. Archives of Dermatological Research 

1994;286(2):107-114. Not sensitivity or specificity of an

identified test 

Hiiragi T, Sasaki H, Nagafuchi A et al. Transglutaminase 

type 1 and its cross-linking activity are concentrated at

adherens junctions in simple epithelial cells. Journal of

Biological Chemistry 1999;274(48):34148-34154. Not 

sensitivity or specificity of an identified test 

Hill A V S. Immunogenetics and genomics. Lancet 

2001;357(9273):2037-2041. Not sensitivity or specificity of 

an identified test

Hill I D. Celiac disease - A never-ending story?. Journal of 

Pediatrics 2003;143(3):289-291. Not sensitivity or

specificity of an identified test

Hill I, Fasano A, Schwartz R et al. The prevalence of celiac 

disease in at-risk groups of children in the United States. 

Journal of Pediatrics 2000;136(1):86-90. Not sensitivity or

specificity of an identified test

Hill P G, Thompson S P, Holmes G K. IgA anti-gliadin

antibodies in adult celiac disease. Clinical Chemistry

1991;37(5):647-650. Improper control group 

Hill R, Cutz E, Cherian G et al. An evaluation of D-xylose 

absorption measurements in children suspected of having

small intestinal disease. Journal of Pediatrics

1981;99(2):245-247. Not sensitivity or specificity of an 

identified test 

Hill S M, Phillips A D, Mearns M et al. Cows' milk 

sensitive enteropathy in cystic fibrosis. Archives of Disease

in Childhood 1989;64(9):1251-1255. Not sensitivity or

specificity of an identified test

Hillert J, Kall T, Olerup O et al. Distribution of HLA-Dw2 

in optic neuritis and multiple sclerosis indicates 

heterogeneity. Acta Neurol Scand 1996;94(3):161-166. Not 

sensitivity or specificity of an identified test 

Hilton D A, Love S, Barber R. Increased endothelial

expression of transglutaminase in glioblastomas. 

Neuropathology and Applied Neurobiology

1997;23(6):507-511. Not sensitivity or specificity of an 

identified test 

Hin H, Bird G, Fisher P et al. Coeliac disease in primary 

care: case finding study. Bmj (Clinical Research Ed.) 

1999;318(7177):164-167. Not sensitivity or specificity of

an identified test

Hines M D, Jin H C, Wheelock M J et al. Inhibition of 

cadherin function differentially affects markers of terminal 

differentiation in cultured human keratinocytes. Journal of

Cell Science 1999;112(Pt 24):4569-4579. Not sensitivity or

specificity of an identified test

Hinks L J, Inwards K D, Lloyd B et al. Body content of

selenium in coeliac disease. Br Med J

1984;288(6434):1862-1863. Not sensitivity or specificity of 

an identified test

Hirao T, Denda M, Takahashi M. Identification of

immature cornified envelopes in the barrier-impaired 

epidermis by characterization of their hydrophobicity and

antigenicities of the components. Experimental 

Dermatology 2001;10(1):35-44. Not sensitivity or

specificity of an identified test

A-386
Hitman G A, Niven M J, Festenstein H et al. HLA class II 

alpha chain gene polymorphisms in patients with insulindependent diabetes mellitus, dermatitis herpetiformis, and 

celiac disease. Journal of Clinical Investigation 

1987;79(2):609-615. Not sensitivity or specificity of an 

identified test 

Hitomi K, Presland R B, Nakayama T et al. Analysis of

epidermal-type transglutaminase (transglutaminase 3) in 

human stratified epithelia and cultured keratinocytes using 

monoclonal antibodies. J Dermatol Sci 2003;32(2):95-103. 

Not sensitivity or specificity of an identified test

Hjelmstrom P, Giscombe R, Lefvert A K et al. TAP

polymorphisms in Swedish myasthenia gravis patients. 

Tissue Antigens 1997;49(2):176-179. Not sensitivity or

specificity of an identified test

Ho G J, Gregory E J, Smirnova I V et al. Cross-linking of 

beta-amyloid protein precursor catalyzed by tissue 

transglutaminase. Febs Letters 1994;349(1):151-154. Not 

sensitivity or specificity of an identified test 

Ho K C, Quarmby V E, French F S et al. Molecular cloning

of rat prostate transglutaminase complementary DNA. The 

major androgen-regulated protein DP1 of rat dorsal prostate 

and coagulating gland. Journal of Biological Chemistry

1992;267(18):12660-12667. Not sensitivity or specificity of 

an identified test

Hodges J R, Isaacson P, Smith C L et al. Malignant 

histiocytosis of the intestine. Digestive Diseases and 

Sciences 1979;24(8):631-638. Not sensitivity or specificity

of an identified test 

Hodges S, Lobo-Yeo A, Donaldson P et al. Autoimmune

chronic active hepatitis in a family. Gut 1991;32(3):299-

302. Not sensitivity or specificity of an identified test 

Hoey J. Irritable bowel syndrome: Could it be celiac 

disease?. Can Med Assoc J 2002;166(4):479-480. Not 

sensitivity or specificity of an identified test 

Hoffbrand A V. Anaemia in adult coeliac disease. Clin

Gastroenterol 1974;3(1):71-89. Not sensitivity or 

specificity of an identified test

Hoffenberg E J, Bao F, Eisenbarth G S et al. 

Transglutaminase antibodies in children with a genetic risk

for celiac disease. Journal of Pediatrics 2000;137(3):356-

360. Unable to extract data 

Hoffenberg E J, Haas J, Drescher A et al. A trial of oats in 

children with newly diagnosed celiac disease. Journal of

Pediatrics 2000;137(3):361-366. Not sensitivity or

specificity of an identified test

Hoffenberg E J, Mackenzie T, Barriga K J et al. A 

prospective study of the incidence of childhood celiac 

disease. Journal of Pediatrics 2003;143(3):308-314. Not 

sensitivity or specificity of an identified test 

Hoffmann M, Vogelsang H, Kletter K et al. 18F-fluorodeoxy-glucose positron emission tomography (18F-FDGPET) for assessment of enteropathy-type T cell lymphoma. 

Gut 2003;52(3):347-351. Not sensitivity or specificity of an 

identified test 

Hogberg L, Falth-Magnusson K, Grodzinsky E et al. 

Familial prevalence of coeliac disease: A twenty-year 

follow-up study. Scandinavian Journal of Gastroenterology

2003;38(1):61-65. Not sensitivity or specificity of an 

identified test 

Hogberg L, Grodzinsky E, Stenhammar L. Better dietary

compliance in patients with coeliac disease diagnosed in 

early childhood. Scandinavian Journal of Gastroenterology

2003;38(7):751-754. Not sensitivity or specificity of an 

identified test 

Hogberg L, Nordwall M, Stenhammar L. One thousand 

small-bowel biopsies in children. A single-port versus a 

double-port capsule. Scandinavian Journal of

Gastroenterology 2001;36(11):1230-1232. Not sensitivity

or specificity of an identified test

Hogberg L, Nordwall M, Stenhammar L. Small bowel 

capsule biopsy in children: parents' opinions on children's 

discomfort. Acta Paediatrica (Oslo, Norway - 1992) 

2001;90(8):876-878. Not sensitivity or specificity of an 

identified test 

Hohenadl C, Mann K, Mayer U et al. Two adjacent Nterminal glutamines of BM-40 (osteonectin, SPARC) act as 

amine acceptor sites in transglutaminaseC-catalyzed 

modification. Journal of Biological Chemistry 

1995;270(40):23415-23420. Not sensitivity or specificity of 

an identified test

Hohl D. Expression patterns of loricrin in dermatological 

disorders. American Journal of Dermatopathology 

1993;15(1):20-27. Not sensitivity or specificity of an 

identified test 

Hohl D, Aeschlimann D, Huber M. In vitro and rapid in 

situ transglutaminase assays for congenital ichthyoses--a 

comparative study. Journal of Investigative Dermatology

1998;110(3):268-271. Not sensitivity or specificity of an

identified test 

Hohl D, de Viragh P A, Amiguet-Barras F et al. The small 

proline-rich proteins constitute a multigene family of 

differentially regulated cornified cell envelope precursor 

proteins. Journal of Investigative Dermatology

1995;104(6):902-909. Not sensitivity or specificity of an

identified test 

Hohl D, Huber M, Frenk E. Analysis of the cornified cell 

envelope in lamellar ichthyosis. Archives of Dermatology

1993;129(5):618-624. Not sensitivity or specificity of an

identified test 

Holdstock D J, Oleesky S. Successful treatment of 

collagenous sprue with combination of prednisolone and

A-387
gluten free diet. Postgrad Med J 1973;49(575):664-667. 

Not sensitivity or specificity of an identified test

Holdstock G. Jejunal biopsy without the need for screening.

Lancet 1978;1(8076):1236-1237. Not sensitivity or 

specificity of an identified test

Holdstock G, Eade O E, Isaacson P et al. Endoscopic 

duodenal biopsies in coeliac disease and duodenitis. 

Scandinavian Journal of Gastroenterology 1979;14(6):717-

720. Unable to extract data 

Holl R W, Grabert M, Heinze E et al. Age at onset and 

long-term metabolic control affect height in type-1 diabetes

mellitus. European Journal of Pediatrics 1998;157(12):972-

977. Not sensitivity or specificity of an identified test 

Hollen E, Hogberg L, Stenhammar L et al. Antibodies to

oat prolamines (avenins) in children with coeliac disease.

Scandinavian Journal of Gastroenterology 2003;38(7):742-

746. Not sensitivity or specificity of an identified test 

Holm K, Maki M, Savilahti E et al. Intraepithelial gamma

delta T-cell-receptor lymphocytes and genetic susceptibility

to coeliac disease. Lancet 1992;339(8808):1500-1503. Not 

sensitivity or specificity of an identified test 

Holm K, Savilahti E, Koskimies S et al. 

Immunohistochemical changes in the jejunum in first 

degree relatives of patients with coeliac disease and the

coeliac disease marker DQ genes. HLA class II antigen

expression, interleukin-2 receptor positive cells and 

dividing crypt cells. Gut 1994;35(1):55-60. Unable to

extract data

Holmes G K. Coeliac disease and Type 1 diabetes mellitus

- the case for screening. Diabetic Medicine - a Journal of

the British Diabetic Association 2001;18(3):169-177. Not

sensitivity or specificity of an identified test 

Holmes G K T. Screening for coeliac disease in type 1 

diabetes. Archives of Disease in Childhood 

2002;87(6):495-498. Not sensitivity or specificity of an 

identified test 

Holmes G K T, Stokes P L, Sorahan T M. Coeliac disease,

gluten free diet, and malignancy. Gut 1976;17(8):612-619. 

Not sensitivity or specificity of an identified test

Holmes G K, Asquith P, Stokes P L et al. Cellular infiltrate

of jejunal biopsies in adult coeliac disease (ACD) in 

relation to gluten withdrawal. Gut 1973;14(5):429Not 

sensitivity or specificity of an identified test 

Holmes G K, Asquith P, Stokes P L et al. Cellular infiltrate

of jejunal biopsies in adult coeliac disease in relation to

gluten withdrawal. Gut 1974;15(4):278-283. Not sensitivity

or specificity of an identified test

Holmgren Peterson K, Falth-Magnusson K, Magnusson K 

E et al. Children with celiac disease express inducible nitric 

oxide synthase in the small intestine during gluten 

challenge. Scandinavian Journal of Gastroenterology

1998;33(9):939-943. Not sensitivity or specificity of an 

identified test 

Holmgren Peterson K, Magnusson K E, Stenhammar L et 

al. Confocal laser scanning microscopy of small-intestinal

mucosa in celiac disease. Scandinavian Journal of

Gastroenterology 1995;30(3):228-234. Not sensitivity or 

specificity of an identified test

Holopainen P, Arvas M, Sistonen P et al. CD28/CTLA4 

gene region on chromosome 2q33 confers genetic 

susceptibility to celiac disease. A linkage and family-based

association study. Tissue Antigens 1999;53(5):470-475. 

Not sensitivity or specificity of an identified test

Holopainen P, Mustalahti K, Uimari P et al. Candidate gene

regions and genetic heterogeneity in gluten sensitivity. Gut 

2001;48(5):696-701. Improper control group 

Honeyman M C, Harrison L C, Drummond B et al. 

Analysis of families at risk for insulin-dependent diabetes 

mellitus reveals that HLA antigens influence progression to 

clinical disease. Molecular Medicine (Cambridge, Mass.) 

1995;1(5):576-582. Not sensitivity or specificity of an 

identified test 

Horejsi V, Nemec M, Angelisova P. Characterization of 

seven new monoclonal antibodies against human DR, DR + 

DP and DQ1 +DQ3 antigens. Tissue Antigens 

1986;28(5):288-297. Not sensitivity or specificity of an 

identified test 

Horikoshi T, Arany I, Rajaraman S et al. Isoforms of 

cathepsin D and human epidermal differentiation.

Biochimie 1998;80(7):605-612. Not sensitivity or

specificity of an identified test

Horvath K, Mehta D I. Celiac disease--a worldwide 

problem. Indian Journal of Pediatrics 2000;67(10):757-763. 

Not sensitivity or specificity of an identified test

Horvath K, Horn G, Bodanszky H et al. Disaccharidases in 

coeliac disease. Acta Paediatrica Hungarica 

1983;24(2):131-136. Not sensitivity or specificity of an 

identified test 

Horvath K, Nagy L, Horn G et al. Intestinal mast cell and 

neutrophil chemotactic activity of serum following a single 

challenge with gluten in celiac children on a gluten-free 

diet. Journal of Pediatric Gastroenterology and Nutrition

1989;9(3):276-280. Not sensitivity or specificity of an 

identified test 

Horvath Karoly, Hill Ivor D. Anti-tissue transglutaminase 

antibody as the first line screening for celiac disease: goodbye antigliadin tests?. American Journal of 

Gastroenterology 2002;97(11):2702-2704. Review article 

Hosokawa K, Hosokawa H, Futamura S et al. Proteins of

the cornified envelope. Journal of Dermatology

1992;19(11):744-748. Not sensitivity or specificity of an

A-388
identified test 

Houlston R S, Ford D. Genetics of coeliac disease. Qjm -

Monthly Journal of the Association of Physicians 

1996;89(10):737-743. Not sensitivity or specificity of an

identified test 

Houlston R S, Tomlinson I P, Ford D et al. Linkage 

analysis of candidate regions for coeliac disease genes.

Human Molecular Genetics 1997;6(8):1335-1339. Not 

sensitivity or specificity of an identified test 

Housseau F, Rouas-Freiss N, Benifla J-L et al. Reaction of

peripheral-blood lymphocytes to the human chorionic 

gonadotropin beta sub-unit in patients with productive 

tumors. Int J Cancer 1995;63(5):633-638. Not sensitivity or 

specificity of an identified test

Hovdenak N. Prevalence and clinical picture of adult 

gluten-induced enteropathy in a Norwegian population.

Scandinavian Journal of Gastroenterology 1980;15(4):401-

404. Not sensitivity or specificity of an identified test 

Hovdenak N, Hovlid E, Aksnes L et al. High prevalence of 

asymptomatic coeliac disease in Norway: a study of blood

donors. European Journal of Gastroenterology & 

Hepatology 1999;11(2):185-187. Not sensitivity or 

specificity of an identified test

Hovell C J, Collett J A, Vautier G et al. High prevalence of 

coeliac disease in a population-based study from Western 

Australia: a case for screening?. Medical Journal of 

Australia 2001;175(5):247-250. Not sensitivity or

specificity of an identified test

Howard M R, Turnbull A J, Morley P et al. A prospective 

study of the prevalence of undiagnosed coeliac disease in

laboratory defined iron and folate deficiency. J Clin Pathol

2002;55(10):754-757. Not sensitivity or specificity of an

identified test 

Howat A J, Mcphie J L, Smith D A et al. Cavitation of 

mesenteric lymph nodes: A rare complication of coeliac 

disease, associated with a poor outcome. Histopathology

1995;27(4):349-354. Not sensitivity or specificity of an 

identified test 

Howdle P D, Blair G E. Molecular biology and coeliac 

disease. Gut 1992;33(5):573-575. Not sensitivity or 

specificity of an identified test

Howdle P D, Bullen A W, Losowsky M S. Cell-mediated 

immunity to gluten within the small intestinal mucosa in

coeliac disease. Gut 1982;23(2):115-122. Not sensitivity or 

specificity of an identified test

Howdle P D, Corazza G R, Bullen A W et al. In vitro 

diagnosis of coeliac disease: an assessment. Gut 

1981;22(11):939-947. Not sensitivity or specificity of an

identified test 

Howell M D, Austin R K, Kelleher D et al. An HLA-D 

region restriction fragment length polymorphism associated

with celiac disease. Journal of Experimental Medicine 

1986;164(1):333-338. Not sensitivity or specificity of an

identified test 

Howell M D, Smith J R, Austin R K et al. An extended 

HLA-D region haplotype associated with celiac disease.

Proc Natl Acad Sci U S A 1988;85(1):222-226. Not 

sensitivity or specificity of an identified test 

Howell W M, Jones D B. The role of human leucocyte 

antigen genes in the development of malignant disease. J 

Clin Pathol Clin Mol Pathol 1995;48(6):M302-M306. Not 

sensitivity or specificity of an identified test 

Howell W M, Calder P C, Grimble R F. Symposium on 

'nutrition in the post-genomic era'. Plenary session 4: 

Genetic variation and diet-related disease: Gene

polymorphisms, inflammatory diseases and cancer. Proc

Nutr Soc 2002;61(4):447-456. Not sensitivity or specificity

of an identified test 

Howell W M, Leung S T, Jones D B et al. HLA-DRB, -

DQA, and -DQB polymorphism in celiac disease and 

enteropathy-associated T-cell lymphoma. Common features 

and additional risk factors for malignancy. Human 

Immunology 1995;43(1):29-37. Improper control group 

Howell W, Martin Calder, Philip C et al. Gene

polymorphisms, inflammatory diseases and cancer. 

Proceedings of the Nutrition Society 2002;61(4):447-456. 

Not sensitivity or specificity of an identified test

Hozyasz K K. Sex ratio variation in offspring of celiac

women - Preliminary report. Pediatr Wspolczesna 

2002;4(3):253-255. Not sensitivity or specificity of an 

identified test 

Hudson D A, Anderson C M. A new experimental system 

for the study of the pathogenesis of coeliac disease. Lancet 

1977;1(8010):511-512. Not sensitivity or specificity of an

identified test 

Huff Thomas, Otto Angela M, Muller Christian S G et al. 

Thymosin beta4 is released from human blood platelets and

attached by factor XIIIa (transglutaminase) to fibrin and

collagen. Faseb Journal - Official Publication of the 

Federation of American Societies for Experimental Biology

2002;16(7):691-696. Not sensitivity or specificity of an 

identified test 

Hummel M, Bonifacio E, Stern M et al. Development of 

celiac disease-associated antibodies in offspring of parents 

with type I diabetes. Diabetologia 2000;43(8):1005-1011. 

Not sensitivity or specificity of an identified test

Hummel M, Ziegler A G, Bonifacio E. Type 1 diabetes

mellitus, celiac disease and their association - Lessons from

antibodies. J Pediatr Endocrinol Metab 2001;14(Suppl 

1):607-610. Not sensitivity or specificity of an identified

test 

A-389
Hummel Michael, Bonifacio Ezio, Naserke Heike E et al.

Elimination of dietary gluten does not reduce titers of type 

1 diabetes-associated autoantibodies in high-risk subjects. 

Diabetes Care 2002;25(7):1111-1116. Not sensitivity or

specificity of an identified test

Hunter I P, Ferguson M M, Scully C et al. Effects of 

dietary gluten elimination in patients with recurrent minor 

aphthous stomatitis and no detectable gluten enteropathy.

Oral Surg Oral Med Oral Pathol 1993;75(5):595-598. Not 

sensitivity or specificity of an identified test 

Huq M I. A simple laboratory method for the diagnosis of 

V. cholerae. Transactions of the Royal Society of Tropical

Medicine and Hygiene 1979;73(5):553-556. Not sensitivity

or specificity of an identified test

Huq M I, Sanyal S C, Samadi A R et al. Comparative

behaviour of classical and El Tor biotypes of Vibrio 

cholerae 01 isolated in Bangladesh during 1982. Journal of

Diarrhoeal Diseases Research 1983;1(1):5-9. Not 

sensitivity or specificity of an identified test 

Husby S. Normal immune responses to ingested foods. 

Journal of Pediatric Gastroenterology and Nutrition 

2000;30(Suppl):s13-s19. Not sensitivity or specificity of an 

identified test 

Hussain G, Ali S, Iqbal M M et al. Study of coeliac disease 

in children. J Coll Phys Surg Pak 1999;9(2):81-84. Not 

sensitivity or specificity of an identified test 

Hwang K C, Gray C D, Sivasubramanian N et al. 

Interaction site of GTP binding Gh (transglutaminase II)

with phospholipase C. Journal of Biological Chemistry

1995;270(45):27058-27062. Not sensitivity or specificity of 

an identified test

Hyams J S, Treem W R, Justinich C J et al.

Characterization of symptoms in children with recurrent 

abdominal pain: resemblance to irritable bowel syndrome. 

Journal of Pediatric Gastroenterology and Nutrition 

1995;20(2):209-214. Not sensitivity or specificity of an 

identified test 

Iacono G, Carroccio A, Montalto G et al. Steatocrit test 

after a standard fatty meal: a new simple and sensitive test 

to detect malabsorption. Journal of Pediatric 

Gastroenterology and Nutrition 1991;13(2):161-167. Not

sensitivity or specificity of an identified test 

Iancu T, Elian E. The intestinal microvillus. Ultrastructural 

variability in coeliac disease and cow's milk intolerance.

Acta Paediatrica Scandinavica 1976;65(1):65-73. Not 

sensitivity or specificity of an identified test 

Ichikawa S, Hatanaka H, Yuuki T et al. Solution structure 

of Der f 2, the major mite allergen for atopic diseases. 

Journal of Biological Chemistry 1998;273(1):356-360. Not 

sensitivity or specificity of an identified test 

Ichinose A, Hendrickson L E, Fujikawa K et al. Amino 

acid sequence of the a subunit of human factor XIII. 

Biochemistry 1986;25(22):6900-6906. Not sensitivity or

specificity of an identified test

Ide A, Eisenbarth G S. Genetic susceptibility in type 1 

diabetes and its associated autoimmune disorders. Rev

Endocr Metab Disord 2003;4(3):243-253. Not sensitivity or 

specificity of an identified test

Ientile R, Merendino R A, Fabiano C et al. Polyamines are

involved in retinoic acid-mediated induction of tissue 

transglutaminase in human peripheral blood monocytes. 

Research Communications in Chemical Pathology and 

Pharmacology 1992;77(3):313-326. Not sensitivity or 

specificity of an identified test

Iijima Junko, Shiina Yoshio, Ohkoudo Mitsuaki et al. 

Usefulness of Auto Cyto Fix (membrane filter method) for

the application of immunohistochemistry. Diagnostic 

Cytopathology 2002;26(1):56-60. Not sensitivity or 

specificity of an identified test

Iismaa S E. Structure and function of tissue 

transglutaminase. Minerva Biotecnol 2002;14(2):113-119. 

Not sensitivity or specificity of an identified test

Ikaheimo I, Silvennoinen-Kassinen S, Tiilikainen A. HLA 

five-locus haplotypes in Finns. Eur J Immunogenet 

1996;23(4):321-328. Not sensitivity or specificity of an 

identified test 

Ikaheimo I, Silvennoinen-Kassinen S, Karvonen J et al. 

Immunogenetic profile of psoriasis vulgaris: Association 

with haplotypes A2,B13,Cw6,DR7,DQA1*0201 and 

A1,B17,Cw6,DR7,DQA1*0201. Arch Dermatol Res 

1996;288(2):63-67. Not sensitivity or specificity of an 

identified test 

Illingworth A L, Young J A, Johnson G D. 

Immunofluorescent staining of metastatic carcinoma cells 

in serious fluid with carcinoembryonic antibody, epithelial 

membrane antibody, AUA-1 and Ber-EP4. Cytopathology - 

Official Journal of the British Society for Clinical Cytology

1994;5(5):270-281. Not sensitivity or specificity of an 

identified test 

Illueca C, Llombart-Bosch A, Ferrando Cucarella J. 

Prognostic factors in Barrett's esophagus: an

immunohistochemical and morphometric study of 120 

cases. Revista Espanola De Enfermedades Digestivas - 

Organo Oficial De La Sociedad Espanola De Patologia 

Digestiva 2000;92(11):726-737. Not sensitivity or

specificity of an identified test

Ilonen J, Merivuori H, Reijonen H et al. Tumour necrosis

factor-beta gene RFLP alleles in Finnish IDDM haplotypes. 

Scand J Immunol 1992;36(6):779-783. Not sensitivity or

specificity of an identified test

Iltanen S, Collin P, Korpela M et al. Celiac disease and

markers of celiac disease latency in patients with primary 

Sjogren's syndrome. American Journal of Gastroenterology

A-390
1999;94(4):1042-1046. Improper control group 

Iltanen S, Holm K, Ashorn M et al. Changing jejunal 

gamma delta T cell receptor (TCR)-bearing intraepithelial 

lymphocyte density in coeliac disease. Clinical and 

Experimental Immunology 1999;117(1):51-55. Not 

sensitivity or specificity of an identified test 

Iltanen S, Rantala I, Laippala P et al. Expression of HSP-65 

in jejunal epithelial cells in patients clinically suspected of

coeliac disease. Autoimmunity 1999;31(2):125-132. 

Improper control group 

Indovina P, Megiorni F, Fontemaggi G et al. Absence of in

vivo DNA-protein interactions in the DQA2 and DQB2 

promoter regions. Hum Immunol 2001;62(5):504-508. Not 

sensitivity or specificity of an identified test 

Isaacson P, Wright D H. Intestinal lymphoma associated 

with malabsorption. Lancet 1978;1(8055):67-70. Not 

sensitivity or specificity of an identified test 

Isaacson P G. Relation between cryptic intestinal

lymphoma and refractory sprue. Lancet 

2000;356(9225):178-179. Not sensitivity or specificity of

an identified test

Isaacson P G. T-cell lymphoma: The real thing. Gut 

1999;45(5):638-639. Not sensitivity or specificity of an 

identified test 

Isbell R G, Carlson H C, Hoffman H N. Roentgenologicpathologic correlation in malabsorption syndromes. 

American Journal of Roentgenology, Radium Therapy, and

Nuclear Medicine 1969;107(1):158-169. Not sensitivity or

specificity of an identified test

Ishido T, Mori N. Primary gastric plasmacytoma: a 

morphological and immunohistochemical study of five 

cases. American Journal of Gastroenterology

1992;87(7):875-878. Not sensitivity or specificity of an 

identified test 

Ivarsson A, Persson L A, Juto P et al. High prevalence of

undiagnosed coeliac disease in adults: a Swedish 

population-based study. Journal of Internal Medicine 

1999;245(1):63-68. Not sensitivity or specificity of an 

identified test 

Ivarsson S A, Carlsson A, Bredberg A et al. Prevalence of 

coeliac disease in Turner syndrome. Acta Paediatrica (Oslo, 

Norway - 1992) 1999;88(9):933-936. Not sensitivity or

specificity of an identified test

 

Iwaki T, Miyazono M, Hitosumatsu T et al. An 

immunohistochemical study of tissue transglutaminase in 

gliomas with reference to their cell dying processes. 

American Journal of Pathology 1994;145(4):776-781. Not 

sensitivity or specificity of an identified test 

Iwanczak F, Iwanczak B, Matusiewicz K et al. Assessment 

of serum antibodies against gliadin, endomysium and tissue 

transglutaminase in diagnosis of celiac disease in children. 

Gastroenterol Pol 2003; 10(4):323-328. Unable to obtain 

full article 

Jabbar A A. HLA and disease associations in Iraq. Disease 

Markers 1993;11(4):161-170. Not sensitivity or specificity

of an identified test 

Jabbari M, Wild G, Goresky C A et al. Scalloped valvulae 

conniventes: an endoscopic marker of celiac sprue. 

Gastroenterology 1988;95(6):1518-1522. Not sensitivity or 

specificity of an identified test

Jabri B, de Serre N P, Cellier C et al. Selective expansion 

of intraepithelial lymphocytes expressing the HLA-Especific natural killer receptor CD94 in celiac disease.

Gastroenterology 2000;118(5):867-879. Not sensitivity or

specificity of an identified test

Jackson D, Walker-Smith J A, Phillips A D. Passive 

diffusion in small intestinal mucosa in childhood. 

Histopathology 1982;6(6):689-702. Not sensitivity or 

specificity of an identified test

Jaeger C, Hatziagelaki E, Petzoldt R et al. Comparative 

analysis of organ-specific autoantibodies and celiac 

disease--associated antibodies in type 1 diabetic patients, 

their first-degree relatives, and healthy control subjects. 

Diabetes Care 2001;24(1):27-32. Not sensitivity or 

specificity of an identified test

Jafarzadeh A, Shokrgozar M A, Khoshnoodi J et al. 

Unresponsiveness to recombinant hepatitis B vaccine in

healthy Iranian neonates: Association with HLA antigens.

Iran J Med Sci 2002;27(2):51-55. Not sensitivity or 

specificity of an identified test

Jagerstad M, Lindstrand K, Norden A et al. The folate

conjugase activity of the intestinal mucosa in celiac

disease. Scandinavian Journal of Gastroenterology

1974;9(3):255-259. Not sensitivity or specificity of an 

identified test 

Jalava T, Maki M, Marttinen A et al. The in vitro response 

to human fibroblast-derived extracellular matrix proteins is 

restricted by specific HLA class II genes. Relevance for

coeliac disease. Hum Immunol 1996;49(2):106-112. Not 

sensitivity or specificity of an identified test 

Jalkanen S, Saari S, Kalimo H et al. Lymphocyte migration 

into the skin: The role of lymphocyte homing receptor 

(CD44) and endothelial cell antigen (HECA-452). J Invest 

Dermatol 1990;94(6):786-792. Not sensitivity or specificity

of an identified test 

James M W, Scott B B. Coeliac disease: the cause of the 

various associated disorders?. European Journal of

Gastroenterology & Hepatology 2001;13(9):1119-1121. 

Not sensitivity or specificity of an identified test

James M W, Scott B B. Evidence-based clinical medicine: 

Application of a diagnostic test using the example of 

A-391
coeliac disease. Cme J Gastroenterol Hepatol Nutr

2001;4(1):28-31. Not sensitivity or specificity of an 

identified test 

Janatkova I, Malic caron, Fu caron et al. Diagnostic asset of

assessment of autoantibodies in gluten-sensitive

enteropathy. Epidemiol Mikrobiol Imunol 2002;51(3):125-

130. Not sensitivity or specificity of an identified test 

Janatuinen E K, Kemppainen T A, Julkunen R J K et al. No 

harm from five year ingestion of oats in coeliac disease.

Gut 2002;50(3):332-335. Not sensitivity or specificity of an 

identified test 

Janatuinen E K, Kemppainen T A, Pikkarainen P H et al. 

Lack of cellular and humoral immunological responses to 

oats in adults with coeliac disease. Gut 2000;46(3):327-

331. Not sensitivity or specificity of an identified test 

Janatuinen E K, Pikkarainen P H, Kemppainen T A et al. A 

comparison of diets with and without oats in adults with 

celiac disease. New England Journal of Medicine 

1995;333(16):1033-1037. Not sensitivity or specificity of

an identified test

Jansen Th T L A, Mulder C J J, Karssen P H Z et al. 

Epidemiological survey of the Dutch Coeliac Disease 

Society: An update 1992. European Journal of 

Gastroenterology & Hepatology 1993;5(2):73-78. Not 

sensitivity or specificity of an identified test 

Jansen J W, Haverkate F, Koopman J et al. Influence of

factor XIIIa activity on human whole blood clot lysis in

vitro. Thrombosis and Haemostasis 1987;57(2):171-175. 

Not sensitivity or specificity of an identified test

Jansson Ulf H G, Kristiansson Bengt, Albertsson-Wikland 

Kerstin et al. Short-term gluten challenge in children with

coeliac disease does not impair spontaneous growth 

hormone secretion. Journal of Pediatric Endocrinology & 

Metabolism - Jpem 2003;16(5):771-778. Not sensitivity or

specificity of an identified test

Jansson U, Johansson C. Down syndrome and celiac 

disease. Journal of Pediatric Gastroenterology and

Nutrition 1995;21(4):443-445. Not sensitivity or specificity

of an identified test 

Jansson U H, Gudjonsdottir A H, Ryd W et al. Two 

different doses of gluten show a dose-dependent response 

of enteropathy but not of serological markers during gluten 

challenge in children with coeliac disease. Acta Paediatrica

(Oslo, Norway - 1992) 2001;90(3):255-259. Not sensitivity

or specificity of an identified test

Jarnik M, Kartasova T, Steinert P M et al. Differential 

expression and cell envelope incorporation of small

proline-rich protein 1 in different cornified epithelia. 

Journal of Cell Science 1996;109(Pt 6):1381-1391. Not 

sensitivity or specificity of an identified test 

Jarvinen Teea T, Kaukinen Katri, Laurila Kaija et al.

Intraepithelial lymphocytes in celiac disease. American

Journal of Gastroenterology 2003;98(6):1332-1337. Unable 

to extract data

Jaskowski T D, Schroder C, Martins T B et al. IgA 

antibodies against endomysium and transglutaminase: a 

comparison of methods. Journal of Clinical Laboratory

Analysis 2001;15(3):108-111. Improper control group 

Jeffries G H, Steinberg H, Sleisenger M H. Chronic 

ulcerative (nongranulomatous) jejunitis. American Journal 

of Medicine 1968;44(1):47-59. Not sensitivity or 

specificity of an identified test

Jeitner T M, Bogdanov M B, Matson W R et al. N(epsilon)-

(gamma-L-glutamyl)-L-lysine (GGEL) is increased in 

cerebrospinal fluid of patients with Huntington's disease.

Journal of Neurochemistry 2001;79(5):1109-1112. Not 

sensitivity or specificity of an identified test 

Jelinkova L, Tuckova L, Sanchez D et al. Increased levels 

of circulating ICAM-1, E-selectin, and IL-2 receptors in 

celiac disease. Digestive Diseases and Sciences

2000;45(2):398-402. Not sensitivity or specificity of an 

identified test 

Jenkins D J A, Taylor R H, Wolever T M S. The diabetic 

diet, dietary carbohydrate and differences in digestibility.

Diabetologia 1982;23(6):477-484. Not sensitivity or 

specificity of an identified test

Jenkins D, Goodall A, Scott B. T-cell and plasma cell 

populations in coeliac small intestinal mucosa in relation to 

dermatitis herpetiformis. Gut 1989;30(7):955-958. Not 

sensitivity or specificity of an identified test 

Jenkins D, Goodall A, Scott B B. T-lymphocyte 

populations in normal and coeliac small intestinal mucosa 

defined by monoclonal antibodies. Gut 1986;27(11):1330-

1337. Not sensitivity or specificity of an identified test 

Jennings J S R, Howdle P D. Celiac disease. Curr Opin 

Gastroenterol 2001;17(2):118-126. Not sensitivity or 

specificity of an identified test

Jennings J S R, Howdle P D. New developments in celiac 

disease. Curr Opin Gastroenterol 2003;19(2):118-129. Not 

sensitivity or specificity of an identified test 

Jennings W, Rowland R, Hecker R. The significance of

lowered jejunal disaccharidase levels. Australian and New 

Zealand Journal of Medicine 1976;6(6):556-560. Not 

sensitivity or specificity of an identified test 

Jensen K, Sollid L M, Scott H et al. Gliadin-specific T cell 

responses in peripheral blood of healthy individuals involve 

T cells restricted by the coeliac disease associated DQ2 

heterodimer. Scandinavian Journal of Immunology

1995;42(1):166-170. Not sensitivity or specificity of an 

identified test 

Jensen M L, Johansen P. Immunocytochemical staining of 

A-392
smears and corresponding cell blocks from serous

effusions: a follow-up and comparative investigation. 

Diagnostic Cytopathology 1996;15(1):33-36. Not 

sensitivity or specificity of an identified test 

Jensen P H, Lorand L, Ebbesen P et al. Type-2 

plasminogen-activator inhibitor is a substrate for

trophoblast transglutaminase and factor XIIIa. 

Transglutaminase-catalyzed cross-linking to cellular and 

extracellular structures. European Journal of Biochemistry / 

Febs 1993;214(1):141-146. Not sensitivity or specificity of 

an identified test

Jeong J M, Murthy S N, Radek J T et al. The fibronectinbinding domain of transglutaminase. Journal of Biological 

Chemistry 1995;270(10):5654-5658. Not sensitivity or 

specificity of an identified test

Jeppesen P B, Mortensen P B. The influence of a preserved

colon on the absorption of medium chain fat in patients

with small bowel resection. Gut 1998;43(4):478-483. Not 

sensitivity or specificity of an identified test 

Jessen B A, Phillips M A, Hovnanian A et al. Role of Sp1

response element in transcription of the human

transglutaminase 1 gene. Journal of Investigative 

Dermatology 2000;115(1):113-117. Not sensitivity or 

specificity of an identified test

Jessurun J, Yardley J H, Giardiello F M et al. Chronic 

colitis with thickening of the subepithelial collagen layer

(collagenous colitis): histopathologic findings in 15 

patients. Human Pathology 1987;18(8):839-848. Not 

sensitivity or specificity of an identified test 

Jevon G P, Dimmick J E, Dohil R et al. Spectrum of 

gastritis in celiac disease in childhood. Pediatric and 

Developmental Pathology - the Official Journal of the 

Society for Pediatric Pathology and the Paediatric

Pathology Society 1999;2(3):221-226. Not sensitivity or

specificity of an identified test

Jewell D P. Celiac disease. Canadian Journal of

Gastroenterology = Journal Canadien De Gastroenterologie 

2000;14(8):665-666. Not sensitivity or specificity of an 

identified test 

Jiang H, Kochhar D M. Induction of tissue 

transglutaminase and apoptosis by retinoic acid in the limb 

bud. Teratology 1992;46(4):333-340. Not sensitivity or

specificity of an identified test

Jing Y, Waxman S, Lopez R. The cellular retinoic acid 

binding protein II is a positive regulator of retinoic acid

signaling in breast cancer cells. Cancer Research

1997;57(9):1668-1672. Not sensitivity or specificity of an

identified test 

Jiskra J, Limanova Z, Vanic caron et al. IgA and IgG 

antigliadin, IgA anti-tissue transglutaminase and

antiendomysial antibodies in patients with autoimmune 

thyroid diseases and their relationship to thyroidal 

replacement therapy. Physiol Res 2003;52(1):79-88. Not 

sensitivity or specificity of an identified test 

Jodl J, Stepan J, Lojda Z. Diagnostic significance of 

determination of serum alkaline phosphatase intestinal 

isoenzyme activity in coeliac sprue in childhood. Acta 

Universitatis Carolinae.Medica.Monographia 1977;78 Pt 

265-70. Not sensitivity or specificity of an identified test 

Johansen B H, Buus S, Vartdal F et al. Binding of peptides 

to HLA-DQ molecules: peptide binding properties of the 

disease-associated HLA-DQ(alpha 1*0501, beta 1*0201) 

molecule. International Immunology 1994;6(3):453-461. 

Not sensitivity or specificity of an identified test

Johansen B H, Gjertsen H A, Vartdal F et al. Binding of 

peptides from the N-terminal region of alpha-gliadin to the 

celiac disease-associated HLA-DQ2 molecule assessed in 

biochemical and T cell assays. Clinical Immunology and 

Immunopathology 1996;79(3):288-293. Not sensitivity or

specificity of an identified test

Johansen B H, Jensen T, Thorpe C J et al. Both alpha and

beta chain polymorphisms determine the specificity of the 

disease-associated HLA-DQ2 molecules, with beta chain

residues being most influential. Immunogenetics 

1996;45(2):142-150. Not sensitivity or specificity of an 

identified test 

Johansen B H, Vartdal F, Eriksen J A et al. Identification of

a putative motif for binding of peptides to HLA-DQ2. 

International Immunology 1996;8(2):177-182. Not 

sensitivity or specificity of an identified test 

Johansson L, Andersson C, Albin M. 

Immunohistochemical study of 158 lung carcinomas. 

Apmis - Acta Pathologica, Microbiologica, Et

Immunologica Scandinavica 1992;100(10):914-921. Not 

sensitivity or specificity of an identified test 

Johansson S, Lie B A, Cambon-Thomsen A et al. No 

evidence of type 1 diabetes susceptibility genes in the

region centromeric of the HLA complex. Hum Immunol 

2003;64(10):951-959. Not sensitivity or specificity of an

identified test 

Johansson S, Lie B A, Pociot F et al. HLA associations in

type 1 diabetes: DPB1 alleles may act as markers of other

HLA-complex susceptibility genes. Tissue Antigens 

2003;61(5):344-351. Not sensitivity or specificity of an 

identified test 

Johnson G V W, Bailey C D C, Tucholski J et al. Tissue 

transglutaminase in neurodegenerative diseases. Minerva 

Biotecnol 2002;14(2):171-176. Not sensitivity or

specificity of an identified test

Johnson G V, Cox T M, Lockhart J P et al. 

Transglutaminase activity is increased in Alzheimer's 

disease brain. Brain Research 1997;751(2):323-329. Not 

sensitivity or specificity of an identified test 

A-393
Johnson K, Hashimoto S, Lotz M et al. Interleukin-1 

induces pro-mineralizing activity of cartilage tissue 

transglutaminase and factor XIIIa. American Journal of

Pathology 2001;159(1):149-163. Not sensitivity or

specificity of an identified test

Johnson T N, Tanner M S, Taylor C J et al. Enterocytic 

CYP3A4 in a paediatric population: Developmental 

changes and the effect of coeliac disease and cystic fibrosis. 

Br J Clin Pharmacol 2001;51(5):451-460. Not sensitivity or 

specificity of an identified test

Johnson T S, El Koraie A F, Skill N J et al. Tissue 

transglutaminase and the progression of human renal 

scarring. J Am Soc Nephrol 2003;14(8):2052-2062. Not 

sensitivity or specificity of an identified test 

Johnson T S, Griffin M, Thomas G L et al. The role of

transglutaminase in the rat subtotal nephrectomy model of 

renal fibrosis. J Clin Invest 1997;99(12):2950-2960. Not 

sensitivity or specificity of an identified test 

Johnson T S, Knight C R, el Alaoui S et al. Transfection of

tissue transglutaminase into a highly malignant hamster 

fibrosarcoma leads to a reduced incidence of primary

tumour growth. Oncogene 1994;9(10):2935-2942. Not 

sensitivity or specificity of an identified test 

Johnston C F, Bell P M, Collins B J et al. Reassessment of 

enteric endocrine cell hyperplasia in celiac disease. HepatoGastroenterology 1988;35(6):285-288. Unable to extract 

data 

Johnston S D, Watson R G P. Small bowel lymphoma in 

unrecognized coeliac disease: A cause for concern?. 

European Journal of Gastroenterology & Hepatology

2000;12(6):645-648. Not sensitivity or specificity of an 

identified test 

Johnston S D, Peter Watson R G, McMillan S A. Soda 

bread provocation test for subjects with transient serology

for coeliac disease 3 years after a population screening 

survey. European Journal of Gastroenterology & 

Hepatology 2000;12(9):1013-1015. Not sensitivity or 

specificity of an identified test

Johnston S D, Ritchie C, Robinson J. Application of red

cell distribution width to screening for coeliac disease in

insulin-dependent diabetes mellitus. Irish Journal of 

Medical Science 1999;168(3):167-170. Not sensitivity or 

specificity of an identified test

Johnston S D, Smye M, Watson R P. Intestinal 

permeability tests in coeliac disease. Clinical Laboratory

2001;47(3-4):143-150. Not sensitivity or specificity of an

identified test 

Johnston S D, Watson R G, McMillan S A et al. 

Serological markers for coeliac disease: changes with time 

and relationship to enteropathy. European Journal of 

Gastroenterology & Hepatology 1998;10(3):259-264. Not 

sensitivity or specificity of an identified test 

Johnston S D, Watson R G, McMillan S A et al. 

Preliminary results from follow-up of a large-scale 

population survey of antibodies to gliadin, reticulin and

endomysium. Acta paediatrica (Oslo, Norway : 

1992).Supplement. 1996;41261-64. Not sensitivity or 

specificity of an identified test

Johnston S D, Watson R G, McMillan S A et al. Coeliac 

disease detected by screening is not silent--simply 

unrecognized. Qjm - Monthly Journal of the Association of

Physicians 1998;91(12):853-860. Not sensitivity or

specificity of an identified test

Johnston S D, Watson R G, Middleton D et al. Genetic, 

morphometric and immunohistochemical markers of latent

coeliac disease. European Journal of Gastroenterology &

Hepatology 1999;11(11):1283-1288. Unable to extract data 

Johnston Simon D, McMillan Stanley A, Collins John S et 

al. A comparison of antibodies to tissue transglutaminase 

with conventional serological tests in the diagnosis of 

coeliac disease. European Journal of Gastroenterology &

Hepatology 2003;15(9):1001-1004. Improper control group 

Jois J, Omagari K, Rowley M J et al. Enzyme inhibitory

antibody to pyruvate dehydrogenase: diagnostic utility in

primary biliary cirrhosis. Annals of Clinical Biochemistry

2000;37(Pt 1):67-73. Not sensitivity or specificity of an 

identified test 

Jokinen J, Peters U, Maki M et al. Celiac sprue in patients 

with chronic oral mucosal symptoms. Journal of Clinical

Gastroenterology 1998;26(1):23-26. Not sensitivity or 

specificity of an identified test

Jonas A. Significance of HLA expression in the mucosa of 

patients with active celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 1987;6(5):821-822. Not

sensitivity or specificity of an identified test 

Jones J G, Elmes M E. The measurement of mucosal nonmyelinated nerve fibre area and endocrine cell area in 

coeliac disease using morphometric analysis. Diagnostic 

Histopathology / Published in Association With the 

Pathological Society of Great Britain and Ireland 

1982;5(3):183-188. Not sensitivity or specificity of an 

identified test 

Jones P E, Gleeson M H. Mucosal ulceration and 

mesenteric lymphadenopathy in coeliac disease. British 

Medical Journal 1973;3(5873):212-213. Not sensitivity or 

specificity of an identified test

Jones P E, Peters T J. DNA synthesis by jejunal mucosa in 

responsive and non-responsive coeliac disease. British 

Medical Journal 1977;1(6069):1130-1131. Not sensitivity

or specificity of an identified test

Jones P E, L'Hirondel C L, Peters T J. Protein synthesis by

cultured jejunal mucosa from control subjects and patients

with coeliac disease. Gut 1981;22(8):623-627. Not 

A-394
sensitivity or specificity of an identified test 

Jones P E, L'Hirondel C, Peters T J. Alkaline phosphatase 

synthesis and properties of subcellular organelles during in

vitro culture of jejunal biopsies from control subjects and 

patients with coeliac disease. Gut 1982;23(2):108-114. Not 

sensitivity or specificity of an identified test 

Jones P E, Pallis C, Peters T J. Morphological and

biochemical findings in jejunal biopsies from patients with

multiple sclerosis. Journal of Neurology, Neurosurgery,

and Psychiatry 1979;42(5):402-406. Not sensitivity or 

specificity of an identified test

Jones R A, Nicholas B, Mian S et al. Reduced expression 

of tissue transglutaminase in a human endothelial cell line 

leads to changes in cell spreading, cell adhesion and 

reduced polymerisation of fibronectin. Journal of Cell 

Science 1997;110(Pt 19):2461-2472. Not sensitivity or

specificity of an identified test

Jordan S C, Sakai R S, Ettenger R B et al. Characterization

of soluble circulating immune complexes by antigenspecific dissociation. Detection in the Raji cell 

radioimmune assay. Clin Immunol Immunopathol 

1983;27(3):357-368. Not sensitivity or specificity of an 

identified test 

Jos J, Labbe F. Ultrastructural localization of IgA globulins 

in normal and coeliac intestinal mucosa using 

immunoenzymatic methods. Biomedicine / Publiee Pour 

L'a.a.i.c.i.g 1976;24(6):425-434. Not sensitivity or

specificity of an identified test

Jos J, Labbe F, Geny B et al. Immunoelectron-microscopic 

localization of immunoglobulin A and secretory component 

in jejunal mucosa from children with coeliac disease. 

Scandinavian Journal of Immunology 1979;9(5):441-450. 

Not sensitivity or specificity of an identified test

Jos J, Lenoir G, Ritis G et al. In vitro pathogenetic studies 

of coeliac disease. Effects of protein digests on coeliac 

intestinal biopsy specimens maintained in culture for 48 

hours. Scandinavian Journal of Gastroenterology

1975;10(2):121-128. Not sensitivity or specificity of an 

identified test 

Joseph B, Lefebvre O, Mereau-Richard C et al. Evidence

for the involvement of both retinoic acid receptor- and 

retinoic X receptor-dependent signaling pathways in the 

induction of tissue transglutaminase and apoptosis in the 

human myeloma cell line RPMI 8226. Blood

1998;91(7):2423-2432. Not sensitivity or specificity of an

identified test 

Joseph Bertrand, Marchetti Philippe, Lefebvre Olga et al. 

The novel retinoid AHPN/CD437 induces a rapid but 

incomplete apoptotic response in human myeloma cells. 

Biochimica Et Biophysica Acta 2003;1593(2-3):277-282. 

Not sensitivity or specificity of an identified test

Joventino L P, Stock W, Lane N J et al. Certain HLA 

antigens are associated with specific morphologic and 

cytogenetic subsets of acute myeloid leukemia. Leukemia 

1995;9(3):433-439. Not sensitivity or specificity of an 

identified test 

Juby L D, Dixon M F, Axon A T. Abnormal intestinal 

permeability and jejunal morphometry. Journal of Clinical 

Pathology 1987;40(7):714-718. Not sensitivity or

specificity of an identified test

Juby L D, Rothwell J, Axon A T. Cellobiose/mannitol 

sugar test--a sensitive tubeless test for coeliac disease:

results on 1010 unselected patients. Gut 1989;30(4):476-

480. Not sensitivity or specificity of an identified test 

Juby L D, Rothwell J, Axon A T. Lactulose/mannitol test: 

an ideal screen for celiac disease. Gastroenterology

1989;96(1):79-85. Not sensitivity or specificity of an 

identified test 

Julkunen H, Siren M-K, Kaaja R et al. Maternal HLA 

antigens and antibodies to SS-A/RO and SS-B/LA. 

Comparison with systemic lupus erythematosus and 

primary Sjogren's syndrome. Br J Rheumatol 

1995;34(10):901-907. Not sensitivity or specificity of an

identified test 

Jung G, Fleckenstein B, von der et al. From combinatorial 

libraries to MHC ligand motifs, T-cell superagonists and 

antagonists. Biologicals - Journal of the International 

Association of Biological Standardization 2001;29(3-

4):179-181. Not sensitivity or specificity of an identified

test 

Junn Eunsung, Ronchetti Ruben D, Quezado Martha M et 

al. Tissue transglutaminase-induced aggregation of alphasynuclein: Implications for Lewy body formation in 

Parkinson's disease and dementia with Lewy bodies. 

Proceedings of the National Academy of Sciences of the

United States of America 2003;100(4):2047-2052. Not 

sensitivity or specificity of an identified test 

Jurado A, Cardaba B, Jara P et al. Autoimmune hepatitis 

type 2 and hepatitis C virus infection: Study of HLA 

antigens. J Hepatol 1997;26(5):983-991. Not sensitivity or

specificity of an identified test

Jurgensen K, Aeschlimann D, Cavin V et al. A new 

biological glue for cartilage-cartilage interfaces: Tissue 

transglutaminase. J Bone Jt Surg Ser A 1997;79(2):185-

193. Not sensitivity or specificity of an identified test 

Just J J. Genetic predisposition to HIV-1 infection and 

acquired immune deficiency virus syndrome: A review of

the literature examining associations with HLA. Hum

Immunol 1995;44(3):156-169. Not sensitivity or specificity

of an identified test 

Juto P, Fredrikzon B, Hernell O. Gliadin-specific serum 

immunoglobulins A, E, G, and M in childhood: relation to

small intestine mucosal morphology. Journal of Pediatric 

Gastroenterology and Nutrition 1985;4(5):723-729. Not

A-395
sensitivity or specificity of an identified test 

Kaczmarek E, Liu Y, Berse B et al. Biosynthesis of plasma

factor XIII: evidence for transcription and translation in

hepatoma cells. Biochimica Et Biophysica Acta

1995;1247(1):127-134. Not sensitivity or specificity of an

identified test 

Kaczmarski M. The disaccharidase activity of jejunal 

mucosa in children with malabsorption syndrome caused

by food intolerance. Roczniki Akademii Medycznej W 

Bialymstoku (1995) 1995;40(3):504-511. Not sensitivity or

specificity of an identified test

Kadokawa Y, Omagari K, Hazama H et al. Evaluation of 

newly developed ELISA using "MESACUP-2 Test

Mitochondrial M2" kit for the diagnosis of primary biliary

cirrhosis. Clin Biochem 2003;36(3):203-210. Not 

sensitivity or specificity of an identified test 

Kadunce D P, McMurry M P, Avots-Avotins A et al. The 

effect of an elemental diet with and without gluten on 

disease activity in dermatitis herpetiformis. Journal of 

Investigative Dermatology 1991;97(2):175-182. Not 

sensitivity or specificity of an identified test 

Kadunce D P, Meyer L J, Zone J J. IgA class antibodies in

dermatitis herpetiformis: reaction with tissue antigens. 

Journal of Investigative Dermatology 1989;93(2):253-258. 

Not sensitivity or specificity of an identified test

Kagnoff M F. Coeliac disease: genetic, immunological and

environmental factors in disease pathogenesis. 

Scandinavian Journal of Gastroenterology.Supplement 

1985;11445-54. Not sensitivity or specificity of an 

identified test 

Kagnoff M F. Immunopathogenesis of celiac disease. 

Immunological Investigations 1989;18(1-4):499-508. Not 

sensitivity or specificity of an identified test 

Kagnoff M F. Understanding the molecular basis of coeliac 

disease. Gut 1990;31(5):497-499. Not sensitivity or 

specificity of an identified test

Kagnoff M F, Harwood J I, Bugawan T L et al. Structural 

analysis of the HLA-DR, -DQ, and -DP alleles on the celiac 

disease-associated HLA-DR3 (DRw17) haplotype. 

Proceedings of the National Academy of Sciences of the

United States of America 1989;86(16):6274-6278. Not 

sensitivity or specificity of an identified test 

Kagnoff M F, Weiss J B, Brown R J et al. Immunoglobulin 

allotype markers in gluten-sensitive enteropathy. Lancet 

1983;1(8331):952-953. Not sensitivity or specificity of an

identified test 

Kagnoff Martin F. Celiac disease pathogenesis: the plot

thickens. Gastroenterology 2002;123(3):939-943. Not 

sensitivity or specificity of an identified test 

Kahn H J, Fekete E, From L. Tenascin differentiates 

dermatofibroma from dermatofibrosarcoma protuberans: 

comparison with CD34 and factor XIIIa. Human Pathology

2001;32(1):50-56. Not sensitivity or specificity of an 

identified test 

Kainulainen H, Rantala I, Collin P et al. Blisters in the 

small intestinal mucosa of coeliac patients contain T cells

positive for cyclooxygenase 2. Gut 2002;50(1):84-89. Not

sensitivity or specificity of an identified test 

Kakar S, Nehra V, Murray J A et al. Significance of 

intraepithelial lymphocytosis in small bowel biopsy

samples with normal mucosal architecture. American

Journal of Gastroenterology 2003;98(9):2027-2033. Not 

sensitivity or specificity of an identified test 

Kalapesi Z, Rees J P R. Coeliac disease in schoolchildren.

Ir Med J 1978;71(6):188-191. Not sensitivity or specificity

of an identified test 

Kallikorm R, Uibo O, Uibo R. Coeliac disease in

spondyloarthropathy: usefulness of serological screening.

Clinical Rheumatology 2000;19(2):118-122. Not sensitivity

or specificity of an identified test

Kalogeropoulos C D, Spyrou P, Stefaniotou M I et al. 

Anticardiolipin antibodies and occlusive vascular disease of

the eye: prospective study. Documenta 

Ophthalmologica.Advances in Ophthalmology

1998;95(2):109-120. Not sensitivity or specificity of an 

identified test 

Kandel L B, Whyard T C, Gonder M J. Monoclonal 

antibody identification of a potentially lithogenic protein

extracted from human renal calculi. Journal of Stone 

Disease 1992;4(4):283-288. Not sensitivity or specificity of 

an identified test

Kanerud L, Engstrom G N, Tarkowski A. Evidence for

differential effects of sulphasalazine on systemic and 

mucosal immunity in rheumatoid arthritis. Annals of the 

Rheumatic Diseases 1995;54(4):256-262. Not sensitivity or 

specificity of an identified test

Kanitakis J, Roca-Miralles M. Factor-XIIIa-expressing 

dermal dendrocytes in Kaposi's sarcoma. A comparison 

between classical and immunosuppression-associated

types. Virchows Archiv.A, Pathological Anatomy and 

Histopathology 1992;420(3):227-231. Not sensitivity or

specificity of an identified test

Kanungo A, Samal K C, Sanjeevi C B. Molecular 

mechanisms involved in the etiopathogenesis of 

malnutrition-modulated diabetes mellitus. Annals of the 

New York Academy of Sciences 2002;958138-143. Not 

sensitivity or specificity of an identified test 

Kanungo A, Shtauvere-Brameus A, Samal K C et al. 

Autoantibodies to tissue transglutaminase in patients from 

eastern India with malnutrition-modulated diabetes 

mellitus, insulin-dependent diabetes mellitus, and noninsulin-dependent diabetes mellitus. Annals of the New 

A-396
York Academy of Sciences 2002;958232-234. Not 

sensitivity or specificity of an identified test 

Kapadia C. The reliability of noninvasive tests for celiac 

disease. Gastroenterology 1995;108(2):608-610. Review 

article 

Kapuscinska A, Zalewski T, Chorzelski T P et al. Disease 

specificity and dynamics of changes in IgA class antiendomysial antibodies in celiac disease. Journal of 

Pediatric Gastroenterology and Nutrition 1987;6(4):529-

534. Improper control group 

Karagen L, Cinnamon Y, Ginsburg M et al. Origin of 

primordial germ cells in the prestreak chick embryo. Dev

Genet 1996;19(4):290-301. Not sensitivity or specificity of 

an identified test

Karagiannis J A, Priddle J D, Jewell D P. Cell-mediated 

immunity to a synthetic gliadin peptide resembling a 

sequence from adenovirus 12. Lancet 1987;1(8538):884-

886. Not sensitivity or specificity of an identified test 

Karagiozoglou-Lampoudi T, Nousia-Arvanitaki S, 

Augoustidou-Savopoulou P et al. Insulin secretion decline 

unrelated to jejunal morphology or exocrine pancreatic 

function in children with celiac disease. J Pediatr

Endocrinol Metab 1996;9(6):585-591. Not sensitivity or

specificity of an identified test

Karban A, Lerner A, Shapiro S. Th1/Th2 cytokine profile 

in celiac disease. Israel Journal of Medical Sciences

1997;33(3):209-214. Not sensitivity or specificity of an 

identified test 

Karczewska K, Lukasik M, Kasner J et al. Familial

occurrence of celiac disease and isolated immunoglobulin a 

deficiency. Med Sci Monit 1998;4(5):836-839. Not 

sensitivity or specificity of an identified test 

Karell K, Holopainen P, Mustalahti K et al. Not all HLA 

DR3 DQ2 haplotypes confer equal susceptibility to coeliac

disease: transmission analysis in families. Scandinavian

Journal of Gastroenterology 2002;37(1):56-61. Improper 

control group 

Karell K, Korponay-Szabo I, Szalai Zs et al. Genetic

dissection between coeliac disease and dermatitis

herpetiformis in sib pairs. Annals of Human Genetics 

2002;66(Pt 5-6):387-392. Not sensitivity or specificity of

an identified test

Karell K, Louka A S, Moodie S J et al. HLA types in celiac 

disease patients not carrying the DQA1 *05-DQB1 *02 

(DQ2) heterodimer: Results from the European genetics 

cluster on celiac disease. Hum Immunol 2003;64(4):469-

477. Improper control group 

Kari J A, Sinnott P, Khan H et al. Familial steroidresponsive nephrotic syndrome and HLA antigens in 

Bengali children. Pediatr Nephrol 2001;16(4):346-349. Not 

sensitivity or specificity of an identified test 

Kariniemi A L, Forsman L, Wahlstrom T et al. Expression 

of differentiation antigens in mammary and extramammary

Paget's disease. British Journal of Dermatology 

1984;110(2):203-210. Not sensitivity or specificity of an

identified test 

Karlsson I J, Dahl M G C, Marks J M. Absence of 

cutaneous IgA in coeliac disease without dermatitis 

herpetiformis. Br J Dermatol 1978;99(6):621-625. Not 

sensitivity or specificity of an identified test 

Karpati S, Burgin-Wolff A, Krieg T et al. Binding to 

human jejunum of serum IgA antibody from children with

coeliac disease. Lancet 1990;336(8727):1335-1338. Not 

sensitivity or specificity of an identified test 

Karpati S, Kosnai I, Torok E et al. Immunoglobulin A 

deposition in jejunal mucosa of children with dermatitis 

herpetiformis. J Invest Dermatol 1988;91(4):336-339. Not 

sensitivity or specificity of an identified test 

Karpati S, Kosnai I, Verkasalo M et al. HLA antigens,

jejunal morphology and associated diseases in children

with dermatitis herpetiformis. Acta Paediatrica 

Scandinavica 1986;75(2):297-301. Not sensitivity or 

specificity of an identified test

Karpati S, Meurer M, Stolz W et al. Ultrastructural binding 

sites of endomysium antibodies from sera of patients with 

dermatitis herpetiformis and coeliac disease. Gut

1992;33(2):191-193. Not sensitivity or specificity of an 

identified test 

Karpati S, Stolz W, Meurer M et al. Extracellular binding 

sites of IgA anti-jejunal antibodies on normal small bowel 

detected by indirect immunoelectronmicroscopy. Journal of 

Investigative Dermatology 1991;96(2):228-233. Not 

sensitivity or specificity of an identified test 

Karska K, Tuckova L, Steiner L et al. Calreticulin--the 

potential autoantigen in celiac disease. Biochemical and 

Biophysical Research Communications 1995;209(2):597-

605. Not sensitivity or specificity of an identified test 

Kartasova T, Darwiche N, Kohno Y et al. Sequence and 

expression patterns of mouse SPR1: Correlation of 

expression with epithelial function. Journal of Investigative 

Dermatology 1996;106(2):294-304. Not sensitivity or 

specificity of an identified test

Kashima K, Yokoyama S, Daa T et al. 

Immunohistochemical study on tissue transglutaminase and 

copper-zinc superoxide dismutase in human myocardium: 

its relevance to apoptosis detected by the nick end labelling 

method. Virchows Archiv - an International Journal of

Pathology 1997;430(4):333-338. Not sensitivity or

specificity of an identified test

Kasner J, Karczewska K, Sulej J et al. Diagnostic value of 

tissue transglutaminase antibodies ((dagger)TG) in celiac 

A-397
disease. Pediatr Wspolczesna 2002; 4(3):269-272. Unable

to obtain full article 

Katona E, Haramura G, Karpati L et al. A simple, quick 

one-step ELISA assay for the determination of complex 

plasma factor XIII (A2B2). Thrombosis and Haemostasis 

2000;83(2):268-273. Not sensitivity or specificity of an 

identified test 

Katz A J, Falchuk Z M. Definitive diagnosis of glutensensitive enteropathy. Use of an in vitro organ culture 

model. Gastroenterology 1978;75(4):695-700. Not 

sensitivity or specificity of an identified test 

Katz A J, Falchuk Z M. Current concepts in gluten

sensitive enteropathy (celiac sprue). Pediatric Clinics of 

North America 1975;22(4):767-785. Not sensitivity or 

specificity of an identified test

Katz A J, Falchuk Z M, Schwachman H. The coexistence 

of cystic fibrosis and celiac disease. Pediatrics

1976;57(5):715-721. Not sensitivity or specificity of an 

identified test 

Katz A J, Falchuk Z M, Strober W et al. Gluten-sensitive

enteropathy. Inhibition by cortisol of the effect of gluten 

protein in vitro. New England Journal of Medicine

1976;295(3):131-135. Not sensitivity or specificity of an

identified test 

Katz K D. Celiac Disease - Current Clinical Considerations

in Treatment and Avoidance of Nutritional Deficiencies.

Today's Ther Trends 2003;21(4):379-389. Not sensitivity

or specificity of an identified test

Katz S I, Hall R P, Lawley T J et al. Dermatitis 

herpetiformis: the skin and the gut. Annals of Internal 

Medicine 1980;93(6):857-874. Not sensitivity or specificity

of an identified test 

Kaufmann H J. Chylous ascites and intestinal muscular 

hypertrophy occurring in the course of celiac sprue. 

American Journal of Digestive Diseases 1975;20(5):494-

497. Not sensitivity or specificity of an identified test 

Kaukinen K, Collin P, Holm K et al. Small-bowel mucosal 

inflammation in reticulin or gliadin antibody-positive 

patients without villous atrophy. Scandinavian Journal of

Gastroenterology 1998;33(9):944-949. Improper control 

group 

Kaukinen K, Collin P, Holm K et al. Wheat starchcontaining gluten-free flour products in the treatment of 

coeliac disease and dermatitis herpetiformis. A long-term

follow-up study. Scandinavian Journal of Gastroenterology

1999;34(2):163-169. Not sensitivity or specificity of an 

identified test 

Kaukinen K, Collin P, Mykkanen A H et al. Celiac disease 

and autoimmune endocrinologic disorders. Digestive 

Diseases and Sciences 1999;44(7):1428-1433. Not 

sensitivity or specificity of an identified test 

Kaukinen K, Halme L, Collin P et al. Celiac disease in

patients with severe liver disease: Gluten-free diet may 

reverse hepatic failure. Gastroenterology 2002;122(4):881-

888. Not sensitivity or specificity of an identified test 

Kaukinen K, Maki M, Partanen J et al. Celiac disease 

without villous atrophy: revision of criteria called for. 

Digestive Diseases and Sciences 2001;46(4):879-887. 

Unable to extract data 

Kaukinen Katri, Partanen Jukka, Maki Markku et al. HLADQ typing in the diagnosis of celiac disease. American

Journal of Gastroenterology 2002;97(3):695-699. Unable to

extract data

Kaukinen Katri, Sulkanen Satu, Maki Markku et al. IgAclass transglutaminase antibodies in evaluating the efficacy

of gluten-free diet in coeliac disease. European Journal of

Gastroenterology & Hepatology 2002;14(3):311-315. Not 

sensitivity or specificity of an identified test 

Kaur Gurvinder, Sarkar N, Bhatnagar S et al. Pediatric 

celiac disease in India is associated with multiple DR3-

DQ2 haplotypes. Human Immunology 2002;63(8):677-682. 

Improper control group 

Kavai M, Csorba S, Szabolcs M et al. Association of 

precipitins and coeliac disease. Acta Allergologica

1977;32(6):395-405. Not sensitivity or specificity of an 

identified test 

Kavai M, Szabolcs M, Csorba S. Circulating antibodies in

coeliac disease. Acta Paediatr Acad Sci Hung 1977;18(3-

4):235-238. Not sensitivity or specificity of an identified

test 

Kavin H. Adult coeliac disease in South Africa. An 

analysis of 20 cases emphasizing atypical presentations. S

Afr Med J 1981;59(18):628-632. Not sensitivity or

specificity of an identified test

Kawabe S, Ikuta T, Ohba M et al. Cholesterol sulfate

activates transcription of transglutaminase 1 gene in normal 

human keratinocytes. Journal of Investigative Dermatology

1998;111(6):1098-1102. Not sensitivity or specificity of an 

identified test 

Kazerounian S, Aho S. Characterization of periphilin, a

widespread, highly insoluble nuclear protein and potential 

constituent of the keratinocyte cornified envelope. J Biol

Chem 2003;278(38):36707-36717. Not sensitivity or 

specificity of an identified test

Keating J, Bjarnason I, Somasundaram S et al. Intestinal 

absorptive capacity, intestinal permeability and jejunal 

histology in HIV and their relation to diarrhoea. Gut 

1995;37(5):623-629. Not sensitivity or specificity of an 

identified test 

A-398
Kedzierska A. Immunogenetic aspects of coeliac disease in

children. Med Sci Monit 1999;5(4):732-740. Not sensitivity 

or specificity of an identified test

Kedzierska A, Turowski G. HLA class I haplotypes in 

families of children with coeliac disease. Medical Science

Monitor - International Medical Journal of Experimental 

and Clinical Research 2000;6(2):336-341. Not sensitivity

or specificity of an identified test

Kedzierska A, Turowski G. HLA class I antigens in 

families with coeliac disease. Medical Science Monitor - 

International Medical Journal of Experimental and Clinical 

Research 2000;6(5):957-963. Not sensitivity or specificity

of an identified test 

Keeling J W, Risdon R A. Proceedings: Quantitation of

small intestinal biopsies from children. Archives of Disease

in Childhood 1974;49(9):747Not sensitivity or specificity

of an identified test 

Kelleher D, Murphy A, Sheils O et al. Tyrosine

phosphorylation in the human duodenum. Gut 

1995;36(1):34-38. Not sensitivity or specificity of an 

identified test 

Kelly C P, Feighery C F, Gallagher R B et al. Diagnosis 

and treatment of gluten-sensitive enteropathy. Advances in 

Internal Medicine 1990;35341-363. Not sensitivity or 

specificity of an identified test

Kelly C P, Feighery C F, Gallagher R B et al. Mucosal and 

systemic IgA anti-gliadin antibody in celiac disease. 

Contrasting patterns of response in serum, saliva, and 

intestinal secretions. Digestive Diseases and Sciences

1991;36(6):743-751. Improper control group 

Kelly C P, O'Shea B, Kelly J. Atopy and childhood coeliac 

disease. Lancet 1987;2(8550):109Not sensitivity or 

specificity of an identified test

Kelly J, O'Farrelly C, Rees J P. alpha-Gliadin antibodies in

childhood coeliac disease. Lancet 1985;2(8454):558-559. 

Not sensitivity or specificity of an identified test

Kelly J, O'Farrelly C, O'Mahony C et al. 

Immunoperoxidase demonstration of the cellular 

composition of the normal and coeliac small bowel.

Clinical and Experimental Immunology 1987;68(1):177-

188. Not sensitivity or specificity of an identified test 

Kelly J, O'Farrelly C, Rees J P et al. Humoral response to 

alpha gliadin as serological screening test for coeliac 

disease. Archives of Disease in Childhood 1987;62(5):469-

473. Serology <1990 

Kelly J, Weir D G, Feighery C. Differential expression of 

HLA-D gene products in the normal and coeliac small 

bowel. Tissue Antigens 1988;31(3):151-160. Not 

sensitivity or specificity of an identified test 

Kelly J, Whelan C A, Weir D G et al. Removal of 

endogenous peroxidase activity from cryostat sections for 

immunoperoxidase visualisation of monoclonal antibodies. 

Journal of Immunological Methods 1987;96(1):127-132. 

Not sensitivity or specificity of an identified test

Kelly M H, Hamilton J R. A micro-technique for the assay

of intestinal alkaline phosphatase. Results in normal 

children and in children with celiac disease. Clinical

Biochemistry 1970;3(1):33-43. Not sensitivity or 

specificity of an identified test

Kemeny D M, Urbanek R, Amlot P L et al. Sub-class of 

IgG in allergic disease. I. IgG sub-class antibodies in 

immediate and non-immediate food allergy. Clinical

Allergy 1986;16(6):571-581. Not sensitivity or specificity

of an identified test 

Kemppainen T A, Kosma V M, Janatuinen E K et al.

Nutritional status of newly diagnosed celiac disease 

patients before and after the institution of a celiac disease 

diet--association with the grade of mucosal villous atrophy.

American Journal of Clinical Nutrition 1998;67(3):482-

487. Not sensitivity or specificity of an identified test 

Kemppainen T, Kroger H, Janatuinen E et al. Bone 

recovery after a gluten-free diet: A 5-year follow-up study.

Bone 1999;25(3):355-360. Not sensitivity or specificity of

an identified test

Kennedy N P, Feighery C. Clinical features of coeliac 

disease today. Biomedicine & Pharmacotherapy =

Biomedecine & Pharmacotherapie 2000;54(7):373-380. 

Not sensitivity or specificity of an identified test

Keogh J P, Zirvi K A, Vossough S et al. Pharmacological 

alterations of cellular transglutaminase activity and 

invasiveness in human colorectal carcinoma cells. Cancer

Biochemistry Biophysics 1993;13(3):209-220. Not 

sensitivity or specificity of an identified test 

Kepczyk T, Kadakia S C. Prospective evaluation of 

gastrointestinal tract in patients with iron-deficiency

anemia. Digestive Diseases and Sciences 1995;40(6):1283-

1289. Not sensitivity or specificity of an identified test 

Kepczyk T, Cremins J E, Long B D et al. A prospective, 

multidisciplinary evaluation of premenopausal women with 

iron-deficiency anemia. American Journal of

Gastroenterology 1999;94(1):109-115. Not sensitivity or 

specificity of an identified test

Kermabon C, Ehrhart A, Volant A et al. Antigliadin 

antibodies in rheumatoid arthritis. Rev Rhum Engl Ed

1993;60(3):157-161. Not sensitivity or specificity of an 

identified test 

Kerttula T O, Holm K, Partanen J et al. Circulating T 

lymphocyte subsets in coeliac disease (CoD) patients and 

healthy family members. Clinical and Experimental

Immunology 1998;111(3):536-540. Not sensitivity or 

specificity of an identified test

A-399
Kett K, Scott H, Fausa O et al. Secretory immunity in 

celiac disease: Cellular expression of immunoglobulin A 

subclass and joining chain. Gastroenterology

1990;99(2):386-392. Not sensitivity or specificity of an 

identified test 

Keuning J J, Pena A S, van Leeuwen A et al. HLA-DW3 

associated with coeliac disease. Lancet 1976;1(7958):506-

508. Not sensitivity or specificity of an identified test 

Keusch G T, Jacewicz M. Primary amines and chloroquine 

inhibit cytotoxic responses to Shigella toxin and permit late 

antibody rescue of toxin treated cells. Biochemical and

Biophysical Research Communications 1984;121(1):69-76. 

Not sensitivity or specificity of an identified test

Khoshoo V, Bhan M K, Arora N K. Gliadin antibodies for 

diagnosis of celiac disease. Indian Journal of Pediatrics 

1984;51(413):669-670. Not sensitivity or specificity of an

identified test 

Khoshoo V, Bhan M K, Puri S et al. Serum anti-gliadin

antibody profile in childhood protracted diarrhoea due to 

coeliac disease and other causes in a developing country. 

Scandinavian Journal of Gastroenterology

1989;24(10):1212-1216. Serology <1990 

Khoshoo V, Bhan M K, Unsworth D J et al. Anti-reticulin

antibodies: useful adjunct to histopathology in diagnosing 

celiac disease, especially in a developing country. Journal 

of Pediatric Gastroenterology and Nutrition 1988;7(6):864-

866. Not sensitivity or specificity of an identified test 

Khulusi S, Rhodes J. Diagnostic dilemmas in colitis. J R

Coll Phys London 1997;31(6):618-623. Not sensitivity or 

specificity of an identified test

Kieffer M. Serum antibodies to gliadin and other cereal 

proteins in patients with coeliac disease and dermatitis 

herpetiformis. Danish Medical Bulletin 1985;32(5):251-

262. Not sensitivity or specificity of an identified test 

Kieffer M, Barnetson R S. Increased gliadin antibodies in

dermatitis herpetiformis and pemphigoid. British Journal of 

Dermatology 1983;108(6):673-678. Not sensitivity or 

specificity of an identified test

Kieffer M, Barnetson StC R. What is the role of gliadin in

bullous pemphigoid?. Lancet 1981;2(8250):806Not 

sensitivity or specificity of an identified test 

Kieffer M, Barnetson R S, Blackwell J N. Sequential

studies of gliadin antibodies in patients with dermatitis 

herpetiformis. Archives of Dermatological Research 

1984;276(2):74-77. Not sensitivity or specificity of an 

identified test 

Kieffer M, Frazier P J, Daniels N W R. Serum antibodies 

(measured by MRSPAH) to alcohol-soluble gliadins in 

adult celiac patients. Journal of Immunological Methods 

1981;42(2):129-136. Not sensitivity or specificity of an 

identified test 

Kieslich M, Errazuriz G, Posselt H G et al. Brain whitematter lesions in celiac disease: a prospective study of 75

diet-treated patients. Pediatrics 2001;108(2):E21Not 

sensitivity or specificity of an identified test 

Kiguchi K, Iwamori M, Yamanouchi S et al. Coexpression 

of cholesterol sulfate and cytokeratin as tumor markers in 

well-differentiated squamous cell carcinoma of the human 

uterine cervix. Clinical Cancer Research - an Official

Journal of the American Association for Cancer Research

1998;4(12):2985-2990. Not sensitivity or specificity of an

identified test 

Kilander A F, Dotevall G, Fallstrom S P et al. Evaluation of

gliadin antibodies for detection of coeliac disease. 

Scandinavian Journal of Gastroenterology 1983;18(3):377-

383. Serology <1990 

Kilander A F, Dotevall G, Lindstedt G et al. Plasma

enteroglucagon related to malabsorption in coeliac disease.

Gut 1984;25(6):629-635. Not sensitivity or specificity of an 

identified test 

Kilander A F, Gillberg R E, Kastrup W et al. Serum

antibodies to gliadin and small-intestinal morphology in

dermatitis herpetiformis. A controlled clinical study of the 

effect of treatment with a gluten-free diet. Scandinavian

Journal of Gastroenterology 1985;20(8):951-958. Not 

sensitivity or specificity of an identified test 

Kilander A F, Nilsson L A, Gillberg R. Serum antibodies to 

gliadin in coeliac disease after gluten withdrawal.

Scandinavian Journal of Gastroenterology 1987;22(1):29-

34. Not sensitivity or specificity of an identified test 

Kilander A F, Stenhammar L, Lindstedt G et al. 

Determination of enteroglucagon in plasma for detection of

celiac disease in children. Clinical Chemistry 

1984;30(1):77-80. Not sensitivity or specificity of an 

identified test 

Kiljanski J I, Peele K, Stachura I et al. Antibodies against

striated muscle, connective tissue and nuclear antigens in

patients with thyroid-associated ophthalmopathy: Should 

Graves' disease be considered a collagen disorder?. J

Endocrinol Invest 1997;20(10):585-591. Not sensitivity or

specificity of an identified test

Kilmartin C, Lynch S, Abuzakouk M et al. Avenin fails to

induce a TH1 response in coeliac tissue following in vitro

culture. Gut 2003;52(1):47-52. Not sensitivity or specificity

of an identified test 

Kilpatrick Z M, Katz J. Occult celiac disease as a cause of 

iron deficiency anemia. Jama - the Journal of the American 

Medical Association 1969;208(6):999-1001. Not sensitivity

or specificity of an identified test

Kim H C, Idler W W, Kim I G et al. The complete amino 

acid sequence of the human transglutaminase K enzyme 

deduced from the nucleic acid sequences of cDNA clones. 

A-400
Journal of Biological Chemistry 1991;266(1):536-539. Not 

sensitivity or specificity of an identified test 

Kim H C, Nemes Z, Idler W W et al. Crystallization and 

preliminary X-ray analysis of human transglutaminase 3

from zymogen to active form. Journal of Structural Biology

2001;135(1):73-77. Not sensitivity or specificity of an 

identified test 

Kim Hyung, Rikihisa Yasuko. Roles of p38 mitogenactivated protein kinase, NF-kappaB, and protein kinase C 

in proinflammatory cytokine mRNA expression by human 

peripheral blood leukocytes, monocytes, and neutrophils in

response to Anaplasma phagocytophila. Infection and 

Immunity 2002;70(8):4132-4141. Not sensitivity or 

specificity of an identified test

Kim I G, Lee S C, Lee J H et al. Structure and organization 

of the human transglutaminase 3 gene: evolutionary

relationship to the transglutaminase family. Journal of

Investigative Dermatology 1994;103(2):137-142. Not 

sensitivity or specificity of an identified test 

Kim I G, McBride O W, Wang M et al. Structure and

organization of the human transglutaminase 1 gene. Journal 

of Biological Chemistry 1992;267(11):7710-7717. Not 

sensitivity or specificity of an identified test 

Kim S Y, Chung S I, Yoneda K et al. Expression of 

transglutaminase 1 in human epidermis. Journal of

Investigative Dermatology 1995;104(2):211-217. Not 

sensitivity or specificity of an identified test 

Kim S Y, Grant P, Lee J H et al. Differential expression of 

multiple transglutaminases in human brain. Increased 

expression and cross-linking by transglutaminases 1 and 2 

in Alzheimer's disease. Journal of Biological Chemistry

1999;274(43):30715-30721. Not sensitivity or specificity of 

an identified test

Kim Soo, Youl Jeitner, Thomas M et al. Transglutaminases 

in disease. Neurochemistry International 2002;40(1):85-

103. Not sensitivity or specificity of an identified test 

Kim Soo, Jeong Eun, Steinert Peter M. IFN-gamma 

induces transglutaminase 2 expression in rat small 

intestinal cells. Journal of Interferon & Cytokine Research - 

the Official Journal of the International Society for 

Interferon and Cytokine Research 2002;22(6):677-682. Not 

sensitivity or specificity of an identified test 

Kim Y J, Park E S, Song K Y et al. Glutathione transferase 

(class pi) and tissue transglutaminase (Tgase C) expression 

in pterygia. Korean Journal of Ophthalmology - Kjo 

1998;12(1):6-13. Not sensitivity or specificity of an 

identified test 

King A L, Ciclitira P J. Celiac disease: strongly heritable,

oligogenic, but genetically complex. Molecular Genetics 

and Metabolism 2000;71(1-2):70-75. Not sensitivity or

specificity of an identified test

King A L, Fraser J S, Moodie S J et al. Coeliac disease: 

follow-up linkage study provides further support for 

existence of a susceptibility locus on chromosome 11p11. 

Annals of Human Genetics 2001;65(Pt 4):377-386. Not 

sensitivity or specificity of an identified test 

King A L, Yiannakou J Y, Brett P M et al. A genome-wide 

family-based linkage study of coeliac disease. Annals of 

Human Genetics 2000;64(Pt 6):479-490. Not sensitivity or

specificity of an identified test

Kingham J G, Parker D R. The association between 

primary biliary cirrhosis and coeliac disease: a study of 

relative prevalences. Gut 1998;42(1):120-122. Not 

sensitivity or specificity of an identified test 

Kirberg A, Latorre J J, Hartard M E. Endoscopic small 

intestinal biopsy in infants and children: its usefulness in 

the diagnosis of celiac disease and other enteropathies. 

Journal of Pediatric Gastroenterology and Nutrition 

1989;9(2):178-181. Not sensitivity or specificity of an 

identified test 

Kirby J, Fielding J F. Very adult coeliac disease! The need

for jejunal biopsy in the middle aged and elderly. Irish 

Medical Journal 1984;77(2):35-36. Not sensitivity or 

specificity of an identified test

Kitahara A, Mikawa H, Ohtsuki H et al. Specific 

localization of tissue-type transglutaminase in 

adrenocorticotropin-producing cells of the human pituitary

gland as demonstrated by immunohistochemistry. Journal 

of Clinical Endocrinology and Metabolism 1987;65(5):885-

890. Not sensitivity or specificity of an identified test 

Kitis G, Lucas M L, Bishop H. Altered jejunal surface pH 

in coeliac disease: Its effect on propranolol and folic acid 

absorption. Clin Sci 1982;63(4):373-380. Not sensitivity or

specificity of an identified test

Klaeveman H L, Gebhard R L, Sessoms C et al. In vitro

studies of ulcerative ileojejunitis. Gastroenterology

1975;68(3):572-582. Not sensitivity or specificity of an 

identified test 

Klein M R, Keet I P M, D'Amaro J et al. Associations

between HLA frequencies and pathogenic features of 

human immunodeficiency virus type 1 infection in 

seroconverters from the Amsterdam cohort of homosexual 

men. J Infect Dis 1994;169(6):1244-1249. Not sensitivity

or specificity of an identified test

Kleinberg-Zissin R, Avigad S, Yahav J et al. Glutensensitive enteropathy: value of oral triglyceride loading test 

in the follow-up of patients on gluten challenge. Israel 

Journal of Medical Sciences 1983;19(4):319-324. Not 

sensitivity or specificity of an identified test 

Kleman J P, Aeschlimann D, Paulsson M et al. 

Transglutaminase-catalyzed cross-linking of fibrils of 

collagen V/XI in A204 rhabdomyosarcoma cells. 

Biochemistry 1995;34(42):13768-13775. Not sensitivity or

A-401
specificity of an identified test

Klemetti P, Savilahti E, Ilonen J et al. T-cell reactivity to 

wheat gluten in patients with insulin-dependent diabetes

mellitus. Scandinavian Journal of Immunology

1998;47(1):48-53. Not sensitivity or specificity of an 

identified test 

Klemola T. Immunohistochemical findings in the intestine 

of IgA-deficient persons: number of intraepithelial T

lymphocytes is increased. Journal of Pediatric 

Gastroenterology and Nutrition 1988;7(4):537-543. Not

sensitivity or specificity of an identified test 

Klemola T, Savilahti E, Arato A et al. 

Immunohistochemical findings in jejunal specimens from 

patients with IgA deficiency. Gut 1995;37(4):519-523. Not 

sensitivity or specificity of an identified test 

Klemola T, Savilahti E, Koskimies S et al. HLA antigens in 

IgA deficient paediatric patients. Tissue Antigens

1988;32(4):218-223. Not sensitivity or specificity of an 

identified test 

Kluge F, Koch H K, Grosse-Wilde H et al. Follow-up of 

treated adult celiac disease: clinical and morphological 

studies. Hepato-Gastroenterology 1982;29(1):17-23. Not 

sensitivity or specificity of an identified test 

Knight C J, Sandhu B K. The investigation of chronic 

diarrhoea. Curr Paediatr 2003;13(2):89-94. Not sensitivity

or specificity of an identified test

Knight C R, Rees R C, Platts A et al. Interleukin-2-

activated human effector lymphocytes mediate cytotoxicity

by inducing apoptosis in human leukaemia and solid 

tumour target cells. Immunology 1993;79(4):535-541. Not 

sensitivity or specificity of an identified test 

Knight R L, Hand D, Piacentini M et al. Characterization of 

the transglutaminase-mediated large molecular weight

polymer from rat liver: Its relationship to apoptosis. Eur J 

Cell Biol 1993;60(1):210-216. Not sensitivity or specificity

of an identified test 

Knudtzon J, Fluge G, Aksnes L. Routine measurements of 

gluten antibodies in children of short stature. Journal of

Pediatric Gastroenterology and Nutrition 1991;12(2):190-

194. Not sensitivity or specificity of an identified test 

Kobayashi H, Takahashi M, Takahashi H et al. CD4SUP+ 

T-cells from peripheral blood of a patient with psoriasis 

recognize keratin 14 peptide but not 'homologous'

streptococcal M-protein epitope. J Dermatol Sci 

2002;30(3):240-247. Not sensitivity or specificity of an 

identified test 

Kocak N, Varzikoglu M, Yuce A et al. Celiac disease in

childhood: Analysis of 41 cases. Turk J Gastroenterol 

1997;8(2):201-205. Not sensitivity or specificity of an 

identified test 

Kochanska-Dziurowicz A, Bukowska C. Estimation of 

serum beta-2-microglobulin in children with malabsorption 

disorders syndrome. Journal of Gastroenterology

1997;32(3):312-317. Not sensitivity or specificity of an 

identified test 

Kockum I, Lernmark A, Dahlquist G et al. Genetic and

immunological findings in patients with newly diagnosed 

insulin-dependent diabetes mellitus. The Swedish 

Childhood Diabetes Study Group and The Diabetes 

Incidence in Sweden Study (DISS) Group. Hormone and

Metabolic Research.Hormon- Und 

Stoffwechselforschung.Hormones Et Metabolisme 

1996;28(7):344-347. Not sensitivity or specificity of an 

identified test 

Kocna P, Fric P, Tlaskalova H et al. Short-term cultivation

of duodenal biopsies in patients with coeliac disease. Effect 

of gluten challenge and gliadin peptides. Advances in 

Experimental Medicine and Biology 1995;371b1367-1370. 

Not sensitivity or specificity of an identified test

Kocna Petr, Vanickova Zdislava, Perusicova Jindriska et al. 

Tissue transglutaminase-serology markers for coeliac

disease. Clinical Chemistry and Laboratory Medicine -

Cclm / Fescc 2002;40(5):485-492. Improper control group 

Koelle D M, Corey L, Burke R L et al. Antigenic

specificities of human CD4sup + T-cell clones recovered 

from recurrent genital herpes simplex virus type 2 lesions. J 

Virol 1994;68(5):2803-2810. Not sensitivity or specificity

of an identified test 

Koelle D M, Johnson M L, Ekstrom A N et al. Preferential 

presentation of herpes simplex virus T-cell antigen by HLA 

DQA1*0501/DQB1*0201 in comparison to HLA 

DQA1*0201/DQB1*0201. Human Immunology

1997;53(2):195-205. Not sensitivity or specificity of an 

identified test 

Kohl D, Ashkenazi A, Ben Shaul Y et al. Tight junctions of

jejunal surface and crypt cells in celiac disease: a freezefracture study. Journal of Pediatric Gastroenterology and 

Nutrition 1987;6(1):57-65. Not sensitivity or specificity of 

an identified test

Koivisto V A, Kuitunen P, Tiilikainen A et al. HLA 

antigens in patients with juvenile diabetes mellitus, coeliac 

disease and both of the diseases. Diabete & Metabolisme

1977;3(1):49-53. Not sensitivity or specificity of an 

identified test 

Koivisto V A, Kuitunen P, Tilikainen A et al. HLA 

antigens, especially B8 and BW15, in patients with juvenile

diabetes mellitus, coeliac disease, and both of these 

diseases [proceedings]. Diabete & Metabolisme

1976;2(3):161Not sensitivity or specificity of an identified

test 

Kojecky Z, Matlocha Z, Pelikan L. Disaccharidase and

LDH isoenzymes of intestinal mucosa. Clinical experiences 

in children and adults. Acta Univpalackiolomucfacmed 

A-402
1972;63(-):239-246. Not sensitivity or specificity of an 

identified test 

Kojima S, Inui T, Muramatsu H et al. Dimerization of 

midkine by tissue transglutaminase and its functional 

implication. Journal of Biological Chemistry 

1997;272(14):9410-9416. Not sensitivity or specificity of

an identified test

Kojima S, Nara K, Rifkin D B. Requirement for

transglutaminase in the activation of latent transforming 

growth factor-beta in bovine endothelial cells. J Cell Biol 

1993;121(2):439-448. Not sensitivity or specificity of an

identified test 

Kokkonen J, Haapalahti M, Laurila K et al. Cow's milk 

protein-sensitive enteropathy at school age. Journal of

Pediatrics 2001;139(6):797-803. Not sensitivity or

specificity of an identified test

Kokkonen J, Holm K, Karttunen T J et al. Children with 

untreated food allergy express a relative increment in the 

density of duodenal gammadelta+ T cells. Scandinavian

Journal of Gastroenterology 2000;35(11):1137-1142. Not 

sensitivity or specificity of an identified test 

Kokkonen J, Simila S, Vuolukka P. The incidence of

coeliac disease and pyloric stenosis in children in Northern

Finland. Ann Clin Res 1982;14(3):123-128. Not sensitivity

or specificity of an identified test

Kolacek S, Booth I W, Taylor C M. Food, mucosal 

immunity, and IgA nephropathy. Journal of Pediatric 

Gastroenterology and Nutrition 1990;11(2):175-178. Not

sensitivity or specificity of an identified test 

Kolek A, Fischerova E, Kos V et al. Application of ELISA 

method to determine antigliadin antibodies in children with 

coeliac disease. Acta Universitatis Palackianae

Olomucensis Facultatis Medicae 1989;122183-192. Not 

sensitivity or specificity of an identified test 

Kolek A, Vospe caron, Her caron et al. Occurrence of 

coeliac disease in children with Down Syndrome in north 

Moravia, Czech Republic. European Journal of Pediatrics 

2003;162(3):207-208. Not sensitivity or specificity of an

identified test 

Koletzko S, Burgin-Wolff A, Koletzko B et al. Prevalence

of coeliac disease in diabetic children and adolescents. A

multicentre study. European Journal of Pediatrics

1988;148(2):113-117. Not sensitivity or specificity of an

identified test 

Kolho K L, Farkkila M A, Savilahti E. Undiagnosed 

coeliac disease is common in Finnish adults. Scandinavian 

Journal of Gastroenterology 1998;33(12):1280-1283. Not 

sensitivity or specificity of an identified test 

Kolho K L, Tiitinen A, Tulppala M et al. Screening for 

coeliac disease in women with a history of recurrent 

miscarriage or infertility. British Journal of Obstetrics and 

Gynaecology 1999;106(2):171-173. Not sensitivity or 

specificity of an identified test

Kolopp-Sarda M N, Massin N, Gobert B et al. Humoral 

immune responses of workers occupationally exposed to 

wheat flour. Am J Ind Med 1994;26(5):671-679. Not 

sensitivity or specificity of an identified test 

Kong Y-C, Flynn J C, Wan Q et al. HLA and H2 class II

transgenic mouse models to study susceptibility and 

protection in autoimmune thyroid disease. Autoimmunity

2003;36(6-7):397-404. Not sensitivity or specificity of an

identified test 

Koninckx C R, Giliams J P, Polanco I et al. IgA antigliadin

antibodies in celiac and inflammatory bowel disease. 

Journal of Pediatric Gastroenterology and Nutrition 

1984;3(5):676-682. Serology <1990 

Koning F. Celiac disease and malignancy: an 

immunological basis?. Journal of Pediatric 

Gastroenterology and Nutrition 1997;24(5):S18-S19. Not 

sensitivity or specificity of an identified test 

Koning F. Immunotherapy of celiac disease: fact or

fallacy?. Netherlands Journal of Medicine 2002;60(7):305-

306. Not sensitivity or specificity of an identified test 

Kontakou M, Przemioslo R T, Sturgess R P et al. 

Expression of tumour necrosis factor-alpha, interleukin-6, 

and interleukin-2 mRNA in the jejunum of patients with 

coeliac disease. Scandinavian Journal of Gastroenterology

1995;30(5):456-463. Not sensitivity or specificity of an 

identified test 

Kontakou M, Przemioslo R T, Sturgess R P et al. Cytokine 

mRNA expression in the mucosa of treated coeliac patients 

after wheat peptide challenge. Gut 1995;37(1):52-57. Not 

sensitivity or specificity of an identified test 

Kontakou M, Sturgess R P, Przemioslo R T et al. Detection

of interferon gamma mRNA in the mucosa of patients with

coeliac disease by in situ hybridisation. Gut

1994;35(8):1037-1041. Not sensitivity or specificity of an

identified test 

Kontiainen S, Schlenzka A, Koskimies S et al.

Autoantibodies and autoimmune diseases in young 

diabetics. Diabetes Research (Edinburgh, Lothian)

1990;13(4):151-156. Not sensitivity or specificity of an 

identified test 

Koop I, Bozkurt T, Adler G et al. Plasma cholecystokinin 

and pancreatic enzyme secretion in patients with coeliac

sprue. Zeitschrift Fur Gastroenterologie 1987;25(2):124-

129. Not sensitivity or specificity of an identified test 

Koop I, Ilchmann R, Izzi L et al. Detection of

autoantibodies against tissue transglutaminase in patients 

with celiac disease and dermatitis herpetiformis. American 

Journal of Gastroenterology 2000;95(8):2009-2014. 

Improper control group 

A-403
Koot V C, Van Straaten M, Hekkens W T et al. Elevated

level of IgA gliadin antibodies in patients with rheumatoid 

arthritis. Clinical and Experimental Rheumatology

1989;7(6):623-626. Not sensitivity or specificity of an 

identified test 

Kordonouri O, Dieterich W, Schuppan D et al. 

Autoantibodies to tissue transglutaminase are sensitive 

serological parameters for detecting silent coeliac disease 

in patients with Type 1 diabetes mellitus. Diabetic

Medicine - a Journal of the British Diabetic Association 

2000;17(6):441-444. Improper control group 

Korhonen M, Ormio M, Burgeson R E et al. Unaltered

distribution of laminins, fibronectin, and tenascin in celiac

intestinal mucosa. Journal of Histochemistry and 

Cytochemistry - Official Journal of the Histochemistry

Society 2000;48(7):1011-1020. Not sensitivity or

specificity of an identified test

Korponay-Szabo I R, Dahlbom I, Laurila K et al. Elevation

of IgG antibodies against tissue transglutaminase as a 

diagnostic tool for coeliac disease in selective IgA 

deficiency. Gut 2003;52(11):1567-1571. Improper control 

group 

Korponay-Szabo I R, Kovacs J B, Czinner A et al. High 

prevalence of silent celiac disease in preschool children

screened with IgA/IgG antiendomysium antibodies. Journal 

of Pediatric Gastroenterology and Nutrition 1999;28(1):26-

30. Not sensitivity or specificity of an identified test 

Korponay-Szabo I R, Kovacs J B, Lorincz M et al. 

Prospective significance of antiendomysium antibody

positivity in subsequently verified celiac disease. Journal of 

Pediatric Gastroenterology and Nutrition 1997;25(1):56-63. 

Improper control group 

Korponay-Szabo I R, Kovacs J B, Lorincz M et al. The 

human appendix: A composite substrate for antiendomysium, anti-reticulin and anti-bowel antibody testing 

in coeliac disease. Med Sci Monit 1997;3(3):285-289. Not 

sensitivity or specificity of an identified test 

Korponay-Szabo I R, Laurila K, Szondy Z et al. Missing 

endomysial and reticulin binding of coeliac antibodies in

transglutaminase 2 knockout tissues. Gut 2003;52(2):199-

204. Not sensitivity or specificity of an identified test 

Korponay-Szabo I R, Sulkanen S, Halttunen T et al. Tissue 

transglutaminase is the target in both rodent and primate 

tissues for celiac disease-specific autoantibodies. Journal of 

Pediatric Gastroenterology and Nutrition 2000;31(5):520-

527. Not sensitivity or specificity of an identified test 

Korponay-Szabo I, Kovacs J, Lorincz M et al. Families 

with multiple cases of gluten-sensitive enteropathy.

Zeitschrift Fur Gastroenterologie 1998;36(7):553-558. Not 

sensitivity or specificity of an identified test 

Kortsik C S, Freudenberg N, Riede U et al. Lectin binding

sites and immunocytochemical characterization of normal 

pleural mesothelium. General & Diagnostic Pathology

1995;141(2):141-146. Not sensitivity or specificity of an

identified test 

Kosnai I, Kuitunen P, Savilahti E. Cell kinetics in the 

jejunal crypt epithelium in malabsorption syndrome with 

cow's milk protein intolerance and in coeliac disease of

childhood. Gut 1980;21(12):1041-1046. Not sensitivity or 

specificity of an identified test

Kosnai I, Kuitunen P, Siimes M A. Iron deficiency in 

children with coeliac disease on treatment with gluten-free 

diet. Role of intestinal blood loss. Arch Dis Child 

1979;54(5):375-378. Not sensitivity or specificity of an 

identified test 

Kosnai I, Kuitunen P, Savilahti E et al. Mast cells and 

eosinophils in the jejunal mucosa of patients with intestinal 

cow's milk allergy and celiac disease of childhood. Journal 

of Pediatric Gastroenterology and Nutrition 1984;3(3):368-

372. Unable to extract data 

Koster-Kamphuis L, van Straaten E A, Kors W A et al. 

Urinary NOx:creatinine ratios during gluten challenge in

children with celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 2003;36(3):372-375. Not

sensitivity or specificity of an identified test 

Kotze Lorete, Maria da, Silva Utiyama et al. IgA class antiendomysial and anti-tissue transglutaminase antibodies in

relation to duodenal mucosa changes in coeliac disease. 

Pathology 2003;35(1):56-60. Improper control group 

Kotze L M, Utiyama S R, Nisihara R M et al.

Antiendomysium antibodies in Brazilian patients with 

celiac disease and their first-degree relatives. Arquivos De 

Gastroenterologia 2001;38(2):94-103. Improper control 

group 

Kowalska E, Wasowska-Krolikowska K, ToporowskaKowalska E. Estimation of antithyroid antibodies 

occurrence in children with coeliac disease. Medical

Science Monitor - International Medical Journal of 

Experimental and Clinical Research 2000;6(4):719-721. 

Not sensitivity or specificity of an identified test

Krasilnikoff P A, Gudman-Hoyer E, Moltke H H.

Diagnostic value of disaccharide tolerance tests in children. 

Acta Paediatrica Scandinavica 1975;64(5):693-698. Not 

sensitivity or specificity of an identified test 

Kraut J R, Lloyd-Still J D. The 1-hr blood xylose test in the 

evaluation of malabsorption in infants and children. 

American Journal of Clinical Nutrition 1980;33(11):2328-

2333. Not sensitivity or specificity of an identified test 

Krawitt E L, Beeken W L. Limitations of the usefulness of 

the d-xylose absorption test. American Journal of Clinical

Pathology 1975;63(2):261-263. Not sensitivity or

specificity of an identified test

A-404
Krig S R, Rice R H. TCDD suppression of tissue 

transglutaminase stimulation by retinoids in malignant 

human keratinocytes. Toxicol Sci 2000;56(2):357-364. Not 

sensitivity or specificity of an identified test 

Krig S R, Chandraratna R A S, Chang M M J et al. Genespecific TCDD suppression of RARalpha- and RXRmediated induction of tissue transglutaminase. Toxicol Sci 

2002;68(1):102-108. Not sensitivity or specificity of an 

identified test 

Krilis S A, Macpherson J L, de Carle D J et al. Small bowel

mucosa from celiac patients generates 15-

hydroxyeicosatetraenoic acid (15-HETE) after in vitro 

challenge with gluten. Journal of Immunology (Baltimore, 

Md.- 1950) 1986;137(12):3768-3771. Not sensitivity or

specificity of an identified test

Krupickova S, Tuckova L, Flegelova Z et al. Identification

of common epitopes on gliadin, enterocytes, and

calreticulin recognised by antigliadin antibodies of patients

with coeliac disease. Gut 1999;44(2):168-173. Not 

sensitivity or specificity of an identified test 

Kubilus J, Baden H P. Isolation of two immunologically

related transglutaminase substrates from cultured human 

keratinocytes. In Vitro 1982;18(5):447-455. Not sensitivity

or specificity of an identified test

Kubilus J, Kvedar J, Baden H P. Identification of new 

components of the cornified envelope of human and bovine

epidermis. Journal of Investigative Dermatology

1987;89(1):44-50. Not sensitivity or specificity of an 

identified test 

Kucera P, Novakova D, Behanova M et al. Gliadin, 

endomysial and thyroid antibodies in patients with latent 

autoimmune diabetes of adults (LADA). Clinical and 

Experimental Immunology 2003;133(1):139-143. Not 

sensitivity or specificity of an identified test 

Kudo S. Role of sperm head syndecan at fertilization in 

fish. Journal of Experimental Zoology 1998;281(6):620-

625. Not sensitivity or specificity of an identified test 

Kuitunen M, Savilahti E. Gut permeability to human alphalactalbumin, beta-lactoglobulin, mannitol, and lactulose in 

celiac disease. Journal of Pediatric Gastroenterology and 

Nutrition 1996;22(2):197-204. Not sensitivity or specificity

of an identified test 

Kuitunen Mikael, Saukkonen Tero, Ilonen Jorma et al. 

Intestinal permeability to mannitol and lactulose in children

with type 1 diabetes with the HLA-DQB1*02 allele. 

Autoimmunity 2002;35(5):365-368. Not sensitivity or 

specificity of an identified test

Kuitunen P, Kosnai I, Savilahti E. Morphometric study of

the jejunal mucosa in various childhood enteropathies with

special reference to intraepithelial lymphocytes. Journal of

Pediatric Gastroenterology and Nutrition 1982;1(4):525-

531. Unable to extract data 

Kuitunen P, Visakorpi J K, Savilahti E et al. Malabsorption 

syndrome with cow's milk intolerance. Clinical findings 

and course in 54 cases. Archives of Disease in Childhood 

1975;50(5):351-356. Not sensitivity or specificity of an 

identified test 

Kuks J B M, Lems S P M, Oosterhuis H J G H. HLA type 

is not indicative for the effect of thymectomy in myasthenia

gravis. J Neuroimmunol 1992;36(2-3):217-224. Not 

sensitivity or specificity of an identified test 

Kull K, Uibo O, Salupere R et al. High frequency of 

antigliadin antibodies and absence of antireticulin and 

antiendomysium antibodies in patients with ulcerative 

colitis. Journal of Gastroenterology 1999;34(1):61-65. Not 

sensitivity or specificity of an identified test 

Kumar P, Bartram C I. Relevance of the barium followthrough examination in the diagnosis of adult celiac 

disease. Gastrointestinal Radiology 1979;4(3):285-289. Not 

sensitivity or specificity of an identified test 

Kumar P, Clark M. Primary biliary cirrhosis and coeliac

disease. Is there an association?. Digestive and Liver 

Disease - Official Journal of the Italian Society of 

Gastroenterology and the Italian Association for the Study

of the Liver 2002;34(4):248-250. Not sensitivity or 

specificity of an identified test

Kumar P J. European and North American populations 

should be screened for coeliac disease. Gut 

2003;52(2):170-171. Not sensitivity or specificity of an 

identified test 

Kumar P J. Clinial pathology of celiac disease. Curr Opin 

Gastroenterol 1991;7(2):232-235. Review article 

Kumar P J, Ferguson A, Lancaster-Smith M et al. Food 

antibodies in patients with dermatitis herpetiformis and 

adult coeliac disease - relationship to jejunal morphology.

Scandinavian Journal of Gastroenterology 1976;11(1):5-9. 

Not sensitivity or specificity of an identified test

Kumar P J, O'Donoghue D P, Stenson K et al. 

Reintroduction of gluten in adults and children with treated

coeliac disease. Gut 1979;20(9):743-749. Not sensitivity or 

specificity of an identified test

Kumar P J, Silk D B A, Marks R. Functional and

morphological changes in response to a gluten free diet and 

corticosteroids in dermatitis herpetiformis and adult coeliac 

disease. Br J Dermatol 1973;89(Suppl 9):13Not sensitivity

or specificity of an identified test

Kumar P J, Silk D B, Rousseau B et al. Assessment of 

jejunal function in patients with dermatitis herpetiformis 

and adult coeliac disease using a perfusion technique. 

Scandinavian Journal of Gastroenterology 1974;9(8):793-

798. Not sensitivity or specificity of an identified test 

Kumar P J, Walker-Smith J, Milla P et al. The teenage

A-405
coeliac: Follow up study of 102 patients. Arch Dis Child

1988;63(8):916-920. Not sensitivity or specificity of an 

identified test 

Kumar R, Lumsden A, Ciclitira P J et al. Human genome 

search in celiac disease using gliadin cDNA as probe. J

Mol Biol 2000;300(5):1155-1167. Not sensitivity or 

specificity of an identified test

Kumar Rajesh, Eastwood Amy L, Brown Milton L et al. 

Human genome search in celiac disease: mutated gliadin Tcell-like epitope in two human proteins promotes T-cell 

activation. Journal of Molecular Biology 2002;319(3):593-

602. Not sensitivity or specificity of an identified test 

Kumar V, Beutner E H, Chorzelski T P. Antiendomysial 

antibody--useful serological indicator of dermatitis 

herpetiformis. Archives of Dermatological Research 

1987;279(7):454-458. Not sensitivity or specificity of an

identified test 

Kumar V, Beutner E H, Chorzelski T P. Distribution of 

monkey esophagus antigens reactive with IgA-class 

antibodies in the sera of dermatitis herpetiformis patients. 

Archives of Dermatological Research 1984;276(5):293-

296. Not sensitivity or specificity of an identified test 

Kumar V, Hemedinger E, Chorzelski T P et al. Reticulin 

and endomysial antibodies in bullous diseases. Comparison 

of specificity and sensitivity. Archives of Dermatology 

1987;123(9):1179-1182. Not sensitivity or specificity of an 

identified test 

Kumar V, Jain N, Beutner E H et al. Detection of 

antigliadin antibodies in bullous diseases and their 

recognition of similar antigenic polypeptides. International 

Archives of Allergy and Applied Immunology

1987;83(2):155-159. Not sensitivity or specificity of an 

identified test 

Kumar V, Jain N, Lerner A et al. Comparative studies of 

different gliadin preparations in detecting antigliadin 

antibodies. Journal of Pediatric Gastroenterology and 

Nutrition 1986;5(5):730-734. Not sensitivity or specificity

of an identified test 

Kumar V, Jarzabek-Chorzelska M, Sulej J et al. Celiac 

disease and immunoglobulin a deficiency: how effective 

are the serological methods of diagnosis?. Clinical and 

Diagnostic Laboratory Immunology 2002;9(6):1295-1300. 

Improper control group 

Kumar V, Jarzabek-Chorzelska M, Sulej J et al. Tissue 

transglutaminase and endomysial antibodies-diagnostic 

markers of gluten-sensitive enteropathy in dermatitis 

herpetiformis. Clinical Immunology (Orlando, Fla.) 

2001;98(3):378-382. Not sensitivity or specificity of an 

identified test 

Kumar V, Rajadhyaksha M, Wortsman J. Celiac diseaseassociated autoimmune endocrinopathies. Clinical and

Diagnostic Laboratory Immunology 2001;8(4):678-685. 

Not sensitivity or specificity of an identified test

Kumar V, Zane H, Kaul N. Serologic markers of glutensensitive enteropathy in bullous diseases. Archives of 

Dermatology 1992;128(11):1474-1478. Not sensitivity or 

specificity of an identified test

Kuncio G S, Tsyganskaya M, Zhu J et al. TNF-alpha 

modulates expression of the tissue transglutaminase gene in

liver cells. American Journal of Physiology 1998;274(2 Pt 

1):G240-G245. Not sensitivity or specificity of an 

identified test 

Kundakc cedil, Oskay T, Olmez U et al. Association of

psoriasis vulgaris with HLA class I and class II antigens in 

the Turkish population, according to the age at onset. Int J 

Dermatol 2002;41(6):345-348. Not sensitivity or specificity

of an identified test 

Kurki P, Heliovaara M, Palosou T et al. Food intolerance 

and rheumatoid arthritis. Lancet 1988;2(8625):1419-1420. 

Not sensitivity or specificity of an identified test

Kuscu N K, Akcali S, Kucukmetin N T. Celiac disease and 

polycystic ovary syndrome. Int J Gynecol Obstet 

2002;79(2):149-150. Not sensitivity or specificity of an 

identified test 

Kutlu T, Brousse N, Rambaud C et al. Numbers of T cell 

receptor (TCR) alpha beta+ but not of TcR gamma delta+

intraepithelial lymphocytes correlate with the grade of 

villous atrophy in coeliac patients on a long term normal 

diet. Gut 1993;34(2):208-214. Improper control group 

Kvedar J C, Manabe M, Phillips S B et al. Characterization

of sciellin, a precursor to the cornified envelope of human 

keratinocytes. Differentiation 1992;Research in Biological 

Diversity; 49(3):195-204. Not sensitivity or specificity of

an identified test

Kvedar J C, Pion I A, Bilodeau E B et al. Detection of 

substrates of keratinocyte transglutaminase in vitro and in 

vivo using a monoclonal antibody to dansylcadaverine. 

Biochemistry 1992;31(1):49-56. Not sensitivity or

specificity of an identified test

Kwok W W, Nepom G T, Raymond F C. HLA-DQ 

polymorphisms are highly selective for peptide binding 

interactions. Journal of Immunology (Baltimore, Md.- 

1950) 1995;155(5):2468-2476. Not sensitivity or specificity

of an identified test 

Kwok W W, Schwarz D, Nepom B S et al. HLA-DQ 

molecules from alpha-beta heterodimers of mixed allotype. 

J Immunol 1988;141(9):3123-3127. Not sensitivity or 

specificity of an identified test

Kwok W W, Thurtle P, Nepom G T. A genetically

controlled pairing anomaly between HLA-DQalpha and 

HLA-DQbeta chains. J Immunol 1989;143(11):3598-3601. 

Not sensitivity or specificity of an identified test

A-406
L'Hirondel C, Doe W F, Peters T J. Biochemical and 

morphological studies on human jejunal mucosa 

maintained in culture. Clinical Science and Molecular 

Medicine 1976;50(5):425-429. Not sensitivity or specificity

of an identified test 

L'Hirondel C, Doe W F, Peters T J. Proceedings: Use of an

improved jejunal culture system for the study of normal 

and coeliac mucosa. Gut 1975;16(5):392Not sensitivity or 

specificity of an identified test

La Seta F, Salerno G, Buccellato A et al. Radiographic 

indicants of adult celiac disease assessed by doublecontrast small bowel enteroclysis. European Journal of

Radiology 1992;15(2):157-162. Not sensitivity or

specificity of an identified test

Labate A, Gambardella A, Messina D et al. Silent celiac 

disease in patients with childhood localization-related

epilepsies. Epilepsia 2001;42(9):1153-1155. Not sensitivity

or specificity of an identified test

Labo G, Gasbarrini G, Migli F et al. Thelio-and 

propriolymphocytes count in normal subjects and in 

primary and secondary enteropathy. G.e.n 1978;32(4):403-

417. Not sensitivity or specificity of an identified test 

LaCelle P T, Lambert A, Ekambaram M C et al. In vitro

cross-linking of recombinant human involucrin. Skin 

Pharmacology and Applied Skin Physiology 1998;11(4-

5):214-226. Not sensitivity or specificity of an identified

test 

Lagerqvist C, Ivarsson A, Juto P et al. Screening for adult 

coeliac disease - which serological marker(s) to use?.

Journal of Internal Medicine 2001;250(3):241-248. 

Improper control group 

Lagrange M, Ferrero J M, Lagrange J L et al. Nonspecifically labelled cells that simulate bone marrow 

metastases in patients with non-metastatic breast cancer. 

Journal of Clinical Pathology 1997;50(3):206-211. Not 

sensitivity or specificity of an identified test 

Lahat E, Broide E, Leshem M et al. Prevalence of celiac 

antibodies in children with neurologic disorders. Pediatr

Neurol 2000;22(5):393-396. Not sensitivity or specificity

of an identified test 

Lahat N, Be-Nun A, Cohen L et al. T cell receptor 

repertoire in the peripheral blood and intestinal mucosa of

coeliac patients. Clinical and Experimental Immunology

1995;101(3):422-427. Not sensitivity or specificity of an

identified test 

Lahdeaho M L, Lehtinen M, Rissa H R et al. Antipeptide 

antibodies to adenovirus E1b protein indicate enhanced risk 

of celiac disease and dermatitis herpetiformis. International

Archives of Allergy and Immunology 1993;101(3):272-

276. Not sensitivity or specificity of an identified test 

Lahteenoja H, Maki M, Viander M et al. Local challenge of

oral mucosa with gliadin in patients with coeliac disease.

Clinical and Experimental Immunology 2000;120(1):38-45. 

Not sensitivity or specificity of an identified test

Lahteenoja H, Toivanen A, Raiha I et al. Salivary 

antigliadin and antiendomysium antibodies in coeliac 

disease. Scandinavian Journal of Immunology

1999;50(5):528-535. Not sensitivity or specificity of an 

identified test 

Lahteenoja H, Toivanen A, Viander M et al. Oral mucosal 

changes in coeliac patients on a gluten-free diet. European

Journal of Oral Sciences 1998;106(5):899-906. Not 

sensitivity or specificity of an identified test 

Lahteenoja H, Toivanen A, Viander M et al. Increase in Tcell subsets of oral mucosa: a late immune response in 

patients with treated coeliac disease?. Scandinavian Journal

of Immunology 2000;52(6):602-608. Not sensitivity or

specificity of an identified test

Lai T S, Bielawska A, Peoples K A et al. 

Sphingosylphosphocholine reduces the calcium ion 

requirement for activating tissue transglutaminase. Journal 

of Biological Chemistry 1997;272(26):16295-16300. Not 

sensitivity or specificity of an identified test 

Lai T S, Hausladen A, Slaughter T F et al. Calcium 

regulates S-nitrosylation, denitrosylation, and activity of

tissue transglutaminase. Biochemistry 2001;40(16):4904-

4910. Not sensitivity or specificity of an identified test 

Lai T S, Slaughter T F, Koropchak C M et al. C-terminal

deletion of human tissue transglutaminase enhances 

magnesium-dependent GTP/ATPase activity. Journal of

Biological Chemistry 1996;271(49):31191-31195. Not 

sensitivity or specificity of an identified test 

Lai T S, Slaughter T F, Peoples K A et al. Regulation of 

human tissue transglutaminase function by magnesiumnucleotide complexes. Identification of distinct binding 

sites for Mg-GTP and Mg-ATP. Journal of Biological 

Chemistry 1998;273(3):1776-1781. Not sensitivity or 

specificity of an identified test

Lamabadusuriya S P, Packer S, Harries J T. Limitations of 

xylose tolerance test as a screening procedure in childhood 

coeliac disease. Archives of Disease in Childhood

1975;50(1):34-39. Not sensitivity or specificity of an 

identified test 

Lamabadusuriya S P, Packer S, Harries J T. Proceedings:

Limitations of xylose tolerance test as screening procedure 

for coeliac disease. Archives of Disease in Childhood 

1974;49(3):244-245. Not sensitivity or specificity of an 

identified test 

Lampasona V, Bazzigaluppi E, Barera G et al. Tissue 

transglutaminase and combined screening for coeliac

disease and type 1 diabetes-associated autoantibodies.

Lancet 1998;352(9135):1192-1193. Not sensitivity or 

specificity of an identified test

A-407
Lampasona V, Bonfanti R, Bazzigaluppi E et al. Antibodies 

to tissue transglutaminase C in type I diabetes. 

Diabetologia 1999;42(10):1195-1198. Not sensitivity or

specificity of an identified test

Lancaster Smith M, Kumar P, Marks R.

Immunofluorescence of the jejunal mucosa in dermatitis 

herpetiformis and adult coeliac disease. Br J Dermatol 

1973;89(Suppl 9):13-14. Not sensitivity or specificity of an 

identified test 

Lancaster-Smith M, Joyce S, Kumar P. Immunoglobulins 

in the jejunal mucosa in adult coeliac disease and dermatitis 

herpetiformis after the reintroduction of dietary gluten. Gut 

1977;18(11):887-891. Not sensitivity or specificity of an

identified test 

Lancaster-Smith M, Kumar P, Clark M L et al.

Antireticulin antibodies in dermatitis herpetiformis and 

adult coeliac disease. Their relationship to a gluten free diet

and jejunal histology. British Journal of Dermatology 

1975;92(1):37-42. Not sensitivity or specificity of an 

identified test 

Lancaster-Smith M, Packer S, Kumar P J et al.

Immunological phenomena in the jejunum and serum after

reintroduction of dietary gluten in children with treated 

coeliac disease. Journal of Clinical Pathology

1976;29(7):592-597. Not sensitivity or specificity of an 

identified test 

Landini M P, Lazzarotto T, La Placa M. The immune 

response to human cytomegalovirus-induced early nuclear

and early membrane antigens and its possible clinical

significance. Journal of Infection 1984;9(3):257-263. Not 

sensitivity or specificity of an identified test 

Lang C C, Brown R M, Kinirons M T et al. Decreased 

intestinal CYP3A in celiac disease: reversal after successful

gluten-free diet: a potential source of interindividual 

variability in first-pass drug metabolism. Clinical

Pharmacology and Therapeutics 1996;59(1):41-46. Not 

sensitivity or specificity of an identified test 

Langman M J, Banwell J G, Stewart J S et al. ABO blood 

groups, secretor status, and intestinal alkaline phosphatase 

concentrations in patients with celiac disease.

Gastroenterology 1969;57(1):19-23. Not sensitivity or 

specificity of an identified test

Lankisch P G, Martinez Schramm A, Petersen F et al.

Diagnostic intervals for recognizing celiac disease. 

Zeitschrift Fur Gastroenterologie 1996;34(8):473-477. Not 

sensitivity or specificity of an identified test 

Lanspa S J, Chan A T, Bell J S et al. Pathogenesis of 

steatorrhea in primary biliary cirrhosis. Hepatology

(Baltimore, Md.) 1985;5(5):837-842. Not sensitivity or 

specificity of an identified test

Lape M L, Baker J A, Chan J K. A comparison of

immunofluorescent assays to detect anti-granulocyte 

antibodies. American Journal of Clinical Pathology

1985;84(4):464-468. Not sensitivity or specificity of an 

identified test 

Lapini M, Lasagni D, Ferrari R. Detection of anti-smooth 

muscle antibodies in the sera of patients with celiac 

disease: Relationship with anti-endomysium antibodies. 

Eur J Lab Med 1998;6(3):174-176. Not sensitivity or 

specificity of an identified test

Lardy N M, Bakas R M, Van der et al. CIS-acting 

regulatory elements abrogate allele-specific HLA class I 

gene expression in healthy individuals. J Immunol 

1992;148(8):2572-2577. Not sensitivity or specificity of an 

identified test 

Larizza D, Calcaterra V, De Giacomo C et al. Celiac 

disease in children with autoimmune thyroid disease. 

Journal of Pediatrics 2001;139(5):738-740. Not sensitivity

or specificity of an identified test

Larizza D, Calcaterra V, Luinetti O et al. Evidence for

immunogenetic predisposition in children with celiac 

disease and autoimmune thyroid disease. Int J Med Biol 

Environ 2001;29(2):143-148. Not sensitivity or specificity

of an identified test 

Larizza D, Martinetti M, Lorini R et al. Parental

segregation of autoimmunity in patients with Turner's 

syndrome: Preferential paternal transmission?. J

Autoimmun 1999;12(1):65-72. Not sensitivity or specificity

of an identified test 

Lasagni D, Ferrari R, Lapini M. Unmasking antiendomysial antibodies in coeliac subjects positive for antismooth muscle antibodies. Acta Paediatrica (Oslo, Norway

- 1992) 1999;88(4):462-464. Not sensitivity or specificity

of an identified test 

Latham S, Becket A J, Chapell D A. Further modifications

in the children's jejunal biopsy capsule. British Medical 

Journal 1969;2(651):243Not sensitivity or specificity of an 

identified test 

Laurent J, Branellec A, Heslan J M et al. An increase in

circulating IgA antibodies to gliadin in IgA mesangial 

glomerulonephritis. American Journal of Nephrology

1987;7(3):178-183. Not sensitivity or specificity of an 

identified test 

Laurie G W, Ciclitira P J, Ellis H J et al. Immunological 

and partial sequence identity of mouse BM180 with wheat 

alpha-gliadin. Biochemical and Biophysical Research 

Communications 1995;217(1):10-15. Not sensitivity or

specificity of an identified test

Laurin P, Falth-Magnusson K, Sundqvist T. Increase in 

nitric oxide urinary products during gluten challenge in

children with coeliac disease. Scandinavian Journal of

Gastroenterology 2003;38(1):55-60. Not sensitivity or 

specificity of an identified test

A-408
Laurin Pia, Wolving Mats, Falth-Magnusson Karin. Even

small amounts of gluten cause relapse in children with 

celiac disease. Journal of Pediatric Gastroenterology and 

Nutrition 2002;34(1):26-30. Not sensitivity or specificity of 

an identified test

Lauritsen K B, Lauritzen J B, Christensen K C. Gastric 

inhibitory polypeptide and insulin release in response to 

oral and intravenous glucose in coeliac disease.

Scandinavian Journal of Gastroenterology 1982;17(2):241-

245. Not sensitivity or specificity of an identified test 

Lauritzen A F. Distinction between cells in serous effusions 

using a panel of antibodies. Virchows Archiv.A, 

Pathological Anatomy and Histopathology

1987;411(3):299-304. Not sensitivity or specificity of an

identified test 

Lavo B, Knutson F, Knutson L et al. Jejunal secretion of 

secretory immunoglobulins and gliadin antibodies in celiac 

disease. Digestive Diseases and Sciences 1992;37(1):53-59. 

Not sensitivity or specificity of an identified test

Lavo B, Knutson L, Loof L et al. Signs of increased 

leakage over the jejunal mucosa during gliadin challenge of

patients with coeliac disease. Gut 1990;31(2):153-157. Not 

sensitivity or specificity of an identified test 

Lawler M, Humphries P, O'Farrelly C et al. Adenovirus 12 

E1A gene detection by polymerase chain reaction in both 

the normal and coeliac duodenum. Gut 1994;35(9):1226-

1232. Not sensitivity or specificity of an identified test 

Lazzari R, Volta U, Bianchi F B et al. R1 reticulin

antibodies: markers of celiac disease in children on a 

normal diet and on gluten challenge. Journal of Pediatric 

Gastroenterology and Nutrition 1984;3(4):516-522. Not

sensitivity or specificity of an identified test 

Le Quellec A, Clapie M, Callamand P et al. Circulating

oxyntomodulin-like immunoreactivity in healthy children

and children with celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 1998;27(5):513-518. Not

sensitivity or specificity of an identified test 

Le Tourneau A, Audouin J, Diebold J. Ultrastructural study

of 4 cases of Ki-1 positive large anaplastic cell malignant 

lymphoma. Virchows Archiv.A, Pathological Anatomy and

Histopathology 1988;413(3):215-222. Not sensitivity or

specificity of an identified test

Lebenthal E, Branski D. Childhood celiac disease--a 

reappraisal. Journal of Pediatrics 1981;98(5):681-690. Not 

sensitivity or specificity of an identified test 

Lebenthal E, Heitlinger L A. Gliadin antibodies in celiac 

disease. Journal of Pediatrics 1983;102(5):711-712. Not 

sensitivity or specificity of an identified test 

Lebenthal E, Antonowicz I, Shwachman H. The 

interrelationship of enterokinase and trypsin activities in 

intractable diarrhea of infancy, celiac disease, and 

intravenous alimentation. Pediatrics 1975;56(4):585-591. 

Not sensitivity or specificity of an identified test

Lebenthal Emanuel, Branski David. Serum anti-endomysial 

and anti-tissue transglutaminase for screening of celiac 

disease. Israel Medical Association Journal - Imaj 

2002;4(8):627-628. Not sensitivity or specificity of an 

identified test 

Lee C H, Lee S K, Chi J G et al. Immunohistochemical 

evaluation of transglutaminase C in tumours of salivary 

glands. European Journal of Cancer.Part B, Oral Oncology

1996;32b(6):401-406. Not sensitivity or specificity of an

identified test 

Lee F I, Prior J, Murray S M. Celiac disease in 

monozygous twin boys. Asynchronous presentation. 

Digestive Diseases and Sciences 1982;27(12):1137-1140. 

Not sensitivity or specificity of an identified test

Lee J H, Jang S I, Yang J M et al. The proximal promoter 

of the human transglutaminase 3 gene. Stratified squamous 

epithelial-specific expression in cultured cells is mediated

by binding of Sp1 and ets transcription factors to a 

proximal promoter element. Journal of Biological 

Chemistry 1996;271(8):4561-4568. Not sensitivity or 

specificity of an identified test

Lee K H, Wucherpfennig K W, Wiley D C. Structure of a 

human insulin peptide-HLA-DQ8 complex and 

susceptibility to type 1 diabetes. Nature Immunology

2001;2(6):501-507. Not sensitivity or specificity of an 

identified test 

Lee K N, Arnold S A, Birckbichler P J et al. Site-directed 

mutagenesis of human tissue transglutaminase: Cys-277 is 

essential for transglutaminase activity but not for GTPase 

activity. Biochimica Et Biophysica Acta 1993;1202(1):1-6. 

Not sensitivity or specificity of an identified test

Lee K N, Birckbichler P J, Fesus L. Purification of human

erythrocyte transglutaminase by immunoaffinity

chromatography. Preparative Biochemistry

1986;16(4):321-335. Not sensitivity or specificity of an 

identified test 

Lee K N, Birckbichler P J, Patterson M K et al. Induction

of cellular transglutaminase biosynthesis by sodium

butyrate. Biochimica Et Biophysica Acta 1987;928(1):22-

28. Not sensitivity or specificity of an identified test 

Lee K N, Lee C S, Tae W-C et al. Cross-linking of wildtype and mutant alphaSUB2-antiplasmins to by activated

factor XIII and by a tissue transglutaminase. J Biol Chem 

2000;275(48):37382-37389. Not sensitivity or specificity of 

an identified test

Lee S K, Chi J G, Jeon Y J et al. Expression of

transglutaminase C during the prenatal development of 

human submandibular glands. Journal of Dental Research

1995;74(11):1812-1816. Not sensitivity or specificity of an 

A-409
identified test 

Lee S K, Chi J G, Park S C et al. Transient expression of 

transglutaminase C during prenatal development of human 

muscles. Journal of Histochemistry and Cytochemistry - 

Official Journal of the Histochemistry Society

2000;48(11):1565-1574. Not sensitivity or specificity of an 

identified test 

Lee Susie K, Lo Winson, Memeo Lorenzo et al. Duodenal 

histology in patients with celiac disease after treatment with

a gluten-free diet. Gastrointestinal Endoscopy

2003;57(2):187-191. Not sensitivity or specificity of an 

identified test 

Lee Y-S, Dlugosz A A, McKay R et al. Definition by

specific antisense oligonucleotides of a role for protein

kinase Calpha in expression of differentiation markers in 

normal and neoplastic mouse epidermal keratinocytes. Mol 

Carcinog 1997;18(1):44-53. Not sensitivity or specificity of 

an identified test

Lefebvre O, Wouters D, Mereau-Richard C et al. Induction

of apoptosis by all-trans retinoic acid in the human 

myeloma cell line RPMI 8226 and negative regulation of 

some of its typical morphological features by

dexamethasone. Cell Death and Differentiation 

1999;6(5):433-444. Not sensitivity or specificity of an 

identified test 

Leffell M S. Is there an immunogenetic basis for Peyronie's 

disease?. J Urol 1997;157(1):295-297. Not sensitivity or

specificity of an identified test

Lehmann F G, Hillert U. Fecal intestinal alkaline 

phosphatase in coeliac disease. Zeitschrift Fur

Gastroenterologie 1980;18(7):381-388. Not sensitivity or 

specificity of an identified test

Leigh R J, Marsh M N, Crowe P et al. Studies of intestinal

lymphoid tissue. IX. Dose-dependent, gluten-induced 

lymphoid infiltration of coeliac jejunal epithelium. 

Scandinavian Journal of Gastroenterology 1985;20(6):715-

719. Not sensitivity or specificity of an identified test 

Lembcke B, Schneider H, Lankisch P G. Is the assay of 

disaccharidase activity in small bowel mucosal biopsy

relevant for clinical gastroenterologists?. Klinische 

Wochenschrift 1989;67(11):568-575. Not sensitivity or

specificity of an identified test

Lemieux B, Boivin M, Brossard J-H et al. Normal

parathyroid function with decreased bone mineral density

in treated celiac disease. Canadian Journal of

Gastroenterology = Journal Canadien De Gastroenterologie 

2001;15(5):302-307. Not sensitivity or specificity of an 

identified test 

Lenoir-Viale M C, Galup C, Darmon M et al. Epidermis

reconstructed from the outer root sheath of human hair

follicle. Effect of retinoic acid. Archives of Dermatological 

Research 1993;285(4):197-204. Not sensitivity or

specificity of an identified test

Lentze M, Schaub J, Harms K. A simple thin-layer

chromatographic technique for the assay of intestinal 

dipeptide hydrolases from human mucosal biopsy material. 

Clinica Chimica Acta 1973;International Journal of Clinical 

Chemistry; 49(1):19-26. Not sensitivity or specificity of an 

identified test 

Leon F, Camarero C, Pena R et al. Anti-transglutaminase 

IgA ELISA: clinical potential and drawbacks in celiac 

disease diagnosis. Scandinavian Journal of 

Gastroenterology 2001;36(8):849-853. Improper control 

group 

Leonard J N, Chorzelski T P, Beutner E H et al. IgA antiendomysial antibody detection in the serum of patients with

dermatitis herpetiformis following gluten challenge. 

Archives of Dermatological Research 1985;277(5):349-

351. Not sensitivity or specificity of an identified test 

Leonard J N, Tucker W F, Fry J S et al. Increased incidence 

of malignancy in dermatitis herpetiformis. British Medical 

Journal (Clinical Research Ed.) 1983;286(6358):16-18. Not 

sensitivity or specificity of an identified test 

Leonard J, Haffenden G, Tucker W. Gluten challenge in

dermatitis herpetiformis. New Engl J Med

1983;308(14):816-819. Not sensitivity or specificity of an

identified test 

Leonard N, Feighery C F, Hourihane D O et al. Peptic 

duodenitis - Does it exist in the second part of the 

duodenum?. J Clin Pathol 1997;50(1):54-58. Not sensitivity 

or specificity of an identified test

Leonard N, Hourihane D O, Whelan A. Neuroproliferation

in the mucosa is a feature of coeliac disease and Crohn's 

disease. Gut 1995;37(6):763-765. Not sensitivity or 

specificity of an identified test

Leong A S, Sormunen R T, Tsui W M et al. Hep Par 1 and

selected antibodies in the immunohistological distinction of

hepatocellular carcinoma from cholangiocarcinoma, 

combined tumours and metastatic carcinoma.

Histopathology 1998;33(4):318-324. Not sensitivity or

specificity of an identified test

Lepage V, Lamm L U, Charron D. Molecular aspects of

HLA class II and some autoimmune diseases. Eur J

Immunogenet 1993;20(3):153-164. Not sensitivity or 

specificity of an identified test

Lepore L, Martelossi S, Pennesi M et al. Prevalence of

celiac disease in patients with juvenile chronic arthritis.

Journal of Pediatrics 1996;129(2):311-313. Not sensitivity

or specificity of an identified test

Lepore L, Pennesi M, Ventura A et al. Anti-alpha-gliadin

antibodies are not predictive of celiac disease in juvenile 

chronic arthritis. Acta Paediatrica (Oslo, Norway - 1992)

1993;82(6-7):569-573. Not sensitivity or specificity of an

A-410
identified test 

Lerner A. The race for the diagnostic autoantibody in celiac 

disease. And the winner is... Israel Medical Association 

Journal - Imaj 2000;2(2):82-83. Not sensitivity or

specificity of an identified test

Lerner A. Factors affecting the clinical presentation and 

time of diagnosis of celiac disease: the Jerusalem and the 

West Bank-Gaza experience. Israel Journal of Medical 

Sciences 1994;30(4):294-295. Not sensitivity or specificity

of an identified test 

Lerner A, Lebenthal E. The controversy of the use of antigluten antibody (AGA) as a diagnostic tool in celiac 

disease. Journal of Pediatric Gastroenterology and

Nutrition 1991;12(4):407-409. Not sensitivity or specificity

of an identified test 

Lerner A, Blank M, Lahat N et al. Increased prevalence of

autoantibodies in celiac disease. Digestive Diseases and 

Sciences 1998;43(4):723-726. Not sensitivity or specificity

of an identified test 

Lerner A, Gruener N, Iancu T C. Serum carnitine 

concentrations in coeliac disease. Gut 1993;34(7):933-935. 

Not sensitivity or specificity of an identified test

Lernmark A. Molecular biology of IDDM. Diabetologia 

1994;37 Suppl 2s73-s81. Not sensitivity or specificity of an 

identified test 

Lernmark A, Kloppel G, Stenger D et al. Heterogeneity of

islet pathology in two infants with recent onset diabetes

mellitus. Virchows Arch 1995;425(6):631-640. Not 

sensitivity or specificity of an identified test 

Leslie D, Lipsky P, Louis Notkins A. Autoantibodies as 

predictors of disease. J Clin Invest 2001;108(10):1417-

1422. Not sensitivity or specificity of an identified test 

Lesort M, Attanavanich K, Zhang J et al. Distinct nuclear

localization and activity of tissue transglutaminase. Journal 

of Biological Chemistry 1998;273(20):11991-11994. Not 

sensitivity or specificity of an identified test 

Lesort M, Chun W, Johnson G V et al. Tissue 

transglutaminase is increased in Huntington's disease brain.

Journal of Neurochemistry 1999;73(5):2018-2027. Not 

sensitivity or specificity of an identified test 

Lesort M, Tucholski J, Miller M L et al. Tissue

transglutaminase: a possible role in neurodegenerative 

diseases. Progress in Neurobiology 2000;61(5):439-463. 

Not sensitivity or specificity of an identified test

Lesort M, Tucholski J, Zhang J et al. Impaired

mitochondrial function results in increased tissue 

transglutaminase activity in situ. Journal of Neurochemistry

2000;75(5):1951-1961. Not sensitivity or specificity of an

identified test 

Lesort Mathieu, Chun WanJoo, Tucholski Janusz et al. 

Does tissue transglutaminase play a role in Huntington's 

disease?. Neurochemistry International 2002;40(1):37-52. 

Not sensitivity or specificity of an identified test

Lesort Mathieu, Lee Matthew, Tucholski Janusz et al.

Cystamine inhibits caspase activity. Implications for the

treatment of polyglutamine disorders. Journal of Biological 

Chemistry 2002;278(6):3825-3830. Not sensitivity or 

specificity of an identified test

Lessof M H, Kemeny D M, Price J F. IgG antibodies to 

food in health and disease. Allergy Proc 1991;12(5):305-

307. Not sensitivity or specificity of an identified test 

Leung A K C, Robson W M. Evaluating the child with 

chronic diarrhea. Am Fam Phys 1996;53(2):635-643. Not 

sensitivity or specificity of an identified test 

Leuven F V, van den, Berghe H et al. Primary amines

inhibit recycling of alphainf 2M receptors in fibroblasts. 

Cell 1980;20(1):37-43. Not sensitivity or specificity of an

identified test 

Levenson S D, Austin R K, Dietler M D et al. Specificity of

antigliadin antibody in celiac disease. Gastroenterology

1985;89(1):1-5. Not sensitivity or specificity of an 

identified test 

Levine A, Bujanover Y, Reif S et al. Comparison of assays

for anti-endomysial and anti-transglutaminase antibodies 

for diagnosis of pediatric celiac disease. Israel Medical 

Association Journal - Imaj 2000; 2(2):122-125. Unable to

obtain full article 

Levine R A. Steatorrhea induced by para-aminosalicylic

acid. Annals of Internal Medicine 1968;68(6):1265-1270. 

Not sensitivity or specificity of an identified test

Levitt M L, Gazdar A F, Oie H K et al. Cross-linked 

envelope-related markers for squamous differentiation in 

human lung cancer cell lines. Cancer Research 

1990;50(1):120-128. Not sensitivity or specificity of an 

identified test 

Lewis C, Book L, Black J et al. Celiac disease and human 

leukocyte antigen genotype: accuracy of diagnosis in selfdiagnosed individuals, dosage effect, and sibling risk. 

Journal of Pediatric Gastroenterology and Nutrition 

2000;31(1):22-27. Improper control group 

Lewis K B, Teller D C, Fry J et al. Crosslinking kinetics of

the human transglutaminase, factor XIII[A2], acting on 

fibrin gels and gamma-chain peptides. Biochemistry

1997;36(5):995-1002. Not sensitivity or specificity of an

identified test 

Lewis-Jones M S, Barnes R M R, Macfarlane A W et al. 

Frequency and isotype distribution of serum antibodies 

reactive with dietary proteins in adults with chronic 

urticaria. Clin Exp Dermatol 1987;12(6):419-423. Not 

sensitivity or specificity of an identified test 

A-411
Li Voon, Chong J S W, Leong K S et al. Is coeliac disease 

more prevalent in young adults with coexisting Type 1

diabetes mellitus and autoimmune thyroid disease

compared with those with Type 1 diabetes mellitus alone?.

Diabetic Medicine - a Journal of the British Diabetic

Association 2002;19(4):334-337. Not sensitivity or 

specificity of an identified test

Licastro F, Mariani R A, Faldella G et al. Immuneendocrine status and coeliac disease in children with Down 

Syndrome: Relationships with zinc and cognitive

efficiency. Brain Res Bull 2001;55(2):313-317. Not 

sensitivity or specificity of an identified test 

Lidang Jensen M, Johansen P. Immunocytochemical 

staining of serous effusions: an additional method in the 

routine cytology practice?. Cytopathology - Official 

Journal of the British Society for Clinical Cytology

1994;5(2):93-103. Not sensitivity or specificity of an 

identified test 

Lie B A, Sollid L M, Ascher H et al. A gene telomeric of

the HLA class I region is involved in predisposition to both 

type 1 diabetes and coeliac disease. Tissue Antigens

1999;54(2):162-168. Not sensitivity or specificity of an 

identified test 

Lifschitz C H, Polanco I, Lobb K. The urinary excretion of

polyethylene glycol as a test for mucosal integrity in 

children with celiac disease: comparison with other 

noninvasive tests. Journal of Pediatric Gastroenterology

and Nutrition 1989;9(1):49-57. Not sensitivity or 

specificity of an identified test

Lilley G R, Griffin M, Bonner P L. Assays for the 

measurement of tissue transglutaminase (type II) mediated

protein crosslinking via epsilon-(gamma-glutamyl) lysine

and N',N'-bis (gamma-glutamyl) polyamine linkages using 

biotin labelled casein. Journal of Biochemical and 

Biophysical Methods 1997;34(1):31-43. Not sensitivity or

specificity of an identified test

Lim S D, Bae S I, Kim I G et al. Tissue transglutaminase is 

not increased during apoptosis of HT-1080 human 

fibrosarcoma cells. Experimental and Toxicologic

Pathology - Official Journal of the Gesellschaft Fur 

Toxikologische Pathologie 1998;50(1):79-82. Not 

sensitivity or specificity of an identified test 

Lin H J, Rotter J I, Conte W J. Use of HLA marker 

associations and HLA haplotype linkage to estimate disease

risks in families with gluten-sensitive enteropathy. Clinical

Genetics 1985;28(3):185-198. Not sensitivity or specificity

of an identified test 

Lin L, Tokunaga K, Nakajima F et al. Both HLA-B*1301 

and B*1302 exist in Asian populations and are associated 

with different haplotypes. Hum Immunol 1995;43(1):51-

56. Not sensitivity or specificity of an identified test 

Lin X R, Wilkinson D I, Farber E M. Camptothecin 

induces differentiation, tissue transglutaminase and 

apoptosis in cultured keratinocytes. Experimental 

Dermatology 1998;7(4):179-183. Not sensitivity or 

specificity of an identified test

Linaker B D, Calam J. Is jejunal biopsy valuable in the 

elderly?. Age and Ageing 1978;7(4):244-245. Not 

sensitivity or specificity of an identified test 

Lindberg J, Ahren C, Iwarson S. Intestinal villous atrophy

in chronic active hepatitis. Scandinavian Journal of 

Gastroenterology 1979;14(8):1015-1018. Not sensitivity or 

specificity of an identified test

Lindberg J, Ahren Chr, Jonsson J. Gluten-free diet in 

chronic active hepatitis associated with intestinal villous 

atrophy. Hepato-Gastroenterology 1982;29(2):52-54. Not 

sensitivity or specificity of an identified test 

Lindberg T, Norden A, Josefsson L. Intestinal dipeptidases. 

Dipeptidase activities in small intestinal biopsy specimens 

from a clinical material. Scandinavian Journal of

Gastroenterology 1968;3(2):177-182. Not sensitivity or

specificity of an identified test

Lindgren S, Sjoberg K, Eriksson S. Unsuspected coeliac 

disease in chronic 'cryptogenic' liver disease. Scandinavian 

Journal of Gastroenterology 1994;29(7):661-664. Not 

sensitivity or specificity of an identified test 

Lindh E, Ljunghall S, Larsson K et al. Screening for 

antibodies against gliadin in patients with osteoporosis. 

Journal of Internal Medicine 1992;231(4):403-406. Not 

sensitivity or specificity of an identified test 

Lindqvist U, Rudsander A, Bostrom A et al. IgA antibodies 

to gliadin and coeliac disease in psoriatic arthritis. 

Rheumatology (Oxford, England) 2002;41(1):31-37. Not 

sensitivity or specificity of an identified test 

Lindstrom C G. Millipore filter as support for fresh frozen

sections of peroral biopsy specimens of small intestine.

Acta Pathologica Et Microbiologica Scandinavica 

1969;77(3):555-556. Not sensitivity or specificity of an 

identified test 

Lindstrom J, Smith K J, Skelton H G et al. Increased 

anticardiolipin antibodies associated with the development 

of anetoderma in HIV-1 disease. Military Medical

Consortium for the Advancement of Retroviral research

(MMCARR). International Journal of Dermatology

1995;34(6):408-415. Not sensitivity or specificity of an 

identified test 

Linnestad P, Erichsen A, Fausa O et al. The release of

human pancreatic polypeptide, gastrin, gastric inhibitory

polypeptide, and somatostatin in celiac disease related to

the histological appearance of jejunal mucosa before and 1 

year after gluten withdrawal. Scandinavian Journal of

Gastroenterology 1983;18(2):169-175. Not sensitivity or 

specificity of an identified test

Linsenmayer T F, Long F, Nurminskaya M et al. Type X 

A-412
collagen and other up-regulated components of the avian

hypertrophic cartilage program. Progress in Nucleic Acid

Research and Molecular Biology 1998;6079-109. Not 

sensitivity or specificity of an identified test 

Lio D, Bonanno C T, D'Anna C et al. Gluten stimulation

induces an in vitro expansion of peripheral blood T gamma 

delta cells from HLA-DQ2-positive subjects of families of 

patients with celiac disease. Experimental and Clinical 

Immunogenetics 1998;15(1):46-55. Improper control group 

Lionetti P. The enteropathy of celiac disease. Journal of

Pediatric Gastroenterology and Nutrition 2002;34(Suppl 

1):S18-S21. Not sensitivity or specificity of an identified

test 

Lionetti P, Pazzaglia A, Moriondo M et al. Differing 

patterns of transforming growth factor-beta expression in 

normal intestinal mucosa and in active celiac disease. 

Journal of Pediatric Gastroenterology and Nutrition 

1999;29(3):308-313. Not sensitivity or specificity of an 

identified test 

Little A-M, Stern P L. Does HLA type predispose some 

individuals to cancer?. Mol Med Today 1999;5(8):337-342. 

Not sensitivity or specificity of an identified test

Little T M. Immunoglobulin levels in families with coeliac 

disease. Lancet 1972;2(7774):400-401. Not sensitivity or 

specificity of an identified test

Littlewood J M. Coeliac disease in childhood. Bailliere's

Clinical Gastroenterology 1995;9(2):295-327. Not 

sensitivity or specificity of an identified test 

Liu E, Bao F, Barriga K et al. Fluctuating transglutaminase 

autoantibodies are related to histologic features of celiac 

disease. Clin Gastroenterol Hepatol 2003;1(5):356-362. 

Improper control group 

Liu Edwin, Eisenbarth George S. Type 1A diabetes 

mellitus-associated autoimmunity. Endocrinology and 

Metabolism Clinics of North America 2002;31(2):391-410, 

Vii. Not sensitivity or specificity of an identified test 

Liu J N, Kung W, Harpel P C et al. Demonstration of 

covalent binding of lipoprotein(a) [Lp(a)] to fibrin and 

endothelial cells. Biochemistry 1998;37(11):3949-3954. 

Not sensitivity or specificity of an identified test

Liu J, Purdy L E, Rabinovitch S et al. Major DQ8-restricted

T-cell epitopes for human GAD65 mapped using human 

CD4, DQA1*0301, DQB1*0302 transgenic IA(null) NOD 

mice. Diabetes 1999;48(3):469-477. Not sensitivity or 

specificity of an identified test

Liu Jianjun, Juo Suh, Holopainen Paivi et al. Genomewide 

linkage analysis of celiac disease in Finnish families. 

American Journal of Human Genetics 2002;70(1):51-59. 

Improper control group 

Liu Shenping, Cerione Richard A, Clardy Jon. Structural 

basis for the guanine nucleotide-binding activity of tissue 

transglutaminase and its regulation of transamidation 

activity. Proceedings of the National Academy of Sciences 

of the United States of America 2002;99(5):2743-2747. Not 

sensitivity or specificity of an identified test 

Liutu M. Helicobacter pylori and chronic urticaria. Forum

Nordic Derm-Venerol 2003;8(2):48-49. Not sensitivity or 

specificity of an identified test

Liutu M, Kalimo K, Uksila J et al. Etiologic aspects of 

chronic urticaria. International Journal of Dermatology

1998;37(7):515-519. Not sensitivity or specificity of an 

identified test 

Lloyd-Still J D, Grand R J, Khaw K T et al. The use of 

corticosteroids in celiac crisis. Journal of Pediatrics 

1972;81(6):1074-1081. Not sensitivity or specificity of an

identified test 

Lock R J, Unsworth D J. Identifying immunoglobulin-A--

deficient children and adults does not necessarily help the 

serologic diagnosis of coeliac disease. Journal of Pediatric 

Gastroenterology and Nutrition 1999;28(1):81-83. Not

sensitivity or specificity of an identified test 

Lock R J, Gilmour J E, Unsworth D J. Anti-tissue 

transglutaminase, anti-endomysium and anti-R1-reticulin

autoantibodies-the antibody trinity of coeliac disease. 

Clinical and Experimental Immunology 1999;116(2):258-

262. Not sensitivity or specificity of an identified test 

Lock R J, Pitcher M C, Unsworth D J. IgA anti-tissue

transglutaminase as a diagnostic marker of gluten sensitive 

enteropathy. Journal of Clinical Pathology 1999;52(4):274-

277. Improper control group 

Loft D E. The epidemiology and diagnosis of coeliac 

disease. European Journal of Gastroenterology & 

Hepatology 1993;5(2):69-72. Not sensitivity or specificity

of an identified test 

Loft D E, Marsh M N, Crowe P T. Rectal gluten challenge

and diagnosis of coeliac disease. Lancet 

1990;335(8701):1293-1295. Not sensitivity or specificity of 

an identified test

Loft D E, Nwokolo C U, Ciclitira P J. The diagnosis of 

gluten sensitivity and coeliac disease--the two are not

mutually inclusive. European Journal of Gastroenterology

& Hepatology 1998;10(11):911-913. Review article 

Logan R F. Screening for coeliac disease--has the time 

come for mass screening?. Acta paediatrica (Oslo, Norway

: 1992).Supplement. 1996;41215-19. Not sensitivity or

specificity of an identified test

Logan R F A, Howarth G F, West J et al. How often is a

positive faecal occult blood test the result of coeliac 

disease?. European Journal of Gastroenterology & 

Hepatology 2003;15(10):1097-1100. Not sensitivity or

specificity of an identified test

A-413
Logan R F, Rifkind E A, Busuttil A et al. Prevalence and 

"incidence" of celiac disease in Edinburgh and the Lothian

region of Scotland. Gastroenterology 1986;90(2):334-342. 

Not sensitivity or specificity of an identified test

Lohiniemi S, Maki M, Kaukinen K et al. Gastrointestinal

symptoms rating scale in coeliac disease patients on wheat

starch-based gluten-free diets. Scandinavian Journal of

Gastroenterology 2000;35(9):947-949. Not sensitivity or 

specificity of an identified test

Lojda Z. Proteinases in pathology. Usefulness of 

histochemical methods. Journal of Histochemistry and 

Cytochemistry - Official Journal of the Histochemistry

Society 1981;29(3a Suppl):481-493. Not sensitivity or 

specificity of an identified test

Lojda Z, Gossrau R. Histochemical demonstration of 

enteropeptidase activity. New method with a synthetic 

substrate and its comparison with the trypsinogen 

procedure. Histochemistry 1983;78(2):251-270. Not 

sensitivity or specificity of an identified test 

Lojda Z, Fric P, Jodl J et al. Cytochemistry of the human 

jejunal mucosa in the norm and in malabsorption

syndrome. Current Topics in Pathology 1970;521-63. Not 

sensitivity or specificity of an identified test 

Lojda Z, Havrankova E, Slaby J. Histochemical 

demonstration of the intestinal hetero beta galactosidase 

(glucosidase). Histochemistry 1974;42(3):271-286. Not 

sensitivity or specificity of an identified test 

Lokshin A, Mayotte J E, Levitt M L. Mechanism of 

interferon beta-induced squamous differentiation and 

programmed cell death in human non-small-cell lung 

cancer cell lines. Journal of the National Cancer Institute

1995;87(3):206-212. Not sensitivity or specificity of an 

identified test 

Lokshin Anna E, Kalinski Pawel, Sassi R et al. Differential 

regulation of maturation and apoptosis of human 

monocyte-derived dendritic cells mediated by MHC class 

II. International Immunology 2002;14(9):1027-1037. Not 

sensitivity or specificity of an identified test 

Lomoschitz F, Schima W, Schober E et al. Enteroclysis in

adult celiac disease: diagnostic value of specific 

radiographic features. European Radiology

2002;13(4):890-896. Not sensitivity or specificity of an 

identified test 

Londei M. The external world of gluten and autoimmunity.

Gut 2001;49(4):463-464. Not sensitivity or specificity of an 

identified test 

Londei M, Quaratino S, Maiuri L. Celiac disease: A model 

autoimmune disease with gene therapy applications. Gene 

Ther 2003;10(10):835-843. Not sensitivity or specificity of 

an identified test

Long F R, Kramer S S, Markowitz R I et al. Duodenitis in 

children: Correlation of radiologic findings with

endoscopic and pathologic findings. Radiology

1998;206(1):103-108. Not sensitivity or specificity of an

identified test 

Lopes J M, Bjerkehagen B, Holm R et al. 

Immunohistochemical profile of synovial sarcoma with

emphasis on the epithelial-type differentiation. A study of 

49 primary tumours, recurrences and metastases.

Pathology, Research and Practice 1994;190(2):168-177. 

Not sensitivity or specificity of an identified test

Lopez-Rodriguez M J, Canal Macias M L, Lavado Garcia J

M et al. Epidemiological changes in diagnosed coeliac 

disease in a population of Spanish children. Acta Paediatr 

Int J Paediatr 2003;92(2):165-169. Not sensitivity or 

specificity of an identified test

Lopez-Vazquez A, Rodrigo L, Fuentes D et al. MHC class

I chain related gene A (MICA) modulates the development 

of coeliac disease in patients with the high risk heterodimer 

DQA1*0501/DQB1*0201. Gut 2002;50(3):336-340. Not 

sensitivity or specificity of an identified test 

Lopez-Vazquez Antonio, Rodrigo Luis, Fuentes Dolores et 

al. MICA-A5.1 allele is associated with atypical forms of 

celiac disease in HLA-DQ2-negative patients. 

Immunogenetics 2002;53(10-11):989-991. Not sensitivity

or specificity of an identified test

Lorand L. Post-translational pathways for generating 

epsilon(gamma-glutamyl)lysine cross-links. Annals of the

New York Academy of Sciences 1983;42110-27. Not 

sensitivity or specificity of an identified test 

Lorand L, Bjerrum O J, Hawkins M et al. Degradation of

transmembrane proteins in Ca2+-enriched human

erythrocytes. An immunochemical study. Journal of 

Biological Chemistry 1983;258(8):5300-5305. Not 

sensitivity or specificity of an identified test 

Lorand L, Dailey J E, Turner P M. Fibronectin as a carrier 

for the transglutaminase from human erythrocytes.

Proceedings of the National Academy of Sciences of the

United States of America 1988;85(4):1057-1059. Not 

sensitivity or specificity of an identified test 

Lorand L, Murthy S N, Velasco P T et al. Identification of 

transglutaminase substrates in inside-out vesicles from 

human erythrocytes: immunoblotting with anti-dansyl 

antibody. Biochemical and Biophysical Research

Communications 1986;134(2):685-689. Not sensitivity or

specificity of an identified test

Lorand L, Parameswaran K N, Velasco P T et al.

Biotinylated peptides containing a factor XIIIa or a tissue 

transglutaminase-reactive glutaminyl residue that block 

protein cross-linking phenomena by becoming incorporated 

into amine donor sites. Bioconjugate Chemistry

1992;3(1):37-41. Not sensitivity or specificity of an 

identified test 

A-414
Lord C, MacGregor G A. Coeliac disease in identical twin 

infants. Postgraduate Medical Journal 1981;57(672):658-

659. Not sensitivity or specificity of an identified test 

Lorini R, Larizza D, Scotta M S et al. HLA in Graves' 

disease coexistent with coeliac disease. European Journal 

of Pediatrics 1986;145(3):241Not sensitivity or specificity

of an identified test 

Lorini R, Scaramuzza A, Vitali L et al. Clinical aspects of

coeliac disease in children with insulin-dependent diabetes

mellitus. Journal of Pediatric Endocrinology & Metabolism

- Jpem 1996;9(Suppl 1):101-111. Not sensitivity or 

specificity of an identified test

Lorini R, Scotta M S, Cortona L et al. Celiac disease and

type I (insulin-dependent) diabetes mellitus in childhood: 

follow-up study. Journal of Diabetes and Its Complications 

1996;10(3):154-159. Not sensitivity or specificity of an 

identified test 

Lotze U, Busch H J, Aschoff A et al. Damaged myocytes as 

detected by the colocalization of DNA fragmentation and 

tissue transglutaminase and their prognostic significance in 

enterovirus-associated dilated cardiomyopathy. European 

Journal of Clinical Investigation 2001;31(9):744-755. Not 

sensitivity or specificity of an identified test 

Louis E J, Payami H, Klitz W et al. A synergistic three 

allele model for the HLA-linked components of coeliac 

disease predisposition. Genetic Epidemiology.Supplement 

1986;1277-282. Not sensitivity or specificity of an 

identified test 

Louis E J, Thomson G, Payami H. The affected sib method. 

II. The intermediate model. Annals of Human Genetics 

1983;47(Pt 3):225-243. Not sensitivity or specificity of an

identified test 

Louka A S, Sollid L M. HLA in coeliac disease: 

Unravelling the complex genetics of a complex disorder. 

Tissue Antigens 2003;61(2):105-117. Not sensitivity or

specificity of an identified test

Louka A S, Moodie S J, Karell K et al. A collaborative 

European search for non-DQA1 *05-DQB1 *02 Celiac 

disease loci on HLA-Dr3 haplotypes: Analysis of

transmission from homozygous parents. Hum Immunol 

2003;64(3):350-358. Not sensitivity or specificity of an 

identified test 

Louka A S, Nilsson S, Olsson M et al. HLA in coeliac 

disease families: a novel test of risk modification by the

'other' haplotype when at least one DQA1*05-DQB1*02 

haplotype is carried. Tissue Antigens 2002;60(2):147-154. 

Not sensitivity or specificity of an identified test

Louka A S, Torinsson Naluai A, D'Alfonso S et al. The 

IL12B gene does not confer susceptibility to coeliac

disease. Tissue Antigens 2002;59(1):70-72. Not sensitivity

or specificity of an identified test

Louka Andrew S, Lie Benedicte A, Talseth Bente et al. 

Coeliac disease patients carry conserved HLA-DR3-DQ2 

haplotypes revealed by association of TNF alleles.

Immunogenetics 2003;55(5):339-343. Not sensitivity or

specificity of an identified test

Lu S, Davies P J. Regulation of the expression of the tissue 

transglutaminase gene by DNA methylation. Proceedings 

of the National Academy of Sciences of the United States 

of America 1997;94(9):4692-4697. Not sensitivity or 

specificity of an identified test

Lu S, Saydak M, Gentile V et al. Isolation and

characterization of the human tissue transglutaminase gene

promoter. Journal of Biological Chemistry 

1995;270(17):9748-9756. Not sensitivity or specificity of

an identified test

Lu X, Xie W, Reed D et al. Nonsteroidal antiinflammatory

drugs cause apoptosis and induce cyclooxygenases in 

chicken embryo fibroblasts. Proc Natl Acad Sci U S A 

1995;92(17):7961-7965. Not sensitivity or specificity of an 

identified test 

Lucas D L, Tanuma S, Davies P J et al. Maturation of 

human promyelocytic leukemia cells induced by

nicotinamide: evidence of a regulatory role for ADPribosylation of chromosomal proteins. Journal of Cellular 

Physiology 1984;121(2):334-340. Not sensitivity or 

specificity of an identified test

Lucas M L, Cooper B T, Lei F H et al. Acid microclimate 

in coeliac and Crohn's disease: a model for folate 

malabsorption. Gut 1978;19(8):735-742. Not sensitivity or 

specificity of an identified test

Luconi M, Muratori M, Maggi M et al. Uteroglobin and 

transglutaminase modulate human sperm functions. Journal 

of Andrology 2000;21(5):676-688. Not sensitivity or 

specificity of an identified test

Ludvigsson J F, Falth-Magnusson K, Ludvigsson J. Tissue 

transglutaminase auto-antibodies in cord blood from

children to become celiacs. Scandinavian Journal of 

Gastroenterology 2001;36(12):1279-1283. Not sensitivity

or specificity of an identified test

Lukacova D, Matsueda G R, Haber E et al. Inhibition of 

factor XIII activation by an anti-peptide monoclonal 

antibody. Biochemistry 1991;30(42):10164-10170. Not 

sensitivity or specificity of an identified test 

Lundin K E A. Coeliac disease--all questions answered?.

Digestive and Liver Disease - Official Journal of the Italian

Society of Gastroenterology and the Italian Association for

the Study of the Liver 2002;34(3):238-242. Not sensitivity

or specificity of an identified test

Lundin K E A. HLA-DQ8 as an Ir gene in coeliac disease. 

Gut 2003;52(1):7-8. Review article 

A-415
Lundin K E A, Sollid L M. Gliadin peptide specific 

intestinal T cells in coeliac disease. Gut 2003;52(2):162Not 

sensitivity or specificity of an identified test 

Lundin K E A, Nilsen E M, Scott H G et al. Oats induced 

villous atrophy in coeliac disease. Gut 2003;52(11):1649-

1652. Not sensitivity or specificity of an identified test 

Lundin K E, Gjertsen H A, Scott H et al. Function of DQ2 

and DQ8 as HLA susceptibility molecules in celiac disease.

Human Immunology 1994;41(1):24-27. Not sensitivity or 

specificity of an identified test

Lundin K E, Qvigstad E, Sollid L M et al. Alloreactive T 

cells recognizing determinants dependent on the DQ beta 

chain of DQw2. Tissue Antigens 1989;34(5):312-316. Not 

sensitivity or specificity of an identified test 

Lundin K E, Scott H, Fausa O et al. T cells from the small 

intestinal mucosa of a DR4, DQ7/DR4, DQ8 celiac disease 

patient preferentially recognize gliadin when presented by

DQ8. Human Immunology 1994;41(4):285-291. Not 

sensitivity or specificity of an identified test 

Lundin K E, Scott H, Hansen T et al. Gliadin-specific, 

HLA-DQ(alpha 1*0501,beta 1*0201) restricted T cells 

isolated from the small intestinal mucosa of celiac disease

patients. Journal of Experimental Medicine

1993;178(1):187-196. Not sensitivity or specificity of an

identified test 

Lundin K E, Sollid L M, Anthonsen D et al. Heterogeneous 

reactivity patterns of HLA-DQ-restricted, small intestinal

T-cell clones from patients with celiac disease.

Gastroenterology 1997;112(3):752-759. Not sensitivity or

specificity of an identified test

Lundin K E, Sollid L M, Qvigstad E et al. T lymphocyte 

recognition of a celiac disease-associated cis- or transencoded HLA-DQ alpha/beta-heterodimer. Journal of 

Immunology (Baltimore, Md.- 1950) 1990;145(1):136-139. 

Not sensitivity or specificity of an identified test

Luostarinen L K, Collin P O, Peraaho M J et al. Coeliac 

disease in patients with cerebellar ataxia of unknown 

origin. Annals of Medicine 2001;33(6):445-449. Not 

sensitivity or specificity of an identified test 

Luostarinen L, Dastidar P, Collin P et al. Association

between coeliac disease, epilepsy and brain atrophy.

European Neurology 2001;46(4):187-191. Not sensitivity

or specificity of an identified test

Luyet C, Burri P H, Schittny J C. Suppression of cell 

proliferation and programmed cell death by dexamethasone 

during postnatal lung development. Am J Physiol Lung 

Cell Mol Physiol 2002;282(3 26-3):L477-L483. Not 

sensitivity or specificity of an identified test 

Luzi Giuseppe, Zullo Angelo, Iebba Filippo et al. Duodenal

pathology and clinical-immunological implications in 

common variable immunodeficiency patients. American 

Journal of Gastroenterology 2003;98(1):118-121. Not 

sensitivity or specificity of an identified test 

Lycke N, Kilander A, Nilsson L A et al. Production of 

antibodies to gliadin in intestinal mucosa of patients with 

coeliac disease: a study at the single cell level. Gut 

1989;30(1):72-77. Not sensitivity or specificity of an 

identified test 

Lynch D A, Sobala G M, Dixon M F et al. Lymphocytic 

gastritis and associated small bowel disease: a diffuse 

lymphocytic gastroenteropathy?. Journal of Clinical 

Pathology 1995;48(10):939-945. Not sensitivity or

specificity of an identified test

Macaubas C, Hallmayer J, Kalil J et al. Extensive

polymorphism of a (CA)(n) microsatellite located in the

HLA- DQA1/DQB1 class II region. Hum Immunol 

1995;42(3):209-220. Not sensitivity or specificity of an 

identified test 

MacDonald T T. Epithelial proliferation in response to 

gastrointestinal inflammation. Annals of the New York 

Academy of Sciences 1992;664202-209. Not sensitivity or

specificity of an identified test

MacDonald T T. The role of activated T lymphocytes in

gastrointestinal disease. Clinical and Experimental Allergy 

- Journal of the British Society for Allergy and Clinical

Immunology 1990;20(3):247-252. Not sensitivity or 

specificity of an identified test

MacDonald T T. Evidence for cell-mediated 

hypersensitivity as an important pathogenetic mechanism in 

food intolerance. Clin Exp Allergy Suppl 1995;25(1):10-

13. Not sensitivity or specificity of an identified test 

MacDonald T T, Spencer J. Cell-mediated immune injury

in the intestine. Gastroenterology Clinics of North America

1992;21(2):367-386. Not sensitivity or specificity of an 

identified test 

MacDonald T T, Spencer J. The role of activated T cells in 

transformed intestinal mucosa. Digestion 1990;46(Suppl 

2):290-296. Not sensitivity or specificity of an identified

test 

Machulla H K G, Muller L P, Schaaf A et al. Association 

of chronic lymphocytic leukemia with specific alleles of the

HLA-DR4:DR53:DQ8 haplotype in German patients. Int J 

Cancer 2001;92(2):203-207. Not sensitivity or specificity

of an identified test 

Mack D G, Johnson J J, Roberts F et al. HLA-class II genes 

modify outcome of Toxoplasma gondii infection. Int J

Parasitol 1999;29(9):1351-1358. Not sensitivity or

specificity of an identified test

Mack R, Chowdary D, Samaan P et al. Prevalence of 

CTLA-4 polymorphism A49G in Ashkenazi Jews. Genet 

Test 2001;5(3):269-271. Not sensitivity or specificity of an 

identified test 

A-416
Mackenzie I R, Gilbert J J. Cysts of the neuraxis of 

endodermal origin. Journal of Neurology, Neurosurgery, 

and Psychiatry 1991;54(7):572-575. Not sensitivity or 

specificity of an identified test

Mackey J, Treem W R, Worley G et al. Frequency of celiac 

disease in individuals with Down syndrome in the United 

States. Clinical Pediatrics 2001;40(5):249-252. Not 

sensitivity or specificity of an identified test 

Mackintosh P, Asquith P. HLA and coeliac disease. British

Medical Bulletin 1978;34(3):291-294. Not sensitivity or

specificity of an identified test

Macpherson A J S, Bjarnason I, Peters T J. The subcellular

distribution and levels of calmodulin in jejunal biopsies 

from control subjects and patients with coeliac disease.

Clin Chim Acta 1986;159(2):133-138. Not sensitivity or

specificity of an identified test

Mader R, Adawi M, Schonfeld S. Malabsorption in 

systemic lupus erythematosus. Clinical and Experimental 

Rheumatology 1997;15(6):659-661. Not sensitivity or 

specificity of an identified test

Madi A, Punyiczki M, di Rao M et al. Biochemical 

characterization and localization of transglutaminase in

wild-type and cell-death mutants of the nematode

Caenorhabditis elegans. European Journal of Biochemistry

/ Febs 1998;253(3):583-590. Not sensitivity or specificity

of an identified test 

Maffei H V, Kingston D, Hill I D et al. Histopathologic 

changes and the immune response within the jejunal 

mucosa in infants and children. Pediatric Research 

1979;13(6):733-736. Not sensitivity or specificity of an 

identified test 

Magaudda A, Dalla Bernadina B, De Marco P et al. 

Bilateral occipital calcification, epilepsy and coeliac 

disease: Clinical and neuroimaging features of a new 

syndrome. J Neurol Neurosurg Psychiatry 1993;56(8):885-

889. Not sensitivity or specificity of an identified test 

Magaudda L, Anastasi G, Arco A et al. Scanning electron 

microscopy of histological relapse after gluten-challenge in 

coeliac disease. Acta Paediatr Scand 1989;78(4):549-554. 

Not sensitivity or specificity of an identified test

Magazzu G, Bottari M, Tuccari G et al. Upper

gastrointestinal endoscopy can be a reliable screening tool 

for celiac sprue in adults. Journal of Clinical 

Gastroenterology 1994;19(3):255-257. Not sensitivity or 

specificity of an identified test

Maggio N, Sellitti S, Capano C P et al. Tissuetransglutaminase in rat and human brain: light and electron

immunocytochemical analysis and in situ hybridization 

study. Brain Research Bulletin 2001;56(3-4):173-182. Not 

sensitivity or specificity of an identified test 

Magliocca F M, Bonamico M, Petrozza V et al. Usefulness

of endoscopic small intestinal biopsies in children with 

coeliac disease. Italian Journal of Anatomy and 

Embryology = Archivio Italiano Di Anatomia Ed 

Embriologia 2001;106(2 Suppl 1):329-335. Unable to

extract data

Magliocca F M, Bonamico M, Petrozza V et al. A new 

morphological classification during follow-up in patients 

with celiac disease: a three-dimensional observation by

scanning electron microscopy. Histology and 

Histopathology 1996;11(2):343-350. Unable to extract data 

Magnaldo T, Bernerd F, Asselineau D et al. Expression of 

loricrin is negatively controlled by retinoic acid in human 

epidermis reconstructed in vitro. Differentiation 

1992;49(1):39-46. Not sensitivity or specificity of an 

identified test 

Mahadeva S, Wyatt J I, Howdle P D. Is a raised 

intraepithelial lymphocyte count with normal duodenal 

villous architecture clinically relevant?. Journal of Clinical

Pathology 2002;55(6):424-428. Not sensitivity or

specificity of an identified test

Mahmoud F, Alsaleh Q, Abul H et al. Association of major 

histocompatibility complex with psoriasis vulgaris in adult 

kuwaitis. Med Princ Pract 1998;7(4):261-263. Not 

sensitivity or specificity of an identified test 

Mahon J, Blair G E, Wood G M et al. Is persistent 

adenovirus 12 infection involved in coeliac disease? A

search for viral DNA using the polymerase chain reaction. 

Gut 1991;32(10):1114-1116. Not sensitivity or specificity

of an identified test 

Mahoney S-A, Wilkinson M, Smith S et al. Stabilization of

neurites in cerebellar granule cells by transglutaminase

activity: Identification of midkine and galectin-3 as 

substrates. Neuroscience 2000;101(1):141-155. Not 

sensitivity or specificity of an identified test 

Mainardi Elsa, Montanelli Alessandro, Dotti Maria et al. 

Thyroid-related autoantibodies and celiac disease: a role for

a gluten-free diet?. Journal of Clinical Gastroenterology

2002;35(3):245-248. Not sensitivity or specificity of an 

identified test 

Mainguet P. Staining methods of the duodenal and 

intestinal mucosae: METHODES DE COLORATIONS 

VITALES DES MUQUEUSES DUODENALES ET 

INTESTINALES. Acta Endosc 2001;31(2):179-182. Not 

sensitivity or specificity of an identified test 

Maiuri L, Auricchio S, Coletta S et al. Blockage of T-cell

costimulation inhibits T-cell action in celiac disease. 

Gastroenterology 1998;115(3):564-572. Not sensitivity or

specificity of an identified test

Maiuri L, Ciacci C, Auricchio S et al. Interleukin 15 

mediates epithelial changes in celiac disease.

Gastroenterology 2000;119(4):996-1006. Not sensitivity or 

A-417
specificity of an identified test

Maiuri L, Ciacci C, Raia V et al. FAS engagement drives 

apoptosis of enterocytes of coeliac patients. Gut 

2001;48(3):418-424. Not sensitivity or specificity of an 

identified test 

Maiuri L, Ciacci C, Vacca L et al. IL-15 drives the specific

migration of CD94+ and TCR-gammadelta+ intraepithelial 

lymphocytes in organ cultures of treated celiac patients.

American Journal of Gastroenterology 2001;96(1):150-156. 

Not sensitivity or specificity of an identified test

Maiuri L, Picarelli A, Boirivant M et al. Definition of the 

initial immunologic modifications upon in vitro gliadin

challenge in the small intestine of celiac patients.

Gastroenterology 1996;110(5):1368-1378. Not sensitivity

or specificity of an identified test

Maiuri L, Troncone R, Fais S et al. Crypt epithelial cells

express the 4F2 antigen in untreated coeliac mucosa. Adv 

Exp Med Biol 1995;371(B):1363-1365. Not sensitivity or

specificity of an identified test

Maiuri L, Troncone R, Mayer M et al. In vitro activities of

A-gliadin-related synthetic peptides: damaging effect on 

the atrophic coeliac mucosa and activation of mucosal 

immune response in the treated coeliac mucosa. 

Scandinavian Journal of Gastroenterology 1996;31(3):247-

253. Not sensitivity or specificity of an identified test 

Maiuri Luigi, Ciacci Carolina, Ricciardelli Ida et al.

Association between innate response to gliadin and 

activation of pathogenic T cells in coeliac disease. Lancet 

2003;362(9377):30-37. Not sensitivity or specificity of an

identified test 

Maiuri M C, De Stefano D, Mele G et al. Nuclear factor 

kappaB is activated in small intestinal mucosa of celiac

patients. J Mol Med 2003;81(6):373-379. Not sensitivity or 

specificity of an identified test

Maki M. The humoral immune system in coeliac disease.

Bailliere's Clinical Gastroenterology 1995;9(2):231-249. 

Not sensitivity or specificity of an identified test

Maki M. Tissue transglutaminase as the autoantigen of 

coeliac disease. Gut 1997;41(4):565-566. Not sensitivity or 

specificity of an identified test

Maki M. Coeliac disease and autoimmunity due to

unmasking of cryptic epitopes?. Lancet 

1996;348(9034):1046-1047. Not sensitivity or specificity of 

an identified test

Maki M. Immunopathogenesis of coeliac disease. Int J 

Immunopathol Pharmacol 1997;10(2 SUPPL.):81-82. Not 

sensitivity or specificity of an identified test 

Maki M, Aine L, Lipsanen V et al. Dental enamel defects

in first-degree relatives of coeliac disease patients. Lancet

1991;337(8744):763-764. Not sensitivity or specificity of

an identified test

Maki M, Hallstrom O, Huupponen T et al. Increased 

prevalence of coeliac disease in diabetes. Archives of 

Disease in Childhood 1984;59(8):739-742. Not sensitivity

or specificity of an identified test

Maki M, Hallstrom O, Vesikari T et al. Evaluation of a 

serum IgA-class reticulin antibody test for the detection of

childhood celiac disease. Journal of Pediatrics 

1984;105(6):901-905. Not sensitivity or specificity of an

identified test 

Maki M, Holm K, Koskimies S et al. Normal small bowel

biopsy followed by coeliac disease. Archives of Disease in 

Childhood 1990;65(10):1137-1141. Improper control group 

Maki M, Huupponen T, Holm K et al. Seroconversion of 

reticulin autoantibodies predicts coeliac disease in insulin 

dependent diabetes mellitus. Gut 1995;36(2):239-242. Not 

sensitivity or specificity of an identified test 

Maki M, Lahdeaho M L, Hallstrom O et al. Postpubertal

gluten challenge in coeliac disease. Archives of Disease in 

Childhood 1989;64(11):1604-1607. Not sensitivity or 

specificity of an identified test

Maki M, Sulkanen S, Collin P. Antibodies in relation to

gluten intake. Digestive Diseases (Basel, Switzerland) 

1998;16(6):330-332. Not sensitivity or specificity of an 

identified test 

Maki Markku, Mustalahti Kirsi, Kokkonen Jorma et al. 

Prevalence of Celiac disease among children in Finland. 

New England Journal of Medicine 2003;348(25):2517-

2524. Not sensitivity or specificity of an identified test 

Maksimak M. A rapid, safe small bowel biopsy technique 

in children. Gastrointest Endosc 1991;37(3):358-361. Not 

sensitivity or specificity of an identified test 

Malik A K, McGee J O. Alpha-1-antitrypsin 

immunoreactivity in the small bowel in coeliac disease. 

Malaysian Journal of Pathology 1993;15(2):151-154. Not 

sensitivity or specificity of an identified test 

Malik A K, Burns J, McGee J O. Immunoperoxidase 

localization of fibronectin in small bowel mucosa. Indian

Journal of Pathology & Microbiology 1992;35(2):88-93. 

Not sensitivity or specificity of an identified test

Malis F, Lojda Z, Fric P et al. Disaccharidases in celiac 

disease and mucoviscidosis. Some correlations between 

histological, histochemical and biochemical studies. 

Digestion 1972;5(1):40-48. Not sensitivity or specificity of 

an identified test

Malizia G, Trejdosiewicz L K, Wood G M et al. The 

microenvironment of coeliac disease: T cell phenotypes

and expression of the T2 'T blast' antigen by small bowel 

lymphocytes. Clinical and Experimental Immunology

1985;60(2):437-446. Not sensitivity or specificity of an 

A-418
identified test 

Mallas E G, Williamson N, Cooper B T et al. IgA class

reticulin antibodies in relatives of patients with coeliac 

disease. Gut 1977;18(8):647-650. Not sensitivity or 

specificity of an identified test

Mallet M. Coeliac disease in the very elderly. Cme J

Geriatr Med 2002;4(2):70-73. Not sensitivity or specificity

of an identified test 

Maluenda C, Phillips A D, Briddon A et al. Quantitative

analysis of small intestinal mucosa in cow's milk-sensitive

enteropathy. Journal of Pediatric Gastroenterology and 

Nutrition 1984;3(3):349-356. Not sensitivity or specificity

of an identified test 

Manabe K, Donaldson P T, Underhill J A et al. Human 

leukocyte antigen A1-B8-DR3-DQ2-DPB1*0401 extended 

haplotype in autoimmune hepatitis. Hepatology

1993;18(6):1334-1337. Not sensitivity or specificity of an

identified test 

Mandal A, Mayberry J. How common is celiac disease in 

South America?. American Journal of Gastroenterology

2000;95(3):579-580. Not sensitivity or specificity of an 

identified test 

Mandrusiak L M, Beitel L K, Wang X et al. 

Transglutaminase potentiates ligand-dependent proteasome 

dysfunction induced by polyglutamine-expanded androgen 

receptor. Hum Mol Genet 2003;12(13):1497-1506. Not

sensitivity or specificity of an identified test 

Manfras B J, Swinyard M, Rudert W A et al. Altered 

CYP21 genes in HLA-haplotypes associated with 

congenital adrenal hyperplasia (CAH): A family study.

Hum Genet 1993;92(1):33-39. Not sensitivity or specificity

of an identified test 

Mann D L, Katz S I, Nelson D L et al. Specific B-cell 

antigens associated with gluten-sensitive enteropathy and

dermatitis herpetiformis. Lancet 1976;1(7951):110-111. 

Not sensitivity or specificity of an identified test

Mannering S I, Purcell A W, Honeyman M C et al. Human 

T-cells recognise N-terminally Fmoc-modified peptide. 

Vaccine 2003;21(25-26):3638-3646. Not sensitivity or 

specificity of an identified test

Mannion A, Stevens F M, McCarthy C F et al. Extended

major histocompatibility complex haplotypes in celiac 

patients in the west of Ireland. American Journal of 

Medical Genetics 1993;45(3):373-377. Not sensitivity or 

specificity of an identified test

Manousos O N, Economidou J C, Georgiadou D E et al. 

Alpha-chain disease with clinical, immunological, and 

histological recovery. British Medical Journal

1974;2(916):409-412. Not sensitivity or specificity of an

identified test 

Mansbridge J N, Knappe A M. Changes in keratinocyte 

maturation during wound healing. J Invest Dermatol 

1987;89(3):253-263. Not sensitivity or specificity of an 

identified test 

Mantile G, Miele L, Cordella-Miele E et al. Human Clara

cell 10-kDa protein is the counterpart of rabbit uteroglobin.

Journal of Biological Chemistry 1993;268(27):20343-

20351. Not sensitivity or specificity of an identified test 

Mantovani V, Corazza G R, Angelini G et al. Molecular 

analysis of HLA-DQ A alleles in coeliac disease lack of a

unique disease-associated sequence. Clinical and 

Experimental Immunology 1991;83(1):74-78. Not 

sensitivity or specificity of an identified test 

Mantovani V, Corazza G R, Bragliani M et al. Asp57-

negative HLA DQ beta chain and DQA1*0501 allele are 

essential for the onset of DQw2-positive and DQw2-

negative coeliac disease. Clinical and Experimental 

Immunology 1993;91(1):153-156. Not sensitivity or 

specificity of an identified test

Mantovani V, Corazza G R, Frisoni M et al. HLA-DP 

polymorphism in northern Italian celiac patients. Tissue 

Antigens 1992;40(4):182-186. Not sensitivity or specificity

of an identified test 

Mantzaris G J, Tsirogianni A, Perivolioti E et al. Sensitivity

and specificity of serum IgA class endomysial antibody in

the diagnosis of coeliac disease. Hell J Gastroenterol 

1996;8(4):308-311. Improper control group 

Manuel P D, Walker-Smith J A, France N E. Patchy

enteropathy in childhood. Gut 1979;20(3):211-215. Not 

sensitivity or specificity of an identified test 

Marek A, Korzon M, Smiatacz T et al. Attempt to evaluate

activation of peripheral blood lymphocytes (CD69) after 

gluten challenge in children with coeliac disease. Med Sci 

Monit 1998;4(5):821-825. Not sensitivity or specificity of

an identified test

Marek Andrzej, Brodzicki Jacek, Liberek Anna et al. TGFbeta (transforming growth factor-beta) in chronic

inflammatory conditions - a new diagnostic and prognostic 

marker?. Medical Science Monitor - International Medical 

Journal of Experimental and Clinical Research

2002;8(7):Ra145-Ra151. Not sensitivity or specificity of an 

identified test 

Mariani P, Carsughi F, Spinozzi F et al. Ligand-induced 

conformational changes in tissue transglutaminase: Monte 

Carlo analysis of small-angle scattering data. Biophysical 

Journal 2000;78(6):3240-3251. Not sensitivity or 

specificity of an identified test

Mariani P, Mazzilli M C, Margutti G et al. Coeliac disease,

enamel defects and HLA typing. Acta Paediatrica (Oslo, 

Norway - 1992) 1994;83(12):1272-1275. Not sensitivity or

specificity of an identified test

A-419
Mariani P, Viti M G, Montuori M et al. The gluten-free 

diet: a nutritional risk factor for adolescents with celiac

disease?. Journal of Pediatric Gastroenterology and 

Nutrition 1998;27(5):519-523. Not sensitivity or specificity

of an identified test 

Marinello D, Rapa A, Osello R et al. Celiac disease

screening: exploring the iceberg with salivary antigliadin 

antibodies. Journal of Pediatric Gastroenterology and 

Nutrition 2001;32(2):227-228. Not sensitivity or specificity

of an identified test 

Marks J, Shuster S. Dermatogenic enteropathy. Gut 

1970;11(4):292-298. Not sensitivity or specificity of an 

identified test 

Marks J, Shuster S. Intestinal malabsorption and the skin. 

Gut 1971;12(11):938-947. Not sensitivity or specificity of

an identified test

Marks J, Shuster S. Skin disease and the gut. British 

Medical Journal 1971;1(740):110-111. Not sensitivity or

specificity of an identified test

Marks J, Birkett D, Shuster S et al. Small intestinal 

mucosal abnormalities in relatives of patients with 

dermatitis herpetiformis. Gut 1970;11(6):493-497. Not 

sensitivity or specificity of an identified test 

Marley N J, Macartney J C, Ciclitira P J. HLA-DR, DP and 

DQ expression in the small intestine of patients with 

coeliac disease. Clinical and Experimental Immunology

1987;70(2):386-393. Not sensitivity or specificity of an 

identified test 

Marn C S, Gore R M, Ghahremani G G. Duodenal 

manifestations of nontropical sprue. Gastrointestinal 

Radiology 1986;11(1):30-35. Not sensitivity or specificity

of an identified test 

Marren P, Yell J, Charnock F M et al. The association

between lichen sclerosus and antigens of the HLA system. 

British Journal of Dermatology 1995;132(2):197-203. Not

sensitivity or specificity of an identified test 

Marsh M N. Studies of intestinal lymphoid tissue: the 

cytology and electron microscopy of gluten-sensitive

enteropathy, with particular reference to its 

immunopathology. Scandinavian Journal of

Gastroenterology.Supplement 1981;7087-106. Not 

sensitivity or specificity of an identified test 

Marsh M N. Studies of intestinal lymphoid tissue. XV. 

Histopathologic features suggestive of cell-mediated 

reactivity in jejunal mucosae of patients with dermatitis 

herpetiformis. Virchows Archiv.A, Pathological Anatomy

and Histopathology 1989;416(2):125-132. Not sensitivity

or specificity of an identified test

Marsh M N. Screening for latent gluten sensitivity:

questions many, but answers few. European Journal of

Gastroenterology & Hepatology 1996;8(1):3-6. Not 

sensitivity or specificity of an identified test 

Marsh M N. Gluten, major histocompatibility complex, and 

the small intestine: A molecular and immunobiologic 

approach to the spectrum of gluten sensitivity ('celiac

sprue'). Gastroenterology 1992;102(1):330-354. Not 

sensitivity or specificity of an identified test 

Marsh M N. Gluten sensitivity and latency: Can patterns of 

intestinal antibody secretion define the great 'silent 

majority?'. Gastroenterology 1993;104(5):1550-1553. Not 

sensitivity or specificity of an identified test 

Marsh M N. The immunopathology of the small intestinal 

reaction in gluten-sensitivity. Immunological Investigations 

1989;18(1-4):509-531. Not sensitivity or specificity of an

identified test 

Marsh M N. The natural history of gluten sensitivity: 

Defining, refining and re-defining. Q J Med 1995;88(1):9-

13. Not sensitivity or specificity of an identified test 

Marsh M N. Transglutaminase, gluten and celiac disease:

Food for thought. Nat Med 1997;3(7):725-726. Not 

sensitivity or specificity of an identified test 

Marsh M N, Haeney M R. Studies of intestinal lymphoid 

tissue. VI. Proliferative response of small intestinal 

epithelial lymphocytes distinguishes gluten-from nongluten-induced enteropathy. J Clin Pathol 1983;36(2):149-

160. Not sensitivity or specificity of an identified test 

Marsh M N, Miller V. Studies of intestinal lymphoid tissue.

VIII. Use of epithelial lymphocyte mitotic indices in 

differentiating untreated celiac sprue mucosa from other 

childhood enteropathies. Journal of Pediatric 

Gastroenterology and Nutrition 1985;4(6):931-935. Unable

to extract data

Marsh M N, Bjarnason I, Shaw J et al. Studies of intestinal

lymphoid tissue. XIV--HLA status, mucosal morphology,

permeability and epithelial lymphocyte populations in first 

degree relatives of patients with coeliac disease. Gut 

1990;31(1):32-36. Not sensitivity or specificity of an 

identified test 

Marsh M N, Loft D E, Garner V G et al. Time/dose 

responses of coeliac mucosae to graded oral challenges 

with Frazer's fraction III of gliadin. European Journal of

Gastroenterology & Hepatology 1992;4(8):667-673. Not 

sensitivity or specificity of an identified test 

Marsh M N, Mathan M, Mathan V I. Studies of intestinal 

lymphoid tissue. VII. The secondary nature of lymphoid 

cell "activation" in the jejunal lesion of tropical sprue. 

American Journal of Pathology 1983;112(3):302-312. Not 

sensitivity or specificity of an identified test 

Martelossi S, Zanatta E, Del Santo E et al. Dental enamel 

defects and screening for coeliac disease. Acta paediatrica 

(Oslo, Norway : 1992).Supplement. 1996;41247-48. Not 

sensitivity or specificity of an identified test 

A-420
Martin-Villa J M, Lopez-Suarez J C, Perez-Blas M et al. 

Coeliac- and enteropathy-associated autoantibodies in 

Spanish insulin-dependent diabetes mellitus patients and 

their relation to HLA antigens. Journal of Diabetes and Its

Complications 2001;15(1):38-43. Unable to extract data 

Martinelli P, Troncone R, Paparo F et al. Coeliac disease 

and unfavourable outcome of pregnancy. Gut 

2000;46(3):332-335. Not sensitivity or specificity of an 

identified test 

Martinet Nadine, Bonnard Lionel, Regnault Veronique et 

al. In vivo transglutaminase type 1 expression in normal 

lung, preinvasive bronchial lesions, and lung cancer. 

American Journal of Respiratory Cell and Molecular 

Biology 2003;28(4):428-435. Not sensitivity or specificity

of an identified test 

Martinetti M, Cuccia M, Daielli C et al. Anti-HBV neonatal

immunization with recombinant vaccine. Part II. Molecular 

basis of the impaired alloreactivity. Vaccine

1995;13(6):555-560. Not sensitivity or specificity of an 

identified test 

Martinetti M, De Silvestri A, Belloni C et al. Humoral 

response to recombinant hepatitis B virus vaccine at birth: 

role of HLA and beyond. Clinical Immunology (Orlando, 

Fla.) 2000;97(3):234-240. Not sensitivity or specificity of

an identified test

Martinez J, Chalupowicz D G, Roush R K et al. 

Transglutaminase-mediated processing of fibronectin by

endothelial cell monolayers. Biochemistry

1994;33(9):2538-2545. Not sensitivity or specificity of an

identified test 

Martinez J, Rich E, Barsigian C. Transglutaminasemediated cross-linking of fibrinogen by human umbilical 

vein endothelial cells. Journal of Biological Chemistry

1989;264(34):20502-20508. Not sensitivity or specificity of 

an identified test

Martini S, Mengozzi G, Aimo G et al. Diagnostic 

accuracies for celiac disease of four tissue transglutaminase

autoantibody tests using human antigen. Clinical Chemistry 

2001;47(9):1722-1725. Improper control group 

Martini Silvia, Mengozzi Giulio, Aimo Giuseppe et al.

Comparative evaluation of serologic tests for celiac disease 

diagnosis and follow-up. Clinical Chemistry 2002;48(6 Pt 

1):960-963. Improper control group 

Marttinen A, Maki M. Purification of fibroblast-derived

celiac disease autoantigen molecules. Pediatric Research

1993;34(4):420-423. Not sensitivity or specificity of an 

identified test 

Marttinen A, Sulkanen S, Maki M. Human fibroblastderived molecules as antigens in enzyme-linked 

immunosorbent assay for coeliac disease-specific IgA. 

European Journal of Clinical Investigation 1997;27(2):135-

140. Not sensitivity or specificity of an identified test 

Martucci S, Biagi F, Di Sabatino A et al. Coeliac disease.

Digestive and Liver Disease - Official Journal of the Italian

Society of Gastroenterology and the Italian Association for

the Study of the Liver 2002;34(Suppl 2):s150-s153. Not 

sensitivity or specificity of an identified test 

Marvin K W, George M D, Fujimoto W et al. Cornifin, a

cross-linked envelope precursor in keratinocytes that is 

down-regulated by retinoids. Proceedings of the National 

Academy of Sciences of the United States of America 

1992;89(22):11026-11030. Not sensitivity or specificity of 

an identified test

Marzari R, Sblattero D, Florian F et al. Molecular

dissection of the tissue transglutaminase autoantibody 

response in celiac disease. Journal of Immunology

(Baltimore, Md.- 1950) 2001;166(6):4170-4176. Not 

sensitivity or specificity of an identified test 

Mascart-Lemone F. Strategy for serological screening of 

celiac disease. Gastroenterol Int 1998;11(3):144-148. Not 

sensitivity or specificity of an identified test 

Mascart-Lemone F, Lambrechts A. Serology of coeliac 

disease: early diagnosis and therapeutic impact. Acta 

Gastro-Enterologica Belgica 1995;58(5-6):388-396. 

Improper control group 

Mascart-Lemone F, Cadranel S, Delacroix D L et al. 

Change in molecular size of antigliadin IgA in serum

related to presence of antigen in the gut. Monographs in 

Allergy 1988;24310-4. Not sensitivity or specificity of an

identified test 

Mascart-Lemone F, Cadranel S, Van den et al. IgA immune 

response patterns to gliadin in serum. Int Arch Allergy

Appl Immunol 1988;86(4):412-419. Not sensitivity or 

specificity of an identified test

Mascart-Lemone F, Van den, Broeck J et al. Serological 

aspects of coeliac disease. Acta Gastro-Enterologica

Belgica 1992;55(2):200-208. Improper control group 

Mascart-Lemone F, Van Pachterbeek T, Duchateau J et al. 

Serum IgA anti-gliadin antibodies (monomeric versus 

dimeric) in childhood coeliac disease. Acta GastroEnterologica Belgica 1986;49(4):415-422. Not sensitivity

or specificity of an identified test

Masclee A A, Jansen J B, Driessen W M et al. Gallbladder 

sensitivity to cholecystokinin in coeliac disease.

Correlation of gallbladder contraction with plasma

cholecystokinin-like immunoreactivity during infusion of 

cerulein. Scandinavian Journal of Gastroenterology

1991;26(12):1279-1284. Not sensitivity or specificity of an 

identified test 

Masevitch C H, Ugolev A M, Zabelinskii E K et al. 

Lumenal and membrane hydrolysis of starch in some 

diseases of the small intestine and pancreas. American

A-421
Journal of Gastroenterology 1975;63(4):299-306. Not 

sensitivity or specificity of an identified test 

Mason M R, Bedrossian C W, Fahey C A. Value of 

immunocytochemistry in the study of malignant effusions. 

Diagnostic Cytopathology 1987;3(3):215-221. Not 

sensitivity or specificity of an identified test 

Masterson J B, Sweeney E C. The role of small bowel 

follow-through examination in the diagnosis of coeliac 

disease. British Journal of Radiology 1976;49(584):660-

664. Not sensitivity or specificity of an identified test 

Mastino A, Grelli S, Piacentini M et al. Correlation 

between induction of lymphocyte apoptosis and

prostaglandin E2 production by macrophages infected with

HIV. Cellular Immunology 1993;152(1):120-130. Not 

sensitivity or specificity of an identified test 

Mather K J, Meddings J B, Beck P L et al. Prevalence of 

IgA-antiendomysial antibody in asymptomatic low bone 

mineral density. American Journal of Gastroenterology

2001;96(1):120-125. Not sensitivity or specificity of an 

identified test 

Mathus-Vliegen E M H. Lymphoma in coeliac disease. J R 

Soc Med 1995;88(12):672-677. Not sensitivity or

specificity of an identified test

Maton P N, Selden A C, Fitzpatrick M L et al. Defective 

gallbladder emptying and cholecystokinin release in celiac 

disease. Reversal by gluten-free diet. Gastroenterology

1985;88(2):391-396. Not sensitivity or specificity of an 

identified test 

Matouskova E, McKay I, Povysil C et al. Characterization

of the differentiated phenotype of an organotypic model of 

skin derived from human keratinocytes and dried porcine 

dermis. Folia Biologica 1998;44(2):59-66. Not sensitivity

or specificity of an identified test

Matsushita S, Nishi T, Oiso M et al. HLA-DQ-binding 

peptide motifs. I. Comparative binding analysis of type II 

collagen-derived peptides to DR and DQ molecules of 

rheumatoid arthritis-susceptible and non-susceptible 

haplotypes. Int Immunol 1996;8(5):757-764. Not 

sensitivity or specificity of an identified test 

Matteoni C A, Goldblum J R, Wang N et al. Celiac disease

is highly prevalent in lymphocytic colitis. Journal of 

Clinical Gastroenterology 2001;32(3):225-227. Not 

sensitivity or specificity of an identified test 

Matteucci E, Cinapri V, Quilici S et al. Screening for 

coeliac disease in families of adults with Type 1 diabetes

based on serological markers. Diabetes, Nutrition & 

Metabolism 2001;14(1):37-42. Not sensitivity or specificity

of an identified test 

Matysiak-Budnik T, Candalh C, Dugave C et al. 

Alterations of the intestinal transport and processing of 

gliadin peptides in celiac disease. Gastroenterology

2003;125(3):696-707. Not sensitivity or specificity of an

identified test 

Maurino E C, Frisoni M, Bai J C et al. alphainf 1-

Antitrypsin clearance cannot be used to predict the severity

of histological intestinal damage in adult coeliac disease.

European Journal of Gastroenterology & Hepatology

1992;4(5):373-376. Not sensitivity or specificity of an 

identified test 

Maurino E, Capizzano H, Niveloni S et al. Value of 

endoscopic markers in celiac disease. Digestive Diseases 

and Sciences 1993;38(11):2028-2033. Not sensitivity or

specificity of an identified test

Maurino Eduardo, Niveloni Sonia, Chernavsky Alejandra 

et al. Azathioprine in refractory sprue: results from a 

prospective, open-label study. American Journal of 

Gastroenterology 2002;97(10):2595-2602. Not sensitivity

or specificity of an identified test

Maury C P, Teppo A M. Demonstration of tissue 90 kD 

glycoprotein as antigen in circulating IgG immune 

complexes in dermatitis herpetiformis and coeliac disease.

Lancet 1984;2(8408):892-894. Not sensitivity or specificity

of an identified test 

Mavromichalis J, Brueton M J, McNeish A S et al. 

Evaluation of the intraepithelial lymphocyte count in the

jejunum in childhood enteropathies. Gut 1976;17(8):600-

603. Not sensitivity or specificity of an identified test 

Mawhinney H, Love A H G. Anti reticulin antibody in 

jejunal juice in coeliac disease. Clinical and Experimental

Immunology 1975;21(3):394-398. Not sensitivity or 

specificity of an identified test

Mayer M, Greco L, Troncone R et al. Compliance of 

adolescents with coeliac disease with a gluten free diet. Gut

1991;32(8):881-885. Not sensitivity or specificity of an 

identified test 

Mayer M, Greco L, Troncone R et al. Early prediction of

relapse during gluten challenge in childhood celiac disease. 

Journal of Pediatric Gastroenterology and Nutrition 

1989;8(4):474-479. Not sensitivity or specificity of an 

identified test 

Maynard E, Ferruchi J T. Neurologic and abdominal 

abnormalities with the malabsorption syndrome. New Engl 

J Med 1973;289(22):1186-1193. Not sensitivity or

specificity of an identified test

Mazzacca G. Diet, coeliac disease and gastrointestinal

neoplasm. Adv Exp Med Biol 1993;348(-):133-136. Not 

sensitivity or specificity of an identified test 

Mazzarella G, Maglio M, Paparo F et al. An 

immunodominant DQ8 restricted gliadin peptide activates 

small intestinal immune response in in vitro cultured 

mucosa from HLA-DQ8 positive but not HLA-DQ8 

negative coeliac patients. Gut 2003;52(1):57-62. Not 

A-422
sensitivity or specificity of an identified test 

Mazzarella Giuseppe, MacDonald Thomas T, Salvati

Virginia M et al. Constitutive activation of the signal 

transducer and activator of transcription pathway in celiac

disease lesions. American Journal of Pathology

2003;162(6):1845-1855. Not sensitivity or specificity of an 

identified test 

Mazzetti di, Pietralata Giorgetti G M, Gregori M et al.

Subclinical coeliac disease. Italian Journal of

Gastroenterology 1992;24(6):352-354. Not sensitivity or 

specificity of an identified test

Mazzilli M C, Ferrante P, Mariani P et al. A study of Italian 

pediatric celiac disease patients confirms that the primary 

HLA association is to the DQ(alpha 1*0501, beta 1*0201) 

heterodimer. Human Immunology 1992;33(2):133-139. 

Improper control group 

Mazzola G, Berrino M, Bersanti M et al. Immunoglobulin 

and HLA-DP genes contribute to the susceptibility to

juvenile dermatitis herpetiformis. Eur J Immunogenet 

1992;19(3):129-139. Not sensitivity or specificity of an 

identified test 

McCarthy C F. The incidence of coeliac disease and its

familial occurrence. Ir Med J 1974;67(15):420-421. Not

sensitivity or specificity of an identified test 

McCarthy C F, Borland J L, Kurtz S M et al. The value of

the dissecting microscope in the diagnosis of nontropical 

sprue. American Journal of Pathology 1964;44(4):585-595. 

Not sensitivity or specificity of an identified test

McCarthy D M, Coleman M. Response of intestinal 

mucosa to gluten challenge in autistic subjects. Lancet

1979;2(8148):877-878. Not sensitivity or specificity of an

identified test 

McCarthy D, Manning N, Rees J P R et al. Hypothyroidism

and coeliac disease. A family study. Ir J Med Sci 

1976;145(7):237-238. Not sensitivity or specificity of an

identified test 

McClean P, Dodge J A, Nunn S et al. Surface features of 

small-intestinal mucosa in childhood diarrheal disorders. 

Journal of Pediatric Gastroenterology and Nutrition 

1996;23(5):538-546. Not sensitivity or specificity of an 

identified test 

McClelland D B, Shearman D J, Lai A et al. In vitro 

synthesis of immunoglobulins, secretory component, 

complement and lysozyme by human gastrointestinal

tissues. II. Pathological tissues. Clinical and Experimental

Immunology 1976;23(1):20-27. Not sensitivity or

specificity of an identified test

McCombs C C, Michalski J P. HLA and immune response. 

Jama - the Journal of the American Medical Association 

1989;262(6):774Not sensitivity or specificity of an 

identified test 

McCombs C C, Leggett A, Ramsey K M et al. The 

association of HLA class II alleles defined by restriction 

fragment length polymorphisms with responsiveness to 

hepatitis B vaccine. Vaccine Res 1993;2(2):105-109. Not

sensitivity or specificity of an identified test 

McCord M L, Hall R P. IgA antibodies against reticulin 

and endomysium in the serum and gastrointestinal 

secretions of patients with dermatitis herpetiformis. 

Dermatology 1994;189(Suppl 1):60-63. Not sensitivity or 

specificity of an identified test

McCormick P A, Feighery C, Dolan C et al. Altered 

gastrointestinal immune response in sarcoidosis. Gut 

1988;29(12):1628-1631. Not sensitivity or specificity of an 

identified test 

McDevitt J, O'Farrelly C, Weir D G et al. Proliferationassociated markers in the coeliac duodenum. European 

Journal of Gastroenterology & Hepatology 1994;6(3):223-

228. Not sensitivity or specificity of an identified test 

McElvaney N G, Duignan R, Fielding J F. Coeliac disease: 

clinical presentations, correlations of dietary compliance,

symptomatic response and repeat biopsy findings. Ulster 

Medical Journal 1992;61(2):134-138. Not sensitivity or

specificity of an identified test

McEwan G T, Lucas M L, Denvir M et al. A combined 

TDDA-PVC pH and reference electrode for use in the 

upper small intestine. Journal of Medical Engineering & 

Technology 1990;14(1):16-20. Not sensitivity or specificity

of an identified test 

McGowan I, Campbell A, Jewell D P. Intestinal mucosal 

abnormality associated with human immunodeficiency

virus infection. European Journal of Gastroenterology & 

Hepatology 1994;6(9):813-819. Not sensitivity or

specificity of an identified test

McGuire E A, Davis A R, Korsmeyer S J. T-cell 

translocation gene 1 (Ttg-1) encodes a nuclear protein

normally expressed in neural lineage cells. Blood 

1991;77(3):599-606. Not sensitivity or specificity of an 

identified test 

McIntyre A S, Long R G. Prospective survey of 

investigations in outpatients referred with iron deficiency

anaemia. Gut 1993;34(8):1102-1107. Not sensitivity or

specificity of an identified test

McIntyre A S, Ng D P, Smith J A et al. The endoscopic 

appearance of duodenal folds is predictive of untreated 

adult celiac disease. Gastrointestinal Endoscopy

1992;38(2):148-151. Not sensitivity or specificity of an 

identified test 

McKelvie P, Friling R, Davey K et al. Changes as the result

of ageing in extraocular muscles: A post-mortem study.

Aust New Zealand J Ophthalmol 1999;27(6):420-425. Not 

sensitivity or specificity of an identified test 

A-423
McKenna R, Stevens F M, McNicholl B et al. Family and 

population studies of HLA and coeliac disease in the West 

of Ireland. Tissue Antigens 1983;22(3):175-181. Not 

sensitivity or specificity of an identified test 

McManus R, Wilson A G, Mansfield J et al. TNF2, a

polymorphism of the tumour necrosis-alpha gene promoter, 

is a component of the celiac disease major 

histocompatibility complex haplotype. European Journal of

Immunology 1996;26(9):2113-2118. Not sensitivity or

specificity of an identified test

McManus Ross, Kelleher Dermot. Celiac disease--the

villain unmasked?. New England Journal of Medicine

2003;348(25):2573-2574. Not sensitivity or specificity of

an identified test

McMillan S A, Dickey W, Douglas J P et al. Transthyretin

values correlate with mucosal recovery in patients with 

coeliac disease taking a gluten free diet. Journal of Clinical

Pathology 2001;54(10):783-786. Not sensitivity or

specificity of an identified test

McMillan S A, Hutchison T, Haire M et al. Antigliadin

antibodies in dermatitis herpetiformis. Ulster Medical 

Journal 1983;52(2):113-117. Not sensitivity or specificity

of an identified test 

McMillan S A, Johnston S D, Watson R G et al. Dietary

intake, smoking, and transient anti-gliadin antibodies. 

Scandinavian Journal of Gastroenterology 1998;33(5):499-

503. Not sensitivity or specificity of an identified test 

McMillan S A, Watson R P, McCrum E E et al. Factors 

associated with serum antibodies to reticulin, endomysium,

and gliadin in an adult population. Gut 1996;39(1):43-47. 

Not sensitivity or specificity of an identified test

McNamee S, McLoughlin R, Stevens F M et al. Coeliac 

disease in the older patient. Rev Clin Gerontol 

2002;12(2):119-126. Not sensitivity or specificity of an 

identified test 

McNeish A S. Diagnosis of coeliac disease in retrospect. 

Archives of Disease in Childhood 1968;43(229):362-364. 

Not sensitivity or specificity of an identified test

McNeish A S, Anderson C M. The disorder in childhood. 

Clin Gastroenterol 1974;3(1):127-144. Not sensitivity or

specificity of an identified test

McNeish A S, Harms H K, Rey J et al. The diagnosis of 

coeliac disease. A commentary on the current practices of

members of the European Society for Paediatric

Gastroenterology and Nutrition (ESPGAN). Archives of 

Disease in Childhood 1979;54(10):783-786. Not sensitivity

or specificity of an identified test

McNicholl B. Coeliac disease: ecology, life history and 

management. Human Nutrition.Applied Nutrition 

1986;40(Suppl 1):55-60. Not sensitivity or specificity of an 

identified test 

McNicholl B, Egan B. Jejunal biopsy in celiac disease.

Clinical Pediatrics 1968;7(9):544-552. Not sensitivity or

specificity of an identified test

McNicholl B, Egan-Mitchell B. Infancy celiac disease 

without diarrhea. Pediatrics 1972;49(1):85-91. Not 

sensitivity or specificity of an identified test 

McNicholl B, Egan Mitchell B, Fottrell P. Early diagnosis 

of coeliac disease. Ir Med J 1975;68(8):187-191. Not 

sensitivity or specificity of an identified test 

McNicholl B, Egan-Mitchell B, Fottrell P F. Variability of 

gluten intolerance in treated childhood coeliac disease. Gut 

1979;20(2):126-132. Not sensitivity or specificity of an 

identified test 

McNicholl B, Egan-Mitchell B, Stevens F et al. Mucosal 

recovery in treated childhood celiac disease (glutensensitive enteropathy). Journal of Pediatrics

1976;89(3):418-424. Not sensitivity or specificity of an 

identified test 

McNiff J M, Glusac E J, Lazova R Z et al. Morphea limited

to the superficial reticular dermis: an underrecognized

histologic phenomenon. American Journal of

Dermatopathology 1999;21(4):315-319. Not sensitivity or

specificity of an identified test

McPherson J R. Jejunal biopsy. Medical Clinics of North 

America 1970;54(4):851-862. Not sensitivity or specificity

of an identified test 

McPherson J R. Jejunal biopsy in the diagnosis of

malabsorption syndromes. Diseases of the Colon and 

Rectum 1965;8(6):425-430. Not sensitivity or specificity of 

an identified test

McPherson R A. Commentary: advances in the laboratory

diagnosis of celiac disease. Journal of Clinical Laboratory

Analysis 2001;15(3):105-107. Not sensitivity or specificity

of an identified test 

McTernan C L, Stewart L C, Mijovic C H et al. Assessment 

of the non-HLA-DR-DQ contribution to IDDM1 in British

Caucasian families: Analysis of LMP7. Diabetic Med 

2000;17(9):661-666. Not sensitivity or specificity of an 

identified test 

Mearin F, Mearin M L, Pena A S. Distribution of IgA 1, 

and IgA 2 immunocytes in the jejunum of adult coeliac 

patients and controls. J Clin Nutr Gastroenterol 

1986;1(2):79-82. Not sensitivity or specificity of an 

identified test 

Mearin M L, Mulder C J J. Endoscopic small bowel biopsy

with a guided capsule. Acta Endosc 1994;24(4):393-401. 

Not sensitivity or specificity of an identified test

Mearin M L, Pena A S. Clinical indications of HLA typing

A-424
and measurement of gliadin antibodies in coeliac disease.

Netherlands Journal of Medicine 1987;31(5-6):279-285. 

Not sensitivity or specificity of an identified test

Mearin M L, Biemond I, Pena A S et al. HLA-DR

phenotypes in Spanish coeliac children: their contribution

to the understanding of the genetics of the disease. Gut 

1983;24(6):532-537. Not sensitivity or specificity of an 

identified test 

Mearin M L, Bouquet J, Mourad N et al. HLA-DR antigens 

and phenotypes in Dutch coeliac children and their 

families. Clinical Genetics 1985;27(1):45-50. Not

sensitivity or specificity of an identified test 

Mearin M L, Koninckx C R, Biemond I et al. Influence of 

genetic factors on the serum levels of antigliadin antibodies 

in celiac disease. Journal of Pediatric Gastroenterology and

Nutrition 1984;3(3):373-377. Not sensitivity or specificity

of an identified test 

Mearin M, Luisa Koning, Frits. Tissue transglutaminase: 

master regulator of celiac disease?. Journal of Pediatric 

Gastroenterology and Nutrition 2003;36(1):9-11. Not 

sensitivity or specificity of an identified test 

Mecham R P, Broekelmann T, Davis E C et al. Elastic fibre

assembly: macromolecular interactions. Ciba Foundation

Symposium 1995;192172-181;Discussion 181-4. Not 

sensitivity or specificity of an identified test 

Meddeb-Garnaoui A, Zeliszewski D, Mougenot J F et al. 

Reevaluation of the relative risk for susceptibility to celiac

disease of HLA-DRB1, -DQA1, -DQB1, -DPB1, and -

TAP2 alleles in a French population. Human Immunology

1995;43(3):190-199. Improper control group 

Mediene S, Hakem S, Bard J M et al. Serum lipoprotein

profile in Algerian patients with celiac disease. Clinica 

Chimica Acta 1995;International Journal of Clinical 

Chemistry; 235(2):189-196. Not sensitivity or specificity of 

an identified test

Mehra N K, Kaur Gurvinder, Kanga Uma et al. 

Immunogenetics of autoimmune diseases in Asian Indians. 

Annals of the New York Academy of Sciences

2002;958333-336. Not sensitivity or specificity of an 

identified test 

Mehta K. High levels of transglutaminase expression in

doxorubicin-resistant human breast carcinoma cells. 

International Journal of Cancer.Journal International Du 

Cancer 1994;58(3):400-406. Not sensitivity or specificity

of an identified test 

Mehta K, Lopez-Berestein G. Expression of tissue 

transglutaminase in cultured monocytic leukemia (THP-1) 

cells during differentiation. Cancer Research 

1986;46(3):1388-1394. Not sensitivity or specificity of an

identified test 

Mehta K, Lopez-Berestein G. Induction of tissue 

transglutaminase (TGase) in human monocytoid cells 

(THP-1) during retinoid and phorbol ester-induced 

differentation. Proc Am Assoc Cancer Res 1985;VOL. 26(-

):No 164Not sensitivity or specificity of an identified test 

Mehta K, Chandrashekar R, Rao U R. Transglutaminasecatalyzed incorporation of host proteins in Brugia malayi

microfilariae. Mol Biochem Parasitol 1996;76(1-2):105-

114. Not sensitivity or specificity of an identified test 

Mehta K, Lopez-Berestein G, Moore W T et al. Interferongamma requires serum retinoids to promote the expression 

of tissue transglutaminase in cultured human blood 

monocytes. Journal of Immunology (Baltimore, Md.- 1950) 

1985;134(4):2053-2056. Not sensitivity or specificity of an 

identified test 

Mehta K, Rao U R, Vickery A C et al. Significance of 

transglutaminase-catalyzed reactions in growth and 

development of filarial parasite, Brugia malayi. Biochem 

Biophys Res Commun 1990;173(3):1051-1057. Not 

sensitivity or specificity of an identified test 

Mehta K, Rao U R, Vickery A C et al. Identification of a

novel transglutaminase from the filarial parasite Brugia 

malayi and its role in growth and development. Mol 

Biochem Parasitol 1992;53(1-2):1-16. Not sensitivity or

specificity of an identified test

Mehta S, Wadhwa U N, Prakash A et al. Small bowel 

function in severe chronic diarrhea in children. Journal of

the Association of Physicians of India 1968;16(6):342-349. 

Not sensitivity or specificity of an identified test

Mehul B, Bernard D, Schmidt R. Calmodulin-like skin 

protein: a new marker of keratinocyte differentiation. 

Journal of Investigative Dermatology 2001;116(6):905-

909. Not sensitivity or specificity of an identified test 

Meijer Jos W R, Wahab Peter J, Mulder Chris J J. Small 

intestinal biopsies in celiac disease: duodenal or jejunal?. 

Virchows Archiv - an International Journal of Pathology

2002;442(2):124-128. Improper control group 

Meinhard E A, Wadbrook D G, Risdon R A. Computer 

card morphometry of jejunal biopsies in childhood coeliac 

disease. Journal of Clinical Pathology 1975;28(2):85-93. 

Not sensitivity or specificity of an identified test

Melino G, Piacentini M. 'Tissue' transglutaminase in cell 

death: a downstream or a multifunctional upstream

effector?. Febs Letters 1998;430(1-2):59-63. Not sensitivity

or specificity of an identified test

Melino G, Annicchiarico-Petruzzelli M, Piredda L et al. 

Tissue transglutaminase and apoptosis: sense and antisense 

transfection studies with human neuroblastoma cells. 

Molecular and Cellular Biology 1994;14(10):6584-6596. 

Not sensitivity or specificity of an identified test

Melino G, Catani M V, Corazzari M et al. Nitric oxide can

inhibit apoptosis or switch it into necrosis. Cellular and 

A-425
Molecular Life Sciences - Cmls 2000;57(4):612-622. Not 

sensitivity or specificity of an identified test 

Melino G, Draoui M, Bellincampi L et al. Retinoic acid

receptors alpha and gamma mediate the induction of 

"tissue" transglutaminase activity and apoptosis in human 

neuroblastoma cells. Experimental Cell Research

1997;235(1):55-61. Not sensitivity or specificity of an 

identified test 

Melino G, Farrace M G, Ceru' M P et al. Correlation 

between transglutaminase activity and polyamine levels in 

human neuroblastoma cells. Effect of retinoic acid and 

alpha-difluoromethylornithine. Experimental Cell Research 

1988;179(2):429-445. Not sensitivity or specificity of an

identified test 

Melone Mariarosa A B, Di Fede, Giuseppe Peluso et al. 

Abnormal accumulation of tTGase products in muscle and

erythrocytes of chorea-acanthocytosis patients. Journal of

Neuropathology and Experimental Neurology

2002;61(10):841-848. Not sensitivity or specificity of an

identified test 

Meloni G F, Dessole S, Vargiu N et al. The prevalence of 

coeliac disease in infertility. Human Reproduction (Oxford, 

England) 1999;14(11):2759-2761. Not sensitivity or 

specificity of an identified test

Meloni G F, Tomasi P A, Bertoncelli A et al. Prevalence of

silent celiac disease in patients with autoimmune thyroiditis 

from Northern Sardinia. Journal of Endocrinological 

Investigation 2001;24(5):298-302. Not sensitivity or 

specificity of an identified test

Meloni G, Dore A, Fanciulli G et al. Subclinical coeliac 

disease in schoolchildren from northern Sardinia. Lancet 

1999;353(9146):37Not sensitivity or specificity of an 

identified test 

Menni S, Cavalli R, Prampolini R et al. Dental enamel

defects in children suffering from dermatitis herpetiformis 

and in their first degree relatives. Eur J Pediatr Dermatol 

1996;6(1):33-38. Not sensitivity or specificity of an 

identified test 

Mention Jean, Ben Ahmed, Melika Begue et al. Interleukin 

15: a key to disrupted intraepithelial lymphocyte 

homeostasis and lymphomagenesis in celiac disease. 

Gastroenterology 2003;125(3):730-745. Not sensitivity or

specificity of an identified test

Menzel E J, Pehamberger H, Holubar K. Demonstration of

antibodies to wheat gliadin in dermatitis herpetiformis 

using sup 1sup 4C-radioimmunoassay. Clin Immunol 

Immunopathol 1978;10(2):193-201. Not sensitivity or 

specificity of an identified test

Menzel J. Radioimmunoassay for antigliadin-antibodies 

using 14C-labelled gliadin. Journal of Immunological 

Methods 1977;18(3-4):257-268. Not sensitivity or

specificity of an identified test

Menzies I S, Laker M F, Pounder R et al. Abnormal 

intestinal permeability to sugars in villous atrophy. Lancet 

1979;2(8152):1107-1109. Not sensitivity or specificity of

an identified test

Mercer J, Eagles M E, Talbot I C. Brush border enzymes in 

coeliac disease: histochemical evaluation. Journal of 

Clinical Pathology 1990;43(4):307-312. Not sensitivity or

specificity of an identified test

Merridew S R, Wilson D V, Williams E J. Antigliadin

antibody measurement by chemiluminescence ELISA in 

the diagnosis of coeliac disease. Journal of Clinical 

Pathology 1995;48(6):509-512. Improper control group 

Merz Hartmut, Lange Karin, Gaiser Timo et al.

Characterization of a novel human anaplastic large cell 

lymphoma cell line tumorigenic in SCID mice. Leukemia 

& Lymphoma 2002;43(1):165-172. Not sensitivity or 

specificity of an identified test

Messing B, Dutra S L, Thuillier F et al. Whole-body

protein metabolism assessed by leucine and glutamine 

kinetics in adult patients with active celiac disease. 

Metabolism- Clinical and Experimental 1998;47(12):1429-

1433. Not sensitivity or specificity of an identified test 

Metha K, Turpin J, Lopez-Berestein G. Induction of tissue 

transglutaminase in human peripheral blood monocytes by

intracellular delivery of retinoids. Journal of Leukocyte 

Biology 1987;41(4):341-348. Not sensitivity or specificity

of an identified test 

Metskula K, Grunberg H, Uibo O et al. Antigliadin 

antibodies and autoantibodies among 9, 12 and 15 year-old 

schoolchildren. Cent-Eur J Immunol 1998;23(3-4):197-202. 

Not sensitivity or specificity of an identified test

Meuli R, Pichler W J, Gaze H et al. Genetic difference in

HLA-DR phenotypes between coeliac disease and

transitory gluten intolerance. Archives of Disease in 

Childhood 1995;72(1):29-32. Not sensitivity or specificity

of an identified test 

Meyer B M, Campbell D R, Curington C W et al. 

Bentiromide test is not affected in patients with small 

bowel disease or liver disease. Pancreas 1987;2(1):44-47. 

Not sensitivity or specificity of an identified test

Mezger J, Endo K, Walter S et al. A pitfall in 

immunocytochemistry: Non-specific staining of 

plasmacytoid cells with immunoalkaline phosphatase 

techniques. J Tumor Marker Oncol 1988;3(1):107-115. Not 

sensitivity or specificity of an identified test 

Mezzogiorno A, Esposito V. Potential role for high and low 

molecular weight tissue transglutaminases in transforming 

mammalian cell properties. Curr Drug Targets Immune 

Endocr Metabol Disord 2001;1(3):223-232. Not sensitivity

or specificity of an identified test

A-426
Mian S, el Alaoui S, Lawry J et al. The importance of the 

GTP-binding protein tissue transglutaminase in the 

regulation of cell cycle progression. Febs Letters 

1995;370(1-2):27-31. Not sensitivity or specificity of an

identified test 

Mic caron, Umek-Bradac caron, Dolins caron et al. 

Ultrasonographic assessment of celiac disease in children: 

Comparison with antiendomysium antibodies and 

histology. Wien Klin Wochenschr Suppl 2001;113(3):27-

31. Not sensitivity or specificity of an identified test 

Michaelsson G, Gerden B, Hagforsen E et al. Psoriasis 

patients with antibodies to gliadin can be improved by a 

gluten-free diet. British Journal of Dermatology 

2000;142(1):44-51. Not sensitivity or specificity of an 

identified test 

Michaelsson G, Gerden B, Ottosson M et al. Patients with

psoriasis often have increased serum levels of IgA 

antibodies to gliadin. British Journal of Dermatology

1993;129(6):667-673. Not sensitivity or specificity of an

identified test 

Michaelsson G, Kraaz W, Gerden B et al. Increased 

lymphocyte infiltration in duodenal mucosa from patients 

with psoriasis and serum IgA antibodies to gliadin. British 

Journal of Dermatology 1995;133(6):896-904. Not 

sensitivity or specificity of an identified test 

Michaelsson G, Kraaz W, Gerden B et al. Patients with 

psoriasis have elevated levels of serum eosinophil cationic 

protein and increased numbers of EG2 positive eosinophils 

in the duodenal stroma. British Journal of Dermatology

1996;135(3):371-378. Not sensitivity or specificity of an

identified test 

Michaelsson G, Kraaz W, Hagforsen E et al. Psoriasis

patients have highly increased numbers of tryptase-positive 

mast cells in the duodenal stroma. Br J Dermatol 

1997;136(6):866-870. Not sensitivity or specificity of an

identified test 

Michalski J P, McCombs C C. Celiac disease: clinical

features and pathogenesis. American Journal of the Medical 

Sciences 1994;307(3):204-211. Not sensitivity or

specificity of an identified test

Michalski J P, McCombs C C, Arai T et al. HLA-DR, DQ 

genotypes of celiac disease patients and healthy subjects 

from the West of Ireland. Tissue Antigens 1996;47(2):127-

133. Improper control group 

Michel S, Demarchez M. Localization and in vivo activity

of epidermal transglutaminase. Journal of Investigative 

Dermatology 1988;90(4):472-474. Not sensitivity or 

specificity of an identified test

Michel S, Bernerd F, Jetten A M et al. Expression of 

keratinocyte transglutamine mRNA revealed by in situ 

hybridization. Journal of Investigative Dermatology

1992;98(3):364-368. Not sensitivity or specificity of an 

identified test 

Michel S, Courseaux A, Miquel C et al. Determination of 

retinoid activity by an enzyme-linked immunosorbent 

assay. Analytical Biochemistry 1991;192(1):232-236. Not 

sensitivity or specificity of an identified test 

Michel S, Reichert U, Isnard J L et al. Retinoic acid 

controls expression of epidermal transglutaminase at the 

pre-translational level. Febs Letters 1989;258(1):35-38. Not 

sensitivity or specificity of an identified test 

Michel S, Schmidt R, Robinson S M et al. Identification 

and subcellular distribution of cornified envelope precursor 

proteins in the transformed human keratinocyte line SVK14. Journal of Investigative Dermatology 1987;88(3):301-

305. Not sensitivity or specificity of an identified test 

Michelsen A E, Santi C, Holme R et al. The chargeheterogeneity of human fibrinogen as investigated by 2D 

electrophoresis. Thrombosis Research 2000;100(6):529-

535. Not sensitivity or specificity of an identified test 

Migheli A, Mongini T, Doriguzzi C et al. Muscle apoptosis 

in humans occurs in normal and denervated muscle, but not 

in myotonic dystrophy, dystrophinopathies or inflammatory

disease. Neurogenetics 1997;1(2):81-87. Not sensitivity or 

specificity of an identified test

Mignot E, Kimura A, Abbal M et al. DQCAR 

microsatellite polymorphisms in three selected HLA class

II-associated diseases. Tissue Antigens 1995;46(4):299-

304. Not sensitivity or specificity of an identified test 

Miletic I D, Miletic V D, Sattely-Miller E A et al. 

Identification of gliadin presence in pharmaceutical 

products. Journal of Pediatric Gastroenterology and 

Nutrition 1994;19(1):27-33. Not sensitivity or specificity of 

an identified test

Miletic I D, Schiffmann S S, Sattely-Miller E A et al. 

Development of ELISA-based assays for detection, 

quantitation and avidity determination of salivary IgA antigliadin antibodies. Jugosl Med Biokem 1995;14(1-2):15-

25. Not sensitivity or specificity of an identified test 

Miller A, Paspaliaris W, Elliott P R et al. Antitransglutaminase antibodies and coeliac disease. Australian 

and New Zealand Journal of Medicine 1999;29(2):239-242. 

Improper control group 

Miller C C, Anderton B H. Transglutaminase and the 

neuronal cytoskeleton in Alzheimer's disease. Journal of

Neurochemistry 1986;46(6):1912-1922. Not sensitivity or 

specificity of an identified test

Miller M L, Johnson G V. Transglutaminase cross-linking 

of the tau protein. Journal of Neurochemistry

1995;65(4):1760-1770. Not sensitivity or specificity of an

identified test 

Milovic V, Stein J, Caspary W F. Intestinal malabsorption: 

A-427
Patophysiology, clinical signs and symptoms, diagnosis and 

treatment (First part). Arch Gastroenterohepatol 1999;18(3-

4):65-74. Not sensitivity or specificity of an identified test 

Ming M E, Daryanani H A, Roberts L P et al. Binding of 

keratin intermediate filaments (K10) to the cornified 

envelope in mouse epidermis: Implicatins for barrier 

function. J Invest Dermatol 1994;103(6):780-784. Not 

sensitivity or specificity of an identified test 

Mino M, Lauwers G Y. Role of lymphocytic 

immunophenotyping in the diagnosis of gluten-sensitive 

enteropathy with preserved villous architecture. Am J Surg 

Pathol 2003;27(9):1237-1242. Unable to extract data 

Minta J O, Pambrun L. In vitro induction of cytologic and 

functional differentiation of the immature human

monocytelike cell line U-937 with phorbol myristate 

acetate. American Journal of Pathology 1985;119(1):111-

126. Not sensitivity or specificity of an identified test 

Mirakian R, Hill S, Richardson A et al. HLA product 

expression and lymphocyte subpopulations in jejunum 

biopsies of children with idiopathic protracted diarrhoea 

and enterocyte autoantibodies. Journal of Autoimmunity

1988;1(3):263-277. Not sensitivity or specificity of an 

identified test 

Mirza A, Liu S-L, Frizell E et al. A role for tissue

transglutaminase in hepatic injury and fibrogenesis, and its 

regulation by NF-kappaB. Am J Physiol Gastrointest Liver 

Physiol 1997;272(2 35-2):G281-G288. Not sensitivity or

specificity of an identified test

Misery L, Boucheron S, Claudy A L. Factor XIIIa 

expression in juvenile xanthogranuloma. Acta DermatoVenereologica 1994;74(1):43-44. Not sensitivity or 

specificity of an identified test

Misra S, Ament M E. Diagnosis of coeliac sprue in 1994. 

Gastroenterology Clinics of North America

1995;24(1):133-143. Not sensitivity or specificity of an 

identified test 

Mitchell R M S, Robinson T J. Monitoring dietary 

compliance in coeliac disease using red cell distribution 

width. International Journal of Clinical Practice

2002;56(4):249-250. Not sensitivity or specificity of an 

identified test 

Mitchison H C, al Mardini H, Gillespie S et al. A pilot

study of fluticasone propionate in untreated coeliac disease.

Gut 1991;32(3):260-265. Not sensitivity or specificity of an 

identified test 

Mitkevich O V, Shainoff J R, DiBello P M et al.

Coagulation factor XIIIa undergoes a conformational 

change evoked by glutamine substrate. Studies on kinetics 

of inhibition and binding of XIIIA by a cross-reacting

antifibrinogen antibody. Journal of Biological Chemistry

1998;273(23):14387-14391. Not sensitivity or specificity of 

an identified test

Mitsunaga S, Oguchi T, Tokunaga K et al. High-resolution

HLA-DQB1 typing by combination of group-specific 

amplification and restriction fragment length 

polymorphism. Hum Immunol 1995;42(4):307-314. Not 

sensitivity or specificity of an identified test 

Mittal K K. Immunobiology of the human major

histocompatibility complex: association of HLA antigens 

with disease. Acta Anthropogenetica 1984;8(3-4):245-268. 

Not sensitivity or specificity of an identified test

Miwa K, Doyle C, Strominger J L. Sequence-specific 

interactions of nuclear factors with conserved sequences of

human class II major histocompatibility complex genes.

Proc Natl Acad Sci U S A 1987;84(14):4939-4943. Not 

sensitivity or specificity of an identified test 

Miyagawa S, Shinohara K, Fujita T et al. Neonatal lupus 

erythematosus: Analysis of HLA class II alleles in mothers

and siblings from seven Japanese families. J Am Acad 

Dermatol 1997;36(2):186-190. Not sensitivity or specificity

of an identified test 

Mizugami T, Mikata A, Hajikano H et al. Childhood 

lymphoma. A clinicopathological and immunohistological 

study of 58 cases. Acta Pathologica Japonica 

1988;38(9):1149-1166. Not sensitivity or specificity of an

identified test 

Moayyedi P, O'Mahony S, Jackson P et al. Small intestine 

in lymphocytic and collagenous colitis: mucosal 

morphology, permeability, and secretory immunity to 

gliadin. Journal of Clinical Pathology 1997;50(6):527-529. 

Not sensitivity or specificity of an identified test

Mobacken H, Andersson H, Dahlberg E et al. Relationship

of dietary gluten intake to dapsone dose in dermatitis 

herpetiformis. Acta Dermato-Venereologica 

1987;67(3):267-270. Not sensitivity or specificity of an 

identified test 

Mobacken H, Kastrup W, Ljunghall K. Linear IgA 

dermatosis: A study of ten adult patients. Acta DermVenereol 1983;63(2):123-128. Not sensitivity or specificity

of an identified test 

Modigliani R, Poitras P, Galian A. Chronic non-specific 

ulcerative duodenojejunoileitis: Report of four cases. Gut 

1979;20(4):318-328. Not sensitivity or specificity of an 

identified test 

Mohan K, Pinto D, Issekutz T B. Identification of tissue 

transglutaminase as a novel molecule involved in human 

CD8SUP+ T cell transendothelial migration. J Immunol 

2003;171(6):3179-3186. Not sensitivity or specificity of an 

identified test 

Mohindra S, Yachha S K, Srivastava A et al. Coeliac 

disease in Indian children: assessment of clinical,

nutritional and pathologic characteristics. Journal of Health,

Population, and Nutrition 2001;19(3):204-208. Not 

A-428
sensitivity or specificity of an identified test 

Mokhallalaty M, Debek A, Naja Z et al. Celiac disease at 

Makassed General Hospital (8 years of experience). Rev 

Med Liban 2002;14(2-3):49-53. Not sensitivity or

specificity of an identified test

Molberg O, Kett K, Scott H et al. Gliadin specific, HLA 

DQ2-restricted T cells are commonly found in small 

intestinal biopsies from coeliac disease patients, but not

from controls. Scandinavian Journal of Immunology

1997;46(1):103-108. Not sensitivity or specificity of an 

identified test 

Molberg O, Lundin K E, Nilsen E M et al. HLA restriction 

patterns of gliadin- and astrovirus-specific CD4+ T cells

isolated in parallel from the small intestine of celiac disease

patients. Tissue Antigens 1998;52(5):407-415. Not 

sensitivity or specificity of an identified test 

Molberg O, McAdam S N, Sollid L M. Role of tissue 

transglutaminase in celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 2000;30(3):232-240. Not

sensitivity or specificity of an identified test 

Molberg O, McAdam S N, Korner R et al. Tissue

transglutaminase selectively modifies gliadin peptides that 

are recognized by gut-derived T cells in celiac disease.

Nature Medicine 1998;4(6):713-717. Not sensitivity or 

specificity of an identified test

Molberg O, McAdam S, Lundin K E et al. T cells from 

celiac disease lesions recognize gliadin epitopes

deamidated in situ by endogenous tissue transglutaminase. 

European Journal of Immunology 2001;31(5):1317-1323. 

Not sensitivity or specificity of an identified test

Molberg Oyvind, Solheim Flaete, Nina Jensen et al. 

Intestinal T-cell responses to high-molecular-weight 

glutenins in celiac disease. Gastroenterology

2003;125(2):337-344. Not sensitivity or specificity of an

identified test 

Monaghan P, Clarke C L, Perusinghe N P et al. Epidermal 

growth factor receptor expression on human breast luminal 

and basal cells in vitro. Epithelial Cell Biology 

1995;4(2):52-62. Not sensitivity or specificity of an 

identified test 

Monos D S, Czanky E, Ono S J et al. L cells expressing DQ 

molecules of the DR3 and DR4 haplotypes: reactivity

patterns with mAbs. Immunogenetics 1995;42(3):172-180. 

Not sensitivity or specificity of an identified test

Monsonego A, Friedmann I, Shani Y et al. GTP-dependent

conformational changes associated with the functional 

switch between Galpha and cross-linking activities in 

brain-derived tissue transglutaminase. Journal of Molecular 

Biology 1998;282(4):713-720. Not sensitivity or specificity

of an identified test 

Montalto M, Cuoco L, Ricci R et al. Immunohistochemical 

analysis of ZO-1 in the duodenal mucosa of patients with 

untreated and treated celiac disease. Digestion 

2002;65(4):227-233. Not sensitivity or specificity of an 

identified test 

Monteiro E, Menezes M L, Magalhaes Ramalho P. Antireticulin antibodies: a diagnostic and monitoring test for 

childhood coeliac disease. Scandinavian Journal of

Gastroenterology 1986;21(8):955-957. Not sensitivity or 

specificity of an identified test

Monteiro M R, Shapiro S S, Takafuta T et al. Von 

Willebrand factor receptor GPIb alpha is expressed by

human factor XIIIa-positive dermal dendrocytes and is 

upregulated by mast cell degranulation. Journal of 

Investigative Dermatology 1999;113(2):272-276. Not 

sensitivity or specificity of an identified test 

Monteleone G, Pender S L F, Alstead E et al. Role of 

interferon alpha in promoting T helper cell type 1 responses 

in the small intestine in coeliac disease. Gut 

2001;48(3):425-429. Not sensitivity or specificity of an 

identified test 

Monteleone G, Pender S L, Wathen N C et al. Interferonalpha drives T cell-mediated immunopathology in the 

intestine. European Journal of Immunology

2001;31(8):2247-2255. Not sensitivity or specificity of an

identified test 

Montgomery A M P, Goka A K J, Kumar P J et al. Low 

gluten diet in the treatment of adult coeliac disease: Effect

on jejunal morphology and serum anti-gluten antibodies. 

Gut 1988;29(11):1564-1568. Serology <1990 

Montgomery R D, Atiyeh M, Scales W R et al. Intestinal

absorption in Saudi Arabia: an evaluation of the one hour 

blood xylose test. Transactions of the Royal Society of 

Tropical Medicine and Hygiene 1982;76(1):25-28. Not 

sensitivity or specificity of an identified test 

Moodie S, Ciclitira P. Coeliac disease: Genetic factors and

antigen presentation: MALADIE CoeLIAQUE: 

FACTEURS GENETIQUES ET PRESENTATION DES

ANTIGENES. Acta Endosc 2001;31(3):255-264. Not 

sensitivity or specificity of an identified test 

Moodie S, Ciclitira P. Recent developments in celiac 

disease. Curr Opin Gastroenterol 2002;18(2):182-186. Not 

sensitivity or specificity of an identified test 

Moodie S J, Norman P J, King A L et al. Analysis of 

candidate genes on chromosome 19 in coeliac disease: an

association study of the KIR and LILR gene clusters. 

European Journal of Immunogenetics - Official Journal of

the British Society for Histocompatibility and

Immunogenetics 2002;29(4):287-291. Not sensitivity or

specificity of an identified test

Moore K G, Goulet F, Sartorelli A C. Purification of 

annexin I and annexin II from human placental membranes 

by high-performance liquid chromatography. Protein

A-429
Expression and Purification 1992;3(1):1-7. Not sensitivity

or specificity of an identified test

Moore R H, Hitman G A, Medcraft J et al. HLA-DP region 

gene polymorphism in primary IgA nephropathy: no 

association. Nephrol Dial Transplant 1992;7(3):200-204. 

Not sensitivity or specificity of an identified test

Mora Barbara, Bonamico Margherita, Indovina Paola et al. 

CTLA-4 +49 A/G dimorphism in Italian patients with 

celiac disease. Human Immunology 2003;64(2):297-301. 

Not sensitivity or specificity of an identified test

Mora S, Barera G, Beccio S et al. A prospective, 

longitudinal study of the long-term effect of treatment on 

bone density in children with celiac disease. Journal of

Pediatrics 2001;139(4):516-521. Not sensitivity or

specificity of an identified test

Morales M, Galvan E, Mery C M et al. Exocrine pancreatic

insufficiency in tropical sprue. Digestion 2001;63(1):30-34. 

Not sensitivity or specificity of an identified test

Mordenti C, Peris K, Concetta Fargnoli M et al. Cutaneous 

metastatic breast carcinoma: A study of 164 patients. Acta 

Dermatovenerol Alp Panonica Adriat 2000;9(4):143-148. 

Not sensitivity or specificity of an identified test

Morellini M, Trabace S, Mazzilli M C et al. A study of 

HLA class II antigens in an Italian paediatric population

with coeliac disease. Disease Markers 1988;6(1):23-28. Not 

sensitivity or specificity of an identified test 

Moretto J C, Soslow R A, Smoller B R. Atypical cells in 

radiation dermatitis express factor XIIIa. American Journal 

of Dermatopathology 1998;20(4):370-372. Not sensitivity

or specificity of an identified test

Morin C L, Roy C C, Lasalle R et al. Small bowel mucosal

dysfunction in patients with cystic fibrosis. Journal of

Pediatrics 1976;88(2):213-216. Not sensitivity or

specificity of an identified test

Morris M A, Ciclitira P J. Coeliac disease. Journal of the

Royal College of Physicians of London 1997;31(6):614-

618. Not sensitivity or specificity of an identified test 

Morris M A, Yiannakou J Y, King A L et al. Coeliac 

disease and Down syndrome: associations not due to

genetic linkage on chromosome 21. Scandinavian Journal 

of Gastroenterology 2000;35(2):177-180. Not sensitivity or 

specificity of an identified test

Morris M-A, Ciclitira P J. Celiac disease. Curr Opin 

Gastroenterol 1998;14(2):107-111. Not sensitivity or 

specificity of an identified test

Morris S J, Rogers A I. Diarrhea after gastrectomy and 

vagotomy. Postgraduate Medicine 1979;65(1):219-22, 225. 

Not sensitivity or specificity of an identified test

Morroni M, Sbarbati A, D'Angelo G et al. Scanning

electron microscopy of the small intestine mucosa in 

children with celiac disease after long-term dietary

treatment. Scanning Microscopy 1989;3(4):1161-1166. Not 

sensitivity or specificity of an identified test 

Mortimer P E, Stewart J S, Norman A P et al. Follow-up 

study of coeliac disease. British Medical Journal 

1968;3(609):7-9. Not sensitivity or specificity of an 

identified test 

Mosher D F. Action of fibrin stabilizing factor on cold 

insoluble globulin and alphainf 2 macroglobulin in clotting

plasma. J Biol Chem 1976;251(6):1639-1645. Not 

sensitivity or specificity of an identified test 

Mosher D F, Johnson R B. In vitro formation of disulfidebonded fibronectin multimers. Journal of Biological

Chemistry 1983;258(10):6595-6601. Not sensitivity or 

specificity of an identified test

Mosnier J F, Larvol L, Barge J et al. Lymphocytic and 

collagenous colitis: an immunohistochemical study.

American Journal of Gastroenterology 1996;91(4):709-713. 

Not sensitivity or specificity of an identified test

Moss S F, Attia L, Scholes J V et al. Increased small

intestinal apoptosis in coeliac disease. Gut 

1996;39(96):811-817. Not sensitivity or specificity of an

identified test 

Moustakas A K, van de, Wal Y et al. Structure of celiac

disease-associated HLA-DQ8 and non-associated HLADQ9 alleles in complex with two disease-specific epitopes.

Int Immunol 2000;12(8):1157-1166. Not sensitivity or 

specificity of an identified test

Mowat A M. Dietary modifications: food dependent 

autoimmunity in coeliac disease. Gut 1998;43(5):599-600. 

Not sensitivity or specificity of an identified test

Mowat A M. Coeliac disease - A future for peptide 

therapy?. Lancet 2000;356(9226):270-271. Not sensitivity

or specificity of an identified test

Mowat Allan, McI. Coeliac disease--a meeting point for

genetics, immunology, and protein chemistry. Lancet 

2003;361(9365):1290-1292. Not sensitivity or specificity of 

an identified test

Moyana T N, Shukoor S. Gastrointestinal endocrine cell 

hyperplasia in celiac disease: a selective proliferative 

process of serotonergic cells. Modern Pathology - an 

Official Journal of the United States and Canadian 

Academy of Pathology, Inc 1991;4(4):419-423. Not 

sensitivity or specificity of an identified test 

Muers M F, Faux J A, Ting A et al. HLA-A, B, C and 

HLA-DR antigens in extrinsic allergic alveolitis 

(budgerigar fancier's lung disease). Clinical Allergy

1982;12(1):47-53. Not sensitivity or specificity of an 

identified test 

A-430
Mugica F, Castiella A, Otazua P et al. Prevalence of coeliac

disease in unexplained chronic hypertransaminasemia.

Revista Espanola De Enfermedades Digestivas - Organo 

Oficial De La Sociedad Espanola De Patologia Digestiva

2001;93(11):707-714. Not sensitivity or specificity of an

identified test 

Mulder C J J. Do we have to screen the general population

for coeliac disease instead of only patients with so-called 

associated diseases?. Digestive and Liver Disease - Official

Journal of the Italian Society of Gastroenterology and the 

Italian Association for the Study of the Liver 

2000;32(9):780-781. Not sensitivity or specificity of an 

identified test 

Mulder C J, van Bergeijk J D, Jansen T L et al. Coeliac 

disease. Diagnostic and therapeutic pitfalls. Scandinavian 

Journal of Gastroenterology.Supplement 1993;20042-47. 

Not sensitivity or specificity of an identified test

Mulder C J, Wahab P J, Meijer J W et al. A pilot study of

recombinant human interleukin-10 in adults with refractory 

coeliac disease. European Journal of Gastroenterology &

Hepatology 2001;13(10):1183-1188. Not sensitivity or

specificity of an identified test

Mulder C J, Wahab P J, Moshaver B et al. Refractory 

coeliac disease: a window between coeliac disease and

enteropathy associated T cell lymphoma. Scandinavian

Journal of Gastroenterology.Supplement 2000;(232):32-37. 

Not sensitivity or specificity of an identified test

Muller W F. Enteroclysis in coeliac disease. Radiologia

Clinica 1976;45(2-4):140-154. Not sensitivity or specificity

of an identified test 

Murch S H. Unusual enteropathies. Gastrointestinal 

Endoscopy Clinics of North America 2001;11(4):741-66, 

Vii. Not sensitivity or specificity of an identified test 

Murdock P J, Owens D L, Chitolie A et al. Development 

and evaluation of ELISAs for factor XIIIA and XIIIB 

subunits in plasma. Thrombosis Research 1992;67(1):73-

79. Not sensitivity or specificity of an identified test 

Murphy M S, Sood M, Johnson T. Use of the lactose 

HSUB2 breath test to monitor mucosal healing in coeliac 

disease. Acta Paediatr Int J Paediatr 2002;91(2):141-144. 

Not sensitivity or specificity of an identified test

Murray I A, Bullimore D W, Long R G. Fasting plasma

nitric oxide products in coeliac disease. European Journal 

of Gastroenterology & Hepatology 2003;15(10):1091-

1095. Not sensitivity or specificity of an identified test 

Murray I A, Coupland K, Smith J A et al. Intestinal 

trehalase activity in a UK population: establishing a normal 

range and the effect of disease. British Journal of Nutrition

2000;83(3):241-245. Not sensitivity or specificity of an 

identified test 

Murray I A, Smith J A, Coupland K et al. Intestinal 

disaccharidase deficiency without villous atrophy may

represent early celiac disease. Scandinavian Journal of

Gastroenterology 2001;36(2):163-168. Not sensitivity or 

specificity of an identified test

Murray Iain A, Daniels Ian, Coupland Kathryn et al. 

Increased activity and expression of iNOS in human 

duodenal enterocytes from patients with celiac disease. 

American Journal of Physiology.Gastrointestinal and Liver

Physiology 2002;283(2):G319-G326. Not sensitivity or

specificity of an identified test

Murray J A. It's not time to put away the biopsy forceps. 

American Journal of Gastroenterology 1999;94(4):869-871. 

Review article 

Murray J A. The widening spectrum of celiac disease. 

American Journal of Clinical Nutrition 1999;69(3):354-

365. Not sensitivity or specificity of an identified test 

Murray J A. Serodiagnosis of celiac disease. Clin Lab Med

1997;17(3):445-464. Not sensitivity or specificity of an 

identified test 

Murray J A, Herlein J, Mitros F et al. Serologic testing for 

celiac disease in the United States: Results of a

multilaboratory comparison study. Clin Diagn Lab 

Immunol 2000;7(4):584-587. Unable to extract data 

Murtaugh M P, Arend W P, Davies P J. Induction of tissue 

transglutaminase in human peripheral blood monocytes. 

Journal of Experimental Medicine 1984;159(1):114-125. 

Not sensitivity or specificity of an identified test

Murtaugh M P, Mehta K, Johnson J et al. Induction of 

tissue transglutaminase in mouse peritoneal macrophages. 

Journal of Biological Chemistry 1983;258(18):11074-

11081. Not sensitivity or specificity of an identified test 

Murthy S N, Lorand L. Cross-linked A alpha.gamma chain

hybrids serve as unique markers for fibrinogen polymerized 

by tissue transglutaminase. Proceedings of the National 

Academy of Sciences of the United States of America 

1990;87(24):9679-9682. Not sensitivity or specificity of an 

identified test 

Murthy S N P, Iismaa Siiri, Begg Gillian et al. Conserved 

tryptophan in the core domain of transglutaminase is 

essential for catalytic activity. Proceedings of the National 

Academy of Sciences of the United States of America 

2002;99(5):2738-2742. Not sensitivity or specificity of an

identified test 

Murthy S N, Wilson J H, Lukas T J et al. Cross-linking 

sites of the human tau protein, probed by reactions with 

human transglutaminase. Journal of Neurochemistry

1998;71(6):2607-2614. Not sensitivity or specificity of an

identified test 

Murthy S N, Wilson J, Guy S L et al. Intramolecular 

crosslinking of monomeric fibrinogen by tissue 

transglutaminase. Proceedings of the National Academy of

A-431
Sciences of the United States of America 

1991;88(23):10601-10604. Not sensitivity or specificity of 

an identified test

Murthy S N, Wilson J, Zhang Y et al. Residue Gln-30 of 

human erythrocyte anion transporter is a prime site for

reaction with intrinsic transglutaminase. Journal of 

Biological Chemistry 1994;269(36):22907-22911. Not 

sensitivity or specificity of an identified test 

Mussche M, Thienpont L. Adult celiac disease complicated 

by intestinal reticulum cell sarcoma with high serum IgA 

level. Acta Clinica Belgica 1974;29(6):388-393. Not 

sensitivity or specificity of an identified test 

Mustafa A S, Shaban F A, Al Attiyah R et al. Human Th1 

cell lines recognize the Mycobacterium tuberculosis ESAT6 antigen and its peptides in association with frequently

expressed HLA class II molecules. Scand J Immunol 

2003;57(2):125-134. Not sensitivity or specificity of an 

identified test 

Mustajoki P, Vuoristo M, Reunala T. Celiac disease or 

dermatitis herpetiformis in three patients with porphyria.

Digestive Diseases and Sciences 1981;26(7):618-621. Not 

sensitivity or specificity of an identified test 

Mustalahti K, Holopainen P, Karell K et al. Genetic

dissection between silent and clinically diagnosed

symptomatic forms of coeliac disease in multiplex families. 

Digestive and Liver Disease - Official Journal of the Italian

Society of Gastroenterology and the Italian Association for

the Study of the Liver 2002;34(12):842-845. Improper 

control group 

Mustalahti K, Sulkanen S, Holopainen P et al. Coeliac 

disease among healthy members of multiple case coeliac 

disease families. Scandinavian Journal of Gastroenterology

2002;37(2):161-165. Not sensitivity or specificity of an 

identified test 

Mustalahti Kirsi, Lohiniemi Susanna, Collin Pekka et al.

Gluten-free diet and quality of life in patients with screendetected celiac disease. Effective Clinical Practice - Ecp 

2002;5(3):105-113. Not sensitivity or specificity of an 

identified test 

Muszbek L, Adany R, Kavai M et al. Monocytes of patients

congenitally deficient in plasma factor XIII lack factor XIII 

subunit a antigen and transglutaminase activity. 

Thrombosis and Haemostasis 1988;59(2):231-235. Not 

sensitivity or specificity of an identified test 

Muszbek L, Adany R, Szegedi G et al. Factor XIII of blood

coagulation in human monocytes. Thrombosis Research 

1985;37(3):401-410. Not sensitivity or specificity of an 

identified test 

Myhre A G, Aarsetoy H, Undlien D E et al. High frequency

of coeliac disease among patients with autoimmune 

adrenocortical failure. Scandinavian Journal of 

Gastroenterology 2003;38(5):511-515. Not sensitivity or 

specificity of an identified test

Myhre Anne, Grethe Undlien, Dag E et al. Autoimmune 

adrenocortical failure in Norway autoantibodies and human 

leukocyte antigen class II associations related to clinical 

features. Journal of Clinical Endocrinology and

Metabolism 2002;87(2):618-623. Not sensitivity or 

specificity of an identified test

Mylotte M, Egan-Mitchell B, Fottrell P F et al. Family

studies in coeliac disease. Quarterly Journal of Medicine 

1974;43(171):359-369. Not sensitivity or specificity of an

identified test 

Mylotte M, Egan-Mitchell B, McCarthy C F et al. 

Incidence of coeliac disease in the West of Ireland. British 

Medical Journal 1973;1(5855):703-705. Not sensitivity or 

specificity of an identified test

Myoung Hee, Park Dong, Hee Whang et al. High resolution

HLA-DQB1 typing by combination of PCR-RFLP and 

PCR-SSCP. Hum Immunol 1999;60(9):901-907. Not 

sensitivity or specificity of an identified test 

Naccarato R, Di Mario F. Italian gastroenterology: Eyes on 

the new millennium. Digestive and Liver Disease - Official

Journal of the Italian Society of Gastroenterology and the 

Italian Association for the Study of the Liver 2000;32(1):3-

8. Not sensitivity or specificity of an identified test 

Nagae S, Lichti U, De Luca L M et al. Effect of retinoic 

acid on cornified envelope formation: Difference between

spontaneous envelope formation in vivo or in vitro and 

expression of envelope competence. J Invest Dermatol 

1987;89(1):51-58. Not sensitivity or specificity of an 

identified test 

Nagasaka T, Nakamura S, Medeiros J et al. Anaplastic

large cell lymphomas presented as bone lesions: A 

clinicopathologic study of six cases and review of the 

literature. Mod Pathol 2000;13(10):1143-1149. Not 

sensitivity or specificity of an identified test 

Nagy L, Saydak M, Shipley N et al. Identification and 

characterization of a versatile retinoid response element 

(retinoic acid receptor response element-retinoid X receptor 

response element) in the mouse tissue transglutaminase 

gene promoter. Journal of Biological Chemistry

1996;271(8):4355-4365. Not sensitivity or specificity of an 

identified test 

Nagy L, Thomazy V A, Chandraratna R A et al. Retinoidregulated expression of BCL-2 and tissue transglutaminase

during the differentiation and apoptosis of human myeloid 

leukemia (HL-60) cells. Leukemia Research 

1996;20(6):499-505. Not sensitivity or specificity of an 

identified test 

Naik S. HLA and gastrointestinal disorders. Indian Journal 

of Gastroenterology - Official Journal of the Indian Society 

of Gastroenterology 1986;5(2):121-124. Not sensitivity or

specificity of an identified test

A-432
Naim H Y. Secretion of human intestinal angiotensinconverting enzyme and its association with the 

differentiation state of intestinal cells. Biochemical Journal 

1996;316(Pt 1):259-264. Not sensitivity or specificity of an 

identified test 

Nakachi K, Swift G, Wilmot D et al. Antibodies to tissue 

transglutaminase: comparison of ELISA and 

immunoprecipitation assay in the presence and in the 

absence of calcium ions. Clinica Chimica Acta

2001;International Journal of Clinical Chemistry; 304(1-

2):75-84. Not sensitivity or specificity of an identified test 

Nakamura T, Nishida K, Dota A et al. Elevated expression 

of transglutaminase 1 and keratinization-related proteins in 

conjunctiva in severe ocular surface disease. Investigative

Ophthalmology & Visual Science 2001;42(3):549-556. Not 

sensitivity or specificity of an identified test 

Nakane H, Ishida-Yamamoto A, Takahashi H et al. Elafin,

a secretory protein, is cross-linked into the cornified cell

envelopes from the inside of psoriatic keratinocytes. J 

Invest Dermatol 2002;119(1):50-55. Not sensitivity or 

specificity of an identified test

Nakshabendi I M, Downie S, Russell R I et al. Increased

rates of duodenal mucosal protein synthesis in vivo in 

patients with untreated coelia disease. Gut 1996;39(2):176-

179. Not sensitivity or specificity of an identified test 

Naluai A T, Nilsson S, Samuelsson L et al. The

CTLA4/CD28 gene region on chromosome 2q33 confers 

susceptibility to celiac disease in a way possibly distinct

from that of type 1 diabetes and other chronic inflammatory

disorders. Tissue Antigens 2000;56(4):350-355. Not 

sensitivity or specificity of an identified test 

Nanda A, Al Saeed K, Dvorak R et al. Clinicopathological 

features and HLA tissue typing in pemphigoid gestationis 

patients in Kuwait. Clin Exp Dermatol 2003;28(3):301-306. 

Not sensitivity or specificity of an identified test

Nara K, Ito S, Ito T et al. Elastase inhibitor elafin is a new 

type of proteinase inhibitor which has a transglutaminasemediated anchoring sequence termed "cementoin". Journal 

of Biochemistry 1994;115(3):441-448. Not sensitivity or

specificity of an identified test

Nardacci Roberta, Lo Iacono, Oreste Ciccosanti et al.

Transglutaminase type II plays a protective role in hepatic 

injury. American Journal of Pathology 2003;162(4):1293-

1303. Not sensitivity or specificity of an identified test 

Natah S S, Hayrinen-Immonen R, Hietanen J et al. Factor

XIIIa-positive dendrocytes are increased in number and

size in recurrent aphthous ulcers (RAU). Journal of Oral 

Pathology & Medicine - Official Publication of the 

International Association of Oral Pathologists and the 

American Academy of Oral Pathology 1997;26(9):408-413. 

Not sensitivity or specificity of an identified test

Nathavitharana K A, Lloyd D R, Raafat F et al. Urinary 

mannitol: lactulose excretion ratios and jejunal mucosal 

structure. Archives of Disease in Childhood 

1988;63(9):1054-1059. Not sensitivity or specificity of an

identified test 

Natter S, Granditsch G, Reichel G L et al. IgA crossreactivity between a nuclear autoantigen and wheat proteins

suggests molecular mimicry as a possible pathomechanism 

in celiac disease. European Journal of Immunology

2001;31(3):918-928. Not sensitivity or specificity of an 

identified test 

Negi M, Colbert M C, Goldsmith L A. High-molecularweight human epidermal transglutaminase. Journal of

Investigative Dermatology 1985;85(1):75-78. Not 

sensitivity or specificity of an identified test 

Nehra V. New clinical issues in celiac disease.

Gastroenterology Clinics of North America

1998;27(2):453-465. Not sensitivity or specificity of an 

identified test 

Nehra V, Angulo P, Buchman A L et al. Nutritional and 

metabolic considerations in the etiology of nonalcoholic 

steatohepatitis. Digestive Diseases and Sciences 

2001;46(11):2347-2352. Not sensitivity or specificity of an 

identified test 

Nelsen David A. Gluten-sensitive enteropathy (celiac

disease): more common than you think. American Family

Physician 2002;66(12):2259-2266. Not sensitivity or 

specificity of an identified test

Nelson E W, Ertan A, Brooks F P et al. Thrombocytosis in

patients with celiac sprue. Gastroenterology

1976;70(6):1042-1044. Not sensitivity or specificity of an

identified test 

Nelson R, McNeish A S, Anderson C M. Coeliac disease in

children of Asian immigrants. Lancet 1973;1(7799):348-

350. Not sensitivity or specificity of an identified test 

Nemes Z, Thomazy V. Diagnostic significance of

histiocyte-related markers in malignant histiocytosis and 

true histiocytic lymphoma. Cancer 1988;62(9):1970-1980. 

Not sensitivity or specificity of an identified test

Nemes Z, Adany R, Thomazy V. Selective visualization of

human dendritic reticulum cells in reactive lymphoid 

follicles by the immunohistochemical demonstration of the 

subunit A of factor XIII (F-XIIIa). Virchows Archiv.B, 

Cell Pathology Including Molecular Pathology

1987;52(5):453-466. Not sensitivity or specificity of an 

identified test 

Nemes Z, Adany R, Balazs M et al. Identification of 

cytoplasmic actin as an abundant glutaminyl substrate for

tissue transglutaminase in HL-60 and U937 cells 

undergoing apoptosis. Journal of Biological Chemistry

1997;272(33):20577-20583. Not sensitivity or specificity of 

an identified test

A-433
Nemes Z, Thomazy V, Adany R et al. Identification of 

histiocytic reticulum cells by the immunohistochemical 

demonstration of factor XIII (F-XIIIa) in human lymph 

nodes. Journal of Pathology 1986;149(2):121-132. Not 

sensitivity or specificity of an identified test 

Nepom G T. MHC genes in HLA-associated disease.

Current Opinion in Immunology 1989;2(4):588-592. Not 

sensitivity or specificity of an identified test 

Nepom G T. Structural variation among major 

histocompatibility complex class-II genes which predispose 

to autoimmunity. Immunol Res 1989;8(1):16-38. Not 

sensitivity or specificity of an identified test 

Nepom G T, Erlich H. MHC class-II molecules and 

autoimmunity. Annu Rev Immunol 1991;9493-525. Not 

sensitivity or specificity of an identified test 

Nestle F O, Zheng X G, Thompson C B et al. 

Characterization of dermal dendritic cells obtained from

normal human skin reveals phenotypic and functionally

distinctive subsets. Journal of Immunology (Baltimore,

Md.- 1950) 1993;151(11):6535-6545. Not sensitivity or

specificity of an identified test

Neuberger J. PBC and the gut: the villi atrophy, the plot

thickens. Gut 1999;44(5):594-595. Not sensitivity or 

specificity of an identified test

Neuhausen Susan L, Feolo Mike, Camp Nicola J et al. 

Genome-wide linkage analysis for celiac disease in North 

American families. American Journal of Medical Genetics

2002;111(1):1-9. Not sensitivity or specificity of an 

identified test 

Neuhausen Susan L, Weizman Zvi, Camp Nicola J et al. 

HLA DQA1-DQB1 genotypes in Bedouin families with 

celiac disease. Human Immunology 2002;63(6):502-507. 

Improper control group 

Nezelof C, Barbey S, Gogusev J et al. Malignant

histiocytosis in childhood: a distinctive CD30-positive 

clinicopathological entity associated with a chromosomal 

translocation involving 5q35. Seminars in Diagnostic 

Pathology 1992;9(1):75-89. Not sensitivity or specificity of 

an identified test

Nicholas D S, Harris S, Wright D H. Lymphocyte 

predominance Hodgkin's disease--an immunohistochemical 

study. Histopathology 1990;16(2):157-165. Not sensitivity

or specificity of an identified test

Nicholl R M, Gamsu H R. Reduced mesenteric blood flow 

velocity in 'AGA' VLBW babies with disproportionate 

growth retardation. Early Hum Dev 1997;49(3):209-210. 

Not sensitivity or specificity of an identified test

Nickoloff B J, Griffiths C E. The spindle-shaped cells in 

cutaneous Kaposi's sarcoma. Histologic simulators include 

factor XIIIa dermal dendrocytes. American Journal of

Pathology 1989;135(5):793-800. Not sensitivity or

specificity of an identified test

Nicolas M E O, Krause P K, Gibson L E et al. Dermatitis 

herpetiformis. International Journal of Dermatology

2003;42(8):588-600. Not sensitivity or specificity of an 

identified test 

Nicolette C C, Tully T E. The duodenum in celiac sprue.

American Journal of Roentgenology, Radium Therapy, and

Nuclear Medicine 1971;113(2):248-254. Not sensitivity or

specificity of an identified test

Nielsen K. Coeliac disease: alpha-1-antitrypsin contents in 

jejunal mucosa before and after gluten-free diet. 

Histopathology 1984;8(5):759-764. Not sensitivity or 

specificity of an identified test

Nieminen U, Kahri A, Savilahti E et al. Duodenal 

disaccharidase activities in the follow-up of villous atrophy 

in coeliac disease. Scandinavian Journal of 

Gastroenterology 2001;36(5):507-510. Not sensitivity or 

specificity of an identified test

Nieto A, Blanco Quiros A, Arranz E et al. Study of HLADQA1 alleles in celiac children. Journal of Investigational 

Allergology & Clinical Immunology - Official Organ of the 

International Association of Asthmology (Interasma) and 

Sociedad Latinoamericana De Alergia E Inmunologia 

1995;5(4):209-215. Unable to extract data 

Nieuwenhuizen W F, Pieters R H H, Knippels L M J et al. 

Is Candida albicans a trigger in the onset of coeliac 

disease?. Lancet 2003;361(9375):2152-2154. Not 

sensitivity or specificity of an identified test 

Nikkels A F, Arrese Estrada J, Pierard-Franchimont C et al. 

CD68 and factor XIIIa expressions in granular-cell tumor 

of the skin. Dermatology (Basel, Switzerland) 

1993;186(2):106-108. Not sensitivity or specificity of an

identified test 

Nilsen E M, Gjertsen H A, Jensen K et al. Gluten activation

of peripheral blood T cells induces a Th0-like cytokine 

pattern in both coeliac patients and controls. Clinical and

Experimental Immunology 1996;103(2):295-303. Not 

sensitivity or specificity of an identified test 

Nilsen E M, Jahnsen F L, Lundin K E et al. Gluten induces

an intestinal cytokine response strongly dominated by

interferon gamma in patients with celiac disease.

Gastroenterology 1998;115(3):551-563. Not sensitivity or

specificity of an identified test

Nilsen E M, Lundin K E, Krajci P et al. Gluten specific,

HLA-DQ restricted T cells from coeliac mucosa produce 

cytokines with Th1 or Th0 profile dominated by interferon

gamma. Gut 1995;37(6):766-776. Not sensitivity or 

specificity of an identified test

Nilssen D E, Brandtzaeg P, Froland S S et al. Subclass 

composition and J-chain expression of the 'compensatory'

A-434
gastrointestinal IgG cell population in selective IgA 

deficiency. Clinical and Experimental Immunology

1992;87(2):237-245. Not sensitivity or specificity of an 

identified test 

Nishida K, Yamanishi K, Yamada K et al. Epithelial

hyperproliferation and transglutaminase 1 gene expression 

in Stevens-Johnson syndrome conjunctiva. American 

Journal of Pathology 1999;154(2):331-336. Not sensitivity

or specificity of an identified test

Nishimura T, Horino K, Nishiura H et al. Apoptotic cells of 

an epithelial cell line, AsPC-1, release monocyte 

chemotactic S19 ribosomal protein dimer. Journal of 

Biochemistry 2001;129(3):445-454. Not sensitivity or 

specificity of an identified test

Nishiura H, Shibuya Y, Yamamoto T. S19 ribosomal 

protein cross-linked dimer causes monocyte-predominant 

infiltration by means of molecular mimicry to complement 

C5a. Laboratory Investigation 1998;A Journal of Technical 

Methods and Pathology; 78(12):1615-1623. Not sensitivity

or specificity of an identified test

Niveloni S, Dezi R, Pedreira S et al. Gluten sensitivity in

patients with primary biliary cirrhosis. American Journal of 

Gastroenterology 1998;93(3):404-408. Not sensitivity or 

specificity of an identified test

Niveloni S, Fiorini A, Dezi R et al. Usefulness of 

videoduodenoscopy and vital dye staining as indicators of

mucosal atrophy of celiac disease: assessment of 

interobserver agreement. Gastrointestinal Endoscopy

1998;47(3):223-229. Not sensitivity or specificity of an 

identified test 

Niveloni S, Pedreira S, Sugai E et al. The natural history of 

gluten sensitivity: report of two new celiac disease patients

resulting from a long-term follow-up of nonatrophic, firstdegree relatives. American Journal of Gastroenterology

2000;95(2):463-468. Not sensitivity or specificity of an 

identified test 

Niveloni S, Weksler-Zangen S, Pedreira S et al. Time

course of nitric oxide synthase generation after gluten 

exposure in the rectal mucosa of gluten-sensitive patients. 

Scandinavian Journal of Gastroenterology

2000;35(11):1150-1156. Not sensitivity or specificity of an 

identified test 

Niven M J, Caffrey C, Moore R H et al. T-cell receptor

beta-subunit gene polymorphism and autoimmune disease. 

Hum Immunol 1990;27(4):360-367. Not sensitivity or 

specificity of an identified test

Noh K W, Poland G A, Murray J A. Hepatitis B Vaccine

Nonresponse and Celiac Disease. American Journal of

Gastroenterology 2003;98(10):2289-2292. Not sensitivity

or specificity of an identified test

Noone C, Menzies I S, Banatvala J E et al. Intestinal 

permeability and lactose hydrolysis in human rotaviral 

gastroenteritis assessed simultaneously by non-invasive 

differential sugar permeation. European Journal of Clinical 

Investigation 1986;16(3):217-225. Not sensitivity or 

specificity of an identified test

Norsgaard H, Clark B F, Rattan S I. Distinction between

differentiation and senescence and the absence of increased

apoptosis in human keratinocytes undergoing cellular aging 

in vitro. Experimental Gerontology 1996;31(5):563-570. 

Not sensitivity or specificity of an identified test

Nosari I, Casati A, Mora C et al. The use of IgAantiendomysial antibody test for screening coeliac disease 

in insulin-dependent diabetes mellitus. Diabetes Nutr 

Metab Clin Exp 1996;9(5):267-272. Not sensitivity or 

specificity of an identified test

Not T, Citta A, Lucchesi A et al. Anti-endomysium 

antibody on human umbilical cord vein tissue: an

inexpensive and sensitive diagnostic tool for the screening 

of coeliac disease. European Journal of Pediatrics

1997;156(8):616-618. Improper control group 

Not T, Horvath K, Hill I D et al. Celiac disease risk in the 

USA: high prevalence of antiendomysium antibodies in

healthy blood donors. Scandinavian Journal of 

Gastroenterology 1998;33(5):494-498. Not sensitivity or 

specificity of an identified test

Not T, Tommasini A, Tonini G et al. Undiagnosed coeliac 

disease and risk of autoimmune disorders in subjects with 

Type I diabetes mellitus. Diabetologia 2001;44(2):151-155. 

Not sensitivity or specificity of an identified test

Not T, Ventura A, Peticarari S et al. A new, rapid, 

noninvasive screening test for celiac disease. Journal of

Pediatrics 1993;123(3):425-427. Improper control group 

Not Tarcisio, Faleschini Elena, Tommasini Alberto et al. 

Celiac disease in patients with sporadic and inherited 

cardiomyopathies and in their relatives. European Heart

Journal 2003;24(15):1455-1461. Not sensitivity or

specificity of an identified test

Nousia-Arvanitakis S, Karagiozoglou-Lamboudes T, 

Aggouridaki C et al. Influence of jejunal morphology

changes on exocrine pancreatic function in celiac disease.

Journal of Pediatric Gastroenterology and Nutrition 

1999;29(1):81-85. Not sensitivity or specificity of an 

identified test 

Novacek G, Miehsler W, Wrba F et al. Prevalence and

clinical importance of hypertransaminasaemia in coeliac

disease. European Journal of Gastroenterology & 

Hepatology 1999;11(3):283-288. Not sensitivity or 

specificity of an identified test

Novak Petr, Man Petr, Tuckova Ludmila et al. Monitoring

of in vitro deamidation of gliadin peptic fragment by mass 

spectrometry may reflect one of the molecular mechanisms

taking place in celiac disease development. Journal of Mass 

Spectrometry - Jms 2002;37(5):507-511. Not sensitivity or

A-435
specificity of an identified test

Nowak T V, Ghishan F K, Schulze-Delrieu K. Celiac sprue

in Down Syndrome: considerations on a pathogenetic link. 

American Journal of Gastroenterology 1983;78(5):280-283. 

Not sensitivity or specificity of an identified test

Nunes I, Gleizes P E, Metz C N et al. Latent transforming 

growth factor-beta binding protein domains involved in

activation and transglutaminase-dependent cross-linking of

latent transforming growth factor-beta. Journal of Cell 

Biology 1997;136(5):1151-1163. Not sensitivity or

specificity of an identified test

Nurminskaya M V, Linsenmayer T F. Immunohistological 

analysis of transglutaminase factor XIIIA expression in

mouse embryonic growth plate. J Orthop Res

2002;20(3):575-578. Not sensitivity or specificity of an 

identified test 

Nuti R, Martini G, Valenti R et al. Prevalence of 

undiagnosed coeliac syndrome in osteoporotic women. 

Journal of Internal Medicine 2001;250(4):361-366. Not 

sensitivity or specificity of an identified test 

Nyren O, Adami H-O, Gustavsson S. The 'epigastric 

distress syndrome'. A possible disease entity identified by

history and endoscopy in patients with nonulcer dyspepsia. 

Journal of Clinical Gastroenterology 1987;9(3):303-309. 

Not sensitivity or specificity of an identified test

O'Brien M, Colwell R. Modified taurocholate-telluritegelatin agar for improved differentiation of Vibrio species. 

Journal of Clinical Microbiology 1985;22(6):1011-1013. 

Not sensitivity or specificity of an identified test

O'Brien R M, Thomas W R, Nicholson I et al. An 

immunogenetic analysis of the T-cell recognition of the 

major house dust mite allergen Der p 2: Identification of

high- and low-responder HLA-DQ alleles and localization 

of T-cell epitopes. Immunology 1995;86(2):176-182. Not 

sensitivity or specificity of an identified test 

O'Donnell B F, O'Neill C M, Francis D M et al. Human 

leucocyte antigen class II associations in chronic idiopathic

urticaria. Br J Dermatol 1999;140(5):853-858. Not 

sensitivity or specificity of an identified test 

O'Driscoll B R, Stevens F M, O'Gorman T A et al. HLA

type of patients with coeliac disease and malignancy in the 

west of Ireland. Gut 1982;23(8):662-665. Not sensitivity or 

specificity of an identified test

O'Farrelly C. Is villous atrophy always and only the result

of gluten sensitive disease of the intestine?. European 

Journal of Gastroenterology & Hepatology 2000;12(6):605-

608. Not sensitivity or specificity of an identified test 

O'Farrelly C, Feighery C, O'Briain D S et al. Humoral 

response to wheat protein in patients with coeliac disease 

and enteropathy associated T cell lymphoma. British 

Medical Journal (Clinical Research Ed.) 

1986;293(6552):908-910. Not sensitivity or specificity of

an identified test

O'Farrelly C, Graeme-Cook F, Hourihane D O et al. 

Histological changes associated with wheat protein 

antibodies in the absence of villous atrophy. Journal of

Clinical Pathology 1987;40(10):1228-1230. Unable to 

extract data

O'Farrelly C, Kelly J, Hekkens W et al. Alpha gliadin

antibody levels: a serological test for coeliac disease. 

British Medical Journal (Clinical Research Ed.)

1983;286(6383):2007-2010. Serology <1990 

O'Farrelly C, O'Mahony C, Graeme-Cook F et al. Gliadin 

antibodies identify gluten-sensitive oral ulceration in the 

absence of villous atrophy. Journal of Oral Pathology &

Medicine - Official Publication of the International 

Association of Oral Pathologists and the American 

Academy of Oral Pathology 1991;20(10):476-478. Not 

sensitivity or specificity of an identified test 

O'Grady J G, Stevens F M, McCarthy C F. Celiac disease:

does hyposplenism predispose to the development of 

malignant disease?. American Journal of Gastroenterology

1985;80(1):27-29. Not sensitivity or specificity of an 

identified test 

O'Grady J G, Stevens F M, McCarthy C F. Genetic

influences on splenic function in coeliac disease. Gut 

1985;26(10):1004-1007. Not sensitivity or specificity of an 

identified test 

O'Grady J G, Stevens F M, Harding B et al. Effect of 

splenectomy and the functional hyposplenism of coeliac 

disease on auto-antibody formation. Irish Journal of 

Medical Science 1984;153(10):351-354. Not sensitivity or

specificity of an identified test

O'Grady J G, Stevens F M, Harding B et al. Hyposplenism 

and gluten-sensitive enteropathy. Natural history,

incidence, and relationship to diet and small bowel 

morphology. Gastroenterology 1984;87(6):1326-1331. Not 

sensitivity or specificity of an identified test 

O'Grady J G, Stevens F M, Keane R et al. Intestinal lactase,

sucrase, and alkaline phosphatase in 373 patients with 

coeliac disease. Journal of Clinical Pathology

1984;37(3):298-301. Not sensitivity or specificity of an 

identified test 

O'Halloran E T, Read M, Morrissey-Walsh E M. Coeliac

disease in children: Problems in diagnosis and

management. Ir Med J 1985;78(7):188-191. Not sensitivity

or specificity of an identified test

O'Halloran E T, Read M, Barry R G et al. The management 

of coeliac disease. Irish Medical Journal 1998;91(6):199-

202. Not sensitivity or specificity of an identified test 

O'Keefe S J. Nutrition and gastrointestinal disease.

Scandinavian Journal of Gastroenterology.Supplement 

A-436
1996;22052-59. Not sensitivity or specificity of an 

identified test 

O'Keeffe J, Lynch S, Whelan A et al. Flow cytometric

measurement of intracellular migration inhibition factor

and tumour necrosis factor alpha in the mucosa of patients

with coeliac disease. Clinical and Experimental

Immunology 2001;125(3):376-382. Not sensitivity or 

specificity of an identified test

O'Keeffe J, Mills K, Jackson J et al. T cell proliferation,

MHC class II restriction and cytokine products of gliadinstimulated peripheral blood mononuclear cells (PBMC). 

Clinical and Experimental Immunology 1999;117(2):269-

276. Not sensitivity or specificity of an identified test 

O'Laughlin J C, Di Giovanni A M. Psoriatic enteropathy:

Report of case and review of literature. J Am Osteopath

Assoc 1979;79(2):107-112. Not sensitivity or specificity of 

an identified test

O'Leary C, Walsh C H, Wieneke P et al. Coeliac disease 

and autoimmune Addison's disease: a clinical pitfall. Qjm - 

Monthly Journal of the Association of Physicians 

2002;95(2):79-82. Not sensitivity or specificity of an 

identified test 

O'Mahony S, Arranz E, Barton J R et al. Dissociation 

between systemic and mucosal humoral immune responses 

in coeliac disease. Gut 1991;32(1):29-35. Not sensitivity or 

specificity of an identified test

O'Mahony S, Barton J R, Crichton S et al. Appraisal of gut 

lavage in the study of intestinal humoral immunity. Gut

1990;31(12):1341-1344. Not sensitivity or specificity of an 

identified test 

O'Mahony S, Vestey J P, Ferguson A. Similarities in 

intestinal humoral immunity in dermatitis herpetiformis 

without enteropathy and in coeliac disease. Lancet 

1990;335(8704):1487-1490. Not sensitivity or specificity of 

an identified test

Oberhuber G. Histopathology of celiac disease. 

Biomedicine & Pharmacotherapy = Biomedecine &

Pharmacotherapie 2000;54(7):368-372. Review article 

Oberhuber G, Granditsch G, Vogelsang H. The 

histopathology of coeliac disease: time for a standardized 

report scheme for pathologists. European Journal of 

Gastroenterology & Hepatology 1999;11(10):1185-1194. 

Not sensitivity or specificity of an identified test

Oberhuber G, Schwarzenhofer M, Vogelsang H. In vitro

model of the pathogenesis of celiac disease. Digestive 

Diseases (Basel, Switzerland) 1998;16(6):341-344. Not 

sensitivity or specificity of an identified test 

Oderda G, Forni M, Morra I et al. Endoscopic and 

histologic findings in the upper gastrointestinal tract of 

children with coeliac disease. Journal of Pediatric 

Gastroenterology and Nutrition 1993;16(2):172-177. Not

sensitivity or specificity of an identified test 

Ofosu M H, Dunston G, Henry L et al. HLA-DQ3 is 

associated with Graves' disease in African-Americans.

Immunological Investigations 1996;25(1-2):103-110. Not 

sensitivity or specificity of an identified test 

Ogawa H, Goldsmith L A. Human epidermal 

transglutaminase. II. Immunologic properties. Journal of

Investigative Dermatology 1977;68(1):32-35. Not 

sensitivity or specificity of an identified test 

Oh J H, MacLean L D. Diseases associated with specific 

HL-A antigens. Canadian Medical Association Journal 

1975;112(11):1315-1318. Not sensitivity or specificity of

an identified test

Ohashi H, Itoh Y, Birckbichler P J et al. Purification and 

characterization of rat brain transglutaminase. Journal of

Biochemistry 1995;118(6):1271-1278. Not sensitivity or

specificity of an identified test

Oiso M, Nishi T, Ishikawa T et al. Differential binding of 

peptides substituted at putative C-terminal anchor residues 

to HLA-DQ8 and DQ9 differing only at betasup 5sup 7. 

Hum Immunol 1997;52(1):47-53. Not sensitivity or 

specificity of an identified test

Okamoto M, Yamamoto T, Matsubara S et al. Factor XIIIdependent generation of 5th complement component(C5)-

derived monocyte chemotactic factor coinciding with 

plasma clotting. Biochimica Et Biophysica Acta

1992;1138(1):53-61. Not sensitivity or specificity of an 

identified test 

Oktedalen O, Skar V, Dahl E et al. Changes in small

intestinal structure and function in HIV-infected patients 

with chronic diarrhoea. Scandinavian Journal of Infectious 

Diseases 1998;30(5):459-463. Not sensitivity or specificity

of an identified test 

Okuno M, Kojima S, Moriwaki H. Chemoprevention of

hepatocellular carcinoma: concept, progress and

perspectives. Journal of Gastroenterology and Hepatology

2001;16(12):1329-1335. Not sensitivity or specificity of an 

identified test 

Okuno M, Sano T, Matsushima-Nishiwaki R et al. 

Apoptosis induction by acyclic retinoid: a molecular basis 

of 'clonal deletion' therapy for hepatocellular carcinoma. 

Japanese Journal of Clinical Oncology 2001;31(8):359-362. 

Not sensitivity or specificity of an identified test

Olaussen R W, Johansen F E, Lundin K E A et al. 

Interferon-gamma-secreting T cells localize to the 

epithelium in coeliac disease. Scand J Immunol 

2002;56(6):652-664. Not sensitivity or specificity of an 

identified test 

Olds G, McLoughlin R, O'Morian C et al. Celiac disease 

for the endoscopist. Gastrointest Endosc 2002;56(3):407-

415. Not sensitivity or specificity of an identified test 

A-437
Olerup O, Olsson R, Hultcrantz R et al. HLA-DR and 

HLA-DQ are not markers for rapid disease progression in 

primary sclerosing cholangitis. Gastroenterology

1995;108(3):870-878. Not sensitivity or specificity of an

identified test 

Oliva A, Armas H, Farina J B. HPLC determination of 

polyethylene glycol 400 in urine: Oligomeric profile in 

healthy and celiac disease subjects. Clinical Chemistry 

1994;40(8):1571-1574. Not sensitivity or specificity of an

identified test 

Oliver R T D. Histocompatibility antigens and human 

disease. Br J Hosp Med 1977;18(5):449-459. Not 

sensitivity or specificity of an identified test 

Oliverio S, Amendola A, Di Sano F et al. Tissue 

transglutaminase-dependent posttranslational modification

of the retinoblastoma gene product in promonocytic cells 

undergoing apoptosis. Mol Cell Biol 1997;17(10):6040-

6048. Not sensitivity or specificity of an identified test 

Oliverio S, Amendola A, Rodolfo C et al. Inhibition of 

"tissue" transglutaminase increases cell survival by

preventing apoptosis. Journal of Biological Chemistry

1999;274(48):34123-34128. Not sensitivity or specificity of 

an identified test

Olives PrJ. Coeliac disease and gluten intolerance: New 

data for a new method of treatment. Rev Med Liban 

2000;12(3):127-128. Not sensitivity or specificity of an 

identified test 

Olorundare O E, Peyruchaud O, Albrecht R M et al. 

Assembly of a fibronectin matrix by adherent platelets

stimulated by lysophosphatidic acid and other agonists. 

Blood 2001;98(1):117-124. Not sensitivity or specificity of 

an identified test

Olsen W A. A pathophysiologic approach to diagnosis of 

malabsorption. American Journal of Medicine 

1979;67(6):1007-1013. Not sensitivity or specificity of an

identified test 

Olsen W A. A practical approach to diagnosis of disorders 

of intestinal absorption. New England Journal of Medicine

1971;285(24):1358-1361. Not sensitivity or specificity of

an identified test

Olson D J, Fujimura M, Swanson P et al. 

Immunohistochemical features of Paget's disease of the 

vulva with and without adenocarcinoma. Int J Gynecol 

Pathol 1991;10(3):285-295. Not sensitivity or specificity of 

an identified test

Olsson R, Kagevi I, Rydberg L. On the concurrence of

primary biliary cirrhosis and intestinal villous atrophy.

Scandinavian Journal of Gastroenterology 1982;17(5):625-

628. Not sensitivity or specificity of an identified test 

Orgad S, Avigad S, Jonas A et al. Immunogenetics of 

childhood celiac disease: the association with HDA DR3 

and DR7 in unrelated patients with multiply affected 

families. Israel Journal of Medical Sciences 

1981;17(11):1041-1044. Not sensitivity or specificity of an 

identified test 

Orru S, Caputo I, D'Amato A et al. Proteomics

identification of acyl-acceptor and acyl-donor substrates for

transglutaminase in a human intestinal epithelial cell line. 

Implications for celiac disease. J Biol Chem

2003;278(34):31766-31773. Not sensitivity or specificity of 

an identified test

Osa A, Almenar L, Palencia M et al. Antigens of the major

histocompatibility system in ischemic heart disease and 

idiopathic dilated cardiomyopathy. Clin Cardiol

1999;22(4):292-296. Not sensitivity or specificity of an 

identified test 

Osman A A, Gunnel T, Dietl A et al. B cell epitopes of 

gliadin. Clinical and Experimental Immunology

2000;121(2):248-254. Not sensitivity or specificity of an

identified test 

Osman A A, Richter T, Stern M et al. The IgA subclass

distributions of endomysium and gliadin antibodies in 

human sera are different. Clinica Chimica Acta

1996;International Journal of Clinical Chemistry;

255(2):145-152. Not sensitivity or specificity of an 

identified test 

Osman A A, Uhlig H, Thamm B et al. Use of the phage 

display technique for detection of epitopes recognized by

polyclonal rabbit gliadin antibodies. Febs Letters 

1998;433(1-2):103-107. Not sensitivity or specificity of an 

identified test 

Osman Awad A, Richter Thomas, Stern Martin et al.

Production of recombinant human tissue transglutaminase 

using the baculovirus expression system, and its application

for serological diagnosis of coeliac disease. European 

Journal of Gastroenterology & Hepatology

2002;14(11):1217-1223. Test-specific exclusion

Otley C, Hall R P. Dermatitis herpetiformis. Dermatol Clin 

1990;8(4):759-769. Not sensitivity or specificity of an 

identified test 

Otley C C, Hall R P. The pathogenesis of dermatitis 

herpetiformis. Clinics in Dermatology 1991;9(3):313-323. 

Not sensitivity or specificity of an identified test

Otley C C, Wenstrup R J, Hall R P. DNA sequence analysis

and restriction fragment length polymorphism (RFLP) 

typing of the HLA-DQw2 alleles associated with dermatitis 

herpetiformis. Journal of Investigative Dermatology

1991;97(2):318-322. Not sensitivity or specificity of an 

identified test 

Ots M, Uibo O, Metskula K et al. IgA-antigliadin

antibodies in patients with IgA nephropathy: the secondary

phenomenon?. American Journal of Nephrology

A-438
1999;19(4):453-458. Not sensitivity or specificity of an 

identified test 

Ott D J. Celiac disease: biopsy or enteroclysis better for

evaluating response to a gluten-free diet?. American 

Journal of Gastroenterology 1997;92(4):715-716. Not 

sensitivity or specificity of an identified test 

Ottaway C A. Activated T cells and genetic restriction in 

celiac disease. Journal of Pediatric Gastroenterology and 

Nutrition 1994;19(2):250-251. Not sensitivity or specificity

of an identified test 

Otto H F, Bettmann I, Weltzien v J et al. Primary intestinal

lymphomas. Virchows Arch Abt A Pathol Anat 

1981;391(1):9-31. Not sensitivity or specificity of an 

identified test 

Owens D W, Brunton V G, Parkinson E K et al. E-cadherin

at the cell periphery is a determinant of keratinocyte 

differentiation in vitro. Biochemical and Biophysical

Research Communications 2000;269(2):369-376. Not 

sensitivity or specificity of an identified test 

Oxentenko A S, Murray J A. Celiac disease and dermatitis 

herpetiformis: The spectrum of gluten-sensitive 

enteropathy. International Journal of Dermatology 

2003;42(8):585-587. Not sensitivity or specificity of an 

identified test 

Oxentenko Amy S, Grisolano Scott W, Murray Joseph A et 

al. The insensitivity of endoscopic markers in celiac 

disease. American Journal of Gastroenterology

2002;97(4):933-938. Not sensitivity or specificity of an 

identified test 

Ozgenc F, Aksu G, Aydogdu S et al. Association between

anti-endomysial antibody and total intestinal villous 

atrophy in children with coeliac disease. Journal of

Postgraduate Medicine 2003;49(1):21-24. Improper control 

group 

Ozkan T, Ozeke T, Meral A. Gliadin-specific IgA 

antibodies in breast milk. Journal of International Medical 

Research 2000;28(5):234-240. Not sensitivity or specificity

of an identified test 

Ozkara C, Altintas A, Yilmaz E et al. An association 

between mesial temporal lobe epilepsy with hippocampal 

sclerosis and human leukocyte antigens. Epilepsia 

2002;43(3):236-239. Not sensitivity or specificity of an 

identified test 

Pacheco L S, Sotto M N. Factor XIIIa+ dermal dendrocytes 

in erythema elevatum diutinum and ordinary cutaneous 

leukocytoclastic vasculitis lesions. Journal of Cutaneous 

Pathology 2000;27(3):136-140. Not sensitivity or

specificity of an identified test

Packer S M, Charlton V, Keeling J W et al. Gluten

challenge in treated coeliac disease. Archives of Disease in

Childhood 1978;53(6):449-455. Not sensitivity or

specificity of an identified test

Packer S, Rowlatt R J, Harries J T. Proceedings: 

Reappraisal of a past diagnosis of "coeliac disease". 

Archives of Disease in Childhood 1974;49(10):819Not 

sensitivity or specificity of an identified test 

Paddenberg R, Flocke K, Elsasser H P et al. Phenotypical

changes of a human pancreatic adenocarcinoma cell line 

after selection on laminin-1/nidogen (LM/Ng) substratum. 

European Journal of Cell Biology 1998;76(4):251-264. Not 

sensitivity or specificity of an identified test 

Padmanabhan Vijayalakshmi, Callas Peter W, Li Shuan C 

et al. Histopathological features of the terminal ileum in 

lymphocytic and collagenous colitis: a study of 32 cases

and review of literature. Modern Pathology - an Official 

Journal of the United States and Canadian Academy of 

Pathology, Inc 2003;16(2):115-119. Not sensitivity or 

specificity of an identified test

Padykula H A, Strauss E W, Ladman A J et al. A 

morphologic and histochemical analysis of the human 

jejunal epithelium in nontropical sprue. Gastroenterology

1968;54(4):SupplUnable to extract data 

Paerregaard A, Vilien M, Krasilnikoff P A et al. Supposed 

coeliac disease during childhood and its presentation 14-38 

years later. Scandinavian Journal of Gastroenterology

1988;23(1):65-70. Not sensitivity or specificity of an 

identified test 

Page S R, Lloyd C A, Hill P G et al. The prevalence of

coeliac disease in adult diabetes mellitus. Qjm - Monthly 

Journal of the Association of Physicians 1994;87(10):631-

637. Not sensitivity or specificity of an identified test 

Paimela L, Kurki P, Leirisalo-Repo M et al. Gliadin 

immune reactivity in patients with rheumatoid arthritis.

Clinical and Experimental Rheumatology 1995;13(5):603-

607. Not sensitivity or specificity of an identified test 

Palavecino E A, Mota A H, Awad J et al. HLA and celiac 

disease in Argentina: involvement of the DQ subregion. 

Disease Markers 1990;8(1):5-10. Improper control group 

Pallet V, Azais-Braesco V, Enderlin V et al. Aging 

decreases retinoic acid and triiodothyronine nuclear 

expression in rat liver: Exogenous retinol and retinoic acid

differentially modulate this decreased expression. Mech 

Ageing Dev 1998;99(2):123-136. Not sensitivity or 

specificity of an identified test

Palosuo K, Alenius H, Varjonen E et al. Rye gamma-70 

and gamma-35 secalins and barley gamma-3 hordein crossreact with omega-5 gliadin, a major allergen in wheatdependent, exercise-induced anaphylaxis. Clinical and 

Experimental Allergy - Journal of the British Society for

Allergy and Clinical Immunology 2001;31(3):466-473. Not 

sensitivity or specificity of an identified test 

Palosuo Kati, Varjonen Elina, Nurkkala Jenni et al. 

A-439
Transglutaminase-mediated cross-linking of a peptic 

fraction of omega-5 gliadin enhances IgE reactivity in

wheat-dependent, exercise-induced anaphylaxis. Journal of 

Allergy and Clinical Immunology 2003;111(6):1386-1392. 

Not sensitivity or specificity of an identified test

Pani M A, Van Autreve J, Van der et al. Non-transmitted 

maternal HLA DQ2 or DQ8 alleles and risk of Type I 

diabetes in offspring: the importance of foetal or post 

partum exposure to diabetogenic molecules. Diabetologia 

2002;45(9):1340-1343. Not sensitivity or specificity of an

identified test 

Pani Michael A, Seidl Christian, Bieda Katrin et al. 

Preliminary evidence that an endogenous retroviral longterminal repeat (LTR13) at the HLA-DQB1 gene locus 

confers susceptibility to Addison's disease. Clinical 

Endocrinology 2002;56(6):773-777. Not sensitivity or 

specificity of an identified test

Pani Michael A, Wood Jeffrey P, Bieda Katrin et al. The 

variable endogenous retroviral insertion in the human 

complement C4 gene: a transmission study in type I 

diabetes mellitus. Human Immunology 2002;63(6):481-

484. Not sensitivity or specificity of an identified test 

Papadatou B, Crino A, Giannotti A et al. Antiendomysial 

and antigliadin antibodies in patients with Down syndrome. 

Dev Brain Dysfunct 1996;9(2-3):129-132. Not sensitivity

or specificity of an identified test

Papadopoulos A J, Schwartz R A, Krysicka Janniger C. 

Alopecia areata: Emerging concepts. Acta Dermatovenerol

Alp Panonica Adriat 2000;9(3):83-90. Not sensitivity or

specificity of an identified test

Papadopoulos G K, Wijmenga C, Koning F. Interplay

between genetics and the environment in the development 

of celiac disease: perspectives for a healthy life. Journal of

Clinical Investigation 2001;108(9):1261-1266. Not 

sensitivity or specificity of an identified test 

Papadopoulos K I, Sjoberg K, Lindgren S et al. Evidence of

gastrointestinal immune reactivity in patients with

sarcoidosis. Journal of Internal Medicine 1999;245(5):525-

531. Not sensitivity or specificity of an identified test 

Papouchado B G, Chapoval S P, Marietta E V et al. 

Cockroach allergen-induced eosinophilic airway

inflammation in HLA-DQ/human CD4SUP+ transgenic 

mice. J Immunol 2001;167(8):4627-4634. Not sensitivity or 

specificity of an identified test

Paranos S, Nikolic G. Lack of cross-reactivity between 

casein and gliadin in sera from coeliac disease patients. 

International Archives of Allergy and Immunology

1998;117(2):152-154. Not sensitivity or specificity of an

identified test 

Pardi D S, Ramnath V R, Loftus E V et al. Lymphocytic 

colitis: Clinical features, treatment, and outcomes. 

American Journal of Gastroenterology 2002;97(11):2829-

2833. Not sensitivity or specificity of an identified test 

Parent D, Bernard B A, Desbas C et al. Spreading of 

psoriatic plaques: alteration of epidermal differentiation

precedes capillary leakiness and anomalies in vascular 

morphology. Journal of Investigative Dermatology

1990;95(3):333-340. Not sensitivity or specificity of an 

identified test 

Parham D M, Coghill G, Robertson A J. Critical evaluation

of monoclonal antibody staining in breast carcinoma. 

Journal of Clinical Pathology 1989;42(8):810-813. Not 

sensitivity or specificity of an identified test 

Park M H, Hwang Y-S, Park K S et al. HLA haplotypes in 

Koreans based on 107 families. Tissue Antigens 1998;51(4 

I):347-355. Not sensitivity or specificity of an identified

test 

Park Y S, Sanjeevi C B, Robles D et al. Additional 

association of intra-MHC genes, MICA and D6S273, with

Addison's disease. Tissue Antigens 2002;60(2):155-163. 

Not sensitivity or specificity of an identified test

Parke A L. Gastrointestinal disorders and rheumatic

diseases. Curr Opin Rheumatol 1993;5(1):79-84. Not 

sensitivity or specificity of an identified test 

Parkkonen P, Hyoty H, Ilonen J et al. Antibody reactivity

to an Epstein-Barr virus BERF4-encoded epitope occurring

also in Asp-57 region of HLA-DQ8 beta chain. Clinical and

Experimental Immunology 1994;95(2):287-293. Not 

sensitivity or specificity of an identified test 

Parmentier L, Blanchet-Bardon C, Nguyen S et al.

Autosomal recessive lamellar ichthyosis: identification of a 

new mutation in transglutaminase 1 and evidence for 

genetic heterogeneity. Human Molecular Genetics 

1995;4(8):1391-1395. Not sensitivity or specificity of an

identified test 

Parnell N, Ciclitira P J. Celiac disease. Curr Opin

Gastroenterol 1999;15(2):120-124. Not sensitivity or 

specificity of an identified test

Parnell N D, Ciclitira P J. Review article: coeliac disease 

and its management. Alimentary Pharmacology &

Therapeutics 1999;13(1):1-13. Not sensitivity or specificity

of an identified test 

Parrot Isabelle, Huang Philip C, Khosla Chaitan. Circular 

dichroism and nuclear magnetic resonance spectroscopic 

analysis of immunogenic gluten peptides and their analogs. 

Journal of Biological Chemistry 2002;277(47):45572-

45578. Not sensitivity or specificity of an identified test 

Parsons K T, Kwok W W, Gaur L K et al. Increased 

frequency of HLA class II alleles DRB1*0301 and 

DQB1*0201 in Lambert-Eaton myasthenic syndrome 

without associated cancer. Hum Immunol 2000;61(8):828-

833. Not sensitivity or specificity of an identified test 

A-440
Partanen J. The HLA-DRB4 gene does not explain genetic 

susceptibility in HLA-DQ2-negative celiac disease. 

Immunogenetics 2000;51(3):249-250. Not sensitivity or

specificity of an identified test

Partanen J, Milner C, Campbell R D et al. HLA-linked 

heat-shock protein 70 (HSP70-2) gene polymorphism and 

celiac disease. Tissue Antigens 1993;41(1):15-19. Not 

sensitivity or specificity of an identified test 

Parveen S, Morshed S A, Arima K et al. Antibodies to 

Ro/La, Cenp-B, and snRNPs antigens in autoimmune 

hepatitis of North America versus Asia: Patterns of 

immunofluorescence, ELISA reactivities, and HLA 

association. Digestive Diseases and Sciences

1998;43(6):1322-1331. Not sensitivity or specificity of an

identified test 

Pasquali D, Rossi V, Prezioso D et al. Changes in tissue 

transglutaminase activity and expression during retinoic 

acid-induced growth arrest and apoptosis in primary

cultures of human epithelial prostate cells. Journal of 

Clinical Endocrinology and Metabolism 1999;84(4):1463-

1469. Not sensitivity or specificity of an identified test 

Passarge E, Valentine-Thon E. Everything the pediatrician 

ever wanted to know about HLA but was afraid to ask. 

European Journal of Pediatrics 1980;133(2):93-100. Not 

sensitivity or specificity of an identified test 

Pasternack A, Collin P, Mustonen J et al. Glomerular IgA

deposits in patients with celiac disease. Clinical

Nephrology 1990;34(2):56-60. Not sensitivity or specificity

of an identified test 

Pastore R A. Celiac disease: Endoscopic observations. 

American Journal of Gastroenterology 1974;61(6):478-480. 

Not sensitivity or specificity of an identified test

Patel R S, Johlin F C, Murray J A. Celiac disease and 

recurrent pancreatitis. Gastrointestinal Endoscopy

1999;50(6):823-827. Not sensitivity or specificity of an 

identified test 

Paterson C R, Burns J. Coeliac disease presenting with 

vitamin D deficiency in the elderly. Eur J Intern Med 

1991;2(2):73-76. Not sensitivity or specificity of an 

identified test 

Patey N, Scoazec J Y, Cuenod-Jabri B et al. Distribution of 

cell adhesion molecules in infants with intestinal epithelial

dysplasia (tufting enteropathy). Gastroenterology

1997;113(3):833-843. Not sensitivity or specificity of an

identified test 

Patey-Mariaud de, Serre Cellier C, Jabri B et al. Distinction

between coeliac disease and refractory sprue: a simple 

immunohistochemical method. Histopathology

2000;37(1):70-77. Not sensitivity or specificity of an 

identified test 

Patinen P, Bjorksten F, Malmstrom M et al. Salivary and

serum IgA antigliadin antibodies in dermatitis

herpetiformis. European Journal of Oral Sciences

1995;103(5):280-284. Not sensitivity or specificity of an

identified test 

Patinen P, Savilahti E, Hietanen J et al. Intraepithelial

lymphocytes bearing the gamma/delta receptor in the oral 

and jejunal mucosa in patients with dermatitis 

herpetiformis. European Journal of Oral Sciences

1997;105(2):130-135. Not sensitivity or specificity of an

identified test 

Patney N L, Srivastava V K, Wahal p k et al. A study of fat 

malabsorption and jejunal muscosal biopsy in diabetic 

neuropathy: a preliminary report. Journal of the Association

of Physicians of India 1973;21(9):777-785. Not sensitivity

or specificity of an identified test

Patterson R N, Johnston S D. Iron deficiency anaemia: Are 

the British Society of Gastroenterology guidelines being

adhered to?. Postgrad Med J 2003;79(930):226-228. Not 

sensitivity or specificity of an identified test 

Paulley J W. Determinants of adult celiac disease. New 

England Journal of Medicine 1971;284(15):916Not 

sensitivity or specificity of an identified test 

Paulsen G, Lundin K E, Gjertsen H A et al. HLA-DQ2-

restricted T-cell recognition of gluten-derived peptides in 

celiac disease. Influence of amino acid substitutions in the 

membrane distal domain of DQ beta 1*0201. Human 

Immunology 1995;42(2):145-153. Not sensitivity or 

specificity of an identified test

Pavone L, Fiumara A, Bottaro G et al. Autism and celiac 

disease: failure to validate the hypothesis that a link might 

exist. Biological Psychiatry 1997;42(1):72-75. Not 

sensitivity or specificity of an identified test 

Pearce Allum B, Sinclair David, Duncan Hamish D et al. 

Use of the anti-endomysial antibody test to diagnose 

coeliac disease in clinical practice. Clinical Laboratory 

2002;48(5-6):319-325. Improper control group 

Peces R, De la, Torre M et al. Prospective analysis of the 

factors influencing the antibody response to hepatitis B

vaccine in hemodialysis patients. Am J Kidney Dis 

1997;29(2):239-245. Not sensitivity or specificity of an 

identified test 

Pecsi G. Genetic associations and immunopathogenesis of 

coeliac disease. Acta Physiologica Hungarica 

2000;87(4):339-353. Not sensitivity or specificity of an 

identified test 

Pehamberger H, Gschnait F, Menzel J et al. Failure to

detect gliadin or gliadin binding sites in the skin of patients

with dermatitis herpetiformis: immunofluorescence, organ

culture and autoradiographic studies. Journal of

Investigative Dermatology 1979;73(2):174-175. Not 

sensitivity or specificity of an identified test 

A-441
Pelkonen P, Savilahti E, Makela A L. Persistent and 

transient IgA deficiency in juvenile rheumatoid arthritis.

Scand J Rheumatol 1983;12(3):273-279. Not sensitivity or

specificity of an identified test

Pellecchia M T, Ambrosio G, Salvatore E et al. Possible 

gluten sensitivity in multiple system atrophy. Neurology 

2002;59(7):1114-1115. Not sensitivity or specificity of an

identified test 

Pellecchia M T, Scala R, Filla A et al. Idiopathic cerebellar 

ataxia associated with celiac disease: lack of distinctive 

neurological features. Journal of Neurology, Neurosurgery, 

and Psychiatry 1999;66(1):32-35. Not sensitivity or 

specificity of an identified test

Pellegrini G, Scotta M S, Soardo S et al. Elevated IgA antigliadin antibodies in juvenile chronic arthritis. Clinical and

Experimental Rheumatology 1991;9(6):653-656. Not 

sensitivity or specificity of an identified test 

Pena A S, Mearin M L. Aetiopathogenesis of coeliac 

disease. Acta Gastroenterol Belg 1986;49(4):428-434. Not 

sensitivity or specificity of an identified test 

Pena A S, Wijmenga C. Genetic factors underlying glutensensitive enteropathy. Current Allergy and Asthma Reports 

2001;1(6):526-533. Not sensitivity or specificity of an 

identified test 

Pena A S, Garrote J A, Crusius J B. Advances in the 

immunogenetics of coeliac disease. Clues for

understanding the pathogenesis and disease heterogeneity. 

Scandinavian Journal of Gastroenterology.Supplement 

1998;22556-58. Not sensitivity or specificity of an 

identified test 

Pena A S, Mann D L, Hague N E et al. Genetic basis of 

gluten-sentitive enteropathy. Gastroenterology

1978;75(2):230-235. Not sensitivity or specificity of an 

identified test 

Pena A S, Mearin M L, Biemond I. Genetics and 

heterogeneity in coeliac disease. Acta Gastro-Enterologica 

Belgica 1984;47(2):134-135. Not sensitivity or specificity

of an identified test 

Pena A S, Truelove S C, Whitehead R. Disaccharidase 

activity and jejunal morphology in coeliac disease. 

Quarterly Journal of Medicine 1972;41(164):457-476. 

Unable to extract data 

Pena A S, Van Nieuwkoop J, Schuit H R E. Transient 

paraproteinaemia in a patient with coeliac disease. Gut

1976;17(9):735-739. Not sensitivity or specificity of an 

identified test 

Pena-Penabad C, de Unamuno P, Garcia Silva J et al. 

Altered expression of immunoreactive involucrin in 

lamellar ichthyosis. European Journal of Dermatology - Ejd

1999;9(3):197-201. Not sensitivity or specificity of an 

identified test 

Penedo-Pita M, Peteiro-Cartelle J. Increased serum levels 

of interleukin-2 and soluble interleukin-2 receptor in celiac 

disease. Journal of Pediatric Gastroenterology and

Nutrition 1991;12(1):56-60. Not sensitivity or specificity of 

an identified test

Penfornis A, Tuomilehto-Wolf E, Faustman D L et al. 

Analysis of TAP2 polymorphisms in finnish individuals 

with type I diabetes. Hum Immunol 2002;63(1):61-70. Not 

sensitivity or specificity of an identified test 

Peng X, Zhang Y, Zhang H et al. Interaction of tissue 

transglutaminase with nuclear transport protein importinalpha3. Febs Letters 1999;446(1):35-39. Not sensitivity or

specificity of an identified test

Pepper H W, Brandborg L L, Shanser J D et al. 

Collagenous sprue. American Journal of Roentgenology,

Radium Therapy, and Nuclear Medicine 1974;121(2):275-

282. Not sensitivity or specificity of an identified test 

Peraaho M, Kaukinen K, Paasikivi K et al. Wheat-starchbased gluten-free products in the treatment of newly

detected coeliac disease: prospective and randomized 

study. Alimentary Pharmacology & Therapeutics

2003;17(4):587-594. Not sensitivity or specificity of an 

identified test 

Peracchi M, Bamonti-Catena F, Faggioli P et al. Duodenal 

mucosa and extracellular cyclic nucleotide pattern in 

coeliac disease. Gut 1993;34(6):769-773. Not sensitivity or 

specificity of an identified test

Peracchi Maddalena, Trovato Cristina, Longhi Massimo et 

al. Tissue transglutaminase antibodies in patients with endstage heart failure. American Journal of Gastroenterology

2002;97(11):2850-2854. Not sensitivity or specificity of an 

identified test 

Perdriger A. Do the HLA-DQ and DP genes play a role in 

rheumatoid arthritis?. Jt Bone Spine 2001;68(1):12-18. Not

sensitivity or specificity of an identified test 

Pereira R M, Yoshinari N H, De Oliveira R M et al.

Antiganglioside antibodies in patients with 

neuropsychiatric systemic lupus erythematosus. Lupus 

1992;1(3):175-179. Not sensitivity or specificity of an 

identified test 

Perera D R, Weinstein W M, Rubin C E. Symposium on 

pathology of the gastrointestinal tract-Part II. Small 

intestinal biopsy. Human Pathology 1975;6(2):157-217. 

Not sensitivity or specificity of an identified test

Perez-Bravo F, Araya M, Mondragon A et al. Genetic 

differences in HLA-DQA1* and DQB1* allelic 

distributions between celiac and control children in 

Santiago, Chile. Human Immunology 1999;60(3):262-267. 

Improper control group 

Perez-Machado Miguel A, Ashwood Paul, Thomson 

A-442
Michael A et al. Reduced transforming growth factorbeta1-producing T cells in the duodenal mucosa of children

with food allergy. European Journal of Immunology

2003;33(8):2307-2315. Not sensitivity or specificity of an

identified test 

Peri A, Cowan B D, Bhartiya D et al. Expression of Clara 

cell 10-kD gene in the human endometrium and its 

relationship to ovarian menstrual cycle. Dna and Cell

Biology 1994;13(5):495-503. Not sensitivity or specificity

of an identified test 

Perichon B, Krishnamoorthy R. Asthma and HLA system. 

Allerg Immunol (Paris) 1991;23(7):301-307. Not 

sensitivity or specificity of an identified test 

Perisic V N, Kokai G. Coeliac disease and

lymphangiectasia. Archives of Disease in Childhood 

1992;67(1):134-136. Not sensitivity or specificity of an 

identified test 

Perkkio M, Savilahti E, Kuitunen P. Semi-quantitative 

analysis of immunoglobulins and complement fractions 3 

and 4 in the jejunal mucosa in coeliac disease and in food

allergy in childhood. Immunohistochemical study by light 

and electron microscopy. Acta Pathologica Et 

Microbiologica Scandinavica.Section a, Pathology 

1981;89(4):343-350. Not sensitivity or specificity of an 

identified test 

Perri F, Pastore M, Festa V et al. Intraduodenal lipase 

activity in celiac disease assessed by means of 13C mixedtriglyceride breath test. Journal of Pediatric 

Gastroenterology and Nutrition 1998;27(4):407-410. Not

sensitivity or specificity of an identified test 

Perrin Christophe, Baran Robert, Pisani Anne et al. The 

onychomatricoma: additional histologic criteria and 

immunohistochemical study. American Journal of

Dermatopathology 2002;24(3):199-203. Not sensitivity or

specificity of an identified test

Perry A, Scheithauer B W, Nascimento A G. The 

immunophenotypic spectrum of meningeal 

hemangiopericytoma: a comparison with fibrous 

meningioma and solitary fibrous tumor of meninges. 

American Journal of Surgical Pathology 1997;21(11):1354-

1360. Not sensitivity or specificity of an identified test 

Persic M, Milin C, Varljen J et al. Intestinal mucosa 

alkaline phosphatase in coeliac disease. Period Biol 

1992;94(2):121-126. Not sensitivity or specificity of an 

identified test 

Persliden J, Pettersson H B L, Falth-Magnusson K. 

Intestinal biopsy in children with coeliac disease; A 

Swedish national study of radiation dose and risk. Radiat 

Prot Dosim 1995;57(1-4):459-462. Not sensitivity or 

specificity of an identified test

Persliden J, Pettersson H B, Falth-Magnusson K. Radiation

dose at small intestinal biopsies in children: results of a 

national study. Acta Paediatrica (Oslo, Norway - 1992) 

1996;85(9):1042-1046. Not sensitivity or specificity of an

identified test 

Persliden J, Pettersson H B, Falth-Magnusson K. Small 

intestinal biopsy in children with coeliac disease:

measurement of radiation dose and analysis of risk. Acta 

Paediatrica (Oslo, Norway - 1992) 1993;82(3):296-299. 

Not sensitivity or specificity of an identified test

Persson B L, Stenberg P, Holmberg L et al. Transamidating

enzymes in maternal plasma and placenta in human 

pregnancies complicated by intrauterine growth retardation.

Journal of Developmental Physiology 1980;2(1-2):37-46. 

Not sensitivity or specificity of an identified test

Perticarari S, Not T, Cauci S et al. ELISA method for 

quantitative measurement of IgA and IgG specific antigliadin antibodies. Journal of Pediatric Gastroenterology

and Nutrition 1992;15(3):302-309. Not sensitivity or 

specificity of an identified test

Perticarari S, Presani G, Trevisan M et al. Serum IgA and 

IgG antibodies to alpha-gliadin: comparison between two

ELISA methods. La Ricerca in Clinica E in Laboratorio

1987;17(4):323-329. Not sensitivity or specificity of an 

identified test 

Perticarari S, Prodan M, Fragonas E et al. CD69 expression 

on alpha-gliadin-specific T cells in coeliac disease. 

European Journal of Histochemistry - Ejh 2002;46(1):13-

22. Not sensitivity or specificity of an identified test 

Pertot W J, Sindres V, Szekeres G et al. Model for 

quantitative immunohistochemical assessment of pulpal 

response to biomaterials. Journal of Biomedical Materials

Research 1997;34(4):457-462. Not sensitivity or specificity

of an identified test 

Pertschuk L P, Cook A W, Gupta J K. Jejunal 

immunopathology in amyotrophic lateral sclerosis and 

multiple sclerosis. Identification of viral antigens by

immunofluorescence. Lancet 1977;1(8022):1119-1123. Not 

sensitivity or specificity of an identified test 

Pervez S, Hasan S H, Aijaz F et al. Changing patterns and

re-distribution of antigen in poorly differentiated 

carcinomas: its implications in tumour diagnosis. Indian 

Journal of Pathology & Microbiology 1998;41(1):55-66. 

Not sensitivity or specificity of an identified test

Pesce G, Pesce F, Fiorino N et al. Intraepithelial 

gamma/delta-positive T lymphocytes and intestinal villous 

atrophy. International Archives of Allergy and

Immunology 1996;110(3):233-237. Not sensitivity or 

specificity of an identified test

Petaros P, Martelossi S, Tommasini A et al. Prevalence of

autoimmune disorders in relatives of patients with celiac 

disease. Digestive Diseases and Sciences 2002;47(7):1427-

1431. Not sensitivity or specificity of an identified test 

A-443
Peters M S, McEvoy M T. IgA antiendomysial antibodies

in dermatitis herpetiformis. Journal of the American 

Academy of Dermatology 1989;21(6):1225-1231. Not 

sensitivity or specificity of an identified test 

Peters T J, Doe W F, Heath J R et al. Lysosomal acid 

hydrolase activity in intestinal biopsies from control 

subjects and patients with coeliac disease. Gut

1973;14(5):430Not sensitivity or specificity of an identified 

test 

Peters T J, Heath J R, Wansbrough-Jones M H et al. 

Enzyme activities and properties of lysosomes and brush 

borders in jejunal biopsies from control subjects and 

patients with coeliac disease. Clinical Science and 

Molecular Medicine 1975;48(4):259-267. Not sensitivity or 

specificity of an identified test

Peters T J, Jones P E, Wells G. Analytical subcellular 

fractionation of jejunal biopsy specimens: enzyme

activities, organelle pathology and response to gluten 

withdrawal in patients with coeliac disease. Clinical

Science and Molecular Medicine 1978;55(3):285-292. Not 

sensitivity or specificity of an identified test 

Peters T J, Jones P E, Jenkins W J et al. Analytical 

subcellular fractionation of jejunal biopsy specimens: 

Enzyme activities, organelle pathology and response to 

corticosteroids in patients with non-responsive coeliac 

disease. Clin Sci Mol Med 1978;55(3):293-300. Not 

sensitivity or specificity of an identified test 

Petit E, Huber M, Rochat A et al. Three novel point 

mutations in the keratinocyte transglutaminase (TGK) gene 

in lamellar ichthyosis: significance for mutant transcript 

level, TGK immunodetection and activity. European 

Journal of Human Genetics - Ejhg 1997;5(4):218-228. Not 

sensitivity or specificity of an identified test 

Petronzelli F, Bonamico M, Ferrante P et al. Genetic 

contribution of the HLA region to the familial clustering of

coeliac disease. Annals of Human Genetics 1997;61(Pt 

4):307-317. Not sensitivity or specificity of an identified

test 

Petronzelli F, Ferrante P, Triglione P et al. Oligotyping of 

celiac multiplex families with the 11th International 

Histocompatibility Workshop reagents. Tissue Antigens 

1991;38(5):238-239. Improper control group 

Petronzelli F, Multari G, Ferrante P et al. Different dose 

effect of HLA-DQ alpha beta heterodimers in insulindependent diabetes mellitus and celiac disease

susceptibility. Human Immunology 1993;36(3):156-162. 

Not sensitivity or specificity of an identified test

Petrovsky N, Harrison L. HLA class II-associated

polymorphism of interferon-gamma production

implications for HLA-disease association. Hum Immunol 

1997;53(1):12-16. Not sensitivity or specificity of an 

identified test 

Pettersson A, Sjoberg K, Lernmark A et al. HLA genotypes

in coeliac disease and healthy individuals carrying gliadin 

antibodies. European Journal of Gastroenterology & 

Hepatology 1993;5(6):445-450. Improper control group 

Pettifor J M. Letter: How different are we?. South African

Medical Journal.Suid-Afrikaanse Tydskrif Vir

Geneeskunde 1974;48(16):669Not sensitivity or specificity

of an identified test 

Pettifor J M. Jejunal biopsy in the diagnosis of coeliac 

disease. S Afr Med J 1974;48(16):669Not sensitivity or

specificity of an identified test

Pham T H, Barr G D. Coeliac disease in adults.

Presentation and management. Australian Family Physician 

1996;25(1):62-65. Not sensitivity or specificity of an 

identified test 

Phelan J J, Stevens F M, McNicholl B N. Chemical studies

of gliadin toxicity. Ir J Med Sci 1975;144(9):364Not 

sensitivity or specificity of an identified test 

Phillips A D, Rice S J, France N E et al. Small intestinal

intraepithelial lymphocyte levels in cow's milk protein

intolerance. Gut 1979;20(6):509-512. Not sensitivity or

specificity of an identified test

Phillips M A, Qin Q, Mehrpouyan M et al. Keratinocyte

transglutaminase membrane anchorage: analysis of sitedirected mutants. Biochemistry 1993;32(41):11057-11063. 

Not sensitivity or specificity of an identified test

Phillips M A, Stewart B E, Qin Q et al. Primary structure of 

keratinocyte transglutaminase. Proceedings of the National 

Academy of Sciences of the United States of America 

1990;87(23):9333-9337. Not sensitivity or specificity of an 

identified test 

Phillips S B, Kubilus J, Grassi A M et al. The pancornulins:

a group of basic low molecular weight proteins in

mammalian epidermis and epithelium that may function as 

cornified envelope precursors. Comparative Biochemistry

and Physiology.B, Comparative Biochemistry

1990;95(4):781-788. Not sensitivity or specificity of an 

identified test 

Philotheou A. Epilogue: What have we learned to improve 

the treatment of children with diabetes mellitus and their 

families?. J Pediatr Endocrinol Metab 2001;14(Suppl 

1):697-700. Not sensitivity or specificity of an identified

test 

Piacentini M. Tissue transglutaminase: a candidate effector 

element of physiological cell death. Current Topics in 

Microbiology and Immunology 1995;200163-175. Not 

sensitivity or specificity of an identified test 

Piacentini M, Autuori F. Immunohistochemical localization

of tissue transglutaminase and Bcl-2 in rat uterine tissues 

during embryo implantation and post-partum involution. 

Differentiation 1994;57(1):51-61. Not sensitivity or 

A-444
specificity of an identified test

Piacentini M, Colizzi V. Tissue transglutaminase: apoptosis 

versus autoimmunity. Immunology Today 1999;20(3):130-

134. Not sensitivity or specificity of an identified test 

Piacentini M, Melino G. Role of tissue transglutaminase in 

neuroblastoma cells undergoing apoptosis. Progress in 

Clinical and Biological Research 1994;385123-129. Not 

sensitivity or specificity of an identified test 

Piacentini M, Annicchiarico-Petruzzelli M, Oliverio S et al. 

Phenotype-specific "tissue" transglutaminase regulation in

human neuroblastoma cells in response to retinoic acid: 

correlation with cell death by apoptosis. International 

Journal of Cancer.Journal International Du Cancer 

1992;52(2):271-278. Not sensitivity or specificity of an 

identified test 

Piacentini M, Autuori F, Dini L et al. 'Tissue' 

transglutaminase is specifically expressed in neonatal rat 

liver cells undergoing apoptosis upon epidermal growth 

factor-stimulation. Cell Tissue Res 1991;263(2):227-235. 

Not sensitivity or specificity of an identified test

Piacentini M, Farrace M G, Hassan C et al. 'Tissue' 

transglutaminase release from apoptotic cells into

extracellular matrix during human liver fibrogenesis. 

Journal of Pathology 1999;189(1):92-98. Not sensitivity or 

specificity of an identified test

Piacentini M, Fesus L, Melino G. Multiple cell cycle access 

to the apoptotic death programme in human neuroblastoma 

cells. Febs Letters 1993;320(2):150-154. Not sensitivity or

specificity of an identified test

Piacentini M, Fesus L, Farrace M G et al. The expression of 

"tissue" transglutaminase in two human cancer cell lines is 

related with the programmed cell death (apoptosis). 

European Journal of Cell Biology 1991;54(2):246-254. Not 

sensitivity or specificity of an identified test 

Piacentini M, Piredda L, Starace D et al. Differential

growth of N- and S-type human neuroblastoma cells 

xenografted into SCID mice. Correlation with apoptosis. J 

Pathol 1996;180(4):415-422. Not sensitivity or specificity

of an identified test 

Piacentini M, Rodolfo C, Farrace M G et al. "Tissue" 

transglutaminase in animal development. International

Journal of Developmental Biology 2000;44(6 Spec 

No):655-662. Not sensitivity or specificity of an identified

test 

Piacentini Mauro, Farrace Maria, Grazia Piredda et al. 

Transglutaminase overexpression sensitizes neuronal cell 

lines to apoptosis by increasing mitochondrial membrane 

potential and cellular oxidative stress. Journal of 

Neurochemistry 2002;81(5):1061-1072. Not sensitivity or 

specificity of an identified test

Picarelli A, Di Tola M, Sabbatella L et al. 31-43 amino acid

sequence of the alpha-gliadin induces anti-endomysial 

antibody production during in vitro challenge. 

Scandinavian Journal of Gastroenterology

1999;34(11):1099-1102. Not sensitivity or specificity of an 

identified test 

Picarelli A, Di Tola M, Sabbatella L et al. Immunologic 

evidence of no harmful effect of oats in celiac disease.

American Journal of Clinical Nutrition 2001;74(1):137-

140. Not sensitivity or specificity of an identified test 

Picarelli A, Di Tola M, Sabbatella L et al. Identification of

a new coeliac disease subgroup: antiendomysial and antitransglutaminase antibodies of IgG class in the absence of

selective IgA deficiency. Journal of Internal Medicine 

2001;249(2):181-188. Improper control group 

Picarelli A, Maiuri L, Frate A et al. Production of

antiendomysial antibodies after in-vitro gliadin challenge of

small intestine biopsy samples from patients with coeliac 

disease. Lancet 1996;348(9034):1065-1067. Not sensitivity

or specificity of an identified test

Picarelli A, Maiuri L, Mazzilli M C et al. Gluten-sensitive

disease with mild enteropathy. Gastroenterology

1996;111(3):608-616. Not sensitivity or specificity of an

identified test 

Picarelli A, Sabbatella L, Di Tola M et al. Forty-eight hours 

of biopsy culture improve the sensitivity of the in vitro 

gliadin challenge in the diagnosis of celiac disease. Clinical 

Chemistry 2001;47(10):1841-1843. Not sensitivity or 

specificity of an identified test

Picarelli A, Triglione P, Mariani P et al. Use of a threshold 

serum level of anti-gliadin antibodies improves diagnostic 

efficiency of the test in adult coeliac disease but is

unreliable as a screening test. Italian Journal of 

Gastroenterology 1996;28(2):70-75. Improper control 

group 

Picarelli Antonio, Sabbatella Luigi, Di Tola et al. 

Antiendomysial antibody detection in fecal supernatants: in

vivo proof that small bowel mucosa is the site of

antiendomysial antibody production. American Journal of

Gastroenterology 2002;97(1):95-98. Not sensitivity or 

specificity of an identified test

Pierard-Franchimont C, Arrese J E, Pierard G E.

Immunohistochemical aspects of the link between

Malassezia ovalis and seborrheic dermatitis. J Eur Acad

Dermatol Venereol 1995;4(1):14-19. Not sensitivity or

specificity of an identified test

Pierard-Franchimont C, Arrese J E, Nikkels A F et al. 

Factor XIIIa-positive dendrocytes and proliferative activity 

of cutaneous cancers. Virchows Archiv - an International 

Journal of Pathology 1996;429(1):43-48. Not sensitivity or 

specificity of an identified test

Pierard-Franchimont C, Dosal F L, Estrada J A et al.

Cutaneous hamartoma with pagetoid cells. American 

A-445
Journal of Dermatopathology 1991;13(2):158-161. Not 

sensitivity or specificity of an identified test 

Pierucci Alessandro, Fofi Claudia, Bartoli Benedetta et al. 

Antiendomysial antibodies in Berger's disease. American 

Journal of Kidney Diseases - the Official Journal of the 

National Kidney Foundation 2002;39(6):1176-1182. Not 

sensitivity or specificity of an identified test 

Pietroletti R, Bishop A E, Carlei F et al. Gut endocrine cell 

population in coeliac disease estimated by

immunocytochemistry using a monoclonal antibody to 

chromogranin. Gut 1986;27(7):838-843. Not sensitivity or 

specificity of an identified test

Pietroletti R, Castro M, Mariani P et al. Prostanoids in 

jejunal biopsy specimens of celiac children with active 

disease and on challenge diet. Radioimmunologic 

evaluation. Scandinavian Journal of Gastroenterology

1987;22(10):1181-1184. Not sensitivity or specificity of an 

identified test 

Pietzak M M, Thomas D W. Childhood malabsorption. 

Pediatr Rev 2003;24(6):195-204. Not sensitivity or 

specificity of an identified test

Pignata C, Troncone R, Monaco G et al. Impaired

suppressor activity in children affected by coeliac disease. 

Gut 1985;26(3):285-290. Not sensitivity or specificity of an 

identified test 

Pileri S, Poggi S, Baglioni P et al. Histology and

immunohistology of bone marrow biopsy in multiple 

myeloma. European Journal of

Haematology.Supplementum 1989;5152-59. Not sensitivity

or specificity of an identified test

Piper J M, Langer O. Is lung maturation related to fetal 

growth in diabetic or hypertensive pregnancies?. European

Journal of Obstetrics, Gynecology, and Reproductive 

Biology 1993;51(1):15-19. Not sensitivity or specificity of 

an identified test

Piper Justin L, Gray Gary M, Khosla Chaitan. High 

selectivity of human tissue transglutaminase for 

immunoactive gliadin peptides: implications for celiac 

sprue. Biochemistry 2002;41(1):386-393. Not sensitivity or 

specificity of an identified test

Piredda L, Farrace M G, Lo Bello M et al. Identification of

'tissue' transglutaminase binding proteins in neural cells 

committed to apoptosis. Faseb Journal - Official

Publication of the Federation of American Societies for 

Experimental Biology 1999;13(2):355-364. Not sensitivity

or specificity of an identified test

Pirmohamed M, Lin K, Chadwick D et al. TNFalpha 

promoter region gene polymorphisms in carbamazepinehypersensitive patients. Neurology 2001;56(7):890-896. 

Not sensitivity or specificity of an identified test

Pisegma J R. A difficult diagnosis: When is irritable bowel 

syndrome really celiac disease?. Med Crossfire 

2002;4(10):46-47. Not sensitivity or specificity of an 

identified test 

Pittman F E, Pittman J C. A light and electron microscopic

study of sigmoid colonic mucosa in adult celiac disease.

Scandinavian Journal of Gastroenterology 1966;1(1):21-27. 

Not sensitivity or specificity of an identified test

Pittschieler K, Ladinser B. Coeliac disease: screened by a 

new strategy. Acta paediatrica (Oslo, Norway : 

1992).Supplement. 1996;41242-45. Improper control group 

Pittschieler K, Gentili L, Niederhofer H. Onset of coeliac

disease: A prospective longitudinal study. Acta Paediatr Int

J Paediatr 2003;92(10):1149-1152. Not sensitivity or 

specificity of an identified test

Pittschieler K, Ladinser B, Petell J K. Reactivity of gliadin 

and lectins with celiac intestinal mucosa. Pediatric 

Research 1994;36(5):635-641. Not sensitivity or specificity

of an identified test 

Pittschieler K, Reissigl H, Mengarda G. Celiac disease in 

two different population groups of South Tirol. Journal of

Pediatric Gastroenterology and Nutrition 1988;7(3):400-

402. Not sensitivity or specificity of an identified test 

Placido R, Mancino G, Amendola A et al. Apoptosis of 

human monocytes/macrophages in Mycobacterium 

tuberculosis infection. Journal of Pathology

1997;181(1):31-38. Not sensitivity or specificity of an 

identified test 

Plenz A, Fritz P, Konig G et al. Immunohistochemical 

detection of factor XIIIa and factor XIIIs in synovial 

membranes of patients with rheumatoid arthritis or 

osteoarthritis. Rheumatology International 1996;16(1):29-

36. Not sensitivity or specificity of an identified test 

Ploski R, Ascher H, Sollid L M. HLA genotypes and the 

increased incidence of coeliac disease in Sweden.

Scandinavian Journal of Gastroenterology

1996;31(11):1092-1097. Improper control group

Ploski R, Ek J, Thorsby E et al. On the HLA-DQ(alpha 

1*0501, beta 1*0201)-associated susceptibility in celiac 

disease: a possible gene dosage effect of DQB1*0201. 

Tissue Antigens 1993;41(4):173-177. Improper control 

group 

Pocecco M, Ventura A. Coeliac disease and insulindependent diabetes mellitus: a causal association?. Acta

Paediatrica (Oslo, Norway - 1992) 1995;84(12):1432-1433. 

Not sensitivity or specificity of an identified test

Pociot F, McDermott M F. Genetics of type 1 diabetes 

mellitus. Genes and Immunity 2002;3(5):235-249. Not

sensitivity or specificity of an identified test 

Poddar S, Davies J A. Induction of tissue transglutaminase 

by structural analogs of trans retinoic acid. Fed Proc 

A-446
1985;44(3):No 2110Not sensitivity or specificity of an 

identified test 

Poddar S, Hong W K, Thacher S M et al. Retinoic acid 

suppression of squamous differentiation in human headand-neck squamous carcinoma cells. International Journal 

of Cancer.Journal International Du Cancer 1991;48(2):239-

247. Not sensitivity or specificity of an identified test 

Poddar U. Celiac disease: clinical features and diagnostic 

criteria. Indian Journal of Pediatrics 1999;66(1 Suppl):S21-

S25. Not sensitivity or specificity of an identified test 

Podolsky D K, LaMont J T. So, where are all the celiacs?.

Gastroenterology 1999;116(2):237Not sensitivity or 

specificity of an identified test

Poelman J R, Netelenbos J C, Van Der et al. Diabetes 

mellitus, diarrhoea and malabsorption. Neth J Med 

1975;18(6):297-306. Not sensitivity or specificity of an 

identified test 

Polak J M, Pearse A G E, Van Noorden S. Secretin cells in 

coeliac disease. Gut 1973;14(11):870-874. Not sensitivity

or specificity of an identified test

Polakowska R R, Eddy R L, Shows T B et al. Epidermal 

type I transglutaminase (TGM1) is assigned to human 

chromosome 14. Cytogenetics and Cell Genetics 

1991;56(2):105-107. Not sensitivity or specificity of an 

identified test 

Polakowska R R, Graf B A, Falciano V et al. Transcription

regulatory elements of the first intron control human 

transglutaminase type I gene expression in epidermal 

keratinocytes. Journal of Cellular Biochemistry

1999;73(3):355-369. Not sensitivity or specificity of an 

identified test 

Polanco I. Clinical relevance of villous atrophy. Pediatric 

Allergy and Immunology - Official Publication of the 

European Society of Pediatric Allergy and Immunology

2001;12(Suppl 14):47-50. Not sensitivity or specificity of

an identified test

Polanco I. Clinical relevance of villus atrophy. Pediatrika

2001;21(10):23-26. Not sensitivity or specificity of an 

identified test 

Polanco I, Mearin M L, Larrauri J et al. Effect of gluten

supplementation in healthy siblings of children with celiac 

disease. Gastroenterology 1987;92(3):678-681. Not 

sensitivity or specificity of an identified test 

Poley J R. The scanning electron microscope: how valuable 

in the evaluation of small bowel mucosal pathology in 

chronic childhood diarrhea?. Scanning Microscopy

1991;5(4):1037-1062. Not sensitivity or specificity of an

identified test 

Poley J R, Bhatia M, Welsh J D. Disaccharidase deficiency

in infants with cow's milk protein intolerance. Response to 

treatment. Digestion 1978;17(2):97-107. Not sensitivity or

specificity of an identified test

Poljac caron, Gajinov Z, Belic caron et al. MHC class II 

antigens in alopecia areata. Acta Dermatovenerol Alp 

Pannonica Adriat 2002;11(2):55-58. Not sensitivity or 

specificity of an identified test

Pollack S. Chronic fatigue syndrome and immune 

dysfunction: Cause or effect?. Isr Med Assoc J 2002;4(11 

SUPPL.):883-885. Not sensitivity or specificity of an 

identified test 

Pollock D J. The liver in coeliac disease. Histopathology 

1977;1(6):421-430. Not sensitivity or specificity of an 

identified test 

Pollock D J, Nagle R E, Jeejeebhoy K N et al. The effect on

jejunal mucosa of withdrawing and adding dietary gluten in

cases of idiopathic steatorrhoea. Gut 1970;11(7):567-575. 

Not sensitivity or specificity of an identified test

Polvi A, Arranz E, Fernandez-Arquero M et al. HLA-DQ2-

negative celiac disease in Finland and Spain. Human 

Immunology 1998;59(3):169-175. Not sensitivity or 

specificity of an identified test

Polvi A, Eland C, Koskimies S et al. HLA DQ and DP in 

Finnish families with celiac disease. European Journal of

Immunogenetics - Official Journal of the British Society for 

Histocompatibility and Immunogenetics 1996;23(3):221-

234. Improper control group 

Polvi A, Garden O A, Elwood C M et al. Canine major 

histocompatibility complex genes DQA and DQB in Irish 

setter dogs. Tissue Antigens 1997;49(3 Pt 1):236-243. Not 

sensitivity or specificity of an identified test 

Polvi A, Maki M, Partanen J. Celiac patients predominantly 

inherit HLA-DPB1*0101 positive haplotype from HLADQ2 homozygous parent. Human Immunology

1997;53(2):156-158. Not sensitivity or specificity of an 

identified test 

Polvi A, Maki M, Collin P et al. TNF microsatellite alleles 

a2 and b3 are not primarily associated with celiac disease in 

the Finnish population. Tissue Antigens 1998;51(5):553-

555. Not sensitivity or specificity of an identified test 

Poon E, Nixon R. Cutaneous spectrum of coeliac disease. 

Australas J Dermatol 2001;42(2):136-138. Not sensitivity

or specificity of an identified test

Popat S, Hearle N, Bevan S et al. Mutational analysis of

CD28 in coeliac disease. Scandinavian Journal of 

Gastroenterology 2002;37(5):536-539. Not sensitivity or 

specificity of an identified test

Popat S, Hearle N, Hogberg L et al. Variation in the 

CTLA4/CD28 gene region confers an increased risk of 

coeliac disease. Annals of Human Genetics 2002;66(Pt 

2):125-137. Not sensitivity or specificity of an identified

A-447
test 

Popat S, Hearle N, Wixey J et al. Analysis of the CTLA4 

gene in Swedish coeliac disease patients. Scandinavian 

Journal of Gastroenterology 2002;37(1):28-31. Improper 

control group 

Popat S, Hogberg L, McGuire S et al. Germline mutations 

in TGM2 do not contribute to coeliac disease susceptibility 

in the Swedish population. European Journal of

Gastroenterology & Hepatology 2001;13(12):1477-1479. 

Not sensitivity or specificity of an identified test

Potolicchio I, Santambrogio L, Strominger J L. Molecular 

interaction and enzymatic activity of macrophage migration

inhibitory factor with immunorelevant peptides. J Biol 

Chem 2003;278(33):30889-30895. Not sensitivity or 

specificity of an identified test

Powis S H, Rosenberg W M, Hall M et al. TAP1 and TAP2 

polymorphism in coeliac disease. Immunogenetics 

1993;38(5):345-350. Not sensitivity or specificity of an 

identified test 

Pozler O, Parizek J, Chylkova V et al. Immunological 

aspects of diagnosis of celiac sprue in children. Sbornik 

Vedeckych Praci Lekarske Fakulty Karlovy University V 

Hradci Kralove 1989;32(2):169-233. Not sensitivity or

specificity of an identified test

Prasad S, Thomas P, Nicholas D S et al. Adult endomysial

antibody-negative coeliac disease and cigarette smoking. 

European Journal of Gastroenterology & Hepatology

2001;13(6):667-671. Not sensitivity or specificity of an 

identified test 

Pratesi R, Gandolfi L, Friedman H et al. Serum IgA 

antibodies from patients with coeliac disease react strongly

with human brain blood-vessel structures. Scandinavian

Journal of Gastroenterology 1998;33(8):817-821. Not 

sensitivity or specificity of an identified test 

Pratesi R, Gandolfi L, Garcia S G et al. Prevalence of 

coeliac disease: Unexplained age-related variation in the

same population. Scandinavian Journal of Gastroenterology

2003;38(7):747-750. Not sensitivity or specificity of an 

identified test 

Pratesi Riccardo, Gandolfi Lenora, Martins Rita C et al. Is 

the prevalence of celiac disease increased among epileptic 

patients?. Arquivos De Neuro-Psiquiatria 2003;61(2b):330-

334. Not sensitivity or specificity of an identified test 

Prati D, Bardella M T, Peracchi M et al. High frequency of

anti-endomysial reactivity in candidates to heart transplant. 

Digestive and Liver Disease - Official Journal of the Italian

Society of Gastroenterology and the Italian Association for

the Study of the Liver 2002;34(1):39-43. Not sensitivity or 

specificity of an identified test

Presani G, Perticarari S, Mangiarotti M A. Flow cytometric

detection of anti-gliadin antibodies. Journal of

Immunological Methods 1989;119(2):197-202. Serology

<1990 

Presland R B, Dale B A. Epithelial structural proteins of the 

skin and oral cavity: function in health and disease. Critical

Reviews in Oral Biology and Medicine - an Official 

Publication of the American Association of Oral Biologists 

2000;11(4):383-408. Not sensitivity or specificity of an 

identified test 

Presotto F, Betterle C. Insulin-dependent diabetes mellitus: 

A constellation of autoimmune diseases. J Pediatr 

Endocrinol Metab 1997;10(5):455-469. Not sensitivity or 

specificity of an identified test

Price H L, Gazzard B G, Dawson A M. Steatorrhoea in the 

elderly. Br Med J 1977;1(6076):1582-1584. Not sensitivity

or specificity of an identified test

Price P, Witt C, Allcock R et al. The genetic basis for the

association of the 8.1 ancestral haplotype (A1, B8, DR3) 

with multiple immunopathological diseases. Immunol Rev

1999;167(-):257-274. Not sensitivity or specificity of an

identified test 

Prieto V G, Reed J A, Shea C R. Immunohistochemistry of 

dermatofibromas and benign fibrous histiocytomas. Journal 

of Cutaneous Pathology 1995;22(4):336-341. Not 

sensitivity or specificity of an identified test 

Priglinger Siegfried G, May Christian A, Neubauer 

Aljoscha S et al. Tissue transglutaminase as a modifying 

enzyme of the extracellular matrix in PVR membranes.

Investigative Ophthalmology & Visual Science 

2003;44(1):355-364. Not sensitivity or specificity of an 

identified test 

Primignani M, Agape D, Ronchi G et al. Prevalence of

duodenal and jejunal lesions in dermatitis herpetiformis. La 

Ricerca in Clinica E in Laboratorio 1987;17(3):243-249. 

Not sensitivity or specificity of an identified test

Prince H E, Norman G L, Binder W L. Immunoglobulin A 

(IgA) deficiency and alternative celiac disease-associated 

antibodies in sera submitted to a reference laboratory for 

endomysial IgA testing. Clinical and Diagnostic Laboratory

Immunology 2000;7(2):192-196. Improper control group 

Prisco A, Troncone R, Mazzarella G et al. Identical T-cell 

receptor beta chain rearrangements are present in T cells

infiltrating the jejunal mucosa of untreated celiac patients. 

Hum Immunol 1997;55(1):22-33. Not sensitivity or 

specificity of an identified test

Probst-Cousin S, Poremba C, Rickert C H et al. Factor

XIIIa expression in granulomatous lesions due to

sarcoidosis or mycobacterial infection. Pathology, Research 

and Practice 1997;193(11-12):741-745. Not sensitivity or 

specificity of an identified test

Provost T T, Talal N, Bias W et al. Ro(SS-A) positive 

Sjogren's/lupus erythematosus (SC/LE) overlap patients are 

A-448
associated with the HLA-DR3 and/or DRw6 phenotypes. J

Invest Dermatol 1988;91(4):369-371. Not sensitivity or

specificity of an identified test

Pruessner H T. Detecting celiac disease in your patients. 

American Family Physician 1998;57(5):1023-34, 1039. Not 

sensitivity or specificity of an identified test 

Przemioslo R T, Kontakou M, Nobili V et al. Raised proinflammatory cytokines interleukin 6 and tumour necrosis 

factor alpha in coeliac disease mucosa detected by

immunohistochemistry. Gut 1994;35(10):1398-1403. Not 

sensitivity or specificity of an identified test 

Przemioslo R T, Lundin K E, Sollid L M et al. Histological 

changes in small bowel mucosa induced by gliadin 

sensitive T lymphocytes can be blocked by anti-interferon

gamma antibody. Gut 1995;36(6):874-879. Not sensitivity

or specificity of an identified test

Przemioslo R, Wright N A, Elia G et al. Analysis of crypt 

cell proliferation in coeliac disease using MI-B1 antibody 

shows an increase in growth fraction. Gut 1995;36(1):22-

27. Not sensitivity or specificity of an identified test 

Pueschel S M, Romano C, Failla P et al. A prevalence

study of celiac disease in persons with Down syndrome

residing in the United States of America. Acta Paediatrica

(Oslo, Norway - 1992) 1999;88(9):953-956. Not sensitivity

or specificity of an identified test

Pynnonen P, Isometsa E, Aalberg V et al. Is coeliac disease 

prevalent among adolescent psychiatric patients?. Acta 

Paediatrica (Oslo, Norway - 1992) 2002;91(6):657-659. 

Not sensitivity or specificity of an identified test

Qari F A. Clinical presentation of adult celiac disease in 

Western Saudi Arabia. Saudi Med J 2002;23(12):1514-

1517. Not sensitivity or specificity of an identified test 

Qiu L, Escalante C R, Aggarwal A K et al. Monomeric 

midkine induces tumor cell proliferation in the absence of

cell-surface proteoglycan binding. Biochemistry

2000;39(20):5977-5987. Not sensitivity or specificity of an 

identified test 

Quarsten H, McAdam S N, Jensen T et al. Staining of 

celiac disease-relevant T cells by peptide-DQ2 multimers. 

Journal of Immunology (Baltimore, Md.- 1950)

2001;167(9):4861-4868. Not sensitivity or specificity of an 

identified test 

Quarsten H, Molberg O, Fugger L et al. HLA binding and

T cell recognition of a tissue transglutaminase-modified

gliadin epitope. European Journal of Immunology

1999;29(8):2506-2514. Not sensitivity or specificity of an

identified test 

Quarsten H, Paulsen G, Johansen B H et al. The P9 pocket 

of HLA-DQ2 (non-Aspbeta57) has no particular preference 

for negatively charged anchor residues found in other type

1 diabetes-predisposing non-Aspbeta57 MHC class II 

molecules. International Immunology 1998;10(8):1229-

1236. Not sensitivity or specificity of an identified test 

Quisel Anna, Gill James M, Westerberg Dyanne. Guideline

for diagnosis of celiac disease. Delaware Medical Journal 

2002;74(5):229-241. Not sensitivity or specificity of an 

identified test 

Rabsztyn A, Green P H, Berti I et al. Macroamylasemia in 

patients with celiac disease. American Journal of 

Gastroenterology 2001;96(4):1096-1100. Not sensitivity or 

specificity of an identified test

Radek J T, Jeong J M, Murthy S N et al. Affinity of human 

erythrocyte transglutaminase for a 42-kDa gelatin-binding 

fragment of human plasma fibronectin. Proceedings of the

National Academy of Sciences of the United States of 

America 1993;90(8):3152-3156. Not sensitivity or

specificity of an identified test

Radisch T, Riechers R, Hertl M. The humanized SCID 

mouse model to study HLA class II-linked autoimmunity to 

desmoglein 3 in pemphigus vulgaris. Br J Dermatol 

2002;146(2):189-193. Not sensitivity or specificity of an

identified test 

Raghunath M, Cankay R, Kubitscheck U et al. 

Transglutaminase activity in the eye: cross-linking in 

epithelia and connective tissue structures. Investigative 

Ophthalmology & Visual Science 1999;40(12):2780-2787. 

Not sensitivity or specificity of an identified test

Raghunath M, Hennies H C, Velten F et al. A novel in situ

method for the detection of deficient transglutaminase 

activity in the skin. Archives of Dermatological Research

1998;290(11):621-627. Not sensitivity or specificity of an

identified test 

Raghunath M, Hopfner B, Aeschlimann D et al. Crosslinking of the dermo-epidermal junction of skin

regenerating from keratinocyte autografts. Anchoring 

fibrils are a target for tissue transglutaminase. Journal of

Clinical Investigation 1996;98(5):1174-1184. Not 

sensitivity or specificity of an identified test 

Rajagopalan G, Kudva Y C, Chen L et al. Autoimmune

diabetes in HLA-DR3/DQ8 transgenic mice expressing the

co-stimulatory molecule B7-1 in the beta cells of islets of 

Langerhans. Int Immunol 2003;15(9):1035-1044. Not 

sensitivity or specificity of an identified test 

Rajagopalan G, Kudva Y C, Flavell R A et al. Accelerated

diabetes in rat insulin promoter-tumor necrosis factor-alpha 

transgenic nonobese diabetic mice lacking major

histocompatibility class II molecules. Diabetes 

2003;52(2):342-347. Not sensitivity or specificity of an 

identified test 

Raju R, Marietta E, Vinasco J et al. Cryptic determinants 

and promiscuous sequences on human acetylcholine 

receptor: HLA-dependent dichotomy in T-cell function.

Hum Immunol 2002;63(4):237-247. Not sensitivity or 

A-449
specificity of an identified test

Ralph D J, Schwartz G, Moore W et al. The genetic and

bacteriological aspects of Peyronie's disease. J Urol 

1997;157(1):291-294. Not sensitivity or specificity of an

identified test 

Ramos-Arroyo M A, Feijoo E, Sanchez-Valverde F et al. 

Heat-shock protein 70-1 and HLA class II gene

polymorphisms associated with celiac disease susceptibility 

in Navarra (Spain). Human Immunology 2001;62(8):821-

825. Not sensitivity or specificity of an identified test 

Ransford Rupert A J, Hayes Mark, Palmer Martin et al. A

controlled, prospective screening study of celiac disease 

presenting as iron deficiency anemia. Journal of Clinical

Gastroenterology 2002;35(3):228-233. Not sensitivity or 

specificity of an identified test

Rantala I, Maki M, Laasonen A et al. Periodate-lysineparaformaldehyde as fixative for the study of duodenal 

mucosa. Morphologic and immunohistochemical results at 

light and electron microscopic levels. Acta Pathologica, 

Microbiologica, Et Immunologica Scandinavica.Section a, 

Pathology 1985;93(4):165-173. Not sensitivity or

specificity of an identified test

Rapoport M J, Bistritzer T, Vardi O et al. Increased 

prevalence of diabetes-related autoantibodies in celiac 

disease. Journal of Pediatric Gastroenterology and

Nutrition 1996;23(5):524-527. Not sensitivity or specificity

of an identified test 

Ratanachaiyavong S, McGregor A M. HLA-DPB1 

polymorphisms on the MHC-extended haplotypes of 

families of patients with Graves' disease: Two distinct

HLA-DR17 haplotypes. Eur J Clin Invest 1994;24(5):309-

315. Not sensitivity or specificity of an identified test 

Rautonen J, Rautonen N, Savilahti E. Antibodies to gliadin

in children with coeliac disease. Acta Paediatrica

Scandinavica 1991;80(12):1200-1206. Improper control 

group 

Rautonen N, Rautonen J, Savilahti E. Influence of the

G2m(n) allotype and age on IgG subclass distribution in

antibodies to dietary proteins in children with coeliac 

disease. Clinical and Experimental Immunology

1990;81(2):306-310. Not sensitivity or specificity of an 

identified test 

Ravaglia Giovanni, Forti Paola, Maioli Fabiola et al.

Increased prevalence of coeliac disease in autoimmune 

thyroiditis is restricted to aged patients. Experimental

Gerontology 2003;38(5):589-595. Not sensitivity or 

specificity of an identified test

Ravelli A M, Tobanelli P, Minelli L et al. Endoscopic 

features of celiac disease in children. Gastrointestinal

Endoscopy 2001;54(6):736-742. Not sensitivity or

specificity of an identified test

Rawashdeh M O, Abu-Farsakh N, Al Jaberi T M. 

Paediatric upper gastro-intestinal endoscopy in developing

countries. Ann Trop Paediatr 1996;16(4):341-346. Not 

sensitivity or specificity of an identified test 

Rawlings J M, Lucas M L, Russell R I. Measurement of 

jejunal surface pH in situ by plastic pH electrode in patients 

with coeliac disease. Scandinavian Journal of

Gastroenterology 1987;22(3):377-384. Not sensitivity or 

specificity of an identified test

Read M, O'Halloran E T, O'Sullivan C. Coeliac disease in

adolescents/young adults: Difficulties in monitoring. Br J 

Biomed Sci 2000;57(3):217-221. Not sensitivity or 

specificity of an identified test

Redondo M J, Eisenbarth G S. Genetic control of

autoimmunity in Type I diabetes and associated disorders.

Diabetologia 2002;45(5):605-622. Not sensitivity or 

specificity of an identified test

Redondo M J, Rewers M, Yu L et al. Genetic determination 

of islet cell autoimmunity in monozygotic twin, dizygotic 

twin, and non-twin siblings of patients with type 1 diabetes: 

prospective twin study. Bmj (Clinical Research Ed.) 

1999;318(7185):698-702. Not sensitivity or specificity of

an identified test

Redondo M J, Yu L, Hawa M et al. Heterogeneity of type I

diabetes: analysis of monozygotic twins in Great Britain

and the United States. Diabetologia 2001;44(3):354-362. 

Not sensitivity or specificity of an identified test

Reen D J, O'Regan D. HLA antigen frequencies in an Irish 

population. Tissue Antigens 1980;15(4):369-372. Not 

sensitivity or specificity of an identified test 

Reeves G E, Burns C, Hall S T et al. The measurement of 

IgA and IgG transglutaminase antibodies in celiac disease: 

a comparison with current diagnostic methods. Pathology

2000;32(3):181-185. Improper control group 

Regan P T, DiMagno E P. Exocrine pancreatic 

insufficiency in celiac sprue: A cause of treatment failure. 

Gastroenterology 1980;78(3):484-487. Not sensitivity or 

specificity of an identified test

Regezi J A, Nickoloff B J, Headington J T. Oral 

submucosal dendrocytes: factor XIIIa+ and CD34+ 

dendritic cell populations in normal tissue and 

fibrovascular lesions. Journal of Cutaneous Pathology

1992;19(5):398-406. Not sensitivity or specificity of an 

identified test 

Regezi J A, Zarbo R J, Daniels T E et al. Oral traumatic 

granuloma. Characterization of the cellular infiltrate. Oral

Surgery, Oral Medicine, and Oral Pathology

1993;75(6):723-727. Not sensitivity or specificity of an 

identified test 

Regnier M, Desbas C, Bailly C et al. Differentiation of 

normal and tumoral human keratinocytes cultured on 

A-450
dermis: reconstruction of either normal or tumoral 

architecture. In Vitro Cellular & Developmental Biology -

Journal of the Tissue Culture Association 1988;24(7):625-

632. Not sensitivity or specificity of an identified test 

Reibel J, Clausen H, Dale B A et al. Immunohistochemical 

analysis of stratum corneum components in oral squamous 

epithelia. Differentiation 1989;Research in Biological 

Diversity; 41(3):237-244. Not sensitivity or specificity of

an identified test

Reichrath J, Rafi L, Muller S M et al.

Immunohistochemical analysis of 1,25-dihydroxyvitamin 

D3 receptor in cervical carcinoma. Histochemical Journal 

1998;30(8):561-567. Not sensitivity or specificity of an 

identified test 

Reichstetter S, Kwok W W, Nepom G T. Impaired binding

of a DQ2 and DQ8-binding HSV VP16 peptide to a 

DQA1*0501/DQB1*0302 trans class II heterodimer. 

Tissue Antigens 1999;53(1):101-105. Not sensitivity or

specificity of an identified test

Reichstetter S, Kwok W W, Kochik S et al. MHC-peptide 

ligand interactions establish a functional threshold for 

antigen-specific T cell recognition. Hum Immunol 

1999;60(7):608-618. Not sensitivity or specificity of an 

identified test 

Reifen R, Buskila D, Maislos M et al. Serum prolactin in

coeliac disease: A marker for disease activity. Arch Dis

Child 1997;77(2):155-157. Not sensitivity or specificity of 

an identified test

Reifen R, Reif S, Buskila D et al. Transthyretin: a marker 

for celiac disease activity. Journal of Medicine 1998;29(1-

2):30-36. Not sensitivity or specificity of an identified test 

Reijonen H, Ilonen J, Knip M et al. Insulin-dependent 

diabetes mellitus associated with dermatitis herpetiformis: 

evidence for heterogeneity of HLA-associated genes.

Tissue Antigens 1991;37(2):94-96. Not sensitivity or 

specificity of an identified test

Reims A, Redfors S, Ascher H et al. Electrogenic ion 

transport in duodenal biopsies from children with coeliac 

disease. Scandinavian Journal of Gastroenterology

2002;37(1):43-50. Not sensitivity or specificity of an 

identified test 

Reina J, Ballesteros F, Gasco J et al. Usefulness of pp65 

antigenemia and viremia in the follow-up of renal 

transplant recipients with cytomegalovirus disease treated 

with ganciclovir. Diagnostic Microbiology and Infectious 

Disease 2000;37(2):83-86. Not sensitivity or specificity of 

an identified test

Rensch M J, Merenich J A, Lieberman M et al. Glutensensitive enteropathy in patients with insulin-dependent

diabetes mellitus. Annals of Internal Medicine

1996;124(6):564-567. Not sensitivity or specificity of an

identified test 

Rensch M J, Szyjkowski R, Shaffer R T et al. The

prevalence of celiac disease autoantibodies in patients with 

systemic lupus erythematosus. American Journal of 

Gastroenterology 2001;96(4):1113-1115. Not sensitivity or 

specificity of an identified test

Rettenbacher T, Hollerweger A, Macheiner P et al. Adult 

celiac disease: US signs. Radiology 1999;211(2):389-394. 

Not sensitivity or specificity of an identified test

Reunala T. Dermatitis herpetiformis: coeliac disease of the 

skin. Annals of Medicine 1998;30(5):416-418. Not 

sensitivity or specificity of an identified test 

Reunala T. Incidence of familial dermatitis herpetiformis. 

Br J Dermatol 1996;134(3):394-398. Not sensitivity or

specificity of an identified test

Reunala T, Chorzelski T P, Viander M et al. IgA antiendomysial antibodies in dermatitis herpetiformis: 

correlation with jejunal morphology, gluten-free diet and

anti-gliadin antibodies. British Journal of Dermatology

1987;117(2):185-191. Not sensitivity or specificity of an

identified test 

Reunala T, Collin P, Holm K et al. Tolerance to oats in

dermatitis herpetiformis. Gut 1998;43(4):490-493. Not 

sensitivity or specificity of an identified test 

Reunala T, Helin H, Pasternack A et al. Renal involvement 

and circulating immune complexes in dermatitis 

herpetiformis. Journal of the American Academy of 

Dermatology 1983;9(2):219-223. Not sensitivity or 

specificity of an identified test

Reunala T, Salmi J, Karvonen J. Dermatitis herpetiformis 

and celiac disease associated with Addison's disease. 

Archives of Dermatology 1987;123(7):930-932. Not 

sensitivity or specificity of an identified test 

Reunala T, Salo O P, Tiilikainen A et al. Histocompatibility

antigens and dermatitis herpetiformis with special reference

to jejunal abnormalities and acetylator phenotype. Br J 

Dermatol 1976;94(2):139-143. Not sensitivity or specificity

of an identified test 

Reunala T, Salo O P, Tiilikainen A et al. Family studies in 

dermatitis herpetiformis. Annals of Clinical Research 

1976;8(4):254-261. Not sensitivity or specificity of an 

identified test 

Reynolds N J, Todd C, Angus B. Overexpression of protein 

kinase C-alpha and -beta isozymes by stromal dendritic

cells in basal and squamous cell carcinoma. British Journal 

of Dermatology 1997;136(5):666-673. Not sensitivity or

specificity of an identified test

Rhyner C, Weichel M, Hubner P et al. Phage display of

human antibodies from a patient suffering from coeliac 

disease and selection of isotype-specific scFv against 

gliadin. Immunology 2003;110(2):269-274. Not sensitivity

A-451
or specificity of an identified test

Ribes C, Pena A S, Pereda A et al. IGA gliadin antibodies, 

a useful screening test for coeliac disease in family

members of children with coeliac disease. J Clin Nutr 

Gastroenterol 1991;6(4):196-202. Not sensitivity or 

specificity of an identified test

Ribes Koninckx C, Pereda Perez R A, Ferrer Calvete J et

al. The value of the measurement of IgA antigliadin

antibodies in a pediatric unit in Spain. A prospective study.

J Clin Nutr Gastroenterol 1986;1(1):26-29. Not sensitivity

or specificity of an identified test

Ribes-Koninckx C, Alfonso P, Ortigosa L et al. A beta-turn 

rich oats peptide as an antigen in an ELISA method for the 

screening of coeliac disease in a paediatric population.

European Journal of Clinical Investigation 2000;30(8):702-

708. Improper control group 

Riccabona M, Rossipal E. Sonographic findings in celiac 

disease. Journal of Pediatric Gastroenterology and

Nutrition 1993;17(2):198-200. Not sensitivity or specificity

of an identified test 

Rice R H, Green H. Presence in human epidermal cells of a 

soluble protein precursor of the cross-linked envelope: 

activation of the cross-linking by calcium ions. Cell 

1979;18(3):681-694. Not sensitivity or specificity of an 

identified test 

Rice R H, Mehrpouyan M, O'Callahan W et al. 

Keratinocyte transglutaminase: differentiation marker and

member of an extended family. Epithelial Cell Biology

1992;1(3):128-137. Not sensitivity or specificity of an 

identified test 

Richiardi P, Borelli I, Malavasi F et al. HLA antigens in 

juvenile dermatitis herpetiformis. Acta DermatoVenereologica 1981;61(3):241-244. Not sensitivity or 

specificity of an identified test

Richter K H, Schnapke R, Clauss M et al. Epidermal Ginf 

1-chalone and transforming growth factor-beta are two 

different endogenous inhibitors of epidermal cell 

proliferation. J Cell Physiol 1990;142(3):496-504. Not 

sensitivity or specificity of an identified test 

Riecken E O, Martini G A. The classification of abnormal 

small intestinal mucosal appearances. Morphology,

function and diagnostic significance. German Medicine

1973;3(3-4):120-127. Not sensitivity or specificity of an

identified test 

Riecken E O, Sahlfeld M, Lorenz-Meyer H. [Quantification 

of the three-dimensional structure of jejunal mucosa in 

healthy subjects and patients with coeliac disease (author's

transl)]: Quantitative Untersuchungen zur

dreidimensionalen Struktur der Dunndarmschleimhaut bei 

Besunden und Patienten mit einheimischer Sprue. Deutsche 

Medizinische Wochenschrift 1976;101(2):51-53. Not 

sensitivity or specificity of an identified test 

Riedy M C, Muirhead K A, Jensen C P et al. Use of a

photolabeling technique to identify nonviable cells in fixed 

homologous or heterologous cell populations. Cytometry - 

the Journal of the Society for Analytical Cytology

1991;12(2):133-139. Not sensitivity or specificity of an 

identified test 

Riestra S, Fernandez E, Rodrigo L et al. Prevalence of

Coeliac disease in the general population of northern Spain.

Strategies of serologic screening. Scandinavian Journal of

Gastroenterology 2000;35(4):398-402. Not sensitivity or 

specificity of an identified test

Rihs H-P, Chen Z, Cremer R et al. HLA class II antigens

DR4 and DQ8 are associated with allergy to hevein, a 

major allergen of Hevea latex. Tissue Antigens

1997;49(1):92-95. Not sensitivity or specificity of an 

identified test 

Rihs H-P, Chen Z, Rueff F et al. HLA-DQ8 and the HLADQ8-DR4 haplotype are positively associated with the

hevein-specific IgE immune response in health care 

workers with latex allergy. J Allergy Clin Immunol 

2002;110(3):507-514. Not sensitivity or specificity of an

identified test 

Rihs H-P, Cremer R, Chen Z et al. Molecular analysis of 

DRB and DQB 1 alleles in German spina bifida patients 

with and without IgE responsiveness to the latex major 

allergen Hev b 1. Clin Exp Allergy 1998;28(2):175-180. 

Not sensitivity or specificity of an identified test

Rinas U, Risse B, Jaenicke R et al. Characterization of 

recombinant factor XIIIa produced in Saccharomyces 

cerevisiae. Bio/Technology (Nature Publishing Company)

1990;8(6):543-546. Not sensitivity or specificity of an 

identified test 

Riordan S M, McIver C J, Wakefield D et al. Luminal 

antigliadin antibodies in small intestinal bacterial

overgrowth. American Journal of Gastroenterology

1997;92(8):1335-1338. Not sensitivity or specificity of an

identified test 

Risch N. Assessing the role of HLA-linked and unlinked

determinants of disease. American Journal of Human 

Genetics 1987;40(1):1-14. Not sensitivity or specificity of 

an identified test

Rischmueller M, Lester S, Chen Z et al. HLA class II 

phenotype controls diversification of the autoantibody 

response in primary Sjogren's syndrome (pSS). Clinical and

Experimental Immunology 1998;111(2):365-371. Not 

sensitivity or specificity of an identified test 

Risdon R A, Keeling J W. Quantitation of the histological 

changes found in small intestinal biopsy specimens from 

children with suspected coeliac disease. Gut 1974;15(1):9-

18. Unable to extract data 

Risdon R A, Meinhard E A, Wadbrook D G et al. Small 

A-452
intestinal biopsy in childhood coeliac disease. Postgraduate 

Medical Journal 1975;51(600):716-721. Not sensitivity or 

specificity of an identified test

Ritter S J, Davies P J. Identification of a transforming 

growth factor-beta1/bone morphogenetic protein 4 (TGFbeta1/BMP4) response element within the mouse tissue 

transglutaminase gene promoter. Journal of Biological 

Chemistry 1998;273(21):12798-12806. Not sensitivity or

specificity of an identified test

Rittmaster R S, Norman R W, Thomas L N et al. Evidence

for atrophy and apoptosis in the prostates of men given

finasteride. Journal of Clinical Endocrinology and 

Metabolism 1996;81(2):814-819. Not sensitivity or 

specificity of an identified test

Rittmaster R S, Thomas L N, Wright A S et al. The utility

of tissue transglutaminase as a marker of apoptosis during 

treatment and progression of prostate cancer. Journal of

Urology 1999;162(6):2165-2169. Not sensitivity or 

specificity of an identified test

Rittner C, DeMarchi M, Mollenhauer E et al. Coeliac 

disease and C4A*QO: an association secondary to HLADR3. Tissue Antigens 1984;23(2):130-134. Not sensitivity

or specificity of an identified test

Robards M F. Changes in plasma nephelometry after oral 

fat loading in children with normal and abnormal small 

intestinal morphology. Archives of Disease in Childhood 

1975;50(8):631-636. Not sensitivity or specificity of an 

identified test 

Robert M E, Ament M E, Weinstein W M. The histologic 

spectrum and clinical outcome of refractory and

unclassified sprue. American Journal of Surgical Pathology

2000;24(5):676-687. Unable to extract data 

Roberts C, Jack F, Angus B et al. Immunohistochemical 

detection of CD30 remains negative in nodular

lymphocyte-predominant Hodgkin's disease using 

enhanced antigen retrieval. Histopathology

2002;40(2):166-170. Not sensitivity or specificity of an 

identified test 

Roberts I M. Workup of the patient with malabsorption. 

Postgraduate Medicine 1987;81(7):32-3, 37. Not sensitivity

or specificity of an identified test

Roberts R K, Campbell C B, Bryant S J et al. Xylose-1-sup 

1sup 4C absorption test: the use of urine, serum and breath 

analysis, and comparison with a colorimetric assay.

Australian and New Zealand Journal of Medicine

1976;6(6):532-536. Not sensitivity or specificity of an 

identified test 

Roberts S H, Heffernan C, Douglas A P. The sialic acid and

carbohydrate content and the synthesis of glycoprotein

from radioactive precursors by tissues of the normal and

diseases upper intestinal tract. Clinica Chimica Acta 

1975;International Journal of Clinical Chemistry;

63(2):121-128. Not sensitivity or specificity of an identified 

test 

Roberts-Thomson I C, Stevens D P, Michel B. Factors

influencing small bowel changes in dermatitis

herpetiformis. Australian and New Zealand Journal of

Medicine 1977;7(4):356-362. Not sensitivity or specificity

of an identified test 

Robertson D A, Bullen A, Field H et al. Suppressor cell 

activity, splenic function and HLA B8 status in man. 

Journal of Clinical & Laboratory Immunology

1982;9(2):133-138. Not sensitivity or specificity of an 

identified test 

Robinson B N, Roberts D F, Mather B A et al. Coeliac 

disease and HLA: a family study. Journal of

Immunogenetics 1980;7(5):381-391. Not sensitivity or 

specificity of an identified test

Robinson D C, Watson A J, Wyatt E H et al. Incidence of

small-intestinal mucosal abnormalities and of clinical 

coeliac disease in the relatives of children with coeliac 

disease. Gut 1971;12(10):789-793. Not sensitivity or 

specificity of an identified test

Robinson T J, Nelson S D, Haire M et al. Jejunal villous 

changes associated with farmer's lung. Postgraduate 

Medical Journal 1981;57(673):697-701. Not sensitivity or 

specificity of an identified test

Robles David T, Fain Pamela R, Gottlieb Peter A et al. The 

genetics of autoimmune polyendocrine syndrome type II. 

Endocrinology and Metabolism Clinics of North America 

2002;31(2):353-68, Vi. Not sensitivity or specificity of an

identified test 

Roch A M, Noel P, el Alaoui S et al. Differential 

expression of isopeptide bonds N epsilon (gammaglutamyl) lysine in benign and malignant human breast 

lesions: an immunohistochemical study. International 

Journal of Cancer.Journal International Du Cancer 

1991;48(2):215-220. Not sensitivity or specificity of an 

identified test 

Rodriguez-Soriano J, Arrieta A, Vallo A et al. IgA 

antigliadin antibodies in children with IgA mesangial

glomerulonephritis. Lancet 1988;1(8594):1109-1110. Not 

sensitivity or specificity of an identified test 

Roep B O, Bontrop R E, Pena A S et al. An HLA-DQ alpha 

allele identified at DNA and protein level is strongly

associated with celiac disease. Hum Immunol 

1988;23(4):271-279. Not sensitivity or specificity of an 

identified test 

Roger M. Influence of host genes on HIV-1 disease 

progression. Faseb J 1998;12(9):625-632. Not sensitivity or 

specificity of an identified test

Rogers A I. Steatorrhea. Postgraduate Medicine 

1971;50(6):123-129. Not sensitivity or specificity of an 

A-453
identified test 

Roggini M, Bonamico M, Capocaccia P et al. Radiological 

changes of the ileum in children with coeliac disease: is

"intestinal adaptation" a specific radiographic sign?. Rivista

Europea Per Le Scienze Mediche E Farmacologiche = 

European Review for Medical and Pharmacological

Sciences = Revue Europeenne Pour Les Sciences

Medicales Et Pharmacologiques 1990;12(3):159-164. Not 

sensitivity or specificity of an identified test 

Rognum T O, Kett K, Fausa O et al. Raised number of

jejunal IgG2-producing cells in untreated adult coeliac 

disease compared with food allergy. Gut

1989;30(11):1574-1580. Not sensitivity or specificity of an 

identified test 

Rokkas T, Vaja S, Murphy G M et al. Postheparin plasma 

diamine oxidase in health and intestinal disease.

Gastroenterology 1990;98(6):1493-1501. Not sensitivity or 

specificity of an identified test

Roldan M B, Barrio R, Roy G et al. Diagnostic value of

serological markers for celiac disease in diabetic children 

and adolescents. Journal of Pediatric Endocrinology & 

Metabolism - Jpem 1998;11(6):751-756. Improper control 

group 

Rollason T P, Byrne P, Williams A et al. Expression of 

epithelial membrane and 3-fucosyl-N-acetyllactosamine 

antigens in cervix uteri with particular reference to

adenocarcinoma in situ. Journal of Clinical Pathology

1988;41(5):547-552. Not sensitivity or specificity of an 

identified test 

Rolles C J. Proceedings: Usefulness of a modified D-xylose 

absorption test in the preliminary diagnosis of coeliac 

disease and its later confirmation. Archives of Disease in 

Childhood 1973;48(10):825Not sensitivity or specificity of 

an identified test

Rolles C J, McNeish A S. Standardised approach to gluten 

challenge in diagnosing childhood coeliac disease. British

Medical Journal 1976;1(6021):1309-1311. Not sensitivity

or specificity of an identified test

Rolles C J, Anderson M, McNeish A S. Confirming 

persistence of gluten intolerance in children diagnosed as

having coeliac disease in infancy. Archives of Disease in

Childhood 1975;50(4):259-263. Not sensitivity or

specificity of an identified test

Rolles C J, Nutter S, Kendall M J et al. One-hour bloodxylose screening-test for coeliac disease in infants and 

young children. Lancet 1973;2(7837):1043-1045. Not 

sensitivity or specificity of an identified test 

Romaldini Ceres C, Barbieri Dorina, Okay Thelma S et al. 

Serum soluble interleukin-2 receptor, interleukin-6, and

tumor necrosis factor-alpha levels in children with celiac 

disease: response to treatment. Journal of Pediatric 

Gastroenterology and Nutrition 2002;35(4):513-517. Not

sensitivity or specificity of an identified test 

Romano Corrado, Pettinato Rosa, Ragusa Letizia et al. Is

there a relationship between zinc and the peculiar

comorbidities of Down syndrome?. Down Syndrome, 

Research and Practice - the Journal of the Sarah Duffen 

Centre / University of Portsmouth 2002;8(1):25-28. Not 

sensitivity or specificity of an identified test 

Ronningen K S. Genetics in the prediction of insulindependent diabetes mellitus: from theory to practice. 

Annals of Medicine 1997;29(5):387-392. Not sensitivity or

specificity of an identified test

Ronningen K S, Keiding N, Green A. Correlations between

the incidence of childhood-onset type I diabetes in Europe 

and HLA genotypes. Diabetologia 2001;44 Suppl 3b51-

b59. Not sensitivity or specificity of an identified test 

Ronningen K S, Undlien D E, Ploski R et al. Linkage 

disequilibrium between TAP2 variants and HLA class II

alleles; no primary association between TAP2 variants and 

insulin-dependent diabetes mellitus. European Journal of

Immunology 1993;23(5):1050-1056. Not sensitivity or

specificity of an identified test

Rood J J, Hooff J P, Keuning J J. Disease predisposition, 

immune responsiveness and the fine structure of the HL-A 

supergene. A need for a reappraisal. Transplantation 

Reviews 1975;2275-104. Not sensitivity or specificity of an 

identified test 

Rorke E A, Jacobberger J W. Transforming growth factorbeta 1 (TGF beta 1) enhances apoptosis in human

papillomavirus type 16-immortalized human ectocervical

epithelial cells. Experimental Cell Research

1995;216(1):65-72. Not sensitivity or specificity of an 

identified test 

Rosa Utiyama S R, Silva Kotze L M, Nisihara R M et al. 

Spectrum of autoantibodies in celiac patients and relatives. 

Digestive Diseases and Sciences 2001;46(12):2624-2630. 

Not sensitivity or specificity of an identified test

Rosales J L, Isseroff R R. Increased expression of a high

molecular weight (130 KD) protein kinase C isoform in a 

differentiation-defective ras-transfected keratinocyte line.

Journal of Cellular Physiology 1995;164(3):509-521. Not 

sensitivity or specificity of an identified test 

Rosch T. Small-bowel endoscopy. Endoscopy

2002;34(11):896-899. Not sensitivity or specificity of an

identified test 

Roschmann E, Wienker T F, Volk B A. Role of T cell 

receptor delta gene in susceptibility to celiac disease. 

Journal of Molecular Medicine (Berlin, Germany) 

1996;74(2):93-98. Not sensitivity or specificity of an 

identified test 

Roschmann E, Wienker T F, Gerok W et al. T-cell receptor 

variable genes and genetic susceptibility to celiac disease:

A-454
an association and linkage study. Gastroenterology

1993;105(6):1790-1796. Not sensitivity or specificity of an 

identified test 

Roschmann E, Wienker T F, Gerok W et al. Analysis of

marker genes contributing to coeliac disease susceptibility.

Advances in Experimental Medicine and Biology

1995;371b1339-1343. Not sensitivity or specificity of an

identified test 

Rosdy M, Clauss L C. Terminal epidermal differentiation

of human keratinocytes grown in chemically defined 

medium on inert filter substrates at the air-liquid interface. 

Journal of Investigative Dermatology 1990;95(4):409-414. 

Not sensitivity or specificity of an identified test

Rose C, Dieterich W, Brocker E B et al. Circulating 

autoantibodies to tissue transglutaminase differentiate 

patients with dermatitis herpetiformis from those with 

linear IgA disease. Journal of the American Academy of 

Dermatology 1999;41(6):957-961. Not sensitivity or 

specificity of an identified test

Rosekrans P C, Lindeman J, Meijer C J. Quantitative 

histological and immunohistochemical findings in jejunal 

biopsy specimens in giardiasis. Virchows Archiv.A, 

Pathological Anatomy and Histology 1981;393(2):145-151. 

Not sensitivity or specificity of an identified test

Rosekrans P C, Meijer C J, Polanco I et al. Long-term 

morphological and immunohistochemical observations on

biopsy specimens of small intestine from children with 

gluten-sensitive enteropathy. Journal of Clinical Pathology

1981;34(2):138-144. Unable to extract data 

Rosenbach Y, Dinari G, Zahavi I et al. Short stature as the 

major manifestation of celiac disease in older children. Clin

Pediatr 1986;25(1):13-16. Not sensitivity or specificity of

an identified test

Rosenberg W M, Moss P A, Bell J I. Molecular aspects of 

autoimmunity: a review. Curr Eye Res 1992;11 Suppl17-

23. Not sensitivity or specificity of an identified test 

Rosenberg W M, Prince C, Kaklamanis L et al. Increased

expression of CD44v6 and CD44v3 in ulcerative colitis but 

not colonic Crohn's disease. Lancet 1995;345(8959):1205-

1209. Not sensitivity or specificity of an identified test 

Rosenberg W M, Wordsworth B P, Jewell D P et al. A 

locus telomeric to HLA-DPB encodes susceptibility to

coeliac disease. Immunogenetics 1989;30(4):307-310. Not 

sensitivity or specificity of an identified test 

Rosenblatt S, Bassuk J A, Alpers C E et al. Differential 

modulation of cell adhesion by interaction between 

adhesive and counter-adhesive proteins: characterization of

the binding of vitronectin to osteonectin (BM40, SPARC). 

Biochemical Journal 1997;324(Pt 1):311-319. Not 

sensitivity or specificity of an identified test 

Rosenthal D S, Roop D R, Huff C A et al. Changes in 

photo-aged human skin following topical application of alltrans retinoic acid. Journal of Investigative Dermatology 

1990;95(5):510-515. Not sensitivity or specificity of an 

identified test 

Rosenthal E, Golan D T, Benderly A. Immunofluorescent 

antigluten antibody test. Titer and profile of gluten

antibodies in celiac disease. Am J Dis Child 

1984;138(7):659-662. Not sensitivity or specificity of an

identified test 

Rossi T M, Tjota A. Serologic indicators of celiac disease.

Journal of Pediatric Gastroenterology and Nutrition 

1998;26(2):205-210. Not sensitivity or specificity of an 

identified test 

Rossi T M, Albini C H, Kumar V. Incidence of celiac

disease identified by the presence of serum endomysial

antibodies in children with chronic diarrhea, short stature, 

or insulin-dependent diabetes mellitus. Journal of Pediatrics 

1993;123(2):262-264. Not sensitivity or specificity of an

identified test 

Rossi T M, Kumar V, Lerner A et al. Relationship of 

endomysial antibodies to jejunal mucosal pathology:

specificity towards both symptomatic and asymptomatic 

celiacs. Journal of Pediatric Gastroenterology and Nutrition 

1988;7(6):858-863. Serology <1990 

Rossiter M A, Van Noorden S. Proceedings: Secretin cells

in childhood coeliac disease. Archives of Disease in 

Childhood 1974;49(3):244Not sensitivity or specificity of

an identified test

Rossiter M A, Barrowman J A, Dand A et al. Amylase 

content of mixed saliva in children. Acta Paediatr Scand 

1974;63(3):389-392. Not sensitivity or specificity of an 

identified test 

Rossiter M A, Palmer T, Evans K et al. The short term

response to a drink of milk, lactose or casein in children

with apparently normal gastrointestinal tracts. Br J Nutr 

1974;32(3):605-613. Not sensitivity or specificity of an 

identified test 

Rostami K, Mulder C J J. Coeliac disease. A challenging

diagnosis. Rom J Gastroenterol 1999;8(2):111-114. Not 

sensitivity or specificity of an identified test 

Rostami K, Kerckhaert J P, Tiemessen R et al. The 

relationship between anti-endomysium antibodies and 

villous atrophy in coeliac disease using both monkey and

human substrate. European Journal of Gastroenterology &

Hepatology 1999;11(4):439-442. Improper control group 

Rostami K, Kerckhaert J, Tiemessen R et al. Sensitivity of

antiendomysium and antigliadin antibodies in untreated 

celiac disease: disappointing in clinical practice. American 

Journal of Gastroenterology 1999;94(4):888-894. Improper 

control group 

Rostami K, Kerckhaert J, von Blomberg B M et al. SAT 

A-455
and serology in adult coeliacs, seronegative coeliac disease

seems a reality. Netherlands Journal of Medicine 

1998;53(1):15-19. Not sensitivity or specificity of an 

identified test 

Rostami K, Mulder C J J, Stapell S et al. Autoantibodies 

and histogenesis of celiac disease. Rom J Gastroenterol 

2003;12(2):101-106. Improper control group 

Rostami K, Mulder C J, van Overbeek F M et al. Should 

relatives of coeliacs with mild clinical complaints undergo 

a small-bowel biopsy despite negative serology?. European

Journal of Gastroenterology & Hepatology 2000;12(1):51-

55. Improper control group 

Rostami K, Mulder C J, Werre J M et al. High prevalence

of celiac disease in apparently healthy blood donors 

suggests a high prevalence of undiagnosed celiac disease in

the Dutch population. Scandinavian Journal of

Gastroenterology 1999;34(3):276-279. Not sensitivity or 

specificity of an identified test

Rostoker G, Delchier J C, Chaumette M T. Increased 

intestinal intra-epithelial T lymphocytes in primary 

glomerulonephritis: a role of oral tolerance breakdown in 

the pathophysiology of human primary

glomerulonephritides?. Nephrology, Dialysis, 

Transplantation - Official Publication of the European 

Dialysis and Transplant Association - European Renal 

Association 2001;16(3):513-517. Not sensitivity or 

specificity of an identified test

Rostoker G, Laurent J, Andre C et al. High levels of IgA 

antigliadin antibodies in patients who have IgA mesangial 

glomerulonephritis but not coeliac disease. Lancet

1988;1(8581):356-357. Not sensitivity or specificity of an

identified test 

Roth E B, Sjoberg K, Stenberg P. Biochemical and 

immuno-pathological aspects of tissue transglutaminase in 

coeliac disease. Autoimmunity 2003;36(4):221-226. Not 

sensitivity or specificity of an identified test 

Rotter J I, Landaw E M. Measuring the genetic contribution

of a single locus to a multilocus disease. Clinical Genetics 

1984;26(6):529-542. Not sensitivity or specificity of an 

identified test 

Roy-Choudhury D C, Cooke W T, Banwell J G et al. 

Multiple jejunal biopsies in adult celiac disease. American 

Journal of Digestive Diseases 1967;12(7):657-663. Unable 

to extract data

Roy-Choudhury D, Cooke W T, Tan D T et al. Jejunal 

biopsy: criteria and significance. Scandinavian Journal of

Gastroenterology 1966;1(1):57-74. Unable to extract data 

Ruan E A, Komorowski R A, Hogan W J et al.

Nongranulomatous chronic idiopathic enterocolitis: 

Clinicopathologic profile and response to corticosteroids. 

Gastroenterology 1996;111(3):629-637. Not sensitivity or

specificity of an identified test

Rubesin S E. Simplified approach to differential diagnosis 

of small bowel abnormalities. Radiol Clin North Am

2003;41(2):343-364. Not sensitivity or specificity of an 

identified test 

Rubin A L, Rice R H. 2,3,7,8-Tetrachlorodibenzo-p-dioxin 

and polycyclic aromatic hydrocarbons suppress retinoidinduced tissue transglutaminase in SCC-4 cultured human 

squamous carcinoma cells. Carcinogenesis 1988;9(6):1067-

1070. Not sensitivity or specificity of an identified test 

Rubin A L, Parenteau N L, Rice R H. Coordination of 

keratinocyte programming in human SCC-13 squamous 

carcinoma and normal epidermal cells. Journal of Cellular

Physiology 1989;138(1):208-214. Not sensitivity or 

specificity of an identified test

Rubin C E, Brandborg L L, Phelps P C et al. Studies of 

celiac disease. I. The apparent identical and specific nature

of the duodenal and proximal jejunal lesion in celiac 

disease and idiopathic sprue. Gastroenterology

1968;54(4):SupplUnable to extract data 

Rubio C A. A simple method to demonstrate duodenal 

gastric metaplasia. Journal of Clinical Pathology 

2002;55(7):520-523. Not sensitivity or specificity of an 

identified test 

Rubio C A, Theorell M, Befrits R et al. The characteristics

of mitotic figures in jejunal mucosa of patients with celiac 

disease. Am J Clin Pathol 1992;98(6):575-578. Not 

sensitivity or specificity of an identified test 

Rudchenko S, Trakht I, Sobel J H. Comparative structural 

and functional features of the human fibrinogen alpha C 

domain and the isolated alpha C fragment. Characterization 

using monoclonal antibodies to defined COOH-terminal A

alpha chain regions. Journal of Biological Chemistry

1996;271(5):2523-2530. Not sensitivity or specificity of an 

identified test 

Rude R K, Olerich M. Magnesium deficiency: Possible role

in osteoporosis associated with gluten-sensitive 

enteropathy. Osteoporosis Int 1996;6(6):453-461. Not 

sensitivity or specificity of an identified test 

Rudolph P, Schubert C, Zelger B G et al. Differential 

expression of CD34 and Ki-M1p in pleomorphic fibroma 

and dermatofibroma with monster cells. American Journal 

of Dermatopathology 1999;21(5):414-419. Not sensitivity

or specificity of an identified test

Rudy G, Lew A M. Limited polymorphism of the HLADQA2 promoter and identification of a variant octamer.

Human Immunology 1994;39(3):225-229. Not sensitivity

or specificity of an identified test

Rueda B, Pascual M, Lopez-Nevot M A et al. A new allele

within the transmembrane region of the human MICA gene 

with seven GCT repeats. Tissue Antigens 2002;60(6):526-

528. Not sensitivity or specificity of an identified test 

A-456
Rueda B, Pascual M, Lopez-Nevot M A et al. Association

of MICA-A5.1 allele with susceptibility to celiac disease in 

a family study. American Journal of Gastroenterology

2003;98(2):359-362. Not sensitivity or specificity of an 

identified test 

Rueda Blanca, Lopez-Nevot Miguel, Angel Pascual et al. 

Polymorphism of the inducible nitric oxide synthase gene 

in celiac disease. Human Immunology 2002;63(11):1062-

1065. Not sensitivity or specificity of an identified test 

Ruiz del, Prado M Y, Olivares Lopez J L et al. HLA 

system. Phenotypic and gene frequencies in celiac and

healthy subjects from the same geographical area. Revista

Espanola De Enfermedades Digestivas - Organo Oficial De

La Sociedad Espanola De Patologia Digestiva

2001;93(2):106-113. Improper control group 

Ruiz M Y, Olivares J L. Three-loci HLA haplotypes in 

Spanish celiac children and healthy subjects: estimation of 

linkage disequilibrium and haplotype frequencies.

American Journal of Gastroenterology 2001;96(5):1455-

1459. Improper control group 

Rujner J, Socha J, Barra E et al. Serum and salivary

antigliadin antibodies and serum IgA anti-endomysium 

antibodies as a screening test for coeliac disease. Acta 

Paediatrica (Oslo, Norway - 1992) 1996;85(7):814-817. 

Improper control group 

Rujner J, Wisniewski A, Gregorek H et al. Coeliac disease 

and HLA-DQ 2 (DQA1* 0501 and DQB1* 0201) in 

patients with Turner syndrome. Journal of Pediatric 

Gastroenterology and Nutrition 2001;32(1):114-115. Not

sensitivity or specificity of an identified test 

Rumbo M, Chirdo F G, Anon M C et al. Detection and 

characterization of antibodies specific to food antigens 

(gliadin, ovalbumin and beta-lactoglobulin) in human 

serum, saliva, colostrum and milk. Clinical and

Experimental Immunology 1998;112(3):453-458. Not 

sensitivity or specificity of an identified test 

Rumbo M, Chirdo F G, Ben R et al. Evaluation of coeliac 

disease serological markers in Down syndrome patients.

Digestive and Liver Disease - Official Journal of the Italian

Society of Gastroenterology and the Italian Association for

the Study of the Liver 2002;34(2):116-121. Not sensitivity

or specificity of an identified test

Runmarker B, Martinsson T, Wahlstrom J et al. HLA and 

prognosis in multiple sclerosis. J Neurol 1994;241(6):385-

390. Not sensitivity or specificity of an identified test 

Russell R I, Atherton S T, Nelson L M. Effect of an 

elemental diet (Vivonex) on the absorption abnormalities

and histological appearances of the jejunum in untreated 

adult coeliac disease. Digestion 1979;19(5):335-339. Not 

sensitivity or specificity of an identified test 

Rust C, Kooy Y, Pena S et al. Phenotypical and functional 

characterization of small intestinal TcR gamma delta + T

cells in coeliac disease. Scandinavian Journal of

Immunology 1992;35(4):459-468. Not sensitivity or 

specificity of an identified test

Rustgi A K, Peppercorn M A. Gluten-sensitive enteropathy 

and systemic lupus erythematosus. Archives of Internal

Medicine 1988;148(7):1583-1584. Not sensitivity or 

specificity of an identified test

Rutgeerts L, Tytgat G, Mainguet P et al. Enterokinase

activity of normal and flat duodenal mucosa. Acta GastroEnterol Belg 1973;36(9):449-455. Not sensitivity or 

specificity of an identified test

Rutz Regula, Ritzler Eva, Fierz Walter et al. Prevalence of 

asymptomatic celiac disease in adolescents of eastern 

Switzerland. Swiss Medical Weekly - Official Journal of

the Swiss Society of Infectious Diseases, the Swiss Society 

of Internal Medicine, the Swiss Society of Pneumology

2002;132(3-4):43-47. Not sensitivity or specificity of an

identified test 

Ryan B M, Kelleher D. Refractory celiac disease.

Gastroenterology 2000;119(1):243-251. Not sensitivity or

specificity of an identified test

Rybakowski J K, Chorzelski T P, Sulej J. Lack of Ig Aclass endomysial antibodies, the specific marker of gluten 

enteropathy, in sera of schizophrenic patients. Med Sci Res 

1990;18(8):311Not sensitivity or specificity of an identified 

test 

Saalman R, Dahlgren U I, Fallstrom S P et al. Avidity 

progression of dietary antibodies in healthy and coeliac 

children. Clinical and Experimental Immunology

2003;134(2):328-334. Not sensitivity or specificity of an

identified test 

Saalman R, Dahlgren U I, Fallstrom S P et al. IgG subclass 

profile of serum antigliadin antibodies and antibodydependent cell-mediated cytotoxicity in young children

with coeliac disease. Scandinavian Journal of Immunology

2001;53(1):92-98. Not sensitivity or specificity of an 

identified test 

Saalman R, Wold A E, Dahlgren U I et al. Antibodydependent cell-mediated cytotoxicity to gliadin-coated cells

with sera from children with coeliac disease. Scandinavian 

Journal of Immunology 1998;47(1):37-42. Not sensitivity

or specificity of an identified test

Saari K M. HLA and coeliac disease. Acta Ophthalmol 

1984;62(Suppl 165):107-109. Not sensitivity or specificity

of an identified test 

Sacchetti L, Ferrajolo A, Salerno G et al. Diagnostic value

of various serum antibodies detected by diverse methods in

childhood celiac disease. Clinical Chemistry

1996;42(11):1838-1842. Improper control group

Sacchetti L, Sarrantonio C, Pastore L et al. Rapid 

A-457
identification of HLA DQA1*0501, DQB1*0201 and 

DRB1*04 alleles in celiac disease by a PCR-based 

methodology. Clinical Chemistry 1997;43(11):2204-2206. 

Not sensitivity or specificity of an identified test

Sacchetti L, Tinto N, Calcagno G et al. Multiplex PCR 

typing of the three most frequent HLA alleles in celiac

disease. Clinica Chimica Acta 2001;International Journal of 

Clinical Chemistry; 310(2):205-207. Not sensitivity or 

specificity of an identified test

Sachdev A, Srinivasan V, Maheswary S et al. Adult onset 

celiac disease in north India. Tropical Gastroenterology - 

Official Journal of the Digestive Diseases Foundation 

2002;23(3):117-119. Not sensitivity or specificity of an 

identified test 

Sachs J A, Awad J, McCloskey D et al. Different HLA 

associated gene combinations contribute to susceptibility 

for coeliac disease and dermatitis herpetiformis. Gut 

1986;27(5):515-520. Not sensitivity or specificity of an 

identified test 

Sacks S H, Bushell A, Rust N A et al. Functional and 

biochemical subtypes of the haplotype HLA-DR3 in 

patients with celiac disease or idiopathic membranous 

nephropathy. Hum Immunol 1987;20(2):175-187. Not 

sensitivity or specificity of an identified test 

Sadikali F, Darwish R, Watson W C. Carnosinase activity 

of human gastrointestinal mucosa. Gut 1975;16(8):585-

589. Not sensitivity or specificity of an identified test 

Safwenberg J, Kollberg H, Lindblom J B. HLA frequencies 

in patients with cystic fibrosis. Tissue Antigens 

1977;10(4):287-290. Not sensitivity or specificity of an 

identified test 

Saga K. Histochemical and immunohistochemical markers 

for human eccrine and apocrine sweat glands: an aid for 

histopathologic differentiation of sweat gland tumors. 

Journal of Investigative Dermatology.Symposium 

Proceedings / the Society for Investigative Dermatology,

Inc.And European Society for Dermatological Research

2001;6(1):49-53. Not sensitivity or specificity of an 

identified test 

Sagaro E, Jimenez N. Family studies of coeliac disease in

Cuba. Archives of Disease in Childhood 1981;56(2):132-

133. Not sensitivity or specificity of an identified test 

Saito S, Ota S, Hashizume K et al. A new HLADQB1(*)0306 allele sharing motifs from DQB1(*)03032 

and DQB1(*)04 sequences. Tissue Antigens 

1996;48(5):580-585. Not sensitivity or specificity of an 

identified test 

Sakai K, Busby W H, Clarke J B et al. Tissue

transglutaminase facilitates the polymerization of insulinlike growth factor-binding protein-1 (IGFBP-1) and leads 

to loss of IGFBP-1's ability to inhibit insulin-like growth 

factor-I-stimulated protein synthesis. Journal of Biological 

Chemistry 2001;276(12):8740-8745. Not sensitivity or 

specificity of an identified test

Salazar de, Sousa Magalhaes, Ramalho P et al. Reaction of

rectal mucosa of celiac patients to direct contact with 

gluten. Journal of Pediatric Gastroenterology and Nutrition

1988;7(3):403-405. Not sensitivity or specificity of an 

identified test 

Salerno Giuseppe, De Franco, Antonio La et al. 

Malabsorption syndromes. Rays 2002;27(1):19-34. Not 

sensitivity or specificity of an identified test 

Salmela M T, Karjalainen-Lindsberg M L, Jeskanen L et al.

Overexpression of tissue inhibitor of metalloproteinases-3 

in intestinal and cutaneous lesions of graft-versus-host 

disease. Mod Pathol 2003;16(2):108-114. Not sensitivity or

specificity of an identified test

Salmela M T, Pender S L, Reunala T et al. Parallel 

expression of macrophage metalloelastase (MMP-12) in 

duodenal and skin lesions of patients with dermatitis 

herpetiformis. Gut 2001;48(4):496-502. Not sensitivity or 

specificity of an identified test

Salur L, Uibo O, Talvik I et al. The high frequency of 

coeliac disease among children with neurological disorders. 

European Journal of Neurology - the Official Journal of the 

European Federation of Neurological Societies 

2000;7(6):707-711. Not sensitivity or specificity of an 

identified test 

Salvati V M, Bajaj-Elliott M, Poulsom R et al. Keratinocyte

growth factor and coeliac disease. Gut 2001;49(2):176-181. 

Not sensitivity or specificity of an identified test

Salvati V M, MacDonald T T, Blanco G D V et al. 

Enhanced expression of interferon regulatory factor-1 in 

the mucosa of children with celiac disease. Pediatric 

Research 2003;54(3):312-318. Not sensitivity or specificity

of an identified test 

Sanchez D, Tuckova L, Sebo P et al. Occurrence of IgA 

and IgG autoantibodies to calreticulin in coeliac disease 

and various autoimmune diseases. Journal of 

Autoimmunity 2000;15(4):441-449. Not sensitivity or 

specificity of an identified test

Sanchez-Albisua I, Storm W, Wascher I et al. How 

frequent is coeliac disease in Down syndrome?. European

Journal of Pediatrics 2002;161(12):683-684. Not sensitivity

or specificity of an identified test

Sanders D S, Carter M J, Hurlstone D P et al. Association 

of adult coeliac disease with irritable bowel syndrome: a 

case-control study in patients fulfilling ROME II criteria

referred to secondary care. Lancet 2001;358(9292):1504-

1508. Not sensitivity or specificity of an identified test 

Sanders D S, Perry I, Hardy R et al. Aberrant P-cadherin 

expression is a feature of clonal expansion in the 

gastrointestinal tract associated with repair and neoplasia.

A-458
Journal of Pathology 2000;190(5):526-530. Not sensitivity

or specificity of an identified test

Sanders David S, Patel Dina, Stephenson Timothy J et al. A 

primary care cross-sectional study of undiagnosed adult 

coeliac disease. European Journal of Gastroenterology &

Hepatology 2003;15(4):407-413. Not sensitivity or 

specificity of an identified test

Sanderson J, Marcantonio J M, Duncan G. A human lens 

model of cortical cataract: Casup 2sup +-induced protein

loss, vimentin cleavage and opacification. Invest 

Ophthalmol Vis Sci 2000;41(8):2255-2261. Not sensitivity

or specificity of an identified test

Sanderson M C, Davis L R, Mowat A P. Failure of

laboratory and radiological studies to predict jejunal 

mucosal atrophy. Archives of Disease in Childhood 

1975;50(7):526-531. Not sensitivity or specificity of an 

identified test 

Sanfilippo G, Patane R, Fusto A et al. Endoscopic approach

to childhood coeliac disease. Acta Gastro-Enterologica 

Belgica 1986;49(4):401-408. Unable to extract data 

Sanjeevi C B. HLA-DQ6-mediated protection in IDDM. 

Human Immunology 2000;61(2):148-153. Not sensitivity

or specificity of an identified test

Sanjeevi C B, DeWeese C, Landin-Olsson M et al. 

Analysis of critical residues of HLA-DQ6 molecules in

insulin-dependent diabetes mellitus. Tissue Antigens

1997;50(1):61-65. Not sensitivity or specificity of an 

identified test 

Sanjeevi C B, Falorni A, Kockum I et al. HLA and 

glutamic acid decarboxylase in human insulin-dependent 

diabetes mellitus. Diabetic Med 1996;13(3):209-217. Not 

sensitivity or specificity of an identified test 

Sanjeevi C B, Hagopian W A, Landin-Olsson M et al. 

Association between autoantibody markers and subtypes of 

DR4 and DR4-DQ in Swedish children with insulindependent diabetes reveals closer association of tyrosine 

pyrophosphatase autoimmunity with DR4 than DQ8. 

Tissue Antigens 1998;51(3):281-286. Not sensitivity or

specificity of an identified test

Sanjeevi C B, Hook P, Landin-Olsson M et al. DR4 

subtypes and their molecular properties in a populationbased study of Swedish childhood diabetes. Tissue 

Antigens 1996;47(4):275-283. Not sensitivity or specificity

of an identified test 

Sanjeevi C B, Kanungo A, Samal K C. Immunogenetic 

studies on malnutrition-modulated diabetes mellitus. 

Annals of the New York Academy of Sciences

2002;958144-147. Not sensitivity or specificity of an 

identified test 

Sanjeevi C B, Kanungo A, Shtauvere A et al. Association 

of HLA class II alleles with different subgroups of diabetes

mellitus in Eastern India identify different associations with

IDDM and malnutrition-related diabetes. Tissue Antigens 

1999;54(1):83-87. Not sensitivity or specificity of an 

identified test 

Sanjeevi C B, Landin-Olsson M, Kockum I et al. The 

combination of several polymorphic amino acid residues in

the DQalpha and DQbeta chains forms a domain structure 

pattern and is associated with insulin-dependent diabetes

mellitus. Annals of the New York Academy of Sciences 

2002;958362-375. Not sensitivity or specificity of an 

identified test 

Sanjeevi C B, Landin-Olsson M, Kockum I et al. Effects of 

the second HLA-DQ haplotype on the association with 

childhood insulin-dependent diabetes mellitus. Tissue 

Antigens 1995;45(2):148-152. Not sensitivity or specificity

of an identified test 

Sanjeevi C B, Lybrand T P, DeWeese C et al. Polymorphic

amino acid variations in HLA-DQ are associated with 

systematic physical property changes and occurrence of

IDDM. Diabetes 1995;44(1):125-131. Not sensitivity or

specificity of an identified test

Sanjeevi C B, Lybrand T P, Landin-Olsson M et al.

Analysis of antibody markers, DRB1, DRB5, DQA1 and 

DQB1 genes and modeling of DR2 molecules in DR2-

positive patients with insulin-dependent diabetes mellitus.

Tissue Antigens 1994;44(2):110-119. Not sensitivity or

specificity of an identified test

Sanjeevi C B, Lybrand T P, Stevanovic S et al. Molecular 

modeling of eluted peptides from DQ6 molecules 

(DQB1*0602 and DQB1*0604) negatively and positively

associated with type 1 diabetes. Annals of the New York 

Academy of Sciences 2002;958317-320. Not sensitivity or

specificity of an identified test

Santos S, Balas A, Lillo R et al. HLA-B14 subtyping by

semi-nested PCR-SSP and haplotype distribution in a

Spanish population. Tissue Antigens 1997;50(6):671-674. 

Not sensitivity or specificity of an identified test

Sapp Heidi, Ithamukkala Sarathehandra, Brien Tom P et al. 

The terminal ileum is affected in patients with lymphocytic 

or collagenous colitis. American Journal of Surgical

Pathology 2002;26(11):1484-1492. Not sensitivity or 

specificity of an identified test

Saputo V, Losi S, Mancosu M et al. Intraepithelial

lymphocytes in jejunal mucosa: diagnostic significance of

changes in their number during chronic intestinal disease,

with particular reference to coeliac disease. Schweizerische

Rundschau Fur Medizin Praxis = Revue Suisse De 

Medecine Praxis 1981;70(30):1342-1348. Unable to extract 

data 

Sardy M, Karpati S, Peterfy F et al. Comparison of a tissue 

transglutaminase ELISA with the endomysium antibody

test in the diagnosis of gluten-sensitive enteropathy. 

Zeitschrift Fur Gastroenterologie 2000;38(5):357-364. 

A-459
Improper control group 

Sardy M, Odenthal U, Karpati S et al. Recombinant human 

tissue transglutaminase ELISA for the diagnosis of glutensensitive enteropathy. Clinical Chemistry 

1999;45(12):2142-2149. Improper control group

Sardy Miklos, Karpati Sarolta, Merkl Barbara et al. 

Epidermal transglutaminase (TGase 3) is the autoantigen of

dermatitis herpetiformis. Journal of Experimental Medicine

2002;195(6):747-757. Not sensitivity or specificity of an

identified test 

Sarles J, Gorvel J P, Olive D et al. Subcellular localization 

of class I (A,B,C) and class II (DR and DQ) MHC antigens 

in jejunal epithelium of children with coeliac disease. 

Journal of Pediatric Gastroenterology and Nutrition 

1987;6(1):51-56. Not sensitivity or specificity of an 

identified test 

Sarsfield P, Jones D B, Wright D H. Accessory cells in

Crohn's disease of the terminal ileum. Histopathology

1996;28(3):213-219. Not sensitivity or specificity of an 

identified test 

Sarsfield P, Rinne A, Jones D B et al. Accessory cells in

physiological lymphoid tissue from the intestine: an 

immunohistochemical study. Histopathology

1996;28(3):205-211. Not sensitivity or specificity of an 

identified test 

Sasado T, Kani S, Washimi K et al. Expression of murine 

early embryonic antigens, SSEA-1 and antigenic 

determinant of EMA-1, in embryos and ovarian follicles of

a teleost medaka (Oryzias latipes). Dev Growth Differ 

1999;41(3):293-302. Not sensitivity or specificity of an 

identified test 

Sategna Guidetti, Carla Scaglione, Nadia Martini et al. Red 

cell distribution width as a marker of coeliac disease: a

prospective study. European Journal of Gastroenterology & 

Hepatology 2002;14(2):177-181. Not sensitivity or 

specificity of an identified test

Sategna-Guidetti C, Grosso S. Changing pattern in adult 

coeliac disease: A 24-year survey. European Journal of

Gastroenterology & Hepatology 1994;6(1):15-19. Not 

sensitivity or specificity of an identified test 

Sategna-Guidetti C, Bruno M, Mazza E et al. Autoimmune 

thyroid diseases and coeliac disease. European Journal of

Gastroenterology & Hepatology 1998;10(11):927-931. Not 

sensitivity or specificity of an identified test 

Sategna-Guidetti C, Bruno M, Pulitano R et al. Disease 

specificity of IgA class anti-endomysium antibodies (IgAEmA) in adult coeliac disease. European Journal of 

Gastroenterology & Hepatology 1991;3(3):251-254. Not 

sensitivity or specificity of an identified test 

Sategna-Guidetti C, Ferfoglia G, Bruno M et al. Do IgA 

antigliadin and IgA antiendomysium antibodies show there 

is latent coeliac disease in primary IgA nephropathy?. Gut 

1992;33(4):476-478. Not sensitivity or specificity of an 

identified test 

Sategna-Guidetti C, Grosso S B, Bruno M et al. Indirect 

immunofluorescence for of anti-jejunum antibody detection 

in celiac disease: comparison among different antigenic 

substrates. Panminerva Medica 1998;40(4):261-263. Not 

sensitivity or specificity of an identified test 

Sategna-Guidetti C, Grosso S B, Bruno M et al. Is human 

umbilical cord the most suitable substrate for the detection

of endomysium antibodies in the screening and follow-up 

of coeliac disease?. European Journal of Gastroenterology

& Hepatology 1997;9(7):657-660. Improper control group 

Sategna-Guidetti C, Grosso S B, Grosso S et al. The effects

of 1-year gluten withdrawal on bone mass, bone 

metabolism and nutritional status in newly-diagnosed adult 

coeliac disease patients. Alimentary Pharmacology & 

Therapeutics 2000;14(1):35-43. Not sensitivity or

specificity of an identified test

Sategna-Guidetti C, Grosso S, Bruno M et al. Reliability of

immunologic markers of celiac sprue in the assessment of 

mucosal recovery after gluten withdrawal. Journal of 

Clinical Gastroenterology 1996;23(2):101-104. Not 

sensitivity or specificity of an identified test 

Sategna-Guidetti C, Grosso S, Pulitano R et al. Celiac 

disease and insulin-dependent diabetes mellitus. Screening 

in an adult population. Digestive Diseases and Sciences 

1994;39(8):1633-1637. Not sensitivity or specificity of an

identified test 

Sategna-Guidetti C, Pulitano R, Grosso S et al. Serum IgA 

antiendomysium antibody titers as a marker of intestinal 

involvement and diet compliance in adult celiac sprue. 

Journal of Clinical Gastroenterology 1993;17(2):123-127. 

Not sensitivity or specificity of an identified test

Sategna-Guidetti C, Volta U, Ciacci C et al. Prevalence of

thyroid disorders in untreated adult celiac disease patients 

and effect of gluten withdrawal: an Italian multicenter

study. American Journal of Gastroenterology

2001;96(3):751-757. Not sensitivity or specificity of an 

identified test 

Satsangi J, Welsh K I, Bunce M et al. Contribution of genes 

of the major histocompatibility complex to susceptibility 

and disease phenotype in inflammatory bowel disease.

Lancet 1996;347(9010):1212-1217. Not sensitivity or 

specificity of an identified test

Saukkonen T, Ilonen J, Akerblom H K et al. Prevalence of 

coeliac disease in siblings of patients with Type I diabetes

is related to the prevalence of DQB1*02 allele. 

Diabetologia 2001;44(8):1051-1053. Improper control 

group 

Saukkonen T, Savilahti E, Reijonen H et al. Coeliac 

disease: frequent occurrence after clinical onset of insulinA-460
dependent diabetes mellitus. Childhood Diabetes in Finland

Study Group. Diabetic Medicine - a Journal of the British

Diabetic Association 1996;13(5):464-470. Not sensitivity

or specificity of an identified test

Savage D A, Middleton D, Trainor F et al. HLA class II

frequencies in celiac disease patients in the west of Ireland.

Human Immunology 1992;34(1):47-52. Not sensitivity or 

specificity of an identified test

Saverymuttu S H, Sabbat J, Burke M et al. Impact of

endoscopic duodenal biopsy on the detection of small 

intestinal villous atrophy. Postgraduate Medical Journal 

1991;67(783):47-49. Unable to extract data 

Savidge T C, Shmakov A N, Walker-Smith J A et al. 

Epithelial cell proliferation in childhood enteropathies. Gut 

1996;39(2):185-193. Not sensitivity or specificity of an 

identified test 

Savilahti E. IgA deficiency in children. Immunoglobulincontaining cells in the intestinal mucosa, immunoglobulins 

in secretions and serum IgA levels. Clinical and 

Experimental Immunology 1973;13(3):395-406. Not 

sensitivity or specificity of an identified test 

Savilahti E, Arato A, Verkasalo M. Intestinal gamma/delta 

receptor-bearing T lymphocytes in celiac disease and 

inflammatory bowel diseases in children. Constant increase 

in celiac disease. Pediatric Research 1990;28(6):579-581. 

Not sensitivity or specificity of an identified test

Savilahti E, Launiala K, Kuitunen P. Jejunal

disaccharidases in children with selective IgA deficiency.

Scandinavian Journal of Gastroenterology 1973;8(5):417-

419. Not sensitivity or specificity of an identified test 

Savilahti E, Ormala T, Arato A et al. Density of

gamma/deltasup + T cells in the jejunal epithelium of 

patients with coeliac disease and dermatitis herpetiformis is 

increased with age. Clinical and Experimental Immunology

1997;109(3):464-467. Not sensitivity or specificity of an

identified test 

Savilahti E, Ormala T, Saukkonen T et al. Jejuna of 

patients with insulin-dependent diabetes mellitus (IDDM) 

show signs of immune activation. Clinical and 

Experimental Immunology 1999;116(1):70-77. Not 

sensitivity or specificity of an identified test 

Savilahti E, Pelkonen P, Verkasalo M et al. Selective 

deficiency of immunoglobulin A in children. Klinische 

Padiatrie 1985;197(4):336-340. Not sensitivity or

specificity of an identified test

Savilahti E, Reunala T, Maki M. Increase of lymphocytes

bearing the gamma/delta T cell receptor in the jejunum of 

patients with dermatitis herpetiformis. Gut 1992;33(2):206-

211. Not sensitivity or specificity of an identified test 

Savilahti E, Simell O, Koskimies S et al. Celiac disease in 

insulin-dependent diabetes mellitus. Journal of Pediatrics 

1986;108(5 Pt 1):690-693. Improper control group 

Savilahti E, Viander M, Perkkio M et al. IgA antigliadin

antibodies: a marker of mucosal damage in childhood 

coeliac disease. Lancet 1983;1(8320):320-322. Not 

sensitivity or specificity of an identified test 

Sblattero D, Florian F, Not T et al. Analyzing the 

peripheral blood antibody repertoire of a celiac disease 

patient using phage antibody libraries. Human Antibodies

2000;9(4):199-205. Not sensitivity or specificity of an 

identified test 

Sblattero Daniele, Florian Fiorella, Azzoni Elisabetta et al. 

The analysis of the fine specificity of celiac disease 

antibodies using tissue transglutaminase fragments. 

European Journal of Biochemistry / Febs 

2002;269(21):5175-5181. Not sensitivity or specificity of

an identified test

Scalici C, Manzoni D, Licastro G et al. Reliability of EMA 

assay in the evaluation of gluten-free diet compliance in 

celiac patients during follow-up. Acta Med Mediterr 

2003;19(1):67-69. Not sensitivity or specificity of an 

identified test 

Schaad U, Gaze H, Hadorn B. Value of 1-hour bloodxylose test in diagnosis of childhood coeliac disease. Arch 

Dis Child 1978;53(5):420-422. Not sensitivity or

specificity of an identified test

Schaffer M, Olerup O. A novel DRB1(*)13 allele 

(DRB1(*)1327) on a DR17,DQ2 haplotype with a 

DRB1(*)0301 sequence motif in the 2nd hyperpolymorphic 

region. Tissue Antigens 1997;49(2):186-188. Not 

sensitivity or specificity of an identified test 

Schattner A, Kozak N, Lassry Y et al. Primary intestinal Tcell lymphoma and sclerosing cholangitis: A cytokinemediated association?. J Intern Med (Gbr) 

1998;244(6):537-541. Not sensitivity or specificity of an

identified test 

Schaumburg-Lever G, Gehring B, Kaiserling E. 

Ultrastructural localization of factor XIIIa. Journal of

Cutaneous Pathology 1994;21(2):129-134. Not sensitivity

or specificity of an identified test

Schenk E A, Samloff I M. Clinical and morphologic 

changes following gluten administration to patients with 

treated celiac dsease. American Journal of Pathology 

1968;52(3):579-593. Unable to extract data 

Schenk E A, Samloff I M, Klipstein F A. Morphologic 

characteristics of jejunal biopsy in celiac disease and 

tropical sprue. American Journal of Pathology

1965;47(5):765-781. Not sensitivity or specificity of an 

identified test 

Schenk E A, Samloff I M, Klipstein F A. Morphology of

small bowel biopsies. American Journal of Clinical 

Nutrition 1968;21(9):944-961. Not sensitivity or specificity

A-461
of an identified test 

Schenker S. Adverse reactions to food. Nutr Bull 

2002;27(2):125-127. Not sensitivity or specificity of an 

identified test 

Scherak O, Smolen J S, Mayr W R. HLA-DRw3 and 

systemic lupus erythematosus. Arthritis Rheum

1980;23(8):954-957. Not sensitivity or specificity of an 

identified test 

Schmid D G, der Mulbe F D, Fleckenstein B et al. 

Broadband detection electrospray ionization Fourier 

transform ion cyclotron resonance mass spectrometry to 

reveal enzymatically and chemically induced deamidation 

reactions within peptides. Analytical Chemistry 

2001;73(24):6008-6013. Not sensitivity or specificity of an 

identified test 

Schmidt R, Michel S, Shroot B et al. Transglutaminases in

normal and transformed human keratinocytes in culture. 

Journal of Investigative Dermatology 1988;90(4):475-479. 

Not sensitivity or specificity of an identified test

Schmitz J. Is celiac disease a lifelong disorder?. Clinical 

and Investigative Medicine.Medecine Clinique Et

Experimentale 1996;19(5):352-356. Not sensitivity or 

specificity of an identified test

Schmitz J. Lack of oats toxicity in coeliac disease. Br Med 

J 1997;314(7075):159-160. Not sensitivity or specificity of 

an identified test

Schneppenheim R, Budde U, Dahlmann N et al. 

Luminography--a new, highly sensitive visualization 

method for electrophoresis. Electrophoresis 

1991;12(5):367-372. Not sensitivity or specificity of an 

identified test 

Schober E, Bittmann B, Granditsch G et al. Screening by

anti-endomysium antibody for celiac disease in diabetic 

children and adolescents in Austria. Journal of Pediatric 

Gastroenterology and Nutrition 2000;30(4):391-396. Not

sensitivity or specificity of an identified test 

Schober Edith, Rami Birgit, Granditsch Gerhard et al. 

Coeliac disease in children and adolescents with type 1 

diabetes mellitus: to screen or not, to treat or not?.

Hormone Research 2002;57(Suppl 1):97-100. Not 

sensitivity or specificity of an identified test 

Scholz S, Albert E. HLA and diseases: involvement of

more than one HLA-linked determinant of disease 

susceptibility. Immunological Reviews 1983;7077-88. Not 

sensitivity or specificity of an identified test 

Schroeder W T, Thacher S M, Stewart-Galetka S et al. 

Type I keratinocyte transglutaminase: expression in human

skin and psoriasis. Journal of Investigative Dermatology

1992;99(1):27-34. Not sensitivity or specificity of an 

identified test 

Schulzke J D, Bentzel C J, Schulzke I et al. Epithelial tight

junction structure in the jejunum of children with acute and 

treated celiac sprue. Pediatric Research 1998;43(4 Pt 

1):435-441. Not sensitivity or specificity of an identified

test 

Schulzke J D, Schulzke I, Fromm M et al. Epithelial barrier

and ion transport in coeliac sprue: electrical measurements

on intestinal aspiration biopsy specimens. Gut 

1995;37(6):777-782. Not sensitivity or specificity of an 

identified test 

Schuppan D, Ciccocioppo R. Coeliac disease and 

secondary autoimmunity. Digestive and Liver Disease - 

Official Journal of the Italian Society of Gastroenterology

and the Italian Association for the Study of the Liver 

2002;34(1):13-15. Not sensitivity or specificity of an 

identified test 

Schuppan D, Hahn E G. Celiac disease and its link to type 

1 diabetes mellitus. Journal of Pediatric Endocrinology & 

Metabolism 2001;14 Suppl 1597-605. Not sensitivity or

specificity of an identified test

Schuppan D, Hahn E G. IgA anti-tissue transglutaminase: 

setting the stage for coeliac disease screening. European 

Journal of Gastroenterology & Hepatology 2001;13(6):635-

637. Not sensitivity or specificity of an identified test 

Schuppan D, Dieterich W, Riecken E O. Exposing gliadin 

as a tasty food for lymphocytes. Nature Medicine 

1998;4(6):666-667. Not sensitivity or specificity of an 

identified test 

Schuppan D, Dieterich W, Ehnis T et al. Identification of 

the autoantigen of celiac disease. Annals of the New York 

Academy of Sciences 1998;859121-126. Not sensitivity or

specificity of an identified test

Schuppan D, Ruehl M, Somasundaram R et al. Matrix as a 

modulator of hepatic fibrogenesis. Seminars in Liver 

Disease 2001;21(3):351-372. Not sensitivity or specificity

of an identified test 

Schuppan Detlef, Hahn Eckhart G. Biomedicine. Gluten

and the gut-lessons for immune regulation. Science 

2002;297(5590):2218-2220. Not sensitivity or specificity of 

an identified test

Schuppan Detlef, Esslinger Birgit, Dieterich Walburga. 

Innate immunity and coeliac disease. Lancet

2003;362(9377):3-4. Not sensitivity or specificity of an 

identified test 

Schutz S M, Stroebel J, Schutz E M et al. Celiac sprue.

Diagnosis and diet: keys to recovery. North Carolina 

Medical Journal 1994;55(1):32-36. Not sensitivity or 

specificity of an identified test

Schwartz F C M, Lunat M, Wolfsdorf J. Blood xylose 

concentrations in protein energy malnutrition. Relationship

to serum albumin and jejunal histology. S Afr Med J 

A-462
1974;48(58):2387-2390. Not sensitivity or specificity of an 

identified test 

Schweiger G D, Murray J A. Postbulbar duodenal 

ulceration and stenosis associated with celiac disease.

Abdom Imaging 1998;23(4):347-349. Not sensitivity or

specificity of an identified test

Schweizer J J, Mearin M L, Pena A S et al. Expression of 

HLA-DQ antigens in the small-intestinal mucosa of 

patients with coeliac disease. Scandinavian Journal of

Gastroenterology 1991;26(6):605-610. Not sensitivity or 

specificity of an identified test

Scoglio Riccardo, Di Pasquale, Giuseppe Pagano et al. Is 

intestinal biopsy always needed for diagnosis of celiac 

disease?. American Journal of Gastroenterology

2003;98(6):1325-1331. Improper control group 

Scott Losowsky B B M S. Coeliac disease with mild 

mucosal abnormalities: a report of our patients. Postgrad 

Med J 1977;53(617):134-138. Improper control group 

Scott B B, Losowsky M S. Patchiness and duodenal-jejunal 

variation of the mucosal abnormality in coeliac disease and 

dermatitis herpetiformis. Gut 1976;17(12):984-992. Unable 

to extract data

Scott B B, Losowsky M S. Proceedings: Patchiness of the 

mucosal abnormality in coeliac disease (CD) and dermatitis 

herpetiformis (DH). Gut 1975;16(5):393Unable to extract 

data 

Scott B B, Fairman M J, Toothill C et al. The expression 

enzyme activity of biopsy tissue from the small intestine.

Digestion 1977;15(3):182-187. Not sensitivity or

specificity of an identified test

Scott B B, Goodall A, Stephenson P et al. Small intestinal 

plasma cells in coeliac disease. Gut 1984;25(1):41-46. Not 

sensitivity or specificity of an identified test 

Scott B B, Goodall A, Stephenson P et al. Duodenal bulb 

plasma cells in duodenitis and duodenal ulceration. Gut

1985;26(10):1032-1037. Not sensitivity or specificity of an 

identified test 

Scott B B, Hardy G J, Losowsky M S. Involvement of the

small intestine in systemic mast cell disease. Gut

1975;16(11):918-924. Not sensitivity or specificity of an

identified test 

Scott B B, Losowsky M S, Rajah S M. Letter: HL-A8 and

HL-A12 in coeliac disease. Lancet 1974;2(7873):171Not 

sensitivity or specificity of an identified test 

Scott B B, Scott D G, Losowsky M S. Jejunal mucosal 

immunoglobulins and complement in untreated coeliac 

disease. J Pathol 1977;121(4):219-223. Not sensitivity or 

specificity of an identified test

Scott B B, Swinburne M L, Rajah S M et al. HL A8 and the 

immune response to gluten. Lancet 1974;2(7877):374-377. 

Not sensitivity or specificity of an identified test

Scott B B, Young S, Rajah S M et al. Coeliac disease and

dermatitis herpetiformis: further studies of their 

relationship. Gut 1976;17(10):759-762. Not sensitivity or 

specificity of an identified test

Scott B B, Young S, Rajah S M et al. Proceedings: The 

incidence of coeliac diseases and HL-A8 in dermatitis

herpetiformis. Gut 1975;16(10):845Not sensitivity or 

specificity of an identified test

Scott H, Brandtzaeg P, Solheim B G et al. Relation 

between HLA-DR-like antigens and secretory component 

(SC) in jejunal epithelium of patients with coeliac disease

or dermatitis herpetiformis. Clinical and Experimental 

Immunology 1981;44(2):233-238. Not sensitivity or 

specificity of an identified test

Scott H, Brandtzaeg P, Thorsby E et al. Mucosal and 

systemic immune response patterns in celiac disease. Ann 

Allergy 1983;51(2 Pt 2):233-239. Not sensitivity or 

specificity of an identified test

Scott H, Ek J, Havnen J et al. Serum antibodies to dietary

antigens: a prospective study of the diagnostic usefulness in

celiac disease of children. Journal of Pediatric 

Gastroenterology and Nutrition 1990;11(2):215-220. Not

sensitivity or specificity of an identified test 

Scott H, Fausa O, Thorsby E. T-lymphocyte activation by a 

gluten fraction, glyc-gli. Studies of adult coeliac patients 

and healthy controls. Scandinavian Journal of Immunology

1983;18(3):185-191. Not sensitivity or specificity of an 

identified test 

Scott H, Fausa O, Ek J et al. Measurements of serum IgA 

and IgG activities to dietary antigens. A prospective study 

of the diagnostic usefulness in adult coeliac disease. 

Scandinavian Journal of Gastroenterology 1990;25(3):287-

292. Not sensitivity or specificity of an identified test 

Scott H, Hirschberg H, Thorsby E. HLA-DR3- and HLADR7-restricted T-cell hyporesponsiveness to gluten 

antigen: a clue to the aetiology of coeliac disease?. Scand J

Immunol 1983;18(2):163-167. Not sensitivity or specificity

of an identified test 

Scott H, Nilsen E, Sollid L M et al. Immunopathology of 

gluten-sensitive enteropathy. Springer Semin 

Immunopathol 1997;18(4):535-553. Not sensitivity or 

specificity of an identified test

Scott H, Sollid L M, Brandtzaeg P et al. Jejunal epithelium

of patients with coeliac disease shows enhanced expression 

of MHC class II subregion products. Adv Exp Med Biol 

1988;237689-693. Not sensitivity or specificity of an 

identified test 

Scott H, Sollid L M, Fausa O et al. Expression of major 

histocompatibility complex class II subregion products by

A-463
jejunal epithelium in patients with coeliac disease.

Scandinavian Journal of Immunology 1987;26(5):563-571. 

Not sensitivity or specificity of an identified test

Scully L J, Toze C, Sengar D P S et al. Early-onset 

autoimmune hepatitis is associated with a C4A gene 

deletion. Gastroenterology 1993;104(5):1478-1484. Not 

sensitivity or specificity of an identified test 

Seah P P, Fry L, Holborow E J et al. Antireticulin antibody:

incidence and diagnostic significance. Gut 1973;14(4):311-

315. Not sensitivity or specificity of an identified test 

Seah P P, Fry L, Kearney J W et al. A comparison of 

histocompatibility antigens in dermatitis herpetiformis and 

adult coeliac disease. British Journal of Dermatology 

1976;94(2):131-138. Not sensitivity or specificity of an 

identified test 

Sebus J, Fernandes J, van der et al. A new twin hole 

capsule for peroral intestinal biopsy in children. Digestion

1968;1(4):193-199. Not sensitivity or specificity of an 

identified test 

Segni M, Pani M A, Pasquino A M et al. Familial 

clustering of juvenile thyroid autoimmunity: Higher risk is 

conferred by human leukocyte antigen DR3-DQ2 and 

thyroid peroxidase antibody status in fathers. J Clin 

Endocrinol Metab 2002;87(8):3779-3782. Not sensitivity or 

specificity of an identified test

Seissler J, Boms S, Wohlrab U et al. Antibodies to human 

recombinant tissue transglutaminase measured by

radioligand assay: evidence for high diagnostic sensitivity

for celiac disease. Hormone and Metabolic

Research.Hormon- Und Stoffwechselforschung.Hormones 

Et Metabolisme 1999;31(6):375-379. Improper control 

group 

Seissler J, Wohlrab U, Wuensche C et al. Autoantibodies 

from patients with coeliac disease recognize distinct 

functional domains of the autoantigen tissue 

transglutaminase. Clinical and Experimental Immunology

2001;125(2):216-221. Not sensitivity or specificity of an

identified test 

Seiving B, Ohlsson K, Linder C et al. Transglutaminase

differentiation during maturation of human blood

monocytes to macrophages. European Journal of

Haematology 1991;46(5):263-271. Not sensitivity or 

specificity of an identified test

Sela B-A. Homocysteine gets to the brain. Isr Med Assoc J 

2002;4(3):204-206. Not sensitivity or specificity of an 

identified test 

Selby R, Barnard J M, Buehler S K et al. Tuberculosis 

associated with HLA--B8, BfS in a Newfoundland 

community study. Tissue Antigens 1978;11(5):403-408. 

Not sensitivity or specificity of an identified test

Selby W. Gluten enteropathy. Aust Prescr 2001;24(2):38-

40+47. Not sensitivity or specificity of an identified test 

Selby W S, Painter D, Collins A et al. Persistent mucosal 

abnormalities in coeliac disease are not related to the 

ingestion of trace amounts of gluten. Scandinavian Journal 

of Gastroenterology 1999;34(9):909-914. Not sensitivity or 

specificity of an identified test

Seliger G, Goldman A B, Firooznia H et al. Ulceration of 

the small intestine complicating celiac disease. American 

Journal of Digestive Diseases 1973;18(9):820-824. Not 

sensitivity or specificity of an identified test 

Selzer G, Sherman G, Callihan T R et al. Primary small 

intestinal lymphomas and alpha-heavy-chain disease. A

study of 43 cases from a pathology department in Israel. 

Israel Journal of Medical Sciences 1979;15(2):111-123. 

Not sensitivity or specificity of an identified test

Semenza G, Bircher J, Mulhaupt E et al. Arbutin absorption 

in human small intestine: a simple procedure for the 

determination of active sugar uptake in peroral biopsy

specimens. Clinica Chimica Acta 1969;International 

Journal of Clinical Chemistry; 25(2):213-219. Not 

sensitivity or specificity of an identified test 

Senarath Yapa R S. Coeliac disease in young and old 

patients. J Clin Exp Gerontol 1991;13(3):95-102. Not 

sensitivity or specificity of an identified test 

Sengar D P S, Goldstein R. Comprehensive typing of 

DQB1 alleles by PCR-RFLP. Tissue Antigens 

1994;43(4):242-248. Not sensitivity or specificity of an 

identified test 

Serebrinsky G, Palermo M, Geffner J et al. Opposite effects 

of amines on lymphocyte- and monocyte-mediated ADCC. 

International Journal of Immunopharmacology

1988;10(5):555-561. Not sensitivity or specificity of an 

identified test 

Serjeantson S W, Court J, Mackay I R et al. HLA-DQ 

genotypes are associated with autoimmunity to glutamic 

acid decarboxylase in insulin-dependent diabetes mellitus 

patients. Human Immunology 1993;38(2):97-104. Not 

sensitivity or specificity of an identified test 

Serrano-Rios M, Gutierrez-Lopez M D, Perez-Bravo F et 

al. HLA-DR, DQ and anti-GAD antibodies in first degree 

relatives of type I diabetes mellitus. Diabetes Res Clin

Pract 1996;34(Suppl):S133-S139. Not sensitivity or 

specificity of an identified test

Shah V H, Rotterdam H, Kotler D P et al. All that scallops 

is not celiac disease. Gastrointestinal Endoscopy

2000;51(6):717-720. Not sensitivity or specificity of an 

identified test 

Shahbazkhani B, Forootan M, Merat S et al. Coeliac 

disease presenting with symptoms of irritable bowel 

syndrome. Alimentary Pharmacology & Therapeutics

2003;18(2):231-235. Not sensitivity or specificity of an 

A-464
identified test 

Shahbazkhani Bijan, Malekzadeh Reza, Sotoudeh Masoud 

et al. High prevalence of coeliac disease in apparently

healthy Iranian blood donors. European Journal of

Gastroenterology & Hepatology 2003;15(5):475-478. Not 

sensitivity or specificity of an identified test 

Shainoff J R, Urbanic D A. Multicolour immuno-staining

of fibrinogen polypeptide chains for identification of their

derivatives in electrophoregrams. Blood Coagulation & 

Fibrinolysis - an International Journal in Haemostasis and 

Thrombosis 1990;1(4-5):479-484. Not sensitivity or 

specificity of an identified test

Shainoff J R, Urbanic D A, DiBello P M. 

Immunoelectrophoretic characterizations of the crosslinking of fibrinogen and fibrin by factor XIIIa and tissue 

transglutaminase. Identification of a rapid mode of hybrid 

alpha-/gamma-chain cross-linking that is promoted by the 

gamma-chain cross-linking. Journal of Biological 

Chemistry 1991;266(10):6429-6437. Not sensitivity or 

specificity of an identified test

Shainoff J R, Valenzuela R, Urbanic D A et al. Fibrinogen 

A alpha and gamma-chain dimers as potential differential

indicators of atherosclerotic and thrombotic vascular 

disease. Blood Coagulation & Fibrinolysis - an 

International Journal in Haemostasis and Thrombosis 

1990;1(4-5):499-503. Not sensitivity or specificity of an

identified test 

Shamir R, Shoenfeld Y, Blank M et al. The prevalence of 

coeliac disease antibodies in patients with the 

antiphospholipid syndrome. Lupus 2003;12(5):394-399. 

Not sensitivity or specificity of an identified test

Shamir Raanan, Eliakim Rami, Lahat Nitza et al. ELISA of 

anti-endomysial antibodies in the diagnosis of celiac 

disease: comparison with immunofluorescence assay of 

anti-endomysial antibodies and tissue transglutaminase 

antibodies. Israel Medical Association Journal - Imaj 

2002;4(8):594-596. Improper control group 

Shamir Raanan, Lerner Aaron, Shinar Eilat et al. The use of 

a single serological marker underestimates the prevalence

of celiac disease in Israel: a study of blood donors.

American Journal of Gastroenterology 2002;97(10):2589-

2594. Not sensitivity or specificity of an identified test 

Shan Lu, Molberg Oyvind, Parrot Isabelle et al. Structural

basis for gluten intolerance in celiac sprue. Science 

2002;297(5590):2275-2279. Not sensitivity or specificity of 

an identified test

Shanahan F, McKenna R, McCarthy C F et al. Coeliac 

disease and diabetes mellitus: a study of 24 patients with 

HLA typing. Quarterly Journal of Medicine 

1982;51(203):329-335. Not sensitivity or specificity of an

identified test 

Shand A G, Ciclitira P J. Celiac disease. Clin Perspect 

Gastroenterol 2002;5(5):277-283. Not sensitivity or 

specificity of an identified test

Shaoul R, Marcon M A, Okada Y et al. Gastric metaplasia:

a frequently overlooked feature of duodenal biopsy

specimens in untreated celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 2000;30(4):397-403. Not

sensitivity or specificity of an identified test 

Sheehan N J, Stanton-King K. Polyautoimmunity in a 

young woman. British Journal of Rheumatology

1993;32(3):254-256. Not sensitivity or specificity of an 

identified test 

Sheldon W, Tempany E. Small intestine peroral biopsy in

coeliac children. Gut 1966;7(5):481-489. Improper control 

group 

Sherman S L. Genetic analysis workshop IV: summary for 

coeliac disease. Genetic Epidemiology.Supplement 

1986;1271-276. Not sensitivity or specificity of an 

identified test 

Sherman S L, Iselius L, Ellis A et al. Combined segregation 

and linkage analysis of coeliac disease. Genetic

Epidemiology.Supplement 1986;1283-288. Not sensitivity

or specificity of an identified test

Sherritt M A, Tait B, Varney M et al. Immunosusceptibility

genes in rheumatoid arthritis. Hum Immunol 

1996;51(1):32-40. Not sensitivity or specificity of an 

identified test 

Sheth K J, Werlin S L, Freeman M E et al. Gastrointestinal

structure and function in Fabry's disease. American Journal

of Gastroenterology 1981;76(3):246-251. Not sensitivity or 

specificity of an identified test

Shibahara M, Nanko H, Shimizu M et al. Dermatitis 

herpetiformis in Japan: An update. Dermatology

2002;204(1):37-42. Not sensitivity or specificity of an 

identified test 

Shidrawi R G, Ciclitira P J. Celiac disease. Curr Opin 

Gastroenterol 1996;12(2):159-163. Not sensitivity or 

specificity of an identified test

Shidrawi R G, Day P, Przemioslo R et al. In vitro toxicity

of gluten peptides in coeliac disease assessed by organ 

culture. Scandinavian Journal of Gastroenterology

1995;30(8):758-763. Not sensitivity or specificity of an 

identified test 

Shidrawi R G, Parnell N D, Ciclitira P J et al. Binding of 

gluten-derived peptides to the HLA-DQ2 (alpha1*0501, 

beta1*0201) molecule, assessed in a cellular assay. Clinical 

and Experimental Immunology 1998;111(1):158-165. Not 

sensitivity or specificity of an identified test 

Shidrawi R G, Przemioslo R, Davies D R et al. Pitfalls in 

diagnosing coeliac disease. Journal of Clinical Pathology

1994;47(8):693-694. Improper control group 

A-465
Shih J-F, Hunninghake G W, Goeken N E et al. The 

relationship between HLA-A, B, DQ, and DR antigens and 

asbestos- induced lung disease. Chest 1993;104(1):26-31. 

Not sensitivity or specificity of an identified test

Shimizu T, Beijer E, Strandvik B. Leukotriene B4 and C4 

metabolism in small intestine mucosa of children with 

celiac disease. Journal of Pediatric Gastroenterology and 

Nutrition 1995;21(4):426-429. Not sensitivity or specificity

of an identified test 

Shimizu T, Beijer E, Ryd W et al. Leukotriene B4 and C4 

generation by small intestinal mucosa in children with 

coeliac disease. Digestion 1994;55(4):239-242. Not 

sensitivity or specificity of an identified test 

Shimoda S S, O'Brien T K, Saunders D R. Fat absorption 

after infusing bile salts into the human small intestine.

Gastroenterology 1974;67(1):7-18. Not sensitivity or 

specificity of an identified test

Shiner M. Coeliac disease. Electron microscopy of jejunal

mucosa. Clinics in Gastroenterology 1974;3(1):33-53. 

Review article 

Shiner M. Ultrastructural changes suggestive of immune

reactions in the jejunal mucosa of coeliac children 

following gluten challenge. Gut 1973;14(1):1-12. Not 

sensitivity or specificity of an identified test 

Shiner M. Ultrastructural features of allergic manifestations 

in the small intestine of children. Scandinavian Journal of

Gastroenterology.Supplement 1981;7049-64. Not 

sensitivity or specificity of an identified test 

Shiner M. Electron microscopy of jejunal mucosa. Clin 

Gastroenterol 1974;3(1):33-53. Not sensitivity or 

specificity of an identified test

Shiner M, Shmerling D H. The immunopathology of 

coeliac disease. Digestion 1972;5(2):69-88. Not sensitivity

or specificity of an identified test

Shiner R J, Ballard J. Mucosal secretory IgA and secretory 

piece in adult coeliac disease. Gut 1973;14(10):778-783. 

Not sensitivity or specificity of an identified test

Shipman R T, Williams A L, Kay R et al. A family study of

coeliac disease. Australian and New Zealand Journal of

Medicine 1975;5(3):250-255. Not sensitivity or specificity

of an identified test 

Shitabata P K, Crouch E C, Fitzgibbon J F et al. Cutaneous 

sclerotic fibroma. Immunohistochemical evidence of a 

fibroblastic neoplasm with ongoing type I collagen 

synthesis. American Journal of Dermatopathology 

1995;17(4):339-343. Not sensitivity or specificity of an 

identified test 

Shmakov A N, Bode J, Kilshaw P J et al. Diverse patterns

of expression of the 67-kD laminin receptor in human small 

intestinal mucosa: potential binding sites for prion

proteins?. Journal of Pathology 2000;191(3):318-322. Not 

sensitivity or specificity of an identified test 

Shmerling D H, Franckx J. Childhood celiac disease: a 

long-term analysis of relapses in 91 patients. Journal of

Pediatric Gastroenterology and Nutrition 1986;5(4):565-

569. Not sensitivity or specificity of an identified test 

Shokrgozar M A, Shokri F. HLA-associated antibody

response to recombinant hepatitis B vaccine in healthy

Iranian adults. Iran J Med Sci 1999;24(3-4):98-103. Not 

sensitivity or specificity of an identified test 

Shtauvere A, Rumba I, Dzivite I et al. HLA-DR and -DQ 

gene polymorphism in Latvian patients with insulindependent diabetes mellitus. Tissue Antigens 

1998;52(4):385-388. Not sensitivity or specificity of an 

identified test 

Shtauvere-Brameus A, Dabadghao P, Rumba I et al. Tumor 

necrosis factor-alpha allele 2 shows an association with 

insulin-dependent diabetes mellitus in Latvians. Annals of 

the New York Academy of Sciences 2002;958357-361. Not 

sensitivity or specificity of an identified test 

Shtauvere-Brameus A, Falorni A, Rumba I et al. Islet 

autoantibodies in Latvian subjects with non-insulindependent diabetes mellitus: slow-onset type 1 diabetes or

polyendocrine autoimmunity?. Annals of the New York 

Academy of Sciences 2002;958259-262. Not sensitivity or

specificity of an identified test

Shtauvere-Brameus A, Ghaderi M, Rumba I et al. 

Microsatellite allele 5 of MHC class I chain-related gene a

increases the risk for insulin-dependent diabetes mellitus in 

latvians. Annals of the New York Academy of Sciences

2002;958349-352. Not sensitivity or specificity of an 

identified test 

Shuster S, Watson A J, Marks J. Coeliac syndrome in

dermatitis herpetiformis. Lancet 1968;1(7552):1101-1106. 

Not sensitivity or specificity of an identified test

Sidney John, del Guercio, Marie Southwood et al. The 

HLA molecules DQA1*0501/B1*0201 and 

DQA1*0301/B1*0302 share an extensive overlap in 

peptide binding specificity. Journal of Immunology

(Baltimore, Md.- 1950) 2002;169(9):5098-5108. Not 

sensitivity or specificity of an identified test 

Siebenlist K R, Mosesson M W. Evidence of 

intramolecular cross-linked A alpha.gamma chain 

heterodimers in plasma fibrinogen. Biochemistry

1996;35(18):5817-5821. Not sensitivity or specificity of an 

identified test 

Siegel L M, Stevens P D, Lightdale C J et al. Combined 

magnification endoscopy with chromoendoscopy in the 

evaluation of patients with suspected malabsorption. 

Gastrointestinal Endoscopy 1997;46(3):226-230. Not 

sensitivity or specificity of an identified test 

A-466
Signer E, Burgin-Wolff A, Berger R et al. Antibodies to

gliadin as a screening test for coeliac disease. A prospective 

study. Helvetica Paediatrica Acta 1979;34(1):41-52. 

Serology <1990

Signore A, Chianelli M, Annovazzi A et al. Imaging active 

lymphocytic infiltration in coeliac disease with iodine-123-

interleukin-2 and the response to diet. European Journal of

Nuclear Medicine 2000;27(1):18-24. Not sensitivity or 

specificity of an identified test

Sigurs N, Johansson C, Elfstrand P O et al. Prevalence of 

coeliac disease in diabetic children and adolescents in 

Sweden. Acta Paediatrica (Oslo, Norway - 1992) 

1993;82(9):748-751. Not sensitivity or specificity of an 

identified test 

Silink M. How should we manage celiac disease in 

childhood diabetes?. Pediatr Diabetes 2001;2(3):95-97. Not 

sensitivity or specificity of an identified test 

Silk D B A, Kumar P J, Perrett D. Amino acid and peptide 

absorption in patients with coeliac disease and dermatitis 

herpetiformis. Gut 1974;15(1):1-8. Not sensitivity or 

specificity of an identified test

Silk D B A, Kumar P J, Webb J P W. Ileal function in 

patients with untreated adult coeliac disease. Gut 

1975;16(4):261-267. Not sensitivity or specificity of an 

identified test 

Siltanen Mirjami, Kajosaari Merja, Savilahti Emma M et

al. IgG and IgA antibody levels to cow's milk are low at

age 10 years in children born preterm. Journal of Allergy

and Clinical Immunology 2002;110(4):658-663. Not 

sensitivity or specificity of an identified test 

Silva E M, Fernandes M I, Galvao L C et al. Human 

leukocyte antigen class II alleles in white Brazilian patients 

with celiac disease. Journal of Pediatric Gastroenterology

and Nutrition 2000;31(4):391-394. Improper control group 

Silva L M, Donadi E A. Is immunogenetic susceptibility to 

neuropsychiatric systemic lupus erythematosus (SLE) 

different from non-neuropsychiatric SLE?. Ann Rheum Dis 

1996;55(8):544-547. Not sensitivity or specificity of an 

identified test 

Silverman J S, Tamsen A. Mammary fibroadenoma and 

some phyllodes tumour stroma are composed of CD34+ 

fibroblasts and factor XIIIa+ dendrophages. Histopathology

1996;29(5):411-419. Not sensitivity or specificity of an 

identified test 

Silvestris F, Anderson W, Goodwin J S et al. Discrepancy

in the expression of autoantibodies in healthy aged

individuals. Clin Immunol Immunopathol 1985;35(2):234-

244. Not sensitivity or specificity of an identified test 

Simon M, Green H. Participation of membrane-associated 

proteins in the formation of the cross-linked envelope of 

the keratinocyte. Cell 1984;36(4):827-834. Not sensitivity

or specificity of an identified test

Simon M, Haftek M, Sebbag M et al. Evidence that 

filaggrin is a component of cornified cell envelopes in 

human plantar epidermis. Biochemical Journal 1996;317(Pt 

1):173-177. Not sensitivity or specificity of an identified

test 

Simpson F G, Bullen A W, Robertson D A et al. HLA-B8 

and cell-mediated immunity to gluten. Gut 1981;22(8):633-

636. Not sensitivity or specificity of an identified test 

Simpson F G, Howdle P D, Robertson D A et al. Jejunal 

biopsy and lymphocyte co-culture in coeliac disease. 

Scandinavian Journal of Gastroenterology 1983;18(6):749-

754. Not sensitivity or specificity of an identified test 

Simu G, Jung J, Vojth V et al. Microscopic observations 

concerning the autoimmune response escalation into 

malignant lymphoma. Morphologie Et Embryologie 

1986;32(2):99-104. Not sensitivity or specificity of an 

identified test 

Sinclair D, Pearce C B, Saas M S L et al. A comparative 

study of tissue transglutaminase antibodies and

endomysium antibody immunofluorescence in routine 

clinical laboratory practice. Ann Clin Biochem 

2003;40(4):411-416. Improper control group 

Singer M A, Hortsch M, Goodman C S et al. Annulin, a 

protein expressed at limb segment boundaries in the 

grasshopper embryo, is homologous to protein crosslinking transglutaminases. Dev Biol 1992;154(1):143-159. 

Not sensitivity or specificity of an identified test

Singer Steven M, Zainelli Gina M, Norlund Maryam A et 

al. Transglutaminase bonds in neurofibrillary tangles and

paired helical filament tau early in Alzheimer's disease.

Neurochemistry International 2002;40(1):17-30. Not 

sensitivity or specificity of an identified test 

Singh U S, Cerione R A. Biochemical effects of retinoic 

acid on GTP-binding Protein/Transglutaminases in HeLa 

cells. Stimulation of GTP-binding and transglutaminase 

activity, membrane association, and phosphatidylinositol 

lipid turnover. Journal of Biological Chemistry

1996;271(44):27292-27298. Not sensitivity or specificity of 

an identified test

Singh U S, Erickson J W, Cerione R A. Identification and 

biochemical characterization of an 80 kilodalton GTPbinding/transglutaminase from rabbit liver nuclei. 

Biochemistry 1995;34(48):15863-15871. Not sensitivity or

specificity of an identified test

Singh U S, Kunar M T, Kao Y L et al. Role of

transglutaminase II in retinoic acid-induced activation of

RhoA-associated kinase-2. Embo Journal 

2001;20(10):2413-2423. Not sensitivity or specificity of an 

identified test 

A-467
Singh U S, Li Q, Cerione R. Identification of the eukaryotic 

initiation factor 5A as a retinoic acid-stimulated cellular

binding partner for tissue transglutaminase II. Journal of

Biological Chemistry 1998;273(4):1946-1950. Not 

sensitivity or specificity of an identified test 

Singh Ugra S, Pan Jing, Kao Yu et al. Tissue 

transglutaminase mediates activation of RhoA and MAP 

kinase pathways during retinoic acid-induced neuronal 

differentiation of SH-SY5Y cells. Journal of Biological

Chemistry 2002;278(1):391-399. Not sensitivity or

specificity of an identified test

Sinnott P J, Livieri C, Sampietro M et al. CYP21/C4 gene 

organisation in Italian 21-hydroxylase deficiency families.

Hum Genet 1992;88(5):545-551. Not sensitivity or 

specificity of an identified test

Sipos A, Csortos C, Sipka S et al. The antigen/receptor 

specificity of antigranulocyte antibodies in patients with 

SLE. Immunology Letters 1988;19(4):329-334. Not 

sensitivity or specificity of an identified test 

Sizemore N, Kasturi L, Gorodeski G et al. Retinoid 

regulation of human ectocervical epithelial cell

transglutaminase activity and keratin gene expression. 

Differentiation 1993;Research in Biological Diversity;

54(3):219-225. Not sensitivity or specificity of an identified 

test 

Sjoberg K, Eriksson S. Regional differences in coeliac 

disease prevalence in Scandinavia?. Scandinavian Journal 

of Gastroenterology 1999;34(1):41-45. Not sensitivity or 

specificity of an identified test

Sjoberg K, Alm R, Ivarsson S A et al. Prevalence and 

clinical significance of gliadin antibodies in healthy

children and adults. Scandinavian Journal of

Gastroenterology 1994;29(3):248-254. Improper control 

group 

Sjoberg K, Eriksson K F, Bredberg A et al. Screening for 

coeliac disease in adult insulin-dependent diabetes mellitus.

Journal of Internal Medicine 1998;243(2):133-140. Not 

sensitivity or specificity of an identified test 

Sjoberg K, Eriksson S, Tenngart B et al. Factor XIII and

tissue transglutaminase antibodies in coeliac and

inflammatory bowel disease. Autoimmunity

2002;35(5):357-364. Not sensitivity or specificity of an 

identified test 

Sjoberg K, Lindgren S, Eriksson S. Frequent occurrence of 

non-specific gliadin antibodies in chronic liver disease. 

Endomysial but not gliadin antibodies predict coeliac 

disease in patients with chronic liver disease. Scandinavian 

Journal of Gastroenterology 1997;32(11):1162-1167. Not 

sensitivity or specificity of an identified test 

Sjoberg K, Wassmuth R, Reichstetter S et al. Gliadin 

antibodies in adult insulin-dependent diabetes--autoimmune 

and immunogenetic correlates. Autoimmunity

2000;32(4):217-228. Not sensitivity or specificity of an 

identified test 

Sjolund K, Ekman R. Plasma motilin in untreated celiac 

disease. Peptides 2003;24(3):483-486. Not sensitivity or

specificity of an identified test

Sjolund K, Alumets J, Berg N O et al. Duodenal endocrine 

cells in adult coeliac disease. Gut 1979;20(7):547-552. Not 

sensitivity or specificity of an identified test 

Sjolund K, Alumets J, Berg N O et al. Enteropathy of 

coeliac disease in adults: increased number of

enterochromaffin cells the duodenal mucosa. Gut 

1982;23(1):42-48. Not sensitivity or specificity of an 

identified test 

Sjolund K, Hakanson R, Lundqvist G et al. Duodenal 

somatostatin in coeliac disease. Scandinavian Journal of

Gastroenterology 1982;17(8):969-976. Not sensitivity or 

specificity of an identified test

Sjostrom H, Lundin K E, Molberg O et al. Identification of

a gliadin T-cell epitope in coeliac disease: general 

importance of gliadin deamidation for intestinal T-cell 

recognition. Scandinavian Journal of Immunology

1998;48(2):111-115. Not sensitivity or specificity of an 

identified test 

Sjostrom H, Noren O, Krasilnikoff P A et al. Intestinal 

peptidases and sucrase in coeliac disease. Clin Chim Acta

1981;109(1):53-58. Not sensitivity or specificity of an 

identified test 

Skeen M B. Neurologic manifestations of gastrointestinal 

disease. Neurol Clin 2002;20(1):195-225. Not sensitivity or 

specificity of an identified test

Skerritt J H, Devery J M, Penttila I A et al. Cellular and

humoral responses in coeliac disease. 2. Protein extracts 

from different cereals. Clinica Chimica Acta

1991;International Journal of Clinical Chemistry; 204(1-

3):109-122. Not sensitivity or specificity of an identified

test 

Skoglosa J, Falth-Magnusson K, Stenhammar L. Conscious 

or deep sedation: a questionnaire regarding the experience 

of parents, children and staff during small bowel biopsy.

Acta Paediatrica (Oslo, Norway - 1992) 2003;92(6):704-

708. Not sensitivity or specificity of an identified test 

Skovbjerg H, Sjostrom H, Noren O B. Coeliac disease - A 

diagnostic and scientific challenge. Ugeskr Laeg

2002;164(25):3329-3333. Not sensitivity or specificity of

an identified test

Slavin G, Sowter C, Robertson K et al. Measurement in 

jejunal biopsies by computer-aided microscopy. Journal of

Clinical Pathology 1980;33(3):254-261. Not sensitivity or

specificity of an identified test

Slavin R G, Hutcheson P S, Chauhan B et al. New insights 

A-468
into the pathogenesis of allergic bronchopulmonary

aspergillosis. Allergy Clin Immunol Int 2003;15(2):79-81. 

Not sensitivity or specificity of an identified test

Slavutsky I, Gomez J C, Pedreira S et al. Increased rDNA 

transcriptional activity in celiac disease. Journal of Clinical 

Gastroenterology 1992;14(1):11-14. Not sensitivity or 

specificity of an identified test

Sleisenger M H, Brandborg L L. Malabsorption. Major 

Problems in Internal Medicine 1977;13v-x,1-261. Not 

sensitivity or specificity of an identified test 

Smecuol E, Bai J C, Vazquez H et al. Gastrointestinal

permeability in celiac disease. Gastroenterology

1997;112(4):1129-1136. Not sensitivity or specificity of an 

identified test 

Smecuol E, Vazquez H, Sugai E et al. Sugar tests detect 

celiac disease among first-degree relatives. American

Journal of Gastroenterology 1999;94(12):3547-3552. Not 

sensitivity or specificity of an identified test 

Smethurst P A, Griffin M. Measurement of tissue 

transglutaminase activity in a permeabilized cell system: its 

regulation by Ca2+ and nucleotides. Biochemical Journal 

1996;313(Pt 3):803-808. Not sensitivity or specificity of an 

identified test 

Smith A D, Bagheri B, Streilein R D et al. Expression of 

interleukin-4 and interferon-gamma in the small bowel of 

patients with dermatitis herpetiformis and isolated glutensensitive enteropathy. Digestive Diseases and Sciences 

1999;44(10):2124-2132. Not sensitivity or specificity of an 

identified test 

Smith K, Mezebish D, Williams J P et al. Cutaneous 

epithelioid schwannomas: A rare variant of a benign 

peripheral nerve sheath tumor. J Cutaneous Pathol

1998;25(1):50-55. Not sensitivity or specificity of an 

identified test 

Smith M E, Costa M J, Weiss S W. Evaluation of CD68 

and other histiocytic antigens in angiomatoid malignant 

fibrous histiocytoma. American Journal of Surgical 

Pathology 1991;15(8):757-763. Not sensitivity or

specificity of an identified test

Smith S. Jejunal biopsy--seeking an alternative. Paediatric

Nursing 1996;8(4):17-19. Not sensitivity or specificity of

an identified test

Smith S E, Littlewood J M. The two-film barium meal in

the exclusion of coeliac disease. Clinical Radiology

1977;28(6):629-634. Not sensitivity or specificity of an 

identified test 

Smoller B R, Apfelberg D B. Infantile (juvenile) capillary

hemangioma: a tumor of heterogeneous cellular elements. 

Journal of Cutaneous Pathology 1993;20(4):330-336. Not 

sensitivity or specificity of an identified test 

Smyth C, Kelleher D, Keeling P W N. Hepatic 

manifestations of gastrointestinal diseases inflammatory

bowel disease, Celiac disease, and Whipple's disease. Clin

Liver Dis 2002;6(4):1013-1032. Not sensitivity or

specificity of an identified test

Snijders A, Elferink D G, Geluk A et al. An HLA-DRB1-

derived peptide associated with protection against 

rheumatoid arthritis is naturally processed by human 

APCsSUP1. J Immunol 2001;166(8):4987-4993. Not 

sensitivity or specificity of an identified test 

Sobel J H, Trakht I, Wu H Q et al. Alpha-Chain crosslinking in fibrin(ogen) Marburg. Blood 1995;86(3):989-

1000. Not sensitivity or specificity of an identified test 

Solheim B G, Ek J, Thune P O et al. HLA antigens in 

dermatitis herpetiformis and coeliac disease. Tissue 

Antigens 1976;7(1):57-59. Not sensitivity or specificity of 

an identified test

Sollid L M. Molecular basis of celiac disease. Annual 

Review of Immunology 2000;1853-81. Not sensitivity or

specificity of an identified test

Sollid L M. Genetics of the immune response to gluten in 

coeliac disease. Digestive Diseases (Basel, Switzerland)

1998;16(6):345-347. Review article 

Sollid L M. Breast milk against coeliac disease. Gut 

2002;51(6):767-768. Not sensitivity or specificity of an 

identified test 

Sollid L M, Lundin K E. Coeliac disease. An inappropriate

immune response. Lancet 2001;358(Suppl):s13Not 

sensitivity or specificity of an identified test 

Sollid L M, Scott H. New tool to predict celiac disease on

its way to the clinics. Gastroenterology 1998;115(6):1584-

1586. Not sensitivity or specificity of an identified test 

Sollid L M, Thorsby E. The primary association of celiac 

disease to a given HLA-DQ alpha/beta heterodimer 

explains the divergent HLA-DR associations observed in

various Caucasian populations. Tissue Antigens 

1990;36(3):136-137. Not sensitivity or specificity of an 

identified test 

Sollid L M, Thorsby E. HLA susceptibility genes in celiac 

disease: genetic mapping and role in pathogenesis. 

Gastroenterology 1993;105(3):910-922. Review article 

Sollid L M, Markussen G, Ek J et al. Evidence for a 

primary association of celiac disease to a particular HLADQ alpha/beta heterodimer. Journal of Experimental 

Medicine 1989;169(1):345-350. Improper control group 

Sollid L M, McAdam S N, Molberg O et al. Genes and 

environment in celiac disease. Acta Odontologica 

Scandinavica 2001;59(3):183-186. Not sensitivity or 

specificity of an identified test

A-469
Sollid L M, Molberg O, McAdam S et al. Autoantibodies in 

coeliac disease: tissue transglutaminase--guilt by

association?. Gut 1997;41(6):851-852. Not sensitivity or

specificity of an identified test

Sollid L M, Scott H, Kolberg J et al. Serum antibodies to

wheat germ agglutinin and gluten in patients with 

dermatitis herpetiformis. Archives of Dermatological

Research 1986;278(6):433-436. Not sensitivity or

specificity of an identified test

Sollid L, Bruserud O, Gaudernack G et al. The role of the 

CD8-positive subset of T cells in proliferative responses to 

soluble antigens. I. Studies of healthy subjects, type 1 

diabetics, and coeliac disease patients. Scandinavian 

Journal of Immunology 1986;23(4):461-467. Not 

sensitivity or specificity of an identified test 

Sollid L, Scott H, Thorsby E. Suppressor-cell activity in

coeliac disease. Lancet 1985;1(8422):229-230. Not 

sensitivity or specificity of an identified test 

Sollid Ludvig M. Coeliac disease: dissecting a complex 

inflammatory disorder. Nature Reviews.Immunology

2002;2(9):647-655. Not sensitivity or specificity of an 

identified test 

Soltoft J. Immunoglobulin-containing cells in non-tropical 

sprue. Clinical and Experimental Immunology

1970;6(3):413-420. Not sensitivity or specificity of an 

identified test 

Soltoft J, Weeke B. Immunoglobulins in serum and jejunal 

biopsies in non-tropical sprue. Acta Medica Scandinavica 

1969;186(5):459-464. Not sensitivity or specificity of an

identified test 

Song Y C, Sheng D, Taubenfeld S M et al. A microtiter 

assay for factor XIII using fibrinogen and

biotinylcadaverine as substrates. Analytical Biochemistry

1994;223(1):88-92. Not sensitivity or specificity of an 

identified test 

Song Y, Taubenfeld S M, Sheng D et al. Characterization 

of a monoclonal antibody directed against the carboxylterminus of human factor XIII. An epitope exposed upon 

denaturation and conserved across species lines. 

Thrombosis and Haemostasis 1994;71(1):62-67. Not 

sensitivity or specificity of an identified test 

Sorell L, Garrote J A, Acevedo B et al. One-step

immunochromatographic assay for screening of coeliac 

disease. Lancet 2002;359(9310):945-946. Improper control 

group 

Soresi M, Amplo M, Agliastro R et al. Screening for 

autoantibodies to tissue transglutaminase reveals a low 

prevalence of celiac disease in blood donors with

cryptogenic hypertransaminasemia. Digestion

2001;64(2):87-91. Not sensitivity or specificity of an 

identified test 

Sorg C, Michels E, Malorny U et al. Migration inhibitory

factors and macrophage differentiation. Springer Seminars 

in Immunopathology 1984;7(4):311-320. Not sensitivity or

specificity of an identified test

Sottrup-Jensen L, Stepanik T M, Kristensen T. Primary

structure of human alphainf 2-macroglobulin. V. The 

complete structure. J Biol Chem 1984;259(13):8318-8327. 

Not sensitivity or specificity of an identified test

Souroujon M, Ashkenazi A, Lupo M et al. Serum ferritin

levels in celiac disease. American Journal of Clinical

Pathology 1982;77(1):82-86. Not sensitivity or specificity

of an identified test 

Spencer J, MacDonald T T, Diss T C et al. Changes in 

intraepithelial lymphocyte subpopulations in coeliac 

disease and enteropathy associated T cell lymphoma

(malignant histiocytosis of the intestine). Gut

1989;30(3):339-346. Not sensitivity or specificity of an 

identified test 

Spiekerkoetter U, Seissler J, Wendel U. General screening 

for celiac disease is advisable in children with type 1 

diabetes. Hormone and Metabolic Research.Hormon- Und 

Stoffwechselforschung.Hormones Et Metabolisme 

2002;34(4):192-195. Not sensitivity or specificity of an 

identified test 

Spurkland A, Ingvarsson G, Falk E S et al. Dermatitis 

herpetiformis and celiac disease are both primarily 

associated with the HLA-DQ (alpha 1*0501, beta 1*02) or

the HLA-DQ (alpha 1*03, beta 1*0302) heterodimers. 

Tissue Antigens 1997;49(1):29-34. Improper control group 

Spurkland A, Sollid L M, Polanco I et al. HLA-DR and -

DQ genotypes of celiac disease patients serologically typed

to be non-DR3 or non-DR5/7. Human Immunology

1992;35(3):188-192. Not sensitivity or specificity of an 

identified test 

Spurkland A, Sollid L M, Ronningen K S et al. 

Susceptibility to develop celiac disease is primarily 

associated with HLA-DQ alleles. Human Immunology

1990;29(3):157-165. Improper control group 

Srinivasan U, Jones E, Weir D G et al. Lactase enzyme, 

detected immunohistochemically, is lost in active celiac 

disease, but unaffected by oats challenge. American Journal

of Gastroenterology 1999;94(10):2936-2941. Not 

sensitivity or specificity of an identified test 

Stachowski J, Kramer J, Fust G et al. Relationship between

the reactivity to hepatitis B virus vaccination and the 

frequency of MHC class I, II and III alleles in 

haemodialysis patients. Scand J Immunol 1995;42(1):60-

65. Not sensitivity or specificity of an identified test 

Stachowski J, Pollok M, Barth C et al. Non-responsiveness 

to hepatitis B vaccination in haemodialysis patients: 

Association with impaired TCR/CD3 antigen receptor 

expression regulating co-stimulatory processes in antigen 

A-470
presentation and recognition. Nephrol Dial Transplant

1994;9(2):144-152. Not sensitivity or specificity of an 

identified test 

Stahlberg M R, Savilahti E, Viander M. Antibodies to

gliadin by ELISA as a screening test for childhood celiac 

disease. Journal of Pediatric Gastroenterology and

Nutrition 1986;5(5):726-729. Serology <1990 

Stallmach A, Belitz H D, Gellermann B et al. Effects of

gliadin peptides B1-B4 in celiac disease. I. Organ culture

studies. Journal of Pediatric Gastroenterology and Nutrition 

1987;6(3):335-340. Not sensitivity or specificity of an 

identified test 

Stancu M, De Petris G, Palumbo T P et al. Collagenous 

gastritis associated with lymphocytic gastritis and celiac 

disease. Arch Pathol Lab Med 2001;125(12):1579-1584. 

Not sensitivity or specificity of an identified test

Stankovic I, Miletic I, Djordjevic B. Determination of antisecalin antibodies in sera from coeliac patients by ELISAbased assay. J Pharm Biomed Anal 1998;18(1-2):255-261. 

Not sensitivity or specificity of an identified test

Stark H J, Baur M, Breitkreutz D et al. Organotypic 

keratinocyte cocultures in defined medium with regular

epidermal morphogenesis and differentiation. Journal of

Investigative Dermatology 1999;112(5):681-691. Not 

sensitivity or specificity of an identified test 

Stark K L, Harris C, Juchau M R. Embryotoxicity elicited

by inhibition of gamma-glutamyltransferase by acivicin and 

transferase antibodies in cultured rat embryos. Toxicol

Appl Pharmacol 1987;89(1):88-96. Not sensitivity or 

specificity of an identified test

Staun M, Jarnum S. Measurement of the 10,000-molecular

weight calcium-binding protein in small-intestinal biopsy 

specimens from patients with malabsorption syndromes. 

Scandinavian Journal of Gastroenterology 1988;23(7):827-

832. Not sensitivity or specificity of an identified test 

Steele J C, Young S P, Goodall J C et al. Structural aspects 

of the interaction between heterogeneic human 

papillomavirus type 1 E4-specific T cell receptors and the 

same peptide/HLA- DQ8 complex. J Immunol 

1998;161(9):4745-4752. Not sensitivity or specificity of an 

identified test 

Steele R J C, Brown M, Eremin O. Characterisation of 

macrophages infiltrating human mammary carcinomas. Br 

J Cancer 1985;51(1):135-138. Not sensitivity or specificity

of an identified test 

Steffan J S, Thompson L M. Targeting aggregation in the 

development of therapeutics for the treatment of

Huntington's disease and other polyglutamine repeat 

diseases. Expert Opin Ther Targets 2003;7(2):201-213. Not 

sensitivity or specificity of an identified test 

Steinert P M, Marekov L N. Initiation of assembly of the 

cell envelope barrier structure of stratified squamous 

epithelia. Molecular Biology of the Cell 1999;10(12):4247-

4261. Not sensitivity or specificity of an identified test 

Stene L C, Magnus P, Ronningen K S et al. Diabetesassociated HLA-DQ genes and birth weight. Diabetes

2001;50(12):2879-2882. Not sensitivity or specificity of an 

identified test 

Stenhammar L. Transient gastro-intestinal disorders during 

infancy and early childhood. A follow-up study with 

special reference to coeliac disease. Acta Paediatrica 

Scandinavica 1981;70(3):383-387. Not sensitivity or 

specificity of an identified test

Stenhammar L, Johansson C G. The incidence of coeliac 

disease in children in south-east Sweden. Acta Paediatrica 

Scandinavica 1981;70(3):379-381. Not sensitivity or 

specificity of an identified test

Stenhammar L, Ascher H, Danielsson L et al. Small bowel 

biopsy in Swedish paediatric clinics. Acta Paediatrica 

(Oslo, Norway - 1992) 2002;91(10):1126-1129. Not 

sensitivity or specificity of an identified test 

Stenhammar L, Brandt A, Wagermark J. A family study of

coeliac disease. Acta Paediatr Scand 1982;71(4):625-628. 

Not sensitivity or specificity of an identified test

Stenhammar L, Fallstrom S P, Jansson G et al. Coeliac 

disease in children of short stature without gastrointestinal 

symptoms. European Journal of Pediatrics 

1986;145(3):185-186. Not sensitivity or specificity of an

identified test 

Stenhammar L, FalthMagnusson K, Jansson G et al. 

Intestinal permeability to inert sugars and different-sized

polyethyleneglycols in children with celiac disease. Journal

of Pediatric Gastroenterology and Nutrition 1989;9(3):281-

289. Not sensitivity or specificity of an identified test 

Stenhammar L, Kilander A F, Nilsson L A et al. Serum 

gliadin antibodies for detection and control of childhood 

coeliac disease. Acta Paediatrica Scandinavica

1984;73(5):657-663. Serology <1990 

Stenhammar L, Stromberg L, Kilander A F et al. Plasma 

enteroglucagon in the control of childhood celiac disease. 

Journal of Pediatric Gastroenterology and Nutrition 

1985;4(2):325-330. Not sensitivity or specificity of an 

identified test 

Stenhammar L, Warngard O, Lewander P et al. Oral versus 

intravenous premedication for small bowel biopsy in

children: effect on procedure and fluoroscopy times. Acta 

Paediatrica (Oslo, Norway - 1992) 1993;82(1):49-51. Not 

sensitivity or specificity of an identified test 

Stenling R, Fredrikzon B, Engberg S et al. Surface 

ultrastructure of the small intestine mucosa in children with 

celiac disease. I. Untreated disease and effects of long-term 

gluten elimination and challenge. Ultrastructural Pathology 

A-471
1984;6(4):295-305. Not sensitivity or specificity of an 

identified test 

Stern M. Comparative evaluation of serologic tests for 

celiac disease: a European initiative toward standardization.

Journal of Pediatric Gastroenterology and Nutrition 

2000;31(5):513-519. Improper control group 

Stern M. Concepts in coeliac disease: is there a receptor for 

gliadin?. Klinische Padiatrie 1985;197(4):349-354. Not 

sensitivity or specificity of an identified test 

Stern M, Dietrich R. Gliadin- and immunoglobulincontaining cells of small intestinal lamina propria in

childhood coeliac disease. European Journal of Pediatrics 

1982;139(1):13-17. Not sensitivity or specificity of an 

identified test 

Stern M, Bender S W, Gruttner R et al. Serum antibodies 

against gliadin and reticulin in a family study of coeliac

disease. European Journal of Pediatrics 1980;135(1):31-36. 

Not sensitivity or specificity of an identified test

Stern M, Dietrich R, Muller J. Small intestinal mucosa in

coeliac disease and cow's milk protein intolerance:

morphometric and immunofluorescent studies. European 

Journal of Pediatrics 1982;139(2):101-105. Not sensitivity

or specificity of an identified test

Stern M, Fischer K, Gruettner R. Gliadin antibodies in 

coeliac disease. Acta Paediatr Belg 1977;30(4):252Not 

sensitivity or specificity of an identified test 

Stern M, Fischer K, Gruttner R. Immunofluorescent serum 

gliadin antibodies in children with coeliac disease and 

various malabsorptive disorders. II. Specificity of Gliadin 

antibodies: immunoglobulin classes, immunogenic 

properties of wheat protein fractions, and pathogenic 

significance of food antibodies in coeliac disease. European

Journal of Pediatrics 1979;130(3):165-172. Serology <1990 

Stern M, Fischer K, Gruttner R. Immunofluorescent serum 

gliadin antibodies in children with coeliac disease and 

various malabsorptive disorders. I. Technique, clinical

evaluation and diagnostic use of a gliadin antibody assay

using pyruvic aldehyde-treated human red cells. European

Journal of Pediatrics 1979;130(3):155-164. Serology <1990 

Stern M, Teuscher M, Wechmann T. Serological screening

for coeliac disease: methodological standards and quality

control. Acta paediatrica (Oslo, Norway : 

1992).Supplement. 1996;41249-51. Improper control group 

Stevens F M. Endoscopic dye-spraying in the diagnosis of 

coeliac disease. Acta Endosc 1978;8(3):173-180. Not 

sensitivity or specificity of an identified test 

Stevens F M, Hitchcock H T. Farmer's lung disease and 

coeliac disease: A prospective study. Ir J Med Sci 

1977;146(10):335-339. Not sensitivity or specificity of an

identified test 

Stevens F M, McCarthy C F. The endoscopic 

demonstration of coeliac disease. Endoscopy

1976;8(4):177-180. Not sensitivity or specificity of an 

identified test 

Stevens F M, Kearns M C, McCarthy C F. Abnormal 

pancreolauryl tests in coeliac disease: lack of correlation 

with the degree of intestinal mucosal damage. Journal of

Clinical Pathology 1997;50(12):1001-1004. Not sensitivity

or specificity of an identified test

Stevens F M, Lloyd R S, Geraghty S M et al. Schizophrenia 

and coeliac disease--the nature of the relationship.

Psychological Medicine 1977;7(2):259-263. Not sensitivity

or specificity of an identified test

Stevens F M, Lloyd R, Egan-Mitchell B et al. Proceedings: 

Antireticulin antibodies in coeliacs and their relatives. Gut 

1973;14(10):829Not sensitivity or specificity of an 

identified test 

Stevens F M, Lloyd R, Egan-Mitchell B et al. Reticulin

antibodies in patients with coeliac disease and their 

relatives. Gut 1975;16(8):598-602. Not sensitivity or 

specificity of an identified test

Stevens H Y, Reeve J, Noble B S. Bcl-2, tissue

transglutaminase and p53 protein expression in the 

apoptotic cascade in ribs of premature infants. Journal of

Anatomy 2000;196(Pt 2):181-191. Not sensitivity or 

specificity of an identified test

Stewart J. Child coeliacs in adult life. Ir Med J

1974;67(15):411-414. Not sensitivity or specificity of an

identified test 

Stewart J S. Clinical and morphologic response to gluten

withdrawal. Clinics in Gastroenterology 1974;3(1):109-

126. Not sensitivity or specificity of an identified test 

Stewart J S, Pollock D J, Hoffbrand A V et al. A study of 

proximal and distal intestinal structure and absorptive

function in idiopathic steatorrhoea. Quarterly Journal of

Medicine 1967;36(143):425-444. Not sensitivity or

specificity of an identified test

Stewart W W, Kerr M A. The measurement of respiratory 

burst induced in polymorphonuclear neutrophils by IgA 

and IgG anti-gliadin antibodies isolated from coeliac 

serum. Immunology 1991;73(4):491-497. Not sensitivity or 

specificity of an identified test

Stockmann A, Hess S, Declerck P et al. Multimeric 

vitronectin. Identification and characterization of

conformation-dependent self-association of the adhesive 

protein. Journal of Biological Chemistry 

1993;268(30):22874-22882. Not sensitivity or specificity of 

an identified test

Stokes P L, Holmes G K T. Malignancy. Clin Gastroenterol 

1974;3(1):159-170. Not sensitivity or specificity of an 

identified test 

A-472
Stokes P L, Asquith P, Cooke W T. Genetics of coeliac 

disease. Clin Gastroenterol 1973;2(3):547-556. Not 

sensitivity or specificity of an identified test 

Stokes P L, Asquith P, Holmes G K et al. Inheritance and

influence of histocompatibility (HL-A) antigens in adult 

coeliac disease. Gut 1973;14(8):627-630. Not sensitivity or 

specificity of an identified test

Stokes P L, Ferguson R, Holmes G K et al. Familial aspects

of coeliac disease. Quarterly Journal of Medicine 

1976;45(180):567-582. Not sensitivity or specificity of an

identified test 

Stokes P L, Holmes G K, Smits B J. Immunoglobulin 

levels in families with coeliac disease. Lancet

1972;2(7777):608Not sensitivity or specificity of an 

identified test 

Stone O J. Dermatitis herpetiformis and gluten sensitive

enteropathy (including celiac disease)--increased

subepithelial extracellular matrix viscosity due to gliadin.

Medical Hypotheses 1990;33(4):283-288. Not sensitivity or 

specificity of an identified test

Storm W. Prevalence and diagnostic significance of gliadin 

antibodies in children with Down syndrome. European 

Journal of Pediatrics 1990;149(12):833-834. Not sensitivity

or specificity of an identified test

Storsrud S, Olsson M, Arvidsson Lenner R et al. Adult 

coeliac patients do tolerate large amounts of oats. European 

Journal of Clinical Nutrition 2003;57(1):163-169. Not 

sensitivity or specificity of an identified test 

Straumfors A, Johansen B H, Vartdal F et al. A peptidebinding assay for the disease-associated HLA-DQ8 

molecule. Scandinavian Journal of Immunology

1998;47(6):561-567. Not sensitivity or specificity of an 

identified test 

Streb H, Posselt H G, Wolter K et al. Aldolase activities of 

the small intestinal mucosa in malabsorption states and 

hereditary fructose intolerance. European Journal of 

Pediatrics 1981;137(1):5-10. Not sensitivity or specificity

of an identified test 

Strobel S, Brydon W G, Ferguson A. Cellobiose/mannitol 

sugar permeability test complements biopsy histopathology

in clinical investigation of the jejunum. Gut 

1984;25(11):1241-1246. Not sensitivity or specificity of an 

identified test 

Strobel S, Busuttil A, Ferguson A. Human intestinal 

mucosal mast cells: expanded population in untreated

coeliac disease. Gut 1983;24(3):222-227. Unable to extract 

data 

Strober W. Genetic and anthropologic factors in glutensensitive enteropathy. American Journal of Physical 

Anthropology 1983;62(1):119-126. Not sensitivity or 

specificity of an identified test

Strober W. Gluten-sensitive enteropathy. Clinics in 

Gastroenterology 1976;5(2):429-452. Not sensitivity or

specificity of an identified test

Strober W, Falchuk Z M, Rogentine G N et al. The 

pathogenesis of gluten-sensitive enteropathy. Annals of 

Internal Medicine 1975;83(2):242-256. Not sensitivity or 

specificity of an identified test

Strocchi A, Corazza G, Furne J et al. Measurements of the 

jejunal unstirred layer in normal subjects and patients with 

celiac disease. American Journal of Physiology 1996;270(3 

Pt 1):G487-G491. Not sensitivity or specificity of an 

identified test 

Strupp M. The humoral response in the pathogenesis of 

"gluten ataxia". J Neurol 2002;249(6):791-792. Not 

sensitivity or specificity of an identified test 

Stuart B M, Gent A E. Atrophy of the coeliac mucosa. 

European Journal of Gastroenterology & Hepatology

1998;10(6):523-525. Not sensitivity or specificity of an 

identified test 

Stuber E, Buschenfeld A, Luttges J et al. The expression of 

OX40 in immunologically mediated diseases of the 

gastrointestinal tract (celiac disease, Crohn's disease, 

ulcerative colitis). Eur J Clin Invest 2000;30(7):594-599. 

Not sensitivity or specificity of an identified test

Stuber Eckhard, Noth Rainer, Dirks Maren et al. The role

of tissue transglutaminase (transglutaminase type II) for the 

intestinal manifestations of murine semi-allogenic graftversus-host disease. Journal of Autoimmunity

2002;18(1):1-8. Not sensitivity or specificity of an 

identified test 

Stulik J, Hernychova L, Porkertova S et al. Identification of

new celiac disease autoantigens using proteomic analysis.

Proteomics 2003;3(6):951-956. Not sensitivity or 

specificity of an identified test

Sturgess R, Ciclitira P J. Pathogenesis and pathophysiology

of celiac disease. Curr Opin Gastroenterol 1993;9(2):242-

245. Not sensitivity or specificity of an identified test 

Sturgess R P, Hooper L B, Spencer J et al. Effects of 

interferon-gamma and tumour necrosis factor-alpha on 

epithelial HLA class-II expression on jejunal mucosal 

biopsy specimens cultured in vitro. Scandinavian Journal of 

Gastroenterology 1992;27(11):907-911. Not sensitivity or

specificity of an identified test

Sturgess R P, Macartney J C, Makgoba M W et al. 

Differential upregulation of intercellular adhesion

molecule-1 in coeliac disease. Clinical and Experimental 

Immunology 1990;82(3):489-492. Not sensitivity or 

specificity of an identified test

Sturgess R, Day P, Ellis H J et al. Wheat peptide challenge 

A-473
in coeliac disease. Lancet 1994;343(8900):758-761. Not 

sensitivity or specificity of an identified test 

Subramanian V S, Krishnaswami C V, Damodaran C. 

HLA, ESD, GLOI, C3 and HP polymorphisms and juvenile 

insulin dependent diabetes mellitus in Tamil Nadu (South 

India). Diabetes Res Clin Pract 1994;25(1):51-59. Not 

sensitivity or specificity of an identified test 

Suedhoff T, Birckbichler P J, Lee K N et al. Differential 

expression of transglutaminase in human erythroleukemia 

cells in response to retinoic acid. Cancer Research

1990;50(24):7830-7834. Not sensitivity or specificity of an 

identified test 

Sueur R, Cerf M, Di Costanzo G et al. Quantitative studies

in vitro on uptake and esterification of palmitate into 

human and rat jejunal mucosa. Digestion 1977;15(1):34-42. 

Not sensitivity or specificity of an identified test

Sugai E, Selvaggio G, Vazquez H et al. Tissue 

transglutaminase antibodies in celiac disease: assessment of 

a commercial kit. American Journal of Gastroenterology

2000;95(9):2318-2322. Improper control group 

Sugai Emilia, Chernavsky Alejandra, Pedreira Silvia et al.

Bone-specific antibodies in sera from patients with celiac 

disease: characterization and implications in osteoporosis. 

Journal of Clinical Immunology 2002;22(6):353-362. Not 

sensitivity or specificity of an identified test 

Sugden P, Andrew J G, Andrew S M et al. Dermal 

dendrocytes in Dupuytren's disease: a link between the skin

and pathogenesis?. Journal of Hand Surgery (Edinburgh, 

Lothian) 1993;18(5):662-666. Not sensitivity or specificity

of an identified test 

Suharjono. Intestinal biopsy and coeliac disease. 

Paediatrica Indonesiana 1971;11(3):116-134. Not 

sensitivity or specificity of an identified test 

Suharjono Sunoto, Damajanti A, Darmawan S et al. Small 

intestine biopsy in protein calorie malnutrition and celiac 

children. Paediatrica Indonesiana 1971;11(5):7-15. Not 

sensitivity or specificity of an identified test 

Sujirachato K, Chiewsilp P, Tsuji K et al. HLA class II 

polymorphism in Thai insulin-dependent diabetes mellitus.

Tokai J Exp Clin Med 1994;19(1-2):73-81. Not sensitivity

or specificity of an identified test

Sulkanen S, Halttunen T, Marttinen A et al. Autoantibodies

in celiac disease: importance of fibroblasts. Journal of 

Pediatric Gastroenterology and Nutrition 1998;27(2):206-

213. Not sensitivity or specificity of an identified test 

Sumi Yoshihiko, Inoue Nobutaka, Azumi Hiroshi et al. 

Expression of tissue transglutaminase and elafin in human 

coronary artery: implication for plaque instability. 

Atherosclerosis 2002;160(1):31-39. Not sensitivity or 

specificity of an identified test

Summey Brett T, Graff Ronald D, Lai Thung et al. Tissue 

transglutaminase localization and activity regulation in the

extracellular matrix of articular cartilage. Journal of 

Orthopaedic Research - Official Publication of the 

Orthopaedic Research Society 2002;20(1):76-82. Not 

sensitivity or specificity of an identified test 

Sumnik Z, Kolouskova S, Cinek O et al. HLA-DQA1*05-

DQB1*0201 positivity predisposes to coeliac disease in

Czech diabetic children. Acta Paediatrica (Oslo, Norway -

1992) 2000;89(12):1426-1430. Improper control group 

Sundqvist T, Laurin P, Falth-Magnusson K et al. 

Significantly increased levels of nitric oxide products in

urine of children with celiac disease. Journal of Pediatric

Gastroenterology and Nutrition 1998;27(2):196-198. Not

sensitivity or specificity of an identified test 

Sung L A, Chien S, Fan Y S et al. Human erythrocyte 

protein 4.2: isoform expression, differential splicing, and 

chromosomal assignment. Blood 1992;79(10):2763-2770. 

Not sensitivity or specificity of an identified test

Sunitha I, Meighen D L, Hartman D P et al. Hepatocyte

growth factor stimulates invasion across reconstituted 

basement membranes by a new human small intestinal cell

line. Clinical & Experimental Metastasis 1994;12(2):143-

154. Not sensitivity or specificity of an identified test 

Suranyi Y, Freier S, Faber J et al. Intestinal mast cells in 

different stages of celiac disease. Israel Journal of Medical

Sciences 1986;22(5):370-375. Unable to extract data 

Susi M, Holopainen P, Mustalahti K et al. Candidate gene

region 15q26 and genetic susceptibility to coeliac disease in

Finnish families. Scandinavian Journal of Gastroenterology

2001;36(4):372-374. Not sensitivity or specificity of an 

identified test 

Sutton G. Coeliac disease: Testing the New Zealand 

iceberg. New Zealand J Med Lab Sci 2000;54(2):46-48. 

Not sensitivity or specificity of an identified test

Suzuki M, Nikaido T, Ikegami M et al. Renal adenoma. 

Clinicopathological and histochemical studies. Acta 

Pathologica Japonica 1989;39(11):731-736. Not sensitivity

or specificity of an identified test

Svendsen M L, Daneels G, Geysen J et al. Proliferation and

differentiation of cultured human keratinocytes is 

modulated by 1,25(OH)2D3 and synthetic vitamin D3 

analogues in a cell density-, calcium- and serum-dependent

manner. Pharmacology & Toxicology 1997;80(1):49-56. 

Not sensitivity or specificity of an identified test

Svensson J, Carlsson A, Ericsson U-B et al. Noonan's

syndrome and autoimmune diseases. J Pediatr Endocrinol 

Metab 2003;16(2):217-218. Not sensitivity or specificity of 

an identified test

Sviridov D D, Izachik N A, Safonova I G et al. Cholesterol 

synthesis in the small intestine of patients with

A-474
malabsorption syndrome. Digestion 1988;40(3):152-156. 

Not sensitivity or specificity of an identified test

Sweeney E C, Masterson J B. Duodenal diaphragm with 

malabsorption. Ir Med J 1974;67(19):510-512. Not 

sensitivity or specificity of an identified test 

Swinson C M, Levi A J. Is coeliac disease 

underdiagnosed?. British Medical Journal 

1980;281(6250):1258-1260. Not sensitivity or specificity of 

an identified test

Swinson C M, Hall P J, Bedford P A et al. HLA antigens in 

coeliac disease associated with malignancy. Gut 

1983;24(10):925-928. Not sensitivity or specificity of an

identified test 

Swinson C M, Slavin G, Coles E C et al. Coeliac disease 

and malignancy. Lancet 1983;1(8316):111-115. Not 

sensitivity or specificity of an identified test 

Sylwestrowicz T, Kelly J K, Hwang W S et al. Collagenous 

colitis and microscopic colitis: The watery diarrhea-colitis

syndrome. American Journal of Gastroenterology

1989;84(7):763-768. Not sensitivity or specificity of an 

identified test 

Szabo B, Jezernicky J, Kavai M. Immunological findings in

primary malabsorption. Acta Paediatr Acad Sci Hung 

1982;23(3):337-342. Not sensitivity or specificity of an 

identified test 

Szabolcs M, Sipka S, Csorba S. In vitro cross-linking of 

gluten into high-molecular-weight polymers with

transglutaminase. Acta Paediatrica Hungarica 1987;28(3-

4):215-227. Not sensitivity or specificity of an identified

test 

Szaflarska-Szczepanik A, Czerwionka-Szaflarska M. The 

frequency of occurrence and clinical picture of celiac 

disease in the parents of children with the disease. Medical

Science Monitor - International Medical Journal of 

Experimental and Clinical Research 2001;7(5):971-976. 

Not sensitivity or specificity of an identified test

Szaflarska-Szczepanik Anna. Assessment of correlation 

between the presence of antiendomysial antibodies and 

small intestine mucosal villous atrophy in the diagnostics of

celiac disease. Medical Science Monitor - International 

Medical Journal of Experimental and Clinical Research

2002;8(3):Cr185-Cr188. Not sensitivity or specificity of an 

identified test 

Szaflarska-Szczepanik A, Romanczuk W, OdrowazSypniewska G et al. Anti tissue transglutaminase antibodies 

(IgA(dagger)TG) for diagnosing of coeliac disease in

children. Pediatr Wspolczesna 2002; 4(3):339-342. Unable

to obtain full article 

Szegezdi E, Szondy Z, Nagy L et al. Apoptosis-linked in

vivo regulation of the tissue transglutaminase gene 

promoter. Cell Death Differ 2000;7(12):1225-1233. Not 

sensitivity or specificity of an identified test 

Tabaqchali S, Hatzioannou J, Booth C C. Bile-salt 

deconjugation and steatorrhoea in patients with the

stagnant-loop syndrome. Lancet 1968;2(7558):12-16. Not 

sensitivity or specificity of an identified test 

Tabbaa M G, Axon A T R, Dixon M F. Enterocyte 

dimensions in patients with abnormal intestinal 

permeability. European Journal of Gastroenterology & 

Hepatology 1994;6(7):607-610. Not sensitivity or

specificity of an identified test

Tabrez S, Roberts I M. Malabsorption and malnutrition.

Primary Care 2001;28(3):505-22, V. Not sensitivity or 

specificity of an identified test

Tait B D, Harrison L C, Drummond B P et al. HLA 

antigens and age at diagnosis of insulin-dependent diabetes 

mellitus. Hum Immunol 1995;42(2):116-122. Not 

sensitivity or specificity of an identified test 

Takahashi H, Aoki N, Nakamura S et al. Cornified cell

envelope formation is distinct from apoptosis in epidermal 

keratinocytes. Journal of Dermatological Science 

2000;23(3):161-169. Not sensitivity or specificity of an 

identified test 

Takahashi H, Isobe T, Horibe S et al. Tissue 

transglutaminase, coagulation factor XIII, and the propolypeptide of von Willebrand factor are all ligands for the

integrins alpha 9beta 1 and alpha 4beta 1. Journal of 

Biological Chemistry 2000;275(31):23589-23595. Not 

sensitivity or specificity of an identified test 

Takahashi M, Tezuka T. Hematoxylin stainable epidermal

protein of the newborn rat. IV. The change of antigenicity

in situ by transglutaminase as determined by an

immunofluorescent study. J Dermatol 1989;16(3):178-183. 

Not sensitivity or specificity of an identified test

Takahashi M, Tezuka T, Katunuma N. Filaggrin linker

segment peptide and cystatin alpha are parts of a complex 

of the cornified envelope of epidermis. Arch Biochem

Biophys 1996;329(1):123-126. Not sensitivity or specificity

of an identified test 

Takahashi M, Tezuka T, Kakegawa H et al. Linkage 

between phosphorylated cystatin alpha and filaggrin by

epiderma) transglutaminase as a model of cornified 

envelope and inhibition of cathepsin L activity by cornified

envelope and the conjugated cystatin alpha. Febs Lett

1994;340(3):173-176. Not sensitivity or specificity of an

identified test 

Takahashi N, Takahashi Y, Putnam F W. Primary structure

of blood coagulation factor XIIIa (fibrinoligase, 

transglutaminase) from human placenta. Proceedings of the

National Academy of Sciences of the United States of 

America 1986;83(21):8019-8023. Not sensitivity or 

specificity of an identified test

A-475
Takaku K, Futamura M, Saitoh S et al. Tissue-type 

transglutaminase is not a tumor-related marker. Journal of

Biochemistry 1995;118(6):1268-1270. Not sensitivity or

specificity of an identified test

Talal A H, Murray J A, Goeken J A et al. Celiac disease in 

an adult population with insulin-dependent diabetes 

mellitus: use of endomysial antibody testing. American 

Journal of Gastroenterology 1997;92(8):1280-1284. Not 

sensitivity or specificity of an identified test 

Talley N J, Kephart G M, McGovern T W et al. Deposition 

of eosinophil granule major basic protein in eosinophilic 

gastroenteritis and celiac disease. Gastroenterology

1992;103(1):137-145. Not sensitivity or specificity of an

identified test 

Talme T, Schultzberg M, Sundqvist K G et al. 

Somatostatin- and factor XIIIa-immunoreactive cells in 

psoriasis during clobetasol propionate and calciprotriol

treatment. Acta Dermato-Venereologica 1999;79(1):44-48. 

Not sensitivity or specificity of an identified test

Tamada Y, Takama H, Kitamura T et al. Expression of 

transglutaminase I in human anagen hair follicles. Acta 

Dermato-Venereologica 1995;75(3):190-192. Not 

sensitivity or specificity of an identified test 

Taminiau J A. Celiac disease. Current Opinion in Pediatrics

1996;8(5):483-486. Not sensitivity or specificity of an 

identified test 

Tanaka N, Fujioka A, Tajima S et al. Levels of proelafin 

peptides in the sera of the patients with generalized pustular

psoriasis and pustulosis palmoplantaris. Acta DermatoVenereologica 2000;80(2):102-105. Not sensitivity or 

specificity of an identified test

Tanay Amir, Brickman Chaim M, Gas Svetlana et al. TG or 

not TG: IgG-anti-tissue transglutaminase in systemic lupus 

erythematosus: new role for an old enzyme. Israel Medical 

Association Journal - Imaj 2002;4(11 Suppl):878-879. Not 

sensitivity or specificity of an identified test 

Tandon N, Shtauvere-Brameus A, Hagopian W A et al. 

Prevalence of ICA-12 and other autoantibodies in north 

Indian patients with early-onset diabetes. Annals of the 

New York Academy of Sciences 2002;958214-217. Not 

sensitivity or specificity of an identified test 

Taneja V, Malaviya A N, Mehra N K. Restriction fragment

length polymorphisms in HLA-DR4-DQ3 haplotypes 

associated with rheumatoid arthritis. Indian J Med Res

1994;99(May):216-222. Not sensitivity or specificity of an 

identified test 

Taresa E, Kedei N, Thomazy V et al. An involucrin-like 

protein in hepatocytes serves as a substrate for tissue 

transglutaminase during apoptosis. Journal of Biological 

Chemistry 1992;267(36):25648-25651. Not sensitivity or

specificity of an identified test

Tarlo S M, Broder I, Prokipchuk E J. Association between

celiac disease and lung disease. Chest 1981;80(6):715-718. 

Not sensitivity or specificity of an identified test

Tarmure Simina, Grigorescu Mircea, Cristea Anca et al.

Antiendomysial and antitissue transglutaminase antibodies

in gluten-induced enteropathy. Romanian Journal of 

Gastroenterology 2002;11(2):91-95. Improper control 

group 

Tate G, Ishizawa M. Structural similarity of the HLA-DQ 

region in DQ3 and DQ4 haplotypes and structural diversity

of the HLA-DQ region in HLA-DR7 haplotypes. Microbiol

Immunol 1992;36(7):737-744. Not sensitivity or specificity

of an identified test 

Taylor B, Sokol G. Cystic fibrosis and coeliac disease. 

Report of two cases. Arch Dis Child 1973;48(9):692-696. 

Not sensitivity or specificity of an identified test

Taylor C J. Predictive value of intraepithelial lymphocyte 

counts in childhood coeliac disease. Journal of Pediatric 

Gastroenterology and Nutrition 1988;7(4):532-536. Unable

to extract data

Taylor C J, Smith S I, Morgan C H et al. HLA and 

Mooren's ulceration. Br J Ophthalmol 2000;84(1):72-75. 

Not sensitivity or specificity of an identified test

Tedeschi A, Tuccari G, Magazzu G et al. 

Immunohistochemical localization of lactoferrin in 

duodenojejunal mucosa from celiac children. Journal of

Pediatric Gastroenterology and Nutrition 1987;6(3):328-

334. Not sensitivity or specificity of an identified test 

Teepe R G, Burger A, Ponec M. Immunohistochemical 

studies on regeneration in cultured epidermal autografts 

used to treat full-thickness burn wounds. Clinical and 

Experimental Dermatology 1994;19(1):16-22. Not 

sensitivity or specificity of an identified test 

Teesalu K, Uibo O, Kalkkinen N et al. Increased levels of

IgA antibodies against desmin in children with coeliac 

disease. International Archives of Allergy and Immunology

2001;126(2):157-166. Not sensitivity or specificity of an

identified test 

ten Dam M, van de, Wal Y et al. Anti-alpha-gliadin 

antibodies (AGA) in the serum of coeliac children and

controls recognize an identical collection of linear epitopes 

of alpha-gliadin. Clinical and Experimental Immunology

1998;114(2):189-195. Not sensitivity or specificity of an

identified test 

Tepper R E, Simon D, Brandt L J et al. Intestinal

permeability in patients infected with the human 

immunodeficiency virus. American Journal of 

Gastroenterology 1994;89(6):878-882. Not sensitivity or 

specificity of an identified test

Teppo A M, Maury C P J. Antibodies to gliadin, gluten and

reticulin glycoprotein in rheumatic diseases: Elevated

A-476
levels in Sjogren's syndrome. Clinical and Experimental 

Immunology 1984;57(1):73-78. Not sensitivity or

specificity of an identified test

ter Steege J, Buurman W, Arends J W et al. Presence of

inducible nitric oxide synthase, nitrotyrosine, CD68, and

CD14 in the small intestine in celiac disease. Laboratory

Investigation 1997;A Journal of Technical Methods and 

Pathology; 77(1):29-36. Not sensitivity or specificity of an 

identified test 

Tessier J L, Davies G A L. Giardiasis. Prim Care Update 

Ob Gyns 1999;6(1):8-11. Not sensitivity or specificity of

an identified test

Thacher S M. Purification of keratinocyte transglutaminase 

and its expression during squamous differentiation. Journal 

of Investigative Dermatology 1989;92(4):578-584. Not 

sensitivity or specificity of an identified test 

Thacher S M, Rice R H. Keratinocyte-specific 

transglutaminase of cultured human epidermal cells:

relation to cross-linked envelope formation and terminal 

differentiation. Cell 1985;40(3):685-695. Not sensitivity or 

specificity of an identified test

Thacher S M, Rice R H. Monoclonal antibody to

transglutaminase in the particulate fraction of human 

keratinocytes. Fed Proc 1984;43(6):No 2164Not sensitivity

or specificity of an identified test

Thain M E, Hamilton J R, Ehrlich R M. Coexistence of

diabetes mellitus and celiac disease. Journal of Pediatrics

1974;85(4):527-529. Not sensitivity or specificity of an 

identified test 

Thapa B R. Celiac disease in India. Indian Journal of 

Pediatrics 1999;66(1 Suppl):S16-S20. Not sensitivity or

specificity of an identified test

Thapa B R. Celiac disease in children: Recent concepts. Jk

Science 2001;3(1):3-12. Not sensitivity or specificity of an 

identified test 

Theintz G E, Nussle D, Cox J et al. Prolactin and the gut: a 

controversy. Journal of Pediatric Gastroenterology and 

Nutrition 1984;3(4):523-528. Not sensitivity or specificity

of an identified test 

Theodor E, Gilon E. Protracted diarrhea of unknown 

etiology in Israeli soldiers. Israel Journal of Medical 

Sciences 1975;11(5):458-464. Not sensitivity or specificity

of an identified test 

Thomas A A, Martin S, Tate D G. An HLA-DQ2 specific 

cytotoxic alloantibody resulting from a failed renal 

transplant: A protocol for identification and verification.

Eur J Immunogenet 1992;19(6):460Not sensitivity or 

specificity of an identified test

Thomas A G, Phillips A D, Walker-Smith J A. The value of 

proximal small intestinal biopsy in the differential

diagnosis of chronic diarrhoea. Archives of Disease in

Childhood 1992;67(6):741-743. Unable to extract data 

Thomas G L, Henley A, Rowland T C et al. Enhanced 

apoptosis in transformed human lung fibroblasts after 

exposure to sodium butyrate. In Vitro Cellular & 

Developmental Biology.Animal 1996;32(8):505-513. Not 

sensitivity or specificity of an identified test 

Thomas L N, Wright A S, Lazier C B et al. Prostatic

involution in men taking finasteride is associated with 

elevated levels of insulin-like growth factor-binding 

proteins (IGFBPs)-2, -4, and -5. Prostate 2000;42(3):203-

210. Not sensitivity or specificity of an identified test 

Thomas P D, Forbes A, Green J et al. Guidelines for the

investigation of chronic diarrhoea, 2nd edition. Gut 

2003;52(Suppl 5):v1-v15. Not sensitivity or specificity of

an identified test

Thomazy V A, Davies P J A. Expression of tissue 

transglutaminase in the developing chicken limb is 

associated both with apoptosis and endochondral 

ossification. Cell Death Differ 1999;6(2):146-154. Not 

sensitivity or specificity of an identified test 

Thomazy V, Fesus L. Differential expression of tissue 

transglutaminase in human cells. An immunohistochemical 

study. Cell and Tissue Research 1989;255(1):215-224. Not 

sensitivity or specificity of an identified test 

Thomazy Vilmos A, Vega Francisco, Medeiros L et al.

Phenotypic modulation of the stromal reticular network in 

normal and neoplastic lymph nodes: tissue 

transglutaminase reveals coordinate regulation of multiple

cell types. American Journal of Pathology

2003;163(1):165-174. Not sensitivity or specificity of an

identified test 

Thompson H. Pathology of coeliac disease. Current Topics

in Pathology 1976;6349-75. Unable to extract data 

Thompson H. The small intestine at autopsy. Clin 

Gastroenterol 1974;3(1):171-181. Not sensitivity or 

specificity of an identified test

Thomson A B, Keelan M, Thiesen A et al. Small bowel 

review: diseases of the small intestine. Digestive Diseases

and Sciences 2001;46(12):2555-2566. Not sensitivity or

specificity of an identified test

Thomson G. HLA disease associations: models for the 

study of complex human genetic disorders. Crit Rev Clin

Lab Sci 1995;32(2):183-219. Not sensitivity or specificity

of an identified test 

Thomson G. Investigation of the mode of inheritance of the 

HLA associated diseases by the method of antigen 

genotype frequencies among diseased individuals. Tissue 

Antigens 1983;21(2):81-104. Not sensitivity or specificity

of an identified test 

A-477
Thornquist H, Jacobsen G S, Dahl L B et al. Coeliac 

disease and gluten-free diet: a following-up study of fifteen 

young adults. Annals of Nutrition & Metabolism

1993;37(6):295-301. Not sensitivity or specificity of an 

identified test 

Thorsby E. Invited anniversary review: HLA associated 

diseases. Hum Immunol 1997;53(1):1-11. Not sensitivity or

specificity of an identified test

Thorsby E, Lundin K E, Ronningen K S et al. Molecular 

basis and functional importance of some disease-associated

HLA polymorphisms. Tissue Antigens 1989;34(1):39-49. 

Not sensitivity or specificity of an identified test

Thurley C A, Kwan W C, Freeman H J et al. T cell receptor 

gene expression and genotypes in celiac disease.

Pathobiology - Journal of Immunopathology, Molecular 

and Cellular Biology 1994;62(5-6):311-318. Not sensitivity

or specificity of an identified test

Tiberti C, Buzzetti R, Anastasi E et al. Autoantibody

negative new onset type 1 diabetic patients lacking high 

risk HLA alleles in a caucasian population: are these type

1b diabetes cases?. Diabetes/Metabolism Research and 

Reviews 2000;16(1):8-14. Not sensitivity or specificity of 

an identified test

Tighe M R, Ciclitira P J. The implications of recent 

advances in coeliac disease. Acta Paediatrica (Oslo, 

Norway - 1992) 1993;82(10):805-810. Not sensitivity or

specificity of an identified test

Tighe M R, Ciclitira P J. The gluten-host interaction. 

Bailliere's Clin Gastroenterol 1995;9(2):211-230. Not 

sensitivity or specificity of an identified test 

Tighe M R, Hall M A, Ashkenazi A et al. Celiac disease 

among Ashkenazi Jews from Israel. A study of the HLA 

class II alleles and their associations with disease 

susceptibility. Human Immunology 1993;38(4):270-276. 

Improper control group 

Tighe M R, Hall M A, Barbado M et al. HLA class II 

alleles associated with celiac disease susceptibility in a 

southern European population. Tissue Antigens 

1992;40(2):90-97. Improper control group 

Tighe M R, Hall M A, Cardi E et al. Associations between 

alleles of the major histocompatibility complex-encoded 

ABC transporter gene TAP2, HLA class II alleles, and

celiac disease susceptibility. Human Immunology

1994;39(1):9-16. Not sensitivity or specificity of an 

identified test 

Tighe R, Ciclitira P J. Molecular biology of coeliac disease.

Archives of Disease in Childhood 1995;73(3):189-191. Not 

sensitivity or specificity of an identified test 

Tighe R, Ciclitira P J. Celiac disease. Curr Opin

Gastroenterol 1995;11(2):112-115. Not sensitivity or 

specificity of an identified test

Tikhonov YuV, Pimenov A M, Uzhevko S A et al. Ion-pair 

high-performance liquid chromatography of purine 

compounds in the small intestinal mucosa of children with

coeliac disease. Journal of Chromatography 1990;520419-

423. Not sensitivity or specificity of an identified test 

Tiltman A J, Allard U. Female adnexal tumours of probable 

Wolffian origin: an immunohistochemical study comparing 

tumours, mesonephric remnants and paramesonephric 

derivatives. Histopathology 2001;38(3):237-242. Not 

sensitivity or specificity of an identified test 

Timms B G, Lee C W, Aumuller G et al. Instructive 

induction of prostate growth and differentiation by a 

defined urogenital sinus mesenchyme. Microsc Res Tech

1995;30(4):319-332. Not sensitivity or specificity of an 

identified test 

Tiwana H, Walmsley R S, Wilson C et al. Characterization

of the humoral immune response to Klebsiella species in

inflammatory bowel disease and ankylosing spondylitis.

British Journal of Rheumatology 1998;37(5):525-531. Not

sensitivity or specificity of an identified test 

Tiwari J L, Betuel H, Gebuhrer L et al. Genetic 

epidemiology of coeliac disease. Genetic Epidemiology

1984;1(1):37-42. Not sensitivity or specificity of an 

identified test 

Toida M, Okumura Y, Swe Win K K et al. Characterization

of cells containing factor XIII subunit a in benign and 

malignant buccal lesions. Histochemical Journal 

1995;27(6):449-456. Not sensitivity or specificity of an 

identified test 

Tomkins A M, Drasar B S, James W P. Bacterial 

colonisation of jejunal mucosa in acute tropical sprue. 

Lancet 1975;1(7898):59-62. Not sensitivity or specificity of 

an identified test

Tomkins A M, James W P, Walters J H et al. 

Malabsorption in overland travellers to India. British 

Medical Journal 1974;3(5927):380-384. Not sensitivity or 

specificity of an identified test

Toner P G, Ferguson A. Intraepithelial cells in the human 

intestinal mucosa. Journal of Ultrastructure Research 

1971;34(3):329-344. Not sensitivity or specificity of an 

identified test 

Tonutti E, Visentini D, Bizzaro N et al. The role of 

antitissue transglutaminase assay for the diagnosis and 

monitoring of coeliac disease: a French-Italian multicentre 

study. Journal of Clinical Pathology 2003;56(5):389-393. 

Improper control group 

Torn C, Gupta M, Zake L N et al. Heterozygosity for 

MICA5.0/MICA5.1 and HLA-DR3-DQ2/DR4-DQ8 are 

independent genetic risk factors for latent autoimmune 

diabetes in adults. Hum Immunol 2003;64(9):902-909. Not 

sensitivity or specificity of an identified test 

A-478
Torrente F, Ashwood P, Day R et al. Small intestinal 

enteropathy with epithelial IgG and complement deposition

in children with regressive autism. Molecular Psychiatry

2002;7(4):375-82, 334. Not sensitivity or specificity of an

identified test 

Toscano V, Conti F G, Anastasi E et al. Importance of

gluten in the induction of endocrine autoantibodies and 

organ dysfunction in adolescent celiac patients. American 

Journal of Gastroenterology 2000;95(7):1742-1748. Not 

sensitivity or specificity of an identified test 

Tosi R, Tanigaki N, Polanco I et al. A radioimmunoassay

typing study of non-DQw2-associated celiac disease.

Clinical Immunology and Immunopathology

1986;39(1):168-172. Not sensitivity or specificity of an 

identified test 

Tosi R, Vismara D, Tanigaki N et al. Evidence that celiac 

disease is primarily associated with a DC locus allelic 

specificity. Clin Immunol Immunopathol 1983;28(3):395-

404. Not sensitivity or specificity of an identified test 

Townley R R. Diagnosis and treatment of coeliac disease in 

childhood. Medical Journal of Australia 1971;1(13):696-

698. Not sensitivity or specificity of an identified test 

Townley R R, Anderson C M. Coeliac disease. A review. 

Ergebnisse Der Inneren Medizin Und Kinderheilkunde 

1967;261-44. Not sensitivity or specificity of an identified

test 

Townley R R, Barnes G L. Intestinal biopsy in childhood. 

Archives of Disease in Childhood 1973;48(6):480-482. Not 

sensitivity or specificity of an identified test 

Trabace S, Cappellacci S, Ciccarone P et al. Psoriatic 

arthritis: A clinical, radiological and genetic study of 58

Italian patients. Acta Derm-Venereol Suppl 1994;-

(186):69-70. Not sensitivity or specificity of an identified 

test 

Trabace S, Giunta A, Rosso M et al. HLA-ABC and DR 

antigens in celiac disease. A study in a pediatric Italian 

population. Vox Sanguinis 1984;46(2):102-106. Not 

sensitivity or specificity of an identified test 

Trejdosiewicz L K, Malizia G, Oakes J et al. Expression of 

the common acute lymphoblastic leukaemia antigen 

(CALLA gp100) in the brush border of normal jejunum and 

jejunum of patients with coeliac disease. Journal of Clinical 

Pathology 1985;38(9):1002-1006. Not sensitivity or 

specificity of an identified test

Trevisiol C, Not T, Berti I et al. Screening for coeliac

disease in healthy blood donors at two immuno-transfusion 

centres in north-east Italy. Italian Journal of

Gastroenterology and Hepatology 1999;31(7):584-586. Not 

sensitivity or specificity of an identified test 

Trevisiol C, Ventura A, Baldas V et al. A reliable screening

procedure for coeliac disease in clinical practice. 

Scandinavian Journal of Gastroenterology 2002;37(6):679-

684. Improper control group 

Trier J S. Diagnostic value of peroral biopsy of the 

proximal small intestine. New England Journal of Medicine 

1971;285(26):1470-1473. Not sensitivity or specificity of

an identified test

Trier J S. Organ-culture methods in the study of 

gastrointestinal-mucosal function and development. New 

England Journal of Medicine 1976;295(3):150-155. Not 

sensitivity or specificity of an identified test 

Trier J S. Medical progress: Celiac sprue. New Engl J Med 

1991;325(24):1709-1719. Not sensitivity or specificity of

an identified test

Trier J S, Browning T H. Epithelial-cell renewal in cultured

duodenal biopsies in celiac sprue. New England Journal of

Medicine 1970;283(23):1245-1250. Not sensitivity or 

specificity of an identified test

Trier J S, Moxey P C, Fordtran J S et al. Ectopic gastric

mucosa in celiac sprue. Gastroenterology 1973;65(5):712-

727. Not sensitivity or specificity of an identified test 

Trieshmann H W, Abraham G N, Santucci E A. The 

characterization of human anti IgG autoantibodies by liquid 

isoelectric focussing. J Immunol 1975;114(1 I):176-181. 

Not sensitivity or specificity of an identified test

Trojani M, de Mascarel I, Coindre J M. Adenoid cystic 

carcinoma of the breast. Value of immunohistochemical 

study in diagnosis. Tumori 1991;77(2):130-135. Not 

sensitivity or specificity of an identified test 

Troncone R. Towards new diagnostic criteria for coeliac

disease. Ital J Pediat 2002;28(4):245-248. Review article 

Troncone R, Ferguson A. Anti-gliadin antibodies. Journal 

of Pediatric Gastroenterology and Nutrition 

1991;12(2):150-158. Not sensitivity or specificity of an 

identified test 

Troncone R, Caputo N, Micillo M et al. Immunologic and

intestinal permeability tests as predictors of relapse during 

gluten challenge in childhood coeliac disease. Scandinavian 

Journal of Gastroenterology 1994;29(2):144-147. Not 

sensitivity or specificity of an identified test 

Troncone R, Catassi C, Lambertini A et al. Latent coeliac

disease in Italy. Acta Paediatr Int J Paediatr

1995;84(11):1252-1257. Improper control group

Troncone R, Esposito C, Auricchio S. The role of tissue 

transglutaminase in the pathophysiology of coeliac disease. 

Minerva Biotecnol 2002;14(2):177-180. Not sensitivity or 

specificity of an identified test

Troncone R, Farris E, Donatiello A et al. In vitro gliadin

antibody production by peripheral blood mononuclear cells 

A-479
from patients with coeliac disease. Journal of Clinical &

Laboratory Immunology 1987;23(4):179-183. Not 

sensitivity or specificity of an identified test 

Troncone R, Gianfrani C, Mazzarella G et al. Majority of

gliadin-specific T-cell clones from celiac small intestinal

mucosa produce interferon-gamma and interleukin-4. 

Digestive Diseases and Sciences 1998;43(1):156-161. Not 

sensitivity or specificity of an identified test 

Troncone R, Greco L, Auricchio S. Gluten-sensitive 

enteropathy. Pediatric Clinics of North America

1996;43(2):355-373. Not sensitivity or specificity of an 

identified test 

Troncone R, Greco L, Mayer M et al. In siblings of celiac 

children, rectal gluten challenge reveals gluten sensitization

not restricted to celiac HLA. Gastroenterology

1996;111(2):318-324. Not sensitivity or specificity of an

identified test 

Troncone R, Greco L, Mayer M et al. Latent and potential 

coeliac disease. Acta paediatrica (Oslo, Norway :

1992).Supplement. 1996;41210-14. Not sensitivity or 

specificity of an identified test

Troncone R, Mayer M, Mugione P et al. 

Cellobiose/mannitol sugar permeability test in children in 

relation to jejunal morphometry. Italian Journal of

Gastroenterology 1995;27(9):489-493. Not sensitivity or 

specificity of an identified test

Troncone R, Mayer M, Spagnuolo F et al. Endomysial 

antibodies as unreliable markers for slight dietary

transgressions in adolescents with celiac disease. Journal of 

Pediatric Gastroenterology and Nutrition 1995;21(1):69-72. 

Not sensitivity or specificity of an identified test

Troncone R, Mazzarella G, Leone N et al. Gliadin activates

mucosal cell mediated immunity in cultured rectal mucosa

from coeliac patients and a subset of their siblings. Gut 

1998;43(4):484-489. Not sensitivity or specificity of an 

identified test 

Troncone R, Pignata C, Farris E. Suppressor cells and 

humoral immune response to gliadin in HLA-DR 3 or -DR 

7 positive healthy subjects. Immunol Clin Sper

1985;4(1):25-32. Not sensitivity or specificity of an 

identified test 

Troncone R, Pignata C, Farris E et al. A solid-phase 

radioimmunoassay for IgG gliadin antibodies using 125Ilabelled staphylococcal protein A. Journal of 

Immunological Methods 1983;63(2):163-170. Serology

<1990 

Troncone R, Starita A, Coletta S et al. Antigliadin

antibody, D-xylose, and cellobiose/mannitol permeability 

tests as indicators of mucosal damage in children with 

coeliac disease. Scandinavian Journal of Gastroenterology

1992;27(8):703-706. Not sensitivity or specificity of an 

identified test 

Troncone R, Vitale M, Donatiello A et al. A sandwich 

enzyme immunoassay for wheat gliadin. Journal of 

Immunological Methods 1986;92(1):21-23. Not sensitivity

or specificity of an identified test

Troncone Riccardo, Franzese Adriana, Mazzarella

Giuseppe et al. Gluten sensitivity in a subset of children

with insulin dependent diabetes mellitus. American Journal

of Gastroenterology 2003;98(3):590-595. Not sensitivity or 

specificity of an identified test

Tsao S W, Chew E C, Yam H F et al. Ultrastructural 

localization of a new surface membrane antigen (SQM1) 

related to squamous differentiation. In Vivo (Athens, 

Greece) 1989;3(6):367-374. Not sensitivity or specificity of 

an identified test

Tshibassu M, Geboes K, Eggermont E et al. Jejunal mucosa

lymphoid cell subsets and the expression of major 

histocompatibility complex antigens in children. European

Journal of Pediatrics 1987;146(3):251-256. Not sensitivity

or specificity of an identified test

Tuccari G, Barresi G. Simultaneous demonstration of 

mucins and lysozyme in duodeno-jejunal biopsies of 

coeliac infants. Basic and Applied Histochemistry

1984;28(2):177-182. Not sensitivity or specificity of an 

identified test 

Tucholski J, Kuret J, Johnson G V. Tau is modified by

tissue transglutaminase in situ: possible functional and

metabolic effects of polyamination. Journal of

Neurochemistry 1999;73(5):1871-1880. Not sensitivity or 

specificity of an identified test

Tucholski J, Lesort M, Johnson G V. Tissue 

transglutaminase is essential for neurite outgrowth in 

human neuroblastoma SH-SY5Y cells. Neuroscience 

2001;102(2):481-491. Not sensitivity or specificity of an

identified test 

Tucholski Janusz, Johnson Gail V. Tissue transglutaminase 

differentially modulates apoptosis in a stimuli-dependent 

manner. Journal of Neurochemistry 2002;81(4):780-791. 

Not sensitivity or specificity of an identified test

Tucholski Janusz, Johnson Gail V. Tissue transglutaminase 

directly regulates adenylyl cyclase resulting in enhanced

cAMP-response element-binding protein (CREB) 

activation. Journal of Biological Chemistry 

2003;278(29):26838-26843. Not sensitivity or specificity of 

an identified test

Tucker N T, Barghuthy F S, Prihoda T J et al. Antigliadin

antibodies detected by enzyme-linked immunosorbent 

assay as a marker of childhood celiac disease. Journal of

Pediatrics 1988;113(2):286-289. Serology <1990

Tuckova L, Karska K, Walters J R et al. Anti-gliadin 

antibodies in patients with celiac disease cross-react with 

enterocytes and human calreticulin. Clinical Immunology

A-480
and Immunopathology 1997;85(3):289-296. Not sensitivity

or specificity of an identified test

Tuckova L, Tlaskalova-Hogenova H, Farre M A et al. 

Molecular mimicry as a possible cause of autoimmune 

reactions in celiac disease? Antibodies to gliadin crossreact with epitopes on enterocytes. Clinical Immunology

and Immunopathology 1995;74(2):170-176. Not sensitivity

or specificity of an identified test

Tumer L, Altuntas B, Hasanoglu A et al. Pattern of human 

leukocyte antigens in Turkish children with celiac disease. 

Pediatrics International - Official Journal of the Japan 

Pediatric Society 2000;42(6):678-681. Improper control 

group 

Tumer L, Hasanoglu A, Aybay C. Endomysium antibodies 

in the diagnosis of celiac disease in short-statured children 

with no gastrointestinal symptoms. Pediatrics International 

- Official Journal of the Japan Pediatric Society 

2001;43(1):71-73. Improper control group 

Tuncyurek M. Immunoglobulin-containing cells on 

intestinal wall in coeliac disease. Aegean Med J 

1979;8(1):31-37. Not sensitivity or specificity of an 

identified test 

Tuomilehto-Wolf E, Tuomilehto J. Is the high incidence of

diabetes in young children diagnosed under the age of 4

years determined by genetic factors in Finland? The DIME 

Study Group. Diabete & Metabolisme 1993;19(1 Pt 2):167-

172. Not sensitivity or specificity of an identified test 

Turcu A, Leveque L, Bielefeld P et al. Adult celiac disease

and hemochromatosis. American Journal of

Gastroenterology 2000;95(12):3661-3662. Not sensitivity

or specificity of an identified test

Turner P M, Lorand L. Complexation of fibronectin with

tissue transglutaminase. Biochemistry 1989;28(2):628-635. 

Not sensitivity or specificity of an identified test

Turowski G, Ke cedil. Soluble HLA class I antigens as a

familial genetic background in coeliac disease. Cent-Eur J 

Immunol 2001;26(1):28-30. Not sensitivity or specificity of 

an identified test

Tursi A, Brandimarte G, Giorgetti G M. Sorbitol H2-breath 

test versus anti-endomysium antibodies for the diagnosis of 

subclinical/silent coeliac disease. Scandinavian Journal of

Gastroenterology 2001;36(11):1170-1172. Improper 

control group 

Tursi A, Brandimarte G, Giorgetti G M. Sorbitol H2-breath 

test versus anti-endomysium antibodies to assess 

histological recovery after gluten-free diet in coeliac 

disease. Digestive and Liver Disease - Official Journal of

the Italian Society of Gastroenterology and the Italian

Association for the Study of the Liver 2002;34(12):846-

850. Not sensitivity or specificity of an identified test 

Tursi A, Brandimarte G, Giorgetti G M. Lack of Usefulness 

of Anti-Transglutaminase Antibodies in Assessing 

Histologic Recovery After Gluten-Free Diet in Celiac 

Disease. Journal of Clinical Gastroenterology

2003;37(5):387-391. Not sensitivity or specificity of an 

identified test 

Tursi A, Brandimarte G, Giorgetti G M et al. Effectiveness

of the sorbitol HSUB2 breath test in detecting histological 

damage among relatives of coeliacs. Scandinavian Journal 

of Gastroenterology 2003;38(7):727-731. Not sensitivity or 

specificity of an identified test

Tursi A, Brandimarte G, Giorgetti G et al. Low prevalence

of antigliadin and anti-endomysium antibodies in

subclinical/silent celiac disease. American Journal of

Gastroenterology 2001;96(5):1507-1510. Improper control 

group 

Tursi A, Giorgetti G, Brandimarte G et al. Prevalence and

clinical presentation of subclinical/silent celiac disease in 

adults: an analysis on a 12-year observation. HepatoGastroenterology 2001;48(38):462-464. Not sensitivity or

specificity of an identified test

Tursi Antonio, Brandimarte Giovanni. The symptomatic

and histologic response to a gluten-free diet in patients with 

borderline enteropathy. Journal of Clinical 

Gastroenterology 2003;36(1):13-17. Not sensitivity or 

specificity of an identified test

Tursi Antonio, Brandimarte Giovanni, Giorgetti Gian et al. 

Prevalence of antitissue transglutaminase antibodies in 

different degrees of intestinal damage in celiac disease.

Journal of Clinical Gastroenterology 2003;36(3):219-221. 

Not sensitivity or specificity of an identified test

Tursi Antonio, Brandimarte Giovanni, Giorgetti 

GianMarco. High prevalence of small intestinal bacterial 

overgrowth in celiac patients with persistence of 

gastrointestinal symptoms after gluten withdrawal. 

American Journal of Gastroenterology 2003;98(4):839-843. 

Not sensitivity or specificity of an identified test

Turton C W, Turner-Warwick M, Owens R et al. Red cell 

folate levels, food antibodies and reticulin antibodies in

farmer's lung--is there an association with coeliac disease?.

British Journal of Diseases of the Chest 1983;77(4):397-

402. Not sensitivity or specificity of an identified test 

Tuysuz B, Dursun A, Kutlu T et al. HLA-DQ alleles in 

patients with celiac disease in Turkey. Tissue Antigens

2001;57(6):540-542. Unable to extract data 

Ueda E, Ohno S, Kuroki T et al. The eta isoform of protein 

kinase C mediates transcriptional activation of the human 

transglutaminase 1 gene. Journal of Biological Chemistry

1996;271(16):9790-9794. Not sensitivity or specificity of

an identified test

Ueki S, Takagi J, Saito Y. Dual functions of

transglutaminase in novel cell adhesion. Journal of Cell 

Science 1996;109 Pt 112727-2735. Not sensitivity or 

A-481
specificity of an identified test

Ugurlu S, Bartley G B, Gibson L E. Necrobiotic 

xanthogranuloma: long-term outcome of ocular and 

systemic involvement. American Journal of Ophthalmology

2000;129(5):651-657. Not sensitivity or specificity of an

identified test 

Uhlig H H, Lichtenfeld J, Osman A A et al. Evidence for

existence of coeliac disease autoantigens apart from tissue 

transglutaminase. European Journal of Gastroenterology &

Hepatology 2000;12(9):1017-1020. Not sensitivity or 

specificity of an identified test

Uhlig H, Osman A A, Tanev I D et al. Role of tissue 

transglutaminase in gliadin binding to reticular extracellular

matrix and relation to coeliac disease autoantibodies. 

Autoimmunity 1998;28(4):185-195. Not sensitivity or 

specificity of an identified test

Uibo O. Childhood celiac disease in Estonia: efficacy of the

IgA-class antigliadin antibody test in the search for new 

cases. Journal of Pediatric Gastroenterology and Nutrition

1994;18(1):53-55. Not sensitivity or specificity of an 

identified test 

Uibo O, Maaroos H I. Hospital screening of coeliac disease

in Estonian children by anti-gliadin antibodies of IgA class. 

Acta Paediatrica (Oslo, Norway - 1992) 1993;82(3):233-

234. Not sensitivity or specificity of an identified test 

Uibo O, Lambrechts A, Mascart-Lemone F. Human 

oesophagus: a convenient antigenic substrate for the 

determination of anti-endomysium antibodies in the 

serological diagnosis of coeliac disease. European Journal 

of Gastroenterology & Hepatology 1995;7(1):37-40. 

Improper control group 

Uibo O, Metskula K, Kukk T et al. Results of coeliac 

disease screening in Estonia in 1990-1994. Acta paediatrica 

(Oslo, Norway : 1992).Supplement. 1996;41239-41. Not 

sensitivity or specificity of an identified test 

Uibo O, Uibo R, Kleimola V et al. Serum IgA anti-gliadin 

antibodies in an adult population sample. High prevalence 

without celiac disease. Digestive Diseases and Sciences 

1993;38(11):2034-2037. Not sensitivity or specificity of an 

identified test 

Uibo R, Sullivan E P, Uibo O et al. Comparison of the 

prevalence of glutamic acid decarboxylase (GAD65) and 

gliadin antibodies (AGA) in a randomly selected adult 

estonian population. Hormone and Metabolic 

Research.Hormon- Und Stoffwechselforschung.Hormones 

Et Metabolisme 2001;33(9):564-567. Not sensitivity or

specificity of an identified test

Uil J J, van Elburg R M, Janssens P M et al. Sensitivity of a

hyperosmolar or "low"-osmolar test solution for sugar 

absorption in recognizing small intestinal mucosal damage 

in coeliac disease. Digestive and Liver Disease - Official

Journal of the Italian Society of Gastroenterology and the 

Italian Association for the Study of the Liver 

2000;32(3):195-200. Not sensitivity or specificity of an 

identified test 

Uil J J, van Elburg R M, Mulder C J et al. The value of the 

D-xylose test compared with the differential sugar 

absorption test in recognizing coeliac disease. Netherlands

Journal of Medicine 1996;49(2):68-72. Not sensitivity or 

specificity of an identified test

Uil J J, van Elburg R M, van Overbeek F M et al. Followup of treated coeliac patients: sugar absorption test and

intestinal biopsies compared. European Journal of

Gastroenterology & Hepatology 1996;8(3):219-223. Not 

sensitivity or specificity of an identified test 

Ukabam S O, Cooper B T. Small intestinal permeability as 

an indicator of jejunal mucosal recovery in patients with 

celiac sprue on a gluten-free diet. Journal of Clinical 

Gastroenterology 1985;7(3):232-236. Not sensitivity or

specificity of an identified test

Ukeda H, Ishii T, Shimizu Y et al. Immunochemical 

approach to characterize post-translational modification of

serum albumin using anti-glutaraldehyde-treated serum

albumin antibodies. Bioscience, Biotechnology, and 

Biochemistry 1997;61(2):341-346. Not sensitivity or 

specificity of an identified test

Umar S, Malavasi F, Mehta K. Post-translational 

modification of CD38 protein into a high molecular weight

form alters its catalytic properties. Journal of Biological 

Chemistry 1996;271(27):15922-15927. Not sensitivity or

specificity of an identified test

Underhill J A, Donaldson P T, Doherty D G et al. HLA 

DPB polymorphism in primary sclerosing cholangitis and 

primary biliary cirrhosis. Hepatology 1995;21(4):959-962. 

Not sensitivity or specificity of an identified test

Undlien D E, Friede T, Rammensee H-G et al. HLAencoded genetic predisposition in IDDM: DR4 subtypes 

may be associated with different degrees of protection.

Diabetes 1997;46(1):143-149. Not sensitivity or specificity

of an identified test 

Undlien D E, Kockum I, Ronningen K S et al. HLA 

associations in type 1 diabetes among patients not carrying

high-risk DR3-DQ2 or DR4-DQ8 haplotypes. Tissue 

Antigens 1999;54(6):543-551. Not sensitivity or specificity

of an identified test 

Unsworth D J. Tissue transglutaminase: The major 

autoantigen in coeliac disease. Cpd Bull Immunol Allergy 

2000;1(2):51-53. Not sensitivity or specificity of an 

identified test 

Unsworth D J, Brown D L. Serological screening suggests 

that adult coeliac disease is underdiagnosed in the UK and

increases the incidence by up to 12%. Gut 1994;35(1):61-

64. Not sensitivity or specificity of an identified test 

A-482
Unsworth D J, Dias J, Walker-Smith J A. Antigliadin and 

antireticulin antibodies in coeliac disease. Lancet 

1988;1(8587):705Not sensitivity or specificity of an 

identified test 

Unsworth D J, Johnson G D, Haffenden G et al. Binding of

wheat gliadin in vitro to reticulum in normal and dermatitis 

herpetiformis skin. Journal of Investigative Dermatology

1981;76(2):88-93. Not sensitivity or specificity of an 

identified test 

Unsworth D J, Kieffer M, Holborow E J et al. IgA antigliadin antibodies in coeliac disease. Clinical and

Experimental Immunology 1981;46(2):286-293. Serology

<1990 

Unsworth D J, Leonard J N, McMinn R M et al. Antigliadin antibodies and small intestinal mucosal damage in

dermatitis herpetiformis. British Journal of Dermatology

1981;105(6):653-658. Not sensitivity or specificity of an

identified test 

Unsworth D J, Lock R J, Harvey R F. Improving the 

diagnosis of coeliac disease in anaemic women. British 

Journal of Haematology 2000;111(3):898-901. Not 

sensitivity or specificity of an identified test 

Unsworth D J, Manuel P D, Walker-Smith J A et al. New 

immunofluorescent blood test for gluten sensitivity.

Archives of Disease in Childhood 1981;56(11):864-868. 

Not sensitivity or specificity of an identified test

Unsworth J, Hutchins P, Mitchell J et al. Flat small 

intestinal mucosa and autoantibodies against the gut 

epithelium. Journal of Pediatric Gastroenterology and 

Nutrition 1982;1(4):503-513. Not sensitivity or specificity

of an identified test 

Upchurch H F, Conway E, Patterson M K et al. 

Localization of cellular transglutaminase on the 

extracellular matrix after wounding: characteristics of the 

matrix bound enzyme. Journal of Cellular Physiology

1991;149(3):375-382. Not sensitivity or specificity of an

identified test 

Upchurch H F, Conway E, Patterson M K et al. Cellular 

transglutaminase has affinity for extracellular matrix. In

Vitro Cellular & Developmental Biology - Journal of the 

Tissue Culture Association 1987;23(11):795-800. Not 

sensitivity or specificity of an identified test 

Uray I P, Davies P J, Fesus L. Pharmacological separation 

of the expression of tissue transglutaminase and apoptosis 

after chemotherapeutic treatment of HepG2 cells.

Molecular Pharmacology 2001;59(6):1388-1394. Not 

sensitivity or specificity of an identified test 

Urbanski S J. Invited review/controversial issue: Can 

duodenal mucosa appear normal in gluten-sensitive 

enteropathy (celiac disease)?. Int J Surg Pathol 

1998;6(1):49-54. Review article 

Urso G, Longo A M, Bruno C M et al. The role of the 

duodenal perendoscopic biopsy in the adult coeliac disease: 

LE ROLE DE LA BIOPSIE DUODENALE 

PERENDOSCOPIQUE DANS LE DIAGNOSTIC DE LA

MALADIE COELIAQUE DE L'ADULTE. Acta Endosc 

1992;22(2):153-158. Not sensitivity or specificity of an 

identified test 

Urven L E, Abbott U K, Erickson C A. Distribution of 

extracellular matrix in the migratory pathway of avian 

primordial germ cells. Anat Rec 1989;224(1):14-21. Not 

sensitivity or specificity of an identified test 

Urven L E, Erickson C A, Abbott U K et al. Analysis of

germ line development in the chick embryo using an 

antimouse EC cell antibody. Development 

1988;103(2):299-304. Not sensitivity or specificity of an

identified test 

Usselmann B, Loft D E. An easy test for coeliac disease 

using human umbilical vein endothelial cells. European 

Journal of Gastroenterology & Hepatology 1996;8(10):947-

950. Review article 

Ussher R, Yeong M L, Stace N. Coeliac disease: incidence

and prevalence in Wellington 1985-92. New Zealand 

Medical Journal 1994;107(978):195-197. Not sensitivity or

specificity of an identified test

Usui T, Takagi J, Saito Y. Propolypeptide of von 

Willebrand factor serves as a substrate for factor XIIIa and

is cross-linked to laminin. Journal of Biological Chemistry

1993;268(17):12311-12316. Not sensitivity or specificity of 

an identified test

Vader L, Willemijn de, Ru Arnoud et al. Specificity of 

tissue transglutaminase explains cereal toxicity in celiac 

disease. Journal of Experimental Medicine

2002;195(5):643-649. Not sensitivity or specificity of an

identified test 

Vader Willemijn, Kooy Yvonne, van Veelen et al. The 

gluten response in children with celiac disease is directed 

toward multiple gliadin and glutenin peptides.

Gastroenterology 2002;122(7):1729-1737. Not sensitivity

or specificity of an identified test

Vahedi Kouroche, Mascart Francoise, Mary Jean et al. 

Reliability of antitransglutaminase antibodies as predictors 

of gluten-free diet compliance in adult celiac disease. 

American Journal of Gastroenterology 2003;98(5):1079-

1087. Not sensitivity or specificity of an identified test 

Vainio E. Immunoblotting analysis of antigliadin

antibodies in the sera of patients with dermatitis

herpetiformis and gluten-sensitive enteropathy.

International Archives of Allergy and Applied Immunology

1986;80(2):157-163. Not sensitivity or specificity of an 

identified test 

Vainio E, Varjonen E. Antibody response against wheat, 

rye, barley, oats and corn: comparison between glutenA-483
sensitive patients and monoclonal antigliadin antibodies. 

International Archives of Allergy and Immunology

1995;106(2):134-138. Not sensitivity or specificity of an

identified test 

Vainio E, Collin P, Lehtonen O P. Avidity of antigliadin 

IgA and IgG antibodies in gluten-sensitive enteropathy and 

dermatitis herpetiformis. Clinical Immunology and 

Immunopathology 1986;41(2):295-300. Not sensitivity or

specificity of an identified test

Vainio E, Kalimo K, Reunala T et al. Circulating IgA- and 

IgG-class antigliadin antibodies in dermatitis herpetiformis 

detected by enzyme-linked immunosorbent assay. Archives

of Dermatological Research 1983;275(1):15-18. Not 

sensitivity or specificity of an identified test 

Vainio E, Kalimo K, Viander M et al. Antigliadin

antibodies and gluten-free diet in dermatitis herpetiformis. 

Acta Dermato-Venereologica 1985;65(4):291-297. Not 

sensitivity or specificity of an identified test 

Vainio E, Kosnai I, Hallstrom O et al. Antigliadin and 

antireticulin antibodies in children with dermatitis

herpetiformis. Journal of Pediatric Gastroenterology and 

Nutrition 1986;5(5):735-739. Not sensitivity or specificity

of an identified test 

Valdimarsson T, Toss G, Lofman O et al. Three years'

follow-up of bone density in adult coeliac disease: 

Significance of secondary hyperparathyroidism. 

Scandinavian Journal of Gastroenterology 2000;35(3):274-

280. Not sensitivity or specificity of an identified test 

Valdimarsson T, Toss G, Ross I et al. Bone mineral density

in coeliac disease. Scandinavian Journal of 

Gastroenterology 1994;29(5):457-461. Not sensitivity or 

specificity of an identified test

Valdovinos M A, Camilleri M, Zimmerman B R. Chronic

diarrhea in diabetes mellitus: mechanisms and an approach

to diagnosis and treatment. Mayo Clinic Proceedings 

1993;68(7):691-702. Not sensitivity or specificity of an 

identified test 

Valentino R, Savastano S, Tommaselli A P et al. 

Prevalence of coeliac disease in patients with thyroid 

autoimmunity. Hormone Research 1999;51(3):124-127. 

Not sensitivity or specificity of an identified test

Valentino Rossella, Savastano Silvia, Maglio Maria et al. 

Markers of potential coeliac disease in patients with 

Hashimoto's thyroiditis. European Journal of

Endocrinology / European Federation of Endocrine 

Societies 2002;146(4):479-483. Not sensitivity or

specificity of an identified test

Valenzuela R, Shainoff J R, DiBello P M et al.

Immunoelectrophoretic and immunohistochemical 

characterizations of fibrinogen derivatives in

atherosclerotic aortic intimas and vascular prosthesis 

pseudo-intimas. American Journal of Pathology

1992;141(4):861-880. Not sensitivity or specificity of an

identified test 

Valerio G, Maiuri L, Troncone R et al. Severe clinical

onset of diabetes and increased prevalence of other 

autoimmune diseases in children with coeliac disease 

diagnosed before diabetes mellitus. Diabetologia 

2002;45(12):1719-1722. Not sensitivity or specificity of an 

identified test 

Valeski J E, Kumar V, Beutner E H et al. Immunology of 

celiac disease: tissue and species specificity of endomysial

and reticulin antibodies. International Archives of Allergy

and Applied Immunology 1990;93(1):1-7. Not sensitivity

or specificity of an identified test

Valet G, Ormerod M G, Warnecke H H et al. Sensitive

three-parameter flow-cytometric detection of abnormal 

cells in human cervical cancers: a pilot study. Journal of

Cancer Research and Clinical Oncology 1981;102(2):177-

184. Not sensitivity or specificity of an identified test 

Valletta E A, Mastella G. Adherence to gluten-free diet and

serum antigliadin antibodies in celiac disease. Digestion 

1990;47(1):20-23. Not sensitivity or specificity of an 

identified test 

Valletta E A, Trevisiol D, Mastella G. IgA anti-gliadin

antibodies in the monitoring of gluten challenge in celiac 

disease. Journal of Pediatric Gastroenterology and

Nutrition 1990;10(2):169-173. Not sensitivity or specificity

of an identified test 

Valnickova Z, Enghild J J. Human procarboxypeptidase U, 

or thrombin-activable fibrinolysis inhibitor, is a substrate

for transglutaminases. Evidence for transglutaminasecatalyzed cross-linking to fibrin. Journal of Biological 

Chemistry 1998;273(42):27220-27224. Not sensitivity or

specificity of an identified test

Van Beers E H, Einerhand A W C, Taminiau J A J M et al. 

Pediatric duodenal biopsies: Mucosal morphology and 

glycohydrolase expression do not change along the 

duodenum. Journal of Pediatric Gastroenterology and 

Nutrition 1998;26(2):186-193. Not sensitivity or specificity

of an identified test 

van Belzen M J, Mulder C J, Pearson P L et al. The tissue 

transglutaminase gene is not a primary factor predisposing 

to celiac disease. American Journal of Gastroenterology

2001;96(12):3337-3340. Not sensitivity or specificity of an 

identified test 

Van Belzen, Martine J, Meijer Jos W R et al. A major nonHLA locus in celiac disease maps to chromosome 19.

Gastroenterology 2003;125(4):1032-1041. Improper 

control group 

Van de, Kamer J H. Coeliac disease: A historical review. Ir

Med J 1974;67(15):405-406. Not sensitivity or specificity

of an identified test 

A-484
van de, Staak W J, van Tongeren J H. Dermatitis 

herpetiformis and pathological changes of the mucous 

membrane of the small intestine. Dermatologica

1970;140(4):231-241. Not sensitivity or specificity of an

identified test 

van de, Wal Y, Kooy Y M et al. Peptide binding

characteristics of the coeliac disease-associated

DQ(alpha1*0501, beta1*0201) molecule. Immunogenetics 

1996;44(4):246-253. Not sensitivity or specificity of an 

identified test 

van de, Wal Y, Kooy Y M et al. Unique peptide binding 

characteristics of the disease-associated DQ(alpha 1*0501, 

beta 1*0201) vs the non-disease-associated DQ(alpha 

1*0201, beta 1*0202) molecule. Immunogenetics 

1997;46(6):484-492. Not sensitivity or specificity of an 

identified test 

van de, Wal Y, Kooy Y M et al. Small intestinal T cells of 

celiac disease patients recognize a natural pepsin fragment 

of gliadin. Proceedings of the National Academy of 

Sciences of the United States of America 

1998;95(17):10050-10054. Not sensitivity or specificity of 

an identified test

van de, Wal Y, Kooy Y M et al. Glutenin is involved in the 

gluten-driven mucosal T cell response. European Journal of

Immunology 1999;29(10):3133-3139. Not sensitivity or

specificity of an identified test

van de, Wal Y, Kooy Y et al. Selective deamidation by

tissue transglutaminase strongly enhances gliadin-specific 

T cell reactivity. Journal of Immunology (Baltimore, Md.- 

1950) 1998;161(4):1585-1588. Not sensitivity or specificity

of an identified test 

van de, Wal Y, Kooy Y et al. Cutting edge: Selective

deamidation by tissue transglutaminase strongly enhances 

gliadin-specific T cell reactivity. J Immunol 

1998;161(4):1585-1588. Not sensitivity or specificity of an 

identified test 

van de, Wal Y, Kooy Y et al. Coeliac disease: it takes three

to tango!. Gut 2000;46(5):734-737. Review article 

van den, Bosch H C, Tham R T et al. Celiac disease: smallbowel enteroclysis findings in adult patients treated with a

gluten-free diet. Radiology 1996;201(3):803-808. Not 

sensitivity or specificity of an identified test 

Van Der, Burg S H, Ressing M E et al. Natural T-helper

immunity against human papillomavirus type 16 (HPV16) 

E7-derived peptide epitopes in patients with HPV16-

positive cervical lesions: Identification of 3 human

leukocyte antigen class II-restricted epitopes. Int J Cancer 

2001;91(5):612-618. Not sensitivity or specificity of an 

identified test 

van der, Zee J M, Heurkens A H et al. Characterization of 

anti-endothelial antibodies in patients with rheumatoid

arthritis complicated by vasculitis. Clinical and 

Experimental Rheumatology 1991;9(6):589-594. Not 

sensitivity or specificity of an identified test 

van der, Zee J M, Miltenburg A M et al. Antiendothelial 

cell antibodies in systemic lupus erythematosus: enhanced 

antibody binding to interleukin-1-stimulated endothelium. 

International Archives of Allergy and Immunology

1994;104(2):131-136. Not sensitivity or specificity of an

identified test 

van Elburg R M, Uil J J, Mulder C J et al. Intestinal

permeability in patients with coeliac disease and relatives

of patients with coeliac disease. Gut 1993;34(3):354-357. 

Not sensitivity or specificity of an identified test

van Lith M, van Ham M, Neefjes J. Novel polymorphisms 

in HLA-DOA and HLA-DOB in B-cell malignancies. 

Immunogenetics 2002;54(8):591-595. Not sensitivity or

specificity of an identified test

Van Mook W N K A, Bourass-Bremer I H D N, Bos L P et 

al. The outcome of esophagogastroduodenoscopy (EGD) in 

asymptomatic outpatients with iron deficiency anemia after

a negative colonoscopy. Eur J Intern Med 2001;12(2):122-

126. Not sensitivity or specificity of an identified test 

van Rood J J. HLA as regulator. Annals of the Rheumatic 

Diseases 1984;43(5):665-672. Not sensitivity or specificity

of an identified test 

van Rood J J. The impact of the major histocompatibility

complex on graft survival and disease susceptibility.

Genetics 1975;79 Suppl277-291. Not sensitivity or 

specificity of an identified test

van Spreeuwel J P, Meijer C J, Rosekrans P C et al.

Immunoglobulin-containing cells in gastrointestinal 

pathology--diagnostic applications. Pathology Annual 

1986;21(Pt 1):295-310. Not sensitivity or specificity of an

identified test 

Van Stirum J, Baerlocher K, Fanconi A. The incidence of 

coeliac disease in children in Switzerland. Helv Paediatr 

Acta 1982;37(5):421-430. Not sensitivity or specificity of

an identified test

van Straaten E A, Koster-Kamphuis L, Bovee-Oudenhoven 

I M et al. Increased urinary nitric oxide oxidation products 

in children with active coeliac disease. Acta Paediatrica

(Oslo, Norway - 1992) 1999;88(5):528-531. Not sensitivity

or specificity of an identified test

van der, Sluijs V, Vermes I. IgG autoantibodies against 

tissue transglutaminase in relation to antinuclear antibodies. 

Clinical Chemistry 2001;47(5):952-954. Not sensitivity or 

specificity of an identified test

Vancikova Z, Chlumecky V, Sokol D et al. The serologic 

screening for celiac disease in the general population 

(blood donors) and in some high-risk groups of adults 

(patients with autoimmune diseases, osteoporosis and 

infertility) in the Czech republic. Folia Microbiologica 

A-485
2002;47(6):753-758. Not sensitivity or specificity of an 

identified test 

Vancikova Z, Kocna P, Tuckova L et al. Characterization

of human, mouse and rabbit anti-gliadin antibodies by

ELISA and western blotting. Folia Microbiologica

1995;40(6):659-664. Not sensitivity or specificity of an 

identified test 

Vandermeeren M, Daneels G, Bergers M et al. 

Development and application of monoclonal antibodies 

against SKALP/elafin and other trappin family members.

Arch Dermatol Res 2001;293(7):343-349. Not sensitivity

or specificity of an identified test

Vardaman C, Albores-Saavedra J. Clear cell carcinomas of 

the gallbladder and extrahepatic bile ducts. American

Journal of Surgical Pathology 1995;19(1):91-99. Not 

sensitivity or specificity of an identified test 

Variend S, Phillips A D, Walker-Smith J A. The small 

intestinal mucosal biopsy in childhood. Perspectives in 

Pediatric Pathology 1984;8(1):57-78. Not sensitivity or

specificity of an identified test

Variend S, Placzek M, Raafat F et al. Small intestinal 

mucosal fat in childhood enteropathies. Journal of Clinical 

Pathology 1984;37(4):373-377. Not sensitivity or

specificity of an identified test

Varjonen E, Kalimo K, Savolainen J et al. IgA and IgG 

binding components of wheat, rye, barley and oats 

recognized by immunoblotting analysis with sera from 

adult atopic dermatitis patients. International Archives of

Allergy and Immunology 1996;111(1):55-63. Not 

sensitivity or specificity of an identified test 

Varjonen E, Vainio E, Kalimo K. Antigliadin IgE--

indicator of wheat allergy in atopic dermatitis. Allergy 

2000;55(4):386-391. Not sensitivity or specificity of an 

identified test 

Varkonyi A, Boda M, Endreffy E et al. Coeliac disease:

always something to discover. Scandinavian Journal of

Gastroenterology.Supplement 1998;228122-129. Not 

sensitivity or specificity of an identified test 

Varljen J, Persic M, Milin C et al. Intestinal alkaline 

phosphatase and disaccharidases in children with gluten

enteropathy. Acta Pharm 1994;44(4):319-324. Not 

sensitivity or specificity of an identified test 

Vartdal F, Johansen B H, Friede T et al. The peptide 

binding motif of the disease associated HLA-DQ (alpha 1* 

0501, beta 1* 0201) molecule. European Journal of 

Immunology 1996;26(11):2764-2772. Not sensitivity or

specificity of an identified test

Vasmant D, Feldmann G, Fontaine J L. Ultrastructural 

localization of concanavalin a surface receptors on brushborder enterocytes in normal children and during coeliac 

disease. Pediatric Research 1982;16(6):441-445. Not 

sensitivity or specificity of an identified test 

Vatay Agnes, Rajczy Katalin, Pozsonyi Eva et al.

Differences in the genetic background of latent 

autoimmune diabetes in adults (LADA) and type 1 diabetes 

mellitus. Immunology Letters 2002;84(2):109-115. Not

sensitivity or specificity of an identified test 

Vazquez H, Cabanne A, Sugai E et al. Serological markers

identify histologically latent coeliac disease among firstdegree relatives. European Journal of Gastroenterology & 

Hepatology 1996;8(1):15-21. Not sensitivity or specificity

of an identified test 

Vazquez H, Sugai E, Pedreira S et al. Screening for 

asymptomatic celiac sprue in families. Journal of Clinical

Gastroenterology 1995;21(2):130-133. Improper control 

group 

Vecchi M, Folli C, Donato M F et al. High rate of positive 

anti-tissue transglutaminase antibodies in chronic liver

disease. Role of liver decompensation and of the antigen 

source. Scandinavian Journal of Gastroenterology

2003;38(1):50-54. Not sensitivity or specificity of an 

identified test 

Vecchi M, Torgano G, De Franchis R et al. Evidence of 

altered structural and secretory glycoconjugates in the 

jejunal mucosa of patients with gluten sensitive enteropathy 

and subtotal villous atrophy. Gut 1989;30(6):804-810. Not 

sensitivity or specificity of an identified test 

Veitch A M, Kelly P, Zulu I S et al. Tropical enteropathy: a

T-cell-mediated crypt hyperplastic enteropathy. European 

Journal of Gastroenterology & Hepatology

2001;13(10):1175-1181. Not sensitivity or specificity of an 

identified test 

Velasco P T, Karush F, Lorand L. Transamidating activities

of factor XIIIa and of transglutaminases, measured by an 

ELISA procedure. Biochemical and Biophysical Research

Communications 1988;152(2):505-511. Not sensitivity or

specificity of an identified test

Velluzzi F, Caradonna A, Boy M F et al. Thyroid and 

celiac disease: clinical, serological, and echographic study.

American Journal of Gastroenterology 1998;93(6):976-979. 

Not sensitivity or specificity of an identified test

Veloso F T, Saleiro J V. Small-bowel changes in recurrent

ulceration of the mouth. Hepato-Gastroenterology

1987;34(1):36-37. Not sensitivity or specificity of an 

identified test 

Ventura A, Martelossi S. The old and new coeliac disease.

Eur J Pediatr Dermatol 1995;5(2):87-94. Not sensitivity or

specificity of an identified test

Ventura A, Facchini S, Amantidu C et al. Searching for 

celiac disease in pediatric general practice. Clin Pediatr 

2001;40(10):575-577. Not sensitivity or specificity of an

A-486
identified test 

Venturini I, Cosenza R, Miglioli L et al. Adult celiac

disease and primary sclerosing cholangitis: two case 

reports. Hepato-Gastroenterology 1998;45(24):2344-2347. 

Not sensitivity or specificity of an identified test

Verbeke S, Gotteland M, Fernandez M et al. Basement 

membrane and connective tissue proteins in intestinal

mucosa of patients with coeliac disease. Journal of Clinical 

Pathology 2002;55(6):440-445. Not sensitivity or

specificity of an identified test

Verderio E A M, Telci D, Okoye A et al. A Novel RGDindependent Cell Adhesion Pathway Mediated by

Fibronectin-bound Tissue Transglutaminase Rescues Cells 

from Anoikis. J Biol Chem 2003;278(43):42604-42614. 

Not sensitivity or specificity of an identified test

Verderio E, Coombes A, Jones R A et al. Role of the crosslinking enzyme tissue transglutaminase in the biological 

recognition of synthetic biodegradable polymers. Journal of 

Biomedical Materials Research 2001;54(2):294-304. Not 

sensitivity or specificity of an identified test 

Verderio E, Nicholas B, Gross S et al. Regulated

expression of tissue transglutaminase in Swiss 3T3 

fibroblasts: effects on the processing of fibronectin, cell 

attachment, and cell death. Experimental Cell Research

1998;239(1):119-138. Not sensitivity or specificity of an

identified test 

Veres G, Helin T, Arato A et al. Increased expression of 

intercellular adhesion molecule-1 and mucosal adhesion 

molecule alpha4beta7 integrin in small intestinal mucosa of 

adult patients with food allergy. Clinical Immunology

(Orlando, Fla.) 2001;99(3):353-359. Not sensitivity or 

specificity of an identified test

Verge C F, Gianani R, Kawasaki E et al. Prediction of type

I diabetes in first-degree relatives using a combination of

insulin, GAD, and ICA512bdc/IA-2 autoantibodies. 

Diabetes 1996;45(3 SUPPL.):926-933. Not sensitivity or 

specificity of an identified test

Verge C F, Howard N J, Rowley M J et al. Anti-glutamate

decarboxylase and other antibodies at the onset of

childhood IDDM: a population-based study. Diabetologia 

1994;37(11):1113-1120. Not sensitivity or specificity of an 

identified test 

Verkarre V, Asnafi V, Lecomte T et al. Refractory coeliac 

sprue is a diffuse gastrointestinal disease. Gut 

2003;52(2):205-211. Not sensitivity or specificity of an 

identified test 

Verkasalo M. HLA and lymphocyte receptors for gliadin

peptides. Klinische Padiatrie 1985;197(4):334-335. Not 

sensitivity or specificity of an identified test 

Verkasalo M A. Adherence of gliadin fractions to

lymphocytes in coeliac disease. Lancet 1982;1(8286):1384-

1386. Not sensitivity or specificity of an identified test 

Verkasalo M A, Arato A, Savilahti E et al. Effect of diet 

and age on jejunal and circulating lymphocyte subsets in 

children with coeliac disease: persistence of CD4-8-

intraepithelial T cells through treatment. Gut 

1990;31(4):422-425. Not sensitivity or specificity of an 

identified test 

Verkasalo M, Kuitunen P, Leisti S et al. Growth failure

from symptomless celiac disease. A study of 14 patients. 

Helvetica Paediatrica Acta 1978;33(6):489-495. Not 

sensitivity or specificity of an identified test 

Verkasalo M, Kuitunen P, Tiilikainen A et al. HLA 

antigens in intestinal cow's milk allergy. Acta Paediatrica

Scandinavica 1983;72(1):19-22. Not sensitivity or

specificity of an identified test

Verkasalo M, Tiilikainen A, Kuitunen P et al. HLA 

antigens and atopy in children with coeliac disease. Gut

1983;24(4):306-310. Not sensitivity or specificity of an 

identified test 

Vermeer B J, Lindeman J, Harst-Oostveen C J et al. The 

immunoglobulin-bearing cells in the lamina propria and the 

clinical response to a gluten-free diet in dermatitis

herpetiformis. Archives for Dermatological 

Research.Archiv Fur Dermatologische Forschung

1977;258(3):223-230. Not sensitivity or specificity of an

identified test 

Vermelin L, Lecolle S, Septier D et al. Apoptosis in human 

and rat dental pulp. European Journal of Oral Sciences 

1996;104(5-6):547-553. Not sensitivity or specificity of an 

identified test 

Verreck F A W, Van De, Poel A et al. Identification of an

HLA-DQ2 peptide binding motif and HLA-DPw3-hound 

self-peptide by pool sequencing. Eur J Immunol 

1994;24(2):375-379. Not sensitivity or specificity of an 

identified test 

Vesy C J, Greenson J K, Papp A C et al. Evaluation of 

celiac disease biopsies for adenovirus 12 DNA using a 

multiplex polymerase chain reaction. Modern Pathology - 

an Official Journal of the United States and Canadian 

Academy of Pathology, Inc 1993;6(1):61-64. Not 

sensitivity or specificity of an identified test 

Vezza R, Habib A, FitzGerald G A. Differential signaling

by the thromboxane receptor isoforms via the novel GTPbinding protein, Gh. Journal of Biological Chemistry

1999;274(18):12774-12779. Not sensitivity or specificity of 

an identified test

Victora C G, Barros F C, Horta B L et al. Short-term

benefits of catch-up growth for small-for-gestational-age 

infants. International Journal of Epidemiology

2001;30(6):1325-1330. Not sensitivity or specificity of an

identified test 

A-487
Vielh P, Validire P, Kheirallah S et al. Paget's disease of

the nipple without clinically and radiologically detectable

breast tumor. Histochemical and immunohistochemical 

study of 44 cases. Pathology, Research and Practice 

1993;189(2):150-155. Not sensitivity or specificity of an

identified test 

Viken H D, Paulsen G, Drover S et al. Influence on

antibody recognition of amino acid substitutions in the cleft

of HLA-DQ2 molecules: Suggestive evidence of peptidedependent epitopes. Hum Immunol 1995;44(2):63-69. Not 

sensitivity or specificity of an identified test 

Viken H D, Paulsen G, Sollid L M et al. Characterization of 

an HLA-DQ2-specific monoclonal antibody. Influence of 

amino acid substitutions in DQ beta 1*0202. Human 

Immunology 1995;42(4):319-327. Not sensitivity or 

specificity of an identified test

Viken H D, Thoresen A B, Thorsby E et al. The cytotoxic 

HLA-DQ3 reactive human hybridoma antibody 4166 that 

may distinguish DQ7+8 from DQ9. Hum Immunol 

1995;42(4):281-288. Not sensitivity or specificity of an 

identified test 

Viken H D, Thorsby E, Gaudernack G. Characterization 

and epitope mapping of four HLA class II reactive mouse 

monoclonal antibodies using transfected L cells and human 

cells transfected with mutants of DQB1(*)0302. Tissue 

Antigens 1995;45(4):250-257. Not sensitivity or specificity

of an identified test 

Vila TJ, Medina ZM, Cusi S, V et al. Computerized 

morphometric analysis of jejunal biopsy: A simple and 

useful method for the routine diagnosis of coeliac disease. J 

Clin Nutr Gastroenterol 1989; 4(4):173-182. Unable to 

obtain full article

Villanacci V, Facchetti F, Pillan N et al. Expression of cell

adhesion molecules in jejunum biopsies of children with 

coeliac disease. Italian Journal of Gastroenterology

1993;25(3):109-116. Not sensitivity or specificity of an 

identified test 

Visakorpi J K. The diagnosis of coeliac disease. Ann Nestle 

1993;51(2):43-49. Not sensitivity or specificity of an 

identified test 

Visakorpi J K, Kuitunen P, Savilahti E. Frequency and 

nature of relapses in children suffering from the 

malabsorption syndrome with gluten intolerance. Acta

Paediatrica Scandinavica 1970;59(5):481-486. Not 

sensitivity or specificity of an identified test 

Viskari H, Paronen J, Keskinen P et al. Humoral beta-cell 

autoimmunity is rare in patients with the congenital rubella 

syndrome. Clinical and Experimental Immunology

2003;133(3):378-383. Not sensitivity or specificity of an

identified test 

Visser H, Vos K, Zanelli E et al. Sarcoid arthritis: Clinical

characteristics, diagnostic aspects, and risk factors. Ann 

Rheum Dis 2002;61(6):499-504. Not sensitivity or

specificity of an identified test

Vitoria J C. Expert's comments. J Postgrad Med 

2003;49(1):24Not sensitivity or specificity of an identified

test 

Vitoria J C, Arrieta A, Arranz C et al. Antibodies to 

gliadin, endomysium, and tissue transglutaminase for the 

diagnosis of celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 1999;29(5):571-574. 

Improper control group 

Vitoria J C, Arrieta A, Astigarraga I et al. Use of

serological markers as a screening test in family members

of patients with celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 1994;19(3):304-309. Not

sensitivity or specificity of an identified test 

Vitoria J C, Castano L, Rica I et al. Association of insulindependent diabetes mellitus and celiac disease: a study 

based on serologic markers. Journal of Pediatric 

Gastroenterology and Nutrition 1998;27(1):47-52. Not

sensitivity or specificity of an identified test 

Vivas Santiago, Ruiz de, Morales Jose M et al. Human 

recombinant anti-transglutaminase antibody testing is

useful in the diagnosis of silent coeliac disease in a selected 

group of at-risk patients. European Journal of 

Gastroenterology & Hepatology 2003;15(5):479-483. Not 

sensitivity or specificity of an identified test 

Vjero Katerina, Martucci Susi, Alvisi Costanza et al.

Defining a proper setting for endoscopy in coeliac disease.

European Journal of Gastroenterology & Hepatology

2003;15(6):675-678. Not sensitivity or specificity of an 

identified test 

Vogelsang H, Hanel S, Steiner B et al. Diagnostic duodenal 

bulb biopsy in celiac disease. Endoscopy 2001;33(4):336-

340. Not sensitivity or specificity of an identified test 

Vogelsang H, Oberhuber G, Wyatt J. Lymphocytic gastritis 

and gastric permeability in patients with celiac disease.

Gastroenterology 1996;111(1):73-77. Not sensitivity or

specificity of an identified test

Vogelsang H, Schwarzenhofer M, Oberhuber G. Changes 

in gastrointestinal permeability in celiac disease. Digestive

Diseases (Basel, Switzerland) 1998;16(6):333-336. Not 

sensitivity or specificity of an identified test 

Vogelsang H, Schwarzenhofer M, Granditsch G et al. In 

vitro production of endomysial antibodies in cultured 

duodenal mucosa from patients with celiac disease. 

American Journal of Gastroenterology 1999;94(4):1057-

1061. Not sensitivity or specificity of an identified test 

Vogelsang H, Schwarzenhofer M, Steiner B et al. In vivo 

and in vitro permeability in coeliac disease. Alimentary 

Pharmacology & Therapeutics 2001;15(9):1417-1425. Not 

sensitivity or specificity of an identified test 

A-488
Vogelsang H, Wyatt J, Penner E et al. Screening for celiac 

disease in first-degree relatives of patients with celiac 

disease by lactulose/mannitol test. American Journal of

Gastroenterology 1995;90(10):1838-1842. Not sensitivity

or specificity of an identified test

Vogelsang Harald, Panzer Simon, Mayr Wolfgang R et al. 

Distribution of HLA class I alleles differs in celiac disease

patients according to age of onset. Digestive Diseases and

Sciences 2003;48(3):611-614. Not sensitivity or specificity

of an identified test 

Vollberg T M, George M D, Nervi C et al. Regulation of 

type I and type II transglutaminase in normal human 

bronchial epithelial and lung carcinoma cells. American 

Journal of Respiratory Cell and Molecular Biology

1992;7(1):10-18. Not sensitivity or specificity of an 

identified test 

Volokhina E B, Hulshof R, Haanen C et al. Tissue 

transglutaminase mRNA expression in apoptotic cell death. 

Apoptosis 2003;8(6):673-679. Not sensitivity or specificity

of an identified test 

Volta U, Bellentani S, Bianchi F B et al. High prevalence

of celiac disease in Italian general population. Digestive 

Diseases and Sciences 2001;46(7):1500-1505. Not 

sensitivity or specificity of an identified test 

Volta U, Bonazzi C, Baldoni A M et al. Clinical

presentation of adult coeliac disease. Ann Med Interne

(Paris) 1988;139(2):123-124. Not sensitivity or specificity

of an identified test 

Volta U, Bonazzi C, Lazzari R et al. Immunoglobulin A 

antigliadin antibodies in jejunal juice: markers of severe 

intestinal damage in coeliac children. Digestion

1988;39(1):35-39. Not sensitivity or specificity of an 

identified test 

Volta U, Bonazzi C, Pisi E et al. Antigliadin and 

antireticulin antibodies in coeliac disease and at onset of 

diabetes in children. Lancet 1987;2(8566):1034-1035. Not 

sensitivity or specificity of an identified test 

Volta U, Cassani F, De Franchis R et al. Antibodies to 

gliadin in adult coeliac disease and dermatitis

herpetiformis. Digestion 1984;30(4):263-270. Serology

<1990 

Volta U, Corazza G R, Frisoni M et al. IgA antigliadin 

antibodies and persistence of jejunal lesions in adult coeliac 

disease. Digestion 1990;47(2):111-114. Not sensitivity or 

specificity of an identified test

Volta U, De Franceschi L, Lari F et al. Coeliac disease 

hidden by cryptogenic hypertransaminasaemia. Lancet

1998;352(9121):26-29. Not sensitivity or specificity of an

identified test 

Volta U, De Franceschi L, Molinaro N et al. Frequency and 

significance of anti-gliadin and anti-endomysial antibodies

in autoimmune hepatitis. Digestive Diseases and Sciences 

1998;43(10):2190-2195. Not sensitivity or specificity of an 

identified test 

Volta U, De Franceschi L, Molinaro N et al. Organ-specific 

autoantibodies in coeliac disease: do they represent an

epiphenomenon or the expression of associated 

autoimmune disorders?. Italian Journal of Gastroenterology

and Hepatology 1997;29(1):18-21. Not sensitivity or 

specificity of an identified test

Volta U, De Giorgio R, Petrolini N et al. Clinical findings

and anti-neuronal antibodies in coeliac disease with 

neurological disorders. Scandinavian Journal of

Gastroenterology 2002;37(11):1276-1281. Not sensitivity

or specificity of an identified test

Volta U, Granito A, De Franceschi L et al. Anti tissue

transglutaminase antibodies as predictors of silent coeliac 

disease in patients with hypertransaminasaemia of

unknown origin. Digestive and Liver Disease - Official 

Journal of the Italian Society of Gastroenterology and the 

Italian Association for the Study of the Liver 

2001;33(5):420-425. Not sensitivity or specificity of an 

identified test 

Volta U, Lazzari R, Bianchi F B et al. Antibodies to dietary 

antigens in coeliac disease. Scandinavian Journal of 

Gastroenterology 1986;21(8):935-940. Not sensitivity or 

specificity of an identified test

Volta U, Lazzari R, Guidetti C S et al. Multicenter study on

the reproducibility of antigliadin (AGA) and 

antiendomysial antibodies (EmA) in celiac sprue screening. 

The Tenue Club Group. Journal of Clinical 

Gastroenterology 1994;19(1):81-82. Improper control 

group 

Volta U, Lenzi M, Lazzari R et al. Antibodies to gliadin 

detected by immunofluorescence and a micro-ELISA 

method: markers of active childhood and adult coeliac 

disease. Gut 1985;26(7):667-671. Improper control group 

Volta U, Molinaro N, De Franceschi L et al. Human 

umbilical cord as substrate for IgA antiendomysial 

antibodies allows large scale screening for celiac sprue. 

Journal of Clinical Gastroenterology 1996;23(1):18-20. 

Improper control group 

Volta U, Molinaro N, De Franceschi L et al. IFL- and 

ELISA-antigliadin antibodies recognize different antigenic 

reactivities from those of R1-antireticulin and

antiendomysial antibodies. Italian Journal of

Gastroenterology 1995;27(2):64-68. Not sensitivity or 

specificity of an identified test

Volta U, Molinaro N, De Franchis R et al. Correlation 

between IgA antiendomysial antibodies and subtotal villous 

atrophy in dermatitis herpetiformis. Journal of Clinical

Gastroenterology 1992;14(4):298-301. Not sensitivity or 

specificity of an identified test

A-489
Volta U, Molinaro N, Fratangelo D et al. IgA antibodies to

jejunum. Specific immunity directed against target organ of

gluten-sensitive enteropathy. Digestive Diseases and 

Sciences 1994;39(9):1924-1929. Not sensitivity or

specificity of an identified test

Volta U, Molinaro N, Fratangelo D et al. IgA subclass 

antibodies to gliadin in serum and intestinal juice of 

patients with coeliac disease. Clinical and Experimental 

Immunology 1990;80(2):192-195. Improper control group 

Volta U, Molinaro N, Fusconi M et al. IgA antiendomysial

antibody test. A step forward in celiac disease screening.

Digestive Diseases and Sciences 1991;36(6):752-756. 

Improper control group 

Volta U, Ravaglia G, Granito A et al. Coeliac disease in

patients with autoimmune thyroiditis. Digestion

2001;64(1):61-65. Not sensitivity or specificity of an 

identified test 

Volta Umberto, Rodrigo Luis, Granito Alessandro et al. 

Celiac disease in autoimmune cholestatic liver disorders.

American Journal of Gastroenterology 2002;97(10):2609-

2613. Not sensitivity or specificity of an identified test 

Voutilainen M, Juhola M, Farkkila M et al. Gastric 

metaplasia and chronic inflammation at the duodenal bulb 

mucosa. Digestive and Liver Disease - Official Journal of

the Italian Society of Gastroenterology and the Italian

Association for the Study of the Liver 2003;35(2):94-98. 

Not sensitivity or specificity of an identified test

Vuoristo M, Miettinen T A. Enhanced synthesis of

cholesterol and its precursors in jejunal mucosa in coeliac 

disease. Gut 1986;27(4):399-404. Not sensitivity or 

specificity of an identified test

Vuoristo M, Tarpila S, Miettinen T A. Serum lipids and 

fecal steroids in patients with celiac disease: Effects of 

gluten-free diet and cholestyramine. Gastroenterology

1980;78(6):1518-1525. Not sensitivity or specificity of an

identified test 

Wachtel M S, Thaler H T, Gangi M D et al.

Immunoperoxidase staining of cervicovaginal smears after 

radiotherapy. Acta Cytologica 1992;36(3):305-309. Not 

sensitivity or specificity of an identified test 

Wade J A F, Hurley C K, Hastings A et al. Combinatorial 

diversity in DR2 haplotypes. Tissue Antigens 

1993;41(3):113-118. Not sensitivity or specificity of an 

identified test 

Wahab P J, Crusius J B, Meijer J W et al. Gluten challenge 

in borderline gluten-sensitive enteropathy. American 

Journal of Gastroenterology 2001;96(5):1464-1469. Not 

sensitivity or specificity of an identified test 

Wahab P J, Crusius J B, Meijer J W et al. Cyclosporin in

the treatment of adults with refractory coeliac disease--an

open pilot study. Alimentary Pharmacology & Therapeutics

2000;14(6):767-774. Not sensitivity or specificity of an 

identified test 

Wahab P J, Meijer J W R, Goerres M S et al. Coeliac

disease: changing views on gluten-sensitive enteropathy.

Scandinavian Journal of Gastroenterology.Supplement 

2002;(236):60-65. Not sensitivity or specificity of an 

identified test 

Wahab P J, Peters W H, Roelofs H M et al. Glutathione Stransferases in small intestinal mucosa of patients with 

coeliac disease. Japanese Journal of Cancer Research -

Gann 2001;92(3):279-284. Not sensitivity or specificity of 

an identified test

Wahab Peter J, Meijer Jos W R, Mulder Chris J J.

Histologic follow-up of people with celiac disease on a 

gluten-free diet: slow and incomplete recovery. American 

Journal of Clinical Pathology 2002;118(3):459-463. Not 

sensitivity or specificity of an identified test 

Wahab Peter J, Meijer Jos W R, Dumitra Daniela et al. 

Coeliac disease: more than villous atrophy. Romanian 

Journal of Gastroenterology 2002;11(2):121-127. Not 

sensitivity or specificity of an identified test 

Wahnschaffe U, Stockmann M, Daum S et al. Intestinal

antibodies against gliadin, tissue-transglutaminase, betalactoglobulin, and ovalbumin in patients with irritable 

bowel syndrome. Annals of the New York Academy of

Sciences 1998;859280-284. Not sensitivity or specificity of 

an identified test

Wahnschaffe U, Ullrich R, Riecken E O et al. Celiac

disease-like abnormalities in a subgroup of patients with 

irritable bowel syndrome. Gastroenterology

2001;121(6):1329-1338. Not sensitivity or specificity of an 

identified test 

Wakita H, Takigawa M. Activation of epidermal growth 

factor receptor promotes late terminal differentiation of

cell-matrix interaction-disrupted keratinocytes. Journal of

Biological Chemistry 1999;274(52):37285-37291. Not 

sensitivity or specificity of an identified test 

Walia B N, Mehta S, Gupte S P. Caeliac disease. Indian 

Pediatrics 1972;9(1):16-19. Not sensitivity or specificity of 

an identified test

Walker A M, Montgomery D W, Saraiya S et al. Prolactinimmunoglobulin G complexes from human serum act as 

costimulatory ligands causing proliferation of malignant B

lymphocytes. Proceedings of the National Academy of 

Sciences of the United States of America 1995;92(8):3278-

3282. Not sensitivity or specificity of an identified test 

Walker Michael G. Z39Ig is co-expressed with activated 

macrophage genes. Biochimica Et Biophysica Acta 

2002;1574(3):387-390. Not sensitivity or specificity of an

identified test 

A-490
Walker Smith J, Kilby A. Small intestinal histology in 

coeliac disease. Lancet 1975;2(7925):132Not sensitivity or 

specificity of an identified test

Walker-Smith J. Cow's milk protein intolerance. Transient 

food intolerance of infancy. Archives of Disease in 

Childhood 1975;50(5):347-350. Not sensitivity or

specificity of an identified test

Walker-Smith J. Transient gluten intolerance. Archives of 

Disease in Childhood 1970;45(242):523-526. Not 

sensitivity or specificity of an identified test 

Walker-Smith J. Food sensitive enteropathy: Overview and

update. Acta Paediatr Jpn Overs Ed 1994;36(5):545-549. 

Not sensitivity or specificity of an identified test

Walker-Smith J A. Small bowel morphology in childhood. 

Medical Journal of Australia 1969;1(8):382-387. Not 

sensitivity or specificity of an identified test 

Walker-Smith J A. Celiac disease and Down syndrome. 

Journal of Pediatrics 2000;137(6):743-744. Not sensitivity

or specificity of an identified test

Walker-Smith J A. Immune function of small bowel and its 

related diseases. Acta Paediatr Taiwan 2000;41(4):177-178. 

Not sensitivity or specificity of an identified test

Walker-Smith J A, Grigor W. Coeliac disease in a diabetic

child. Lancet 1969;1(7603):1021Not sensitivity or

specificity of an identified test

Walker-Smith J A, Reye R D. Small intestinal morphology

in aboriginal children. Australian and New Zealand Journal 

of Medicine 1971;1(4):377-384. Not sensitivity or

specificity of an identified test

Walker-Smith J A, Guandalini S, Schmitz J et al. Revised 

criteria for diagnosis of coeliac disease. Arch Dis Child 

1990;65(8):909-911. Serology <1990 

Walker-Smith J A, Vines R, Grigor W. Coeliac disease and

diabetes. Lancet 1969;2(7621):650Not sensitivity or 

specificity of an identified test

Walker-Smith J, Kilby A. Letter: Small-intestinal histology 

in coeliac disease. Lancet 1975;2(7925):132Not sensitivity

or specificity of an identified test

Walker-Smith J, Walker W A. The development of

pediatric gastroenterology: A historical overview. Pediatric 

Research 2003;53(4):706-715. Not sensitivity or specificity

of an identified test 

Walkowiak J, Herzig K H. Fecal elastase-1 is decreased in 

villous atrophy regardless of the underlying disease. 

European Journal of Clinical Investigation 2001;31(5):425-

430. Not sensitivity or specificity of an identified test 

Wall A J, Levinson J D, Refetoff S. Hyperthyroidism and 

adult celiac disease. American Journal of Gastroenterology

1973;60(4):387-393. Not sensitivity or specificity of an 

identified test 

Wallaschofski H, Meyer A, Tuschy U et al. HLADQA1*0301-associated susceptibility for autoimmune 

polyglandular syndrome type II and III. Hormone and 

Metabolic Research.Hormon- Und 

Stoffwechselforschung.Hormones Et Metabolisme 

2003;35(2):120-124. Not sensitivity or specificity of an 

identified test 

Walsh C H, Cooper B T, Wright A D et al. Diabetes

mellitus and coeliac disease: a clinical study. Quarterly 

Journal of Medicine 1978;47(185):89-100. Not sensitivity

or specificity of an identified test

Walsh L J, Goerdt S, Pober J S et al. MS-1 sinusoidal 

endothelial antigen is expressed by factor XIIIa+, HLADR+ dermal perivascular dendritic cells. Laboratory

Investigation 1991;A Journal of Technical Methods and 

Pathology; 65(6):732-741. Not sensitivity or specificity of

an identified test

Walter M, Albert E, Conrad M et al. IDDM2/insulin VNTR 

modifies risk conferred by IDDM1/HLA for development 

of Type 1 diabetes and associated autoimmunity.

Diabetologia 2003;46(5):712-720. Not sensitivity or 

specificity of an identified test

Walters J R, Banks L M, Butcher G P et al. Detection of 

low bone mineral density by dual energy x ray

absorptiometry in unsuspected suboptimally treated coeliac 

disease. Gut 1995;37(2):220-224. Not sensitivity or 

specificity of an identified test

Walz R, Koch H K. Malignant pleural mesothelioma: some

aspects of epidemiology, differential diagnosis and 

prognosis. Histological and immunohistochemical 

evaluation and follow-up of mesotheliomas diagnosed from

1964 to January 1985. Pathology, Research and Practice 

1990;186(1):124-134. Not sensitivity or specificity of an

identified test 

Wan X H, Lee E H, Koh H J et al. Enhanced expression of 

transglutaminase 2 in anterior polar cataracts and its 

induction by TGF-beta in vitro. British Journal of

Ophthalmology 2002;86(11):1293-1298. Not sensitivity or

specificity of an identified test

Wang M, Kim I G, Steinert P M et al. Assignment of the

human transglutaminase 2 (TGM2) and transglutaminase 3

(TGM3) genes to chromosome 20q11.2. Genomics 

1994;23(3):721-722. Not sensitivity or specificity of an 

identified test 

Wang N, Dumot J A, Achkar E et al. Colonic epithelial 

lymphocytosis without a thickened subepithelial collagen 

table: a clinicopathologic study of 40 cases supporting a 

heterogeneous entity. American Journal of Surgical 

Pathology 1999;23(9):1068-1074. Not sensitivity or 

specificity of an identified test

A-491
Wankiewicz Anna, Iwan-Zietek Iza, Gwiezdzinski Zenon 

et al. Levels of F(1+2) prothrombin fragments and

thrombin - antithrombin III (TAT) complexes in patients 

with dermatitis herpetiformis. Medical Science Monitor -

International Medical Journal of Experimental and Clinical 

Research 2002;8(8):Br324-Br327. Not sensitivity or 

specificity of an identified test

Warngard O, Stenhammar L, Ascher H et al. Small bowel

biopsy in Swedish paediatric clinics. Acta Paediatrica 

(Oslo, Norway - 1992) 1996;85(2):240-241. Not sensitivity

or specificity of an identified test

Warshaw A L, Laster L. Protein synthesis by human 

intestinal mucosa: variations with diseases of the gut.

Journal of Surgical Research 1973;14(4):285-293. Not 

sensitivity or specificity of an identified test 

Watson A J, Parkin J M. Jejunal-biopsy findings during 

prodromal stage of measles in a child with coeliac disease.

Lancet 1970;2(7683):1134-1135. Not sensitivity or 

specificity of an identified test

Watson A J, Wright N A. Morphology and cell kinetics of 

the jejunal mucosa in untreated patients. Clin Gastroenterol 

1974;3(1):11-31. Not sensitivity or specificity of an 

identified test 

Watson A J, Appleton D R, Wright N A. Adaptive cellproliferative changes in the small-intestinal mucosa in 

coeliac disease. Scandinavian Journal of

Gastroenterology.Supplement 1982;74115-127. Not 

sensitivity or specificity of an identified test 

Watson R G, McMillan S A, Dickey W et al. Detection of

undiagnosed coeliac disease with atypical features using 

antireticulin and antigliadin antibodies. Quarterly Journal 

of Medicine 1992;84(305):713-718. Not sensitivity or 

specificity of an identified test

Watson R G, McMillan S A, Dolan C et al. Gliadin 

antibody detection in gluten enteropathy. Ulster Medical 

Journal 1986;55(2):160-164. Serology <1990 

Wauters E A. Clinical diagnosis of coeliac disease. Irish 

Medical Journal 1974;67(15):406-411. Not sensitivity or

specificity of an identified test

Wauters E A, Jansen J, Houwen R H et al. Serum IgG and

IgA anti-gliadin antibodies as markers of mucosal damage 

in children with suspected celiac disease upon gluten 

challenge. Journal of Pediatric Gastroenterology and 

Nutrition 1991;13(2):192-196. Not sensitivity or specificity

of an identified test 

Weetman A P, McCorkle R. Evidence against extended

DR3-related haplotypes in Graves' disease. Journal of

Immunogenetics 1990;17(6):403-407. Not sensitivity or

specificity of an identified test

Wehbi Nizar K, Dugger Ashley L, Bonner Rebecca B et al. 

Pan-cadherin as a high level phenotypic biomarker for

prostate cancer. Journal of Urology 2002;167(5):2215-

2221. Not sensitivity or specificity of an identified test 

Wei L, Debets R, Hegmans J J et al. IL-1 beta and IFNgamma induce the regenerative epidermal phenotype of

psoriasis in the transwell skin organ culture system. IFNgamma up-regulates the expression of keratin 17 and 

keratinocyte transglutaminase via endogenous IL-1

production. Journal of Pathology 1999;187(3):358-364. Not 

sensitivity or specificity of an identified test 

Weile B. Aspects of classic symptomatic childhood coeliac 

disease in Denmark: Retrospectively illustrated by local,

regional, and national studies. Apmis Suppl 

2003;111(113):5-46. Not sensitivity or specificity of an 

identified test 

Weile B, Grodzinsky E, Skogh T et al. Screening Danish 

blood donors for antigliadin and antiendomysium 

antibodies. Acta paediatrica (Oslo, Norway : 

1992).Supplement. 1996;41246Not sensitivity or specificity

of an identified test 

Weile B, Hansen B F, Hagerstrand I et al. Interobserver 

variation in diagnosing coeliac disease. A joint study by

Danish and Swedish pathologists. Apmis - Acta

Pathologica, Microbiologica, Et Immunologica 

Scandinavica 2000;108(5):380-384. Unable to extract data 

Weile Birgitte, Heegaard Niels H H, Hoier-Madsen Mimi 

et al. Tissue transglutaminase and endomysial 

autoantibodies measured in an historical cohort of children

and young adults in whom coeliac disease was suspected. 

European Journal of Gastroenterology & Hepatology

2002;14(1):71-76. Improper control group 

Weile I, Grodzinsky E, Skogh T et al. High prevalence 

rates of adult silent coeliac disease, as seen in Sweden,

must be expected in Denmark. Apmis - Acta Pathologica, 

Microbiologica, Et Immunologica Scandinavica 

2001;109(11):745-750. Not sensitivity or specificity of an

identified test 

Weinberg J B, Pippen A M, Greenberg C S. Extravascular

fibrin formation and dissolution in synovial tissue of 

patients with osteoarthritis and rheumatoid arthritis. 

Arthritis and Rheumatism 1991;34(8):996-1005. Not 

sensitivity or specificity of an identified test 

Weinshenker B G, Santrach P, Bissonet A S et al. Major 

histocompatibility complex class II alleles and the course

and outcome of MS: a population-based study. Neurology

1998;51(3):742-747. Not sensitivity or specificity of an 

identified test 

Weinstein W M. Latent celiac sprue. Gastroenterology

1974;66(4):489-493. Not sensitivity or specificity of an 

identified test 

Weinstein W M, Brow J R, Parker F et al. The small 

intestinal mucosa in dermatitis herpetiformis. II. 

Relationship of the small intestinal lesion to gluten. 

A-492
Gastroenterology 1971;60(3):362-369. Not sensitivity or 

specificity of an identified test

Weinstein W M, Saunders D R, Tytgat G N et al. 

Collagenous sprue--an unrecognized type of malabsorption. 

New England Journal of Medicine 1970;283(24):1297-

1301. Not sensitivity or specificity of an identified test 

Weir D G, Hourihane D O. Coeliac disease during the

teenage period: the value of serial serum folate estimations.

Gut 1974;15(6):450-457. Not sensitivity or specificity of an 

identified test 

Weiser M M, Douglas A P. An alternative mechanism for 

gluten toxicity in coeliac disease. Lancet 

1976;1(7959):567-569. Not sensitivity or specificity of an

identified test 

Weiss J B, Austin R K, Schanfield M S et al. Glutensensitive enteropathy. Immunoglobulin G heavy-chain

(Gm) allotypes and the immune response to wheat gliadin.

Journal of Clinical Investigation 1983;72(1):96-101. Not 

sensitivity or specificity of an identified test 

Weizman Z, Ben Zion Y Z, Binsztok M et al. Correlation 

of clinical characteristics and small bowel histopathology

in celiac disease. Journal of Pediatric Gastroenterology and

Nutrition 1997;24(5):555-558. Not sensitivity or specificity

of an identified test 

Weizman Z, Stringer D A, Durie P R. Radiologic 

manifestations of malabsorption: a nonspecific finding. 

Pediatrics 1984;74(4):530-533. Not sensitivity or

specificity of an identified test

Weizman Z, Vardi O, Binsztok M. Dermatoglyphic 

(fingerprint) patterns in celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 1990;10(4):451-453. Not

sensitivity or specificity of an identified test 

Welcher B C, Carra J H, DaSilva L et al. Lethal shock 

induced by streptococcal pyrogenic exotoxin A in mice 

transgenic for human leukocyte antigen-DQ8 and human 

CD4 receptors: Implications for development of vaccines

and therapeutics. J Infect Dis 2002;186(4):501-510. Not 

sensitivity or specificity of an identified test 

Weller M, Esser P, Bresgen M et al. Thrombospondin: a 

new attachment protein in preretinal traction membranes.

European Journal of Ophthalmology 1992;2(1):10-14. Not 

sensitivity or specificity of an identified test 

Wellman-Bednawska M, Artur Y, Siest G. Variations in 

sialic acid content of gamma-glutamyltransferase: a

consequence for immunochemical determinations?. Clinica 

Chimica Acta 1985;International Journal of Clinical 

Chemistry; 148(1):21-30. Not sensitivity or specificity of

an identified test

Wells C A, Heryet A, Brochier J et al. The 

immunocytochemical detection of axillary micrometastases 

in breast cancer. British Journal of Cancer 1984;50(2):193-

197. Not sensitivity or specificity of an identified test 

Welsh J D, Zschiesche O M, Anderson J et al. Intestinal 

disaccharidase activity in celiac sprue (gluten-sensitive

enteropathy). Archives of Internal Medicine

1969;123(1):33-38. Not sensitivity or specificity of an 

identified test 

West J, Lloyd C A, Hill P G et al. IgA-antitissue 

transglutaminase: validation of a commercial assay for 

diagnosing coeliac disease. Clinical Laboratory 2002;48(5-

6):241-246. Improper control group 

West J, Logan R F A, Hill P G et al. Seroprevalence,

correlates, and characteristics of undetected coeliac disease 

in England. Gut 2003;52(7):960-965. Not sensitivity or

specificity of an identified test

Westergaard H. The sprue syndromes. American Journal of 

the Medical Sciences 1985;290(6):249-262. Not sensitivity

or specificity of an identified test

Westerholm-Ormio M, Garioch J, Ketola I et al. 

Inflammatory cytokines in small intestinal mucosa of 

patients with potential coeliac disease. Clinical and 

Experimental Immunology 2002;128(1):94-101. Not 

sensitivity or specificity of an identified test 

Westerholm-Ormio Mia, Vaarala Outi, Pihkala Paivi et al.

Immunologic activity in the small intestinal mucosa of 

pediatric patients with type 1 diabetes. Diabetes

2003;52(9):2287-2295. Not sensitivity or specificity of an

identified test 

Westphal J R, Boerbooms A M, Schalwijk C J et al. Antiendothelial cell antibodies in sera of patients with 

autoimmune diseases: comparison between ELISA and 

FACS analysis. Clinical and Experimental Immunology

1994;96(3):444-449. Not sensitivity or specificity of an 

identified test 

Wharton B A. Coeliac disease in childhood. Br J Hosp Med 

1974;12(4):452-466. Not sensitivity or specificity of an 

identified test 

White A G, Barnetson R S C, Da Costa J A G et al. The 

incidence of HL A antigens in dermatitis herpetiformis. Br 

J Dermatol 1973;89(2):133-136. Not sensitivity or

specificity of an identified test

Whitlow M B, Ramm L E, Mayer M M. Penetration of C8

and C9 in the C5b-9 complex across the erythrocyte 

membrane into the cytoplasmic space. Journal of Biological 

Chemistry 1985;260(2):998-1005. Not sensitivity or 

specificity of an identified test

Whyard T C, Ablin R J. A tissue type transglutaminase in 

human seminal plasma. American Journal of Reproductive 

Immunology (New York, N.y.- 1989) 1997;38(6):391-399. 

Not sensitivity or specificity of an identified test

Whyard T C, Ablin R J. A modified assay for blood 

A-493
coagulation factor XIII using enzyme immobilisation on 

Staphylococcus aureus: Preliminary evaluation.

Fibrinolysis 1991;5(2):127-130. Not sensitivity or

specificity of an identified test

Wiedmann M, Liebert U G, Oesen U et al. Decreased 

immunogenicity of recombinant hepatitis B vaccine in

chronic hepatitis C. Hepatology 2000;31(1):230-234. Not 

sensitivity or specificity of an identified test 

Willems D, Cadranel S, Jacobs W. Measurement of urinary 

sugars by HPLC in the estimation of intestinal

permeability: Evaluation in pediatric clinical practice. 

Clinical Chemistry 1993;39(5):888-890. Not sensitivity or 

specificity of an identified test

Williams A J, Annis P, Lock R J et al. Evaluation of a highthroughput second antibody radiobinding assay for 

measuring IgA antibodies to human tissue 

transglutaminase. Journal of Immunological Methods 

1999;228(1-2):81-85. Improper control group 

Williams A J, Norcross A J, Lock R J et al. The high 

prevalence of autoantibodies to tissue transglutaminase in 

first-degree relatives of patients with type 1 diabetes is not

associated with islet autoimmunity. Diabetes Care

2001;24(3):504-509. Not sensitivity or specificity of an 

identified test 

Williams C N. Celiac disease: Past, present and future.

Canadian Journal of Gastroenterology = Journal Canadien 

De Gastroenterologie 1997;11(8):647-649. Not sensitivity

or specificity of an identified test

Williams C N. Collagenous colitis. Canadian Journal of

Gastroenterology = Journal Canadien De Gastroenterologie 

1998;12(1):23-24. Not sensitivity or specificity of an 

identified test 

Williamson Debbie, Marsh Michael N. Celiac disease.

Molecular Biotechnology 2002;22(3):293-299. Not 

sensitivity or specificity of an identified test 

Williamson N, Asquith P, Stokes L et al. Anticonnective 

tissue and other antitissue 'antibodies' in the sera of patients

with coeliac disease compared with the findings in a mixed 

hospital population. Journal of Clinical Pathology

1976;29(6):484-494. Not sensitivity or specificity of an 

identified test 

Willoughby J M T, Laitner S M. Audit of the investigation

of iron deficiency anaemia in a distinct general hospital,

with sample guidelines for future practice. Postgrad Med J 

2000;76(894):218-222. Not sensitivity or specificity of an

identified test 

Wills A J, Turner B, Lock R J et al. Dermatitis 

herpetiformis and neurological dysfunction. Journal of

Neurology, Neurosurgery, and Psychiatry 2002;72(2):259-

261. Not sensitivity or specificity of an identified test 

Wilson A G, Clay F E, Crane A M et al. Comparative 

genetic association of human leukocyte antigen class II and 

tumor necrosis factor-alpha with dermatitis herpetiformis. J 

Invest Dermatol 1995;104(5):856-858. Not sensitivity or

specificity of an identified test

Wilson A G, Symons J A, McDowell T L et al. Effects of a 

polymorphism in the human tumor necrosis factor alpha 

promoter on transcriptional activation. Proc Natl Acad Sci

U S A 1997;94(7):3195-3199. Not sensitivity or specificity

of an identified test 

Wilson C, Eade O E, Elstein M et al. Subclinical coeliac

disease and infertility. Br Med J 1976;2(6029):215-216. 

Not sensitivity or specificity of an identified test

Wilson W B. Clinical and laboratory evaluation of

malabsorption. Journal of the Mississippi State Medical 

Association 1978;19(10):183-185. Not sensitivity or 

specificity of an identified test

Wingren U, Hallert C, Norrby K et al. Histamine and 

mucosal mast cells in gluten enteropathy. Agents and 

Actions 1986;18(1-2):266-268. Not sensitivity or

specificity of an identified test

Winklhofer-Roob B M, Rossipal E, Lanzer G. Human 

leucocyte class I and II antigens in coeliac disease: a study 

in an Austrian paediatric population. European Journal of

Pediatrics 1991;150(10):704-707. Not sensitivity or 

specificity of an identified test

Wirtz P W, Roep B O, Schreuder G M T et al. HLA class I 

and II in Lambert-Eaton myasthenic syndrome without 

associated tumor. Hum Immunol 2001;62(8):809-813. Not 

sensitivity or specificity of an identified test 

Witas H W. Genetic background of coeliac disease. CentEur J Immunol 2000;25(4):222-226. Not sensitivity or 

specificity of an identified test

Witas H W, Mlynarski W, Niewiadomska H et al. Immune 

response in coeliac disease: Involvement of costimulatory

molecules during activation of lymphocytes infiltrating the 

intestine. Cent-Eur J Immunol 2000;25(4):180-184. Not 

sensitivity or specificity of an identified test 

Witas H W, Mlynarski W, Rozalski M et al. Study of 

Polish coeliac patients: HLA-DQ amino acid variants 

involved in antigen presentation. Cent-Eur J Immunol 

1997;22(4):266-271. Not sensitivity or specificity of an 

identified test 

Witas H W, Sychowski R, Mlynarski W et al. Does TNF 

locus contribute to coeliac disease as the independent 

genetic factor or linked to particular HLA-haplotype?.

Cent-Eur J Immunol 2000;25(2):57-62. Not sensitivity or 

specificity of an identified test

Wolber R, Owen D, Freeman H. Colonic lymphocytosis in

patients with celiac sprue. Human Pathology

1990;21(11):1092-1096. Not sensitivity or specificity of an 

identified test 

A-494
Wolber R, Owen D, DelBuono L et al. Lymphocytic 

gastritis in patients with celiac sprue or spruelike intestinal

disease. Gastroenterology 1990;98(2):310-315. Not 

sensitivity or specificity of an identified test 

Wong F S, Wen L. The study of HLA class II and 

autoimmune diabetes. Curr Mol Med 2003;3(1):1-15. Not 

sensitivity or specificity of an identified test 

Wong R C W, Steele R H, Reeves G E M et al. Antibody

and genetic testing in coeliac disease. Pathology 

2003;35(4):285-304. Not sensitivity or specificity of an 

identified test 

Wong R C W, Wilson R J, Steele R H et al. A comparison 

of 13 guinea pig and human anti-tissue transglutaminase 

antibody ELISA kits. Journal of Clinical Pathology

2002;55(7):488-494. Improper control group 

Wood G M, Howdle P D, Trejdosiewicz L K et al. Jejunal 

plasma cells and in vitro immunoglobulin production in

adult coeliac disease. Clinical and Experimental

Immunology 1987;69(1):123-132. Not sensitivity or 

specificity of an identified test

Wood G M, Shires S, Howdle P D et al. Immunoglobulin 

production by coeliac biopsies in organ culture. Gut 

1986;27(10):1151-1160. Not sensitivity or specificity of an 

identified test 

Woodley J F. Pyrrolidonecarboxylyl peptidase activity in

normal intestinal biopsies and those from coeliac patients. 

Clinica Chimica Acta 1972;International Journal of Clinical 

Chemistry; 42(1):211-213. Not sensitivity or specificity of 

an identified test

Woolley N, Holopainen P, Bourgain C et al. CD80 (B7-1) 

and CD86 (B7-2) genes and genetic susceptibility to 

coeliac disease. European Journal of Immunogenetics - 

Official Journal of the British Society for

Histocompatibility and Immunogenetics 2002;29(4):331-

333. Not sensitivity or specificity of an identified test 

Woolley Niina, Holopainen Paivi, Ollikainen Vesa et al. A 

new locus for coeliac disease mapped to chromosome 15 in

a population isolate. Human Genetics 2002;111(1):40-45. 

Not sensitivity or specificity of an identified test

Wordsworth B P, Salmon M. The HLA class II component 

of susceptibility to rheumatoid arthritis. Bailliere's Clin 

Rheumatol 1992;6(2):325-336. Not sensitivity or 

specificity of an identified test

Wordsworth P. PCR-SSO typing in HLA-disease 

association studies. European Journal of Immunogenetics -

Official Journal of the British Society for

Histocompatibility and Immunogenetics 1991;18(1-2):139-

146. Not sensitivity or specificity of an identified test 

Wozniak M, Fausto A, Carron C P et al. Mechanically

strained cells of the osteoblast lineage organize their 

extracellular matrix through unique sites of alphavbeta3-

integrin expression. Journal of Bone and Mineral Research

- the Official Journal of the American Society for Bone and

Mineral Research 2000;15(9):1731-1745. Not sensitivity or 

specificity of an identified test

Wray D. Gluten-sensitive recurrent aphthous stomatitis. 

Digestive Diseases and Sciences 1981;26(8):737-740. Not 

sensitivity or specificity of an identified test 

Wright D H. Enteropathy associated T cell lymphoma. 

Cancer Surveys 1997;30249-261. Not sensitivity or 

specificity of an identified test

Wright N A, Morley A R, Appleton D R et al. 

Measurement of cell production rate in the human small 

bowel. Pathologia Et Microbiologia 1973;39(3):251-253. 

Not sensitivity or specificity of an identified test

Wright N, Watson A, Morley A et al. Cell kinetics in flat

(avillous) mucosa of the human small intestine. Gut 

1973;14(9):701-710. Not sensitivity or specificity of an 

identified test 

Wright P H, Menzies I S, Pounder R E et al. Adult 

idiopathic pulmonary haemosiderosis and coeliac disease.

Quarterly Journal of Medicine 1981;50(197):95-102. Not 

sensitivity or specificity of an identified test 

Wu T T, Hamilton S R. Lymphocytic gastritis: association

with etiology and topology. American Journal of Surgical 

Pathology 1999;23(2):153-158. Not sensitivity or

specificity of an identified test

Wucherpfennig K W. Insights into autoimmunity gained 

from structural analysis of MHC-peptide complexes.

Current Opinion in Immunology 2001;13(6):650-656. Not 

sensitivity or specificity of an identified test 

Wurm P, Wicks A C. Iron deficiency anaemia - A clinical

challenge. Postgrad Med J 2000;76(894):193-194. Not 

sensitivity or specificity of an identified test 

Wyckoff E E, Croall D E, Ehrenfeld E. The p220 

component of eukaryotic initiation factor 4F is a substrate 

for multiple calcium-dependent enzymes. Biochemistry

1990;29(43):10055-10061. Not sensitivity or specificity of 

an identified test

Yadollahi-Farsani Masoud, Davies Donald S, Boobis Alan 

R. The mutational signature of alpha-hydroxytamoxifen at 

Hprt locus in Chinese hamster cells. Carcinogenesis 

2002;23(11):1947-1952. Not sensitivity or specificity of an 

identified test 

Yagui-Beltran A, Craig A L, Lawrie L et al. The human 

oesophageal squamous epithelium exhibits a novel type of 

heat shock protein response. European Journal of

Biochemistry / Febs 2001;268(20):5343-5355. Not 

sensitivity or specificity of an identified test 

Yamada K, Matsuki M, Morishima Y et al. Activation of 

A-495
the human transglutaminase 1 promoter in transgenic mice: 

terminal differentiation-specific expression of the TGM1-

lacZ transgene in keratinized stratified squamous epithelia. 

Human Molecular Genetics 1997;6(13):2223-2231. Not 

sensitivity or specificity of an identified test 

Yamada K, Yamanishi K, Kakizuka A et al. Transcriptional

regulation of human transglutaminase1 gene by signaling

systems of protein kinase C, RAR/RXR and Jun/Fos in 

keratinocytes. Biochemistry and Molecular Biology

International 1994;34(4):827-836. Not sensitivity or 

specificity of an identified test

Yamada T, Yoshiyama Y, Kawaguchi N et al. Possible 

roles of transglutaminases in Alzheimer's disease.

Dementia and Geriatric Cognitive Disorders 

1998;9(2):103-110. Not sensitivity or specificity of an 

identified test 

Yamanishi K, Inazawa J, Liew F M et al. Structure of the

gene for human transglutaminase 1. Journal of Biological 

Chemistry 1992;267(25):17858-17863. Not sensitivity or

specificity of an identified test

Yan S D, Huang C C. Lymphotoxin in human middle ear

cholesteatoma. Laryngoscope 1991;101(4 Pt 1):411-415. 

Not sensitivity or specificity of an identified test

Yan S D, Huang C C. Tumor necrosis factor alpha in

middle ear cholesteatoma and its effect on keratinocytes in 

vitro. Annals of Otology, Rhinology, and Laryngology

1991;100(2):157-161. Not sensitivity or specificity of an

identified test 

Yan Z H, Noonan S, Nagy L et al. Retinoic acid induction

of the tissue transglutaminase promoter is mediated by a

novel response element. Mol Cell Endocrinol 

1996;120(2):203-212. Not sensitivity or specificity of an

identified test 

Yanagawa T, Mangklabruks A, Chang Y-B et al. Human 

histocompatibility leukocyte antigen-DQA1*0501 allele 

associated with genetic susceptibility to Graves' disease in 

a Caucasian population. J Clin Endocrinol Metab

1993;76(6):1569-1574. Not sensitivity or specificity of an

identified test 

Yang H, Goluszko E, David C et al. Induction of 

myasthenia gravis in HLA transgenic mice by

immunization with human acetylcholine receptors. Ann 

New York Acad Sci 2003;998(-):375-378. Not sensitivity

or specificity of an identified test

Yao Z, Kimura A, Hartung K et al. Polymorphism of the 

DQA1 promoter region (QAP) and DRB1, QAP, DQA1,

DQB1 haplotypes in systemic lupus erythematosus. 

Immunogenetics 1993;38(6):421-429. Not sensitivity or

specificity of an identified test

Yaqoob N. Coeliac disease: A local perspective. J Coll 

Phys Surg Pak 1999;9(12):526-528. Not sensitivity or 

specificity of an identified test

Yazdanbakhsh M, Sartono E, Kruize Y C M et al. HLA and 

elephantiasis in lymphatic filariasis. Hum Immunol 

1995;44(1):58-61. Not sensitivity or specificity of an 

identified test 

Yeboah F A, White D. AlphaB-crystallin expression in 

celiac disease - a preliminary study. Croatian Medical 

Journal 2001;42(5):523-526. Not sensitivity or specificity

of an identified test 

Yelamos J, Garcia-Lozano J R, Moreno I et al. Association 

of HLA-DR4-Dw15 (DRB1*0405) and DR10 with 

rheumatoid arthritis in a Spanish population. Arthritis 

Rheum 1993;36(6):811-814. Not sensitivity or specificity

of an identified test 

Yiannakou J Y, Brett P M, Morris M A et al. Family

linkage study of the T-cell receptor genes in coeliac 

disease. Italian Journal of Gastroenterology and 

Hepatology 1999;31(3):198-201. Not sensitivity or 

specificity of an identified test

Yiannakou J Y, Dell'Olio D, Saaka M et al. Detection and

characterisation of anti-endomysial antibody in coeliac 

disease using human umbilical cord. International Archives 

of Allergy and Immunology 1997;112(2):140-144. 

Improper control group 

Yiu C Y, Baker L A, Boulos P B. Immunolocalisation of an 

anti-EMA monoclonal antibody to a renal carcinoma 

xenograft. Anticancer Research 1990;10(6):1775-1778. Not 

sensitivity or specificity of an identified test 

Yoneda K, Akiyama M, Morita K et al. Expression of 

transglutaminase 1 in human hair follicles, sebaceous 

glands and sweat glands. British Journal of Dermatology 

1998;138(1):37-44. Not sensitivity or specificity of an 

identified test 

Yoneda K, Akiyama M, Shimizu H et al. Transglutaminase

1 in human hair follicle. Experimental Dermatology

1999;8(4):368-369. Not sensitivity or specificity of an 

identified test 

Yoshiie K, Kim H-Y, Mott J et al. Intracellular infection by

the human granulocytic ehrlichiosis agent inhibits human 

neutrophil apoptosis. Infect Immun 2000;68(3):1125-1133. 

Not sensitivity or specificity of an identified test

Young G P, Hebbard G S. Diagnostic techniques for small 

intestinal disease. Curr Opin Gastroenterol 1992;8(2):232-

238. Not sensitivity or specificity of an identified test 

Young G P, Koberts S K. Diagnostic studies of the small 

intestine. Curr Opin Gastroenterol 1991;7(2):256-262. Not 

sensitivity or specificity of an identified test 

Young V L, Nemecek J R, Schwartz B D et al. HLA typing 

in women with breast implants. Plast Reconstr Surg 

1995;96(7):1497-1520. Not sensitivity or specificity of an

identified test 

A-496
Younoszai M K, Ranshaw J C. Quantitation of intestinaltissue layers from their histology. American Journal of

Digestive Diseases 1975;20(8):764-770. Not sensitivity or 

specificity of an identified test

Yu B, Gauthier L, Hausmann D H et al. Binding of 

conserved islet peptides by human and murine MHC class 

II molecules associated with susceptibility to type I 

diabetes. European Journal of Immunology

2000;30(9):2497-2506. Not sensitivity or specificity of an

identified test 

Yu L, Brewer K W, Gates S et al. DRB1*04 and DQ 

alleles: expression of 21-hydroxylase autoantibodies and

risk of progression to Addison's disease. Journal of Clinical 

Endocrinology and Metabolism 1999;84(1):328-335. Not 

sensitivity or specificity of an identified test 

Yunis J J, Salazar M, Delgado M B et al. HLA-DQA1,

DQB1 and DPB1 alleles on HLA-DQ2- and DQ9-carrying 

extended haplotypes. Tissue Antigens 1993;41(1):37-41. 

Not sensitivity or specificity of an identified test

Zaccari G, Mazzetti di, Pietralata Paone F M et al. A

proposal for coeliac disease screening of all infants at the 

age of fifteen months. Gastroenterol Int 1996;9(1):11-15. 

Not sensitivity or specificity of an identified test

Zacchi Paola, Sblattero Daniele, Florian Fiorella et al. 

Selecting open reading frames from DNA. Genome 

Research 2003;13(5):980-990. Not sensitivity or specificity

of an identified test 

Zachor D A, Mroczek-Musulman E, Brown P. Prevalence

of celiac disease in Down syndrome in the United States. 

Journal of Pediatric Gastroenterology and Nutrition 

2000;31(3):275-279. Not sensitivity or specificity of an 

identified test 

Zaitoun A, Record C O. Morphometric studies in duodenal 

biopsies from patients with coeliac disease: the effect of the

steroid fluticasone propionate. Alimentary Pharmacology &

Therapeutics 1991;5(2):151-160. Not sensitivity or 

specificity of an identified test

Zauli D, Grassi A, Granito A et al. Prevalence of silent

coeliac disease in atopics. Digestive and Liver Disease -

Official Journal of the Italian Society of Gastroenterology

and the Italian Association for the Study of the Liver 

2000;32(9):775-779. Not sensitivity or specificity of an 

identified test 

Zeeuwen P L J M, Vlijmen-Willems I M J J, Egami H et al. 

Cystatin M / E expression in inflammatory and neoplastic 

skin disorders. British Journal of Dermatology 

2002;147(1):87-94. Not sensitivity or specificity of an 

identified test 

Zeeuwen P L J M, Vlijmen-Willems I M J J, Jansen B J H 

et al. Cystatin M/E expression is restricted to differentiated 

epidermal keratinocytes and sweat glands: A new skinspecific proteinase inhibitor that is a target for cross-linking 

by transglutaminase. J Invest Dermatol 2001;116(5):693-

701. Not sensitivity or specificity of an identified test 

Zeher M, Szegedi G, Csiki Z et al. Fibrinolysis-resistant

fibrin deposits in minor labial salivary glands of patients 

with Sjogren's syndrome. Clinical Immunology and 

Immunopathology 1994;71(2):149-155. Not sensitivity or

specificity of an identified test

Zelger B, Weinlich G, Zelger B. Perineuroma. A frequently

unrecognized entity with emphasis on a plexiform variant. 

Advances in Clinical Pathology - the Official Journal of

Adriatic Society of Pathology 2000;4(1):25-33. Not 

sensitivity or specificity of an identified test 

Zemaitaitis M O, Lee J M, Troncoso J C et al. 

Transglutaminase-induced cross-linking of tau proteins in 

progressive supranuclear palsy. Journal of Neuropathology

and Experimental Neurology 2000;59(11):983-989. Not 

sensitivity or specificity of an identified test 

Zettergren J G, Peterson L L, Wuepper K D. Keratolinin:

the soluble substrate of epidermal transglutaminase from

human and bovine tissue. Proceedings of the National 

Academy of Sciences of the United States of America 

1984;81(1):238-242. Not sensitivity or specificity of an 

identified test 

Zhang H, Koty P P, Mayotte J et al. Induction of multiple

programmed cell death pathways by IFN-beta in human 

non-small-cell lung cancer cell lines. Experimental Cell 

Research 1999;247(1):133-141. Not sensitivity or

specificity of an identified test

Zhang H, Yousem S A, Franklin W A et al. Differentiation

and programmed cell death-related intermediate biomarkers 

for the development of non-small cell lung cancer: a pilot 

study. Human Pathology 1998;29(9):965-971. Not 

sensitivity or specificity of an identified test 

Zhang J, Guttmann R P, Johnson G V. Tissue 

transglutaminase is an in situ substrate of calpain:

regulation of activity. Journal of Neurochemistry

1998;71(1):240-247. Not sensitivity or specificity of an 

identified test 

Zhang J, Lesort M, Guttmann R P et al. Modulation of the 

in situ activity of tissue transglutaminase by calcium and 

GTP. Journal of Biological Chemistry 1998;273(4):2288-

2295. Not sensitivity or specificity of an identified test 

Zhang J, Tucholski J, Lesort M et al. Novel bimodal effects 

of the G-protein tissue transglutaminase on adrenoreceptor 

signalling. Biochemical Journal 1999;343(Pt 3):541-549. 

Not sensitivity or specificity of an identified test

Zhang L X, Mills K J, Dawson M I et al. Evidence for the 

involvement of retinoic acid receptor RAR alpha-dependent

signaling pathway in the induction of tissue 

transglutaminase and apoptosis by retinoids. Journal of

Biological Chemistry 1995;270(11):6022-6029. Not 

A-497
sensitivity or specificity of an identified test 

Zhang Rulin, Tremblay Tammy, McDermid Angela et al. 

Identification of differentially expressed proteins in human 

glioblastoma cell lines and tumors. Glia 2003;42(2):194-

208. Not sensitivity or specificity of an identified test 

Zhang W, Johnson B R, Bjornsson T D. Pharmacologic 

inhibition of transglutaminase-induced cross-linking of 

Alzheimer's amyloid beta-peptide. Life Sciences

1997;60(25):2323-2332. Not sensitivity or specificity of an 

identified test 

Zhang W, Johnson B R, Suri D E et al. 

Immunohistochemical demonstration of tissue 

transglutaminase in amyloid plaques. Acta 

Neuropathologica 1998;96(4):395-400. Not sensitivity or 

specificity of an identified test

Zhong F, McCombs C C, Olson J M et al. An autosomal 

screen for genes that predispose to celiac disease in the

western counties of Ireland. Nature Genetics

1996;14(3):329-333. Not sensitivity or specificity of an 

identified test 

Zhu T H, Bodem J, Keppel E et al. A single ancestral gene

of the human LIM domain oncogene family LMO in 

Drosophila: characterization of the Drosophila Dlmo gene. 

Oncogene 1995;11(7):1283-1290. Not sensitivity or 

specificity of an identified test

Zhu Y, Tassi L, Lane W et al. Specific binding of the 

transglutaminase, platelet factor XIII, to HSP27. Journal of 

Biological Chemistry 1994;269(35):22379-22384. Not 

sensitivity or specificity of an identified test 

Ziegler Anette, Schmid Sandra, Huber Doris et al. Early

infant feeding and risk of developing type 1 diabetesassociated autoantibodies. Jama - the Journal of the 

American Medical Association 2003;290(13):1721-1728. 

Not sensitivity or specificity of an identified test

Zimmer K P, Naim H, Weber P et al. Targeting of gliadin 

peptides, CD8, alpha/beta-TCR, and gamma/delta-TCR to 

Golgi complexes and vacuoles within celiac disease 

enterocytes. Faseb Journal - Official Publication of the 

Federation of American Societies for Experimental Biology

1998;12(13):1349-1357. Not sensitivity or specificity of an 

identified test 

Zimmer K P, Poremba C, Weber P et al. Translocation of 

gliadin into HLA-DR antigen containing lysosomes in 

coeliac disease enterocytes. Gut 1995;36(5):703-709. Not 

sensitivity or specificity of an identified test 

Zins B J, Tremaine W J, Carpenter H A. Collagenous 

colitis: mucosal biopsies and association with fecal 

leukocytes. Mayo Clinic Proceedings 1995;70(5):430-433. 

Not sensitivity or specificity of an identified test

Zipser R D, Patel S, Yahya K Z et al. Presentations of adult 

celiac disease in a nationwide patient support group. 

Digestive Diseases and Sciences 2003;48(4):761-764. Not 

sensitivity or specificity of an identified test 

Zubillaga P, Vitoria J C, Arrieta A et al. Down Syndrome 

and celiac disease. Journal of Pediatric Gastroenterology

and Nutrition 1993;16(2):168-171. Not sensitivity or 

specificity of an identified test

Zubillaga Paul, Vidales Maria, Concepcion Zubillaga et al. 

HLA-DQA1 and HLA-DQB1 genetic markers and clinical 

presentation in celiac disease. Journal of Pediatric 

Gastroenterology and Nutrition 2002;34(5):548-554. 

Improper control group 

Zuin G, Fontana M, Morelli A et al. Antigliadin antibodies

in HIV-infected children. Pediatric Aids and Hiv Infection 

1996;7(6):409-412. Not sensitivity or specificity of an 

identified test

Objective 2 – Prevalence and Incidence of CD 

Abdulkarim A S, Murray J A. Review article: The 

diagnosis of coeliac disease. Aliment Pharmacol Ther 

2003;17(8):987-995. No prevalence or incidence 

reported 

Abdullah A M. Aetiology of chronic diarrhoea in

children: experience at King Khalid University

Hospital, Riyadh, Saudi Arabia. Ann Trop Paediatr 

1994;14(2):111-117. Not a relevant screening 

geography

Abele M, Schols L, Schwartz S et al. Prevalence of 

antigliadin antibodies in ataxia patients. Neurology

2003;60(10):1674-1675. No prevalence or incidence 

reported 

Acalovschi M. Coeliac disease and lymphoma. Rom J 

Gastroenterol 2001;10(4):317-320. No prevalence or 

incidence reported 

Addolorato G, Capristo E, Ghittoni G et al. Anxiety

but not depression decreases in coeliac patients after 

one-year gluten-free diet: a longitudinal study. Scand J 

Gastroenterol 2001;36(5):502-506. No prevalence or 

incidence reported 

Addolorato G, Stefanini G F, Capristo E et al. Anxiety

and depression in adult untreated celiac subjects and in 

patients affected by inflammatory bowel disease: A 

personality 'trait' or a reactive illness?. 

Hepatogastroenterology 1996;43(12):1513-1517. No 

prevalence or incidence reported

A-498
Adeniji O A, DiPalma J A. Food allergy. Pract 

Gastroenterol 2003;27(4):49-56. No prevalence or

incidence reported 

Agardh D, Nilsson A, Carlsson A et al. Tissue 

transglutaminase autoantibodies and human leucocyte 

antigen in Down Syndrome patients with coeliac 

disease. Acta Paediatr 2002;91(1):34-38. No

prevalence or incidence reported

Agrawal S, Gupta A, Yachha S K et al. Association of 

human leucocyte-DR and DQ antigens in coeliac 

disease: a family study. J Gastroenterol Hepatol 

2000;15(7):771-774. No prevalence or incidence 

reported 

Agreus L, Svardsudd K, Tibblin G et al. Endomysium 

antibodies are superior to gliadin antibodies in

screening for coeliac disease in patients presenting 

supposed functional gastrointestinal symptoms. Scand 

J Prim Health Care 2000;18(2):105-110. No 

prevalence or incidence reported

Aguirre J M, Rodriguez R, Oribe D et al. Dental 

enamel defects in celiac patients. Oral Surg Oral Med 

Oral Pathol Oral Radiol Endod 1997;84(6):646-650. 

No prevalence or incidence reported 

Ahmed A R, Hameed A. Bullous pemphigoid and

dermatitis herpetiformis. Clin Dermatol 

1993;11(1):47-52. No prevalence or incidence 

reported 

Aine L, Maki M, Collin P et al. Dental enamel defects 

in celiac disease. Journal of Oral Pathology & 

Medicine - Official Publication of the International 

Association of Oral Pathologists and the American 

Academy of Oral Pathology 1990;19(6):241-245. No 

prevalence or incidence reported

Aine L, Maki M, Reunala T. Coeliac-type dental 

enamel defects in patients with dermatitis

herpetiformis. Acta Derm Venereol 1992;72(1):25-27. 

No prevalence or incidence reported 

Aine L. Coeliac-type permanent-tooth enamel defects.

Ann Med 1996;28(1):9-12. No prevalence or

incidence reported 

Akerblom H K, Knip M. Putative environmental 

factors in Type 1 diabetes. Diabetes Metab Rev

1998;14(1):31-67. No prevalence or incidence 

reported 

Al Ashwal A A, Shabib S M, Sakati N A et al. 

Prevalence and characteristics of celiac disease in type

I diabetes mellitus in Saudi Arabia. Saudi Med J 

2003;24(10):1113-1115. No prevalence or incidence 

reported 

Al Attas R A. How common is celiac disease in

Eastern Saudi Arabia?. Ann Saudi Med 2002;22(5-

6):315-319. No prevalence or incidence reported

Al Bayatti S M. Etiology of chronic diarrhea. Saudi 

Med J 2002;23(6):675-679. No prevalence or

incidence reported 

Al Mondhiry H. Primary lymphomas of the small 

intestine: east-west contrast. Am J Hematol 

1986;22(1):89-105. No prevalence or incidence 

reported 

al Tawaty A I, Elbargathy S M. Coeliac disease in

north-eastern Libya. Ann Trop Paediatr 

1998;18(1):27-30. Not a relevant screening geography

Albert E D, Harms K, Wank R et al. Segregation

analysis of HL-A antigens and haplotypes in 50

families of patients with coeliac disease. Transplant 

Proc 1973;5(4):1785-1789. No prevalence or

incidence reported 

Alper C A, Awdeh Z L, Yunis E J. Complotypes, 

extended haplotypes, male segregation distortion, and

disease markers. Hum Immunol 1986;15(4):366-373. 

No prevalence or incidence reported 

Alper C A, Fleischnick E, Awdeh Z et al. Extended 

major histocompatibility complex haplotypes in

patients with gluten-sensitive enteropathy. Eur J Clin 

Invest 1987;79(1):251-256. No prevalence or

incidence reported 

Alpers D H. The role of nutritional deficiency in the 

osteopenia and osteoporosis of gastrointestinal 

diseases. Curr Opin Gastroenterol 2002;18(2):203-

208. No prevalence or incidence reported 

Altmann D M, Sansom D, Marsh S G. What is the 

basis for HLA-DQ associations with autoimmune 

disease?. Immunol Today 1991;12(8):267-270. No 

prevalence or incidence reported

Altmann D M. HLA-DQ associations with 

autoimmune disease. Autoimmunity 1992;14(1):79-

83. No prevalence or incidence reported 

Altuntas B, Kansu A, Ensari A et al. Celiac disease in

Turkish short-statured children and the value of

antigliadin antibody in diagnosis. Nippon Shonika 

Gakkai Zasshi 1998;40(5):457-460. Not a relevant 

screening geography

Altuntas cedil, Filik B, Ensari A et al. Can zinc

deficiency be used as a marker for the diagnosis of 

celiac disease in Turkish children with short stature?.

Pediatr Int 2000;42(6):682-684. No prevalence or

incidence reported 

Alvarez D, Vazquez H, Bai J C et al. Superior 

mesenteric artery blood flow in celiac disease. Dig Dis 

A-499
Sci 1993;38(7):1175-1182. No prevalence or

incidence reported 

Amann S T, Bishop M, Curington C et al. Fecal 

pancreatic elastase 1 is inaccurate in the diagnosis of 

chronic pancreatitis. Pancreas 1996;13(3):226-230. No 

prevalence or incidence reported

Ament M E, Perera D R, Esther L J. Sucraseisomaltase deficiency-a frequently misdiagnosed 

disease. Eur J Pediatr 1973;83(5):721-727. No 

prevalence or incidence reported

Amin Rakesh, Murphy Nuala, Edge Julie et al. A 

longitudinal study of the effects of a gluten-free diet 

on glycemic control and weight gain in subjects with 

type 1 diabetes and celiac disease. Diabetes Care

2002;25(7):1117-1122. No prevalence or incidence 

reported 

Amirhakimi G H, Samloff I M, Bryson M F et al.

Intestinal lymphangiectasia. Metabolic studies. Am J 

Dis Child 1969;117(2):178-185. No prevalence or

incidence reported 

Ammann R W, Hammer B, Fumagalli I. Chronic 

pancreatitis in Zurich, 1963-1972. Clinical findings 

and follow-up studies of 102 cases. Digestion 

1973;9(5):404-415. No prevalence or incidence 

reported 

Anand A C, Elias E, Neuberger J M. End-stage 

primary biliary cirrhosis in a first generation migrant 

south Asian population. Eur J Gastroenterol Hepatol 

1996;8(7):663-666. No prevalence or incidence 

reported 

Anderson J A. The clinical spectrum of food allergy in 

adults. Clin Exp Allergy Suppl 1991;21(1):304-315. 

No prevalence or incidence reported 

Anderson R P, Degano P, Godkin A J et al. In vivo 

antigen challenge in celiac disease identifies a single 

transglutaminase-modified peptide as the dominant Agliadin T-cell epitope. Nat Med 2000;6(3):337-342. 

No prevalence or incidence reported 

Andersson-Wenckert I, Blomquist H K, Fredrikzon B. 

Oral health in coeliac disease and cow's milk protein 

intolerance. Swed Dent J 1984;8(1):9-14. No

prevalence or incidence reported

Andre F, Andre C, Colin L et al. Role of new allergens

and of allergens consumption in the increased 

incidence of food sensitizations in France. Toxicology

1994;93(1):77-83. No prevalence or incidence 

reported 

Annibale B, Capurso G, Delle Fave G. The stomach 

and iron deficiency anaemia: a forgotten link.

Digestive and Liver Disease - Official Journal of the 

Italian Society of Gastroenterology and the Italian 

Association for the Study of the Liver 2003;35(4):288-

295. No prevalence or incidence reported 

Annibale B, Severi C, Chistolini A et al. Efficacy of 

gluten-free diet alone on recovery from iron 

deficiency anemia in adult celiac patients. Am J

Gastroenterol 2001;96(1):132-137. No prevalence or 

incidence reported 

Anonymous. A guide for patients. Pract Gastroenterol 

2002;26(11):58-61. No prevalence or incidence 

reported 

Anonymous. A long-term survey of coeliac disease. 

Med J Aust 1971;2(20):992No prevalence or

incidence reported 

Anonymous. American Gastroenterological 

Association medical position statement: Celiac Sprue. 

Gastroenterology 2001;120(6):1522-1525. No 

prevalence or incidence reported

Anonymous. American Gastroenterological 

Association medical position statement: guidelines on 

osteoporosis in gastrointestinal diseases. 

Gastroenterology 2003;124(3):791-794. No 

prevalence or incidence reported

Anonymous. American Thoracic Society/European 

Respiratory Society statement: Standards for the

diagnosis and management of individuals with alpha-1 

antitrypsin deficiency. Am J Respir Crit Care Med

2003;168(7):818-900. No prevalence or incidence 

reported 

Anonymous. Are your GI symptoms linked to wheat?.

Johns Hopkins Med Lett Health After 50 

2003;15(5):3, 7No prevalence or incidence reported 

Anonymous. Catch-up growth in celiac disease. Nutr 

Rev 1973;31(1):13-14. No prevalence or incidence 

reported 

Anonymous. Celiac disease and how to live with it. 

Harvard Women's Health Watch 2001;8(9):3-4. No

prevalence or incidence reported

Anonymous. Celiac disease. Am Fam Phys

1998;57(5):1039-1041. No prevalence or incidence 

reported 

Anonymous. Coeliac disease in the West of Ireland. 

Br Med J 1973;2(5864):484-485. No prevalence or

incidence reported 

Anonymous. Coeliac disease. Br Med J

1970;4(726):1-2. No prevalence or incidence reported 

Anonymous. Editorial: Drop-outs' diarrhoea. Br Med J 

1974;3(5927):373No prevalence or incidence reported 

A-500
Anonymous. Giardia lamblia and coeliac disease.

Lancet 1973;2(7821):138No prevalence or incidence 

reported 

Anonymous. Highly inheritable coeliac disease. Med 

Today 2002;3(7):15No prevalence or incidence 

reported 

Anonymous. Hypophosphataemic osteomalacia in 

adults. Lancet 1971;1(7713):1343No prevalence or 

incidence reported 

Anonymous. Irritable bowel syndrome. Merec Bull 

2000;11(11):41-44. No prevalence or incidence 

reported 

Anonymous. M2A(R) capsule endoscopy common 

diseases & current data: Including results from 

Digestive Disease Week (DDW) 2002, San Francisco, 

May 19th-22nd. Endoscopy 2002;34(7):I-V. No 

prevalence or incidence reported

Anonymous. Minerva. Br Med J 

1996;312(7040):1238No prevalence or incidence 

reported 

Anonymous. Patient support organisations: The 

coeliac society of Australia. Aust Prescr 

2001;24(2):40No prevalence or incidence reported 

Anonymous. RCN Paediatric and Adolescent Diabetes

Group 2002 Conference. Pract Diabetes Int 

2003;20(2):77No prevalence or incidence reported 

Anonymous. Sedondary effects of iron deficiency. 

Nutr Rev 1969;27(2):41-43. No prevalence or

incidence reported 

Anonymous. Summary and recommendations: 

Classification of gastrointestinal manifestations due to

immunologic reactions to foods in infants and young 

children. J Pediatr Gastroenterol Nutr 2000;30(Suppl 

1):S87-S94. No prevalence or incidence reported

Anonymous. Thyroid disease in young diabetics. 

Lancet 1982;1(8284):1285-1286. No prevalence or

incidence reported 

Anonymous. What you need to know about ... coeliac 

disease. Nurs Times 2003;99(10):30No prevalence or 

incidence reported 

Ansaldi-Balocco N, Santini B, Sarchi C. Efficacy of 

pancreatic enzyme supplementation in children with 

cystic fibrosis: comparison of two preparations by

random crossover study and a retrospective study of 

the same patients at two different ages. J Pediatr

Gastroenterol Nutr 1988;7(Suppl 1):s40-s45. No 

prevalence or incidence reported

Anson O, Weizman Z, Zeevi N. Celiac disease:

parental knowledge and attitudes of dietary

compliance. Pediatrics 1990;85(1):98-103. No

prevalence or incidence reported

Anton H C. Thinning of the clavicular cortex in adults 

under the age of 45 in osteomalacia and 

hyperparathyroidism. Clin Radiol 1979;30(3):307-

310. No prevalence or incidence reported 

Arato A, Savilahti E, Tainio V M et al. HLA-DR 

expression, natural killer cells and IgE containing cells 

in the jejunal mucosa of coeliac children. Gut

1987;28(8):988-994. No prevalence or incidence 

reported 

Araya M, Henderson-Smart D. Letter: Coeliac disease:

an undiagnosed disorder with important implications. 

Med J Aust 1974;1(14):549No prevalence or

incidence reported 

Araya M, Mondragon A, Perez-Bravo F et al. Celiac 

disease in a Chilean population carrying Amerindian 

traits. J Pediatr Gastroenterol Nutr 2000;31(4):381-

386. No prevalence or incidence reported 

Arden Nigel K, Cooper Cyrus. Assessment of the risk 

of fracture in patients with gastrointestinal disease.

Eur J Gastroenterol Hepatol 2003;15(8):865-868. No 

prevalence or incidence reported

Armentia A, Martin-Santos J M, Quintero A et al.

Bakers' asthma: prevalence and evaluation of

immunotherapy with a wheat flour extract. Ann 

Allergy 1990;65(4):265-272. No prevalence or

incidence reported 

Armentia A, Tapias J, Barber D et al. Sensitization to 

the storage mite Lepidoglyphus destructor in wheat 

flour respiratory allergy. Ann Allergy 1992;68(5):398-

403. No prevalence or incidence reported 

Armes J, Gee D C, Macrae F A et al. Collagenous

colitis: jejunal and colorectal pathology. J Clin Pathol

1992;45(9):784-787. No prevalence or incidence 

reported 

Arnala I, Kemppainen T, Kroger H et al. Bone

histomorphometry in celiac disease. Ann Chir 

Gynaecol 2001;90(2):100-104. No prevalence or

incidence reported 

Arnason J A, Gudjonsson H, Freysdottir J et al. Do 

adults with high gliadin antibody concentrations have 

subclinical gluten intolerance?. Gut 1992;33(2):194-

197. No prevalence or incidence reported 

Arnott I D, McDonald D, Williams A et al. Clinical

use of Infliximab in Crohn's disease: the Edinburgh 

experience. Aliment Pharmacol Ther 

A-501
2001;15(10):1639-1646. No prevalence or incidence 

reported 

Arranz E, Ferguson A. Intestinal antibody pattern of 

celiac disease: occurrence in patients with normal

jejunal biopsy histology. Gastroenterology

1993;104(5):1263-1272. No prevalence or incidence 

reported 

Arranz E, Telleria J J, Sanz A et al. HLA-DQA1*0501 

and DQB1*02 homozygosity and disease 

susceptibility in Spanish coeliac patients. Exp Clin

Immunogenet 1997;14(4):286-290. No prevalence or 

incidence reported 

Arshad S H, Matthews S, Gant C et al. Effect of

allergen avoidance on development of allergic 

disorders in infancy. Lancet 1992;339(8808):1493-

1497. No prevalence or incidence reported 

Arshad S H. Food allergen avoidance in primary 

prevention of food allergy. Allergy Eur J Allergy Clin

Immunol Suppl 2001;56(67):113-116. No prevalence 

or incidence reported 

Ascher H, Hahn-Zoric M, Hanson L A et al. Value of 

serologic markers for clinical diagnosis and population

studies of coeliac disease. Scand J Gastroenterol 

1996;31(1):61-67. No prevalence or incidence 

reported 

Ascher H, Holm K, Kristiansson B et al. Different

features of coeliac disease in two neighbouring 

countries. Arch Dis Child 1993;69(3):375-380. No 

prevalence or incidence reported

Ascher H, Krantz I, Kristiansson B. Increasing

incidence of coeliac disease in Sweden. Arch Dis

Child 1991;66(5):608-611. Serology screen <1990 

Ascher H, Krantz I, Rydberg L et al. Influence of

infant feeding and gluten intake on coeliac disease.

Arch Dis Child 1997;76(2):113-117. Not a relevant 

screening test 

Ascher H, Kristiansson B. The highest incidence of 

celiac disease in Europe: the Swedish experience. J

Pediatr Gastroenterol Nutr 1997;24(5):S3-S6. No 

prevalence or incidence reported

Ascher H. Coeliac disease and type 1 diabetes: an

affair still with much hidden behind the veil. Acta 

Paediatr 2001;90(11):1217-1220. No prevalence or

incidence reported 

Ascher H. Paediatric aspects of coeliac disease: old 

challenges and new ones... Digestive and Liver 

Disease - Official Journal of the Italian Society of 

Gastroenterology and the Italian Association for the 

Study of the Liver 2002;34(3):216-224. No prevalence 

or incidence reported 

Ashabani A, Errabtea H, Shapan A et al. Serologic 

markers of untreated celiac disease in Libyan children: 

antigliadin, antitransglutaminase, antiendomysial, and 

anticalreticulin antibodies. J Pediatr Gastroenterol 

Nutr 2001;33(3):276-282. No prevalence or incidence 

reported 

Ashabani Abdelhakim, Abushofa Umaima, Abusrewill 

Suliman et al. The prevalence of coeliac disease in

Libyan children with type 1 diabetes mellitus.

Diabetes Metab Res Rev 2003;19(1):69-75. Not a 

relevant screening geography

Ashkenazi A, Cooper M, Nissim F et al. Occurrence 

of celiac disease in children in a defined area of Israel. 

Isr J Med Sci 1983;19(1):63-66. Not a relevant 

screening geography

Ashorn M. Gastrointestinal diseases in the paediatric

age groups in Europe: Epidemiology and impact on 

healthcare. Aliment Pharmacol Ther Suppl 

2003;18(3):80-83. No prevalence or incidence 

reported 

Askling Johan, Linet Martha, Gridley Gloria et al. 

Cancer incidence in a population-based cohort of

individuals hospitalized with celiac disease or 

dermatitis herpetiformis. Gastroenterology

2002;123(5):1428-1435. No prevalence or incidence 

reported 

Asquith P. Adult coeliac disease and malignancy. Ir 

Med J 1974;67(15):417-420. No prevalence or 

incidence reported 

Aukee S, Jussila J, Saikku L A et al. The functional 

state of the gastrointestinal tract before and after 

selective surgery. Scand J Gastroenterol 

1969;4(3):241-248. No prevalence or incidence 

reported 

Auricchio S, Buffolano W, Ciccimarra F et al. In vitro 

proliferation of lymphocytes from celiac children and 

their first-degree relatives in response to wheat

gliadin-derived peptides. J Pediatr Gastroenterol Nutr 

1982;1(4):515-524. No prevalence or incidence 

reported 

Auricchio S, Follo D, de Ritis G et al. Does breast 

feeding protect against the development of clinical

symptoms of celiac disease in children?. J Pediatr 

Gastroenterol Nutr 1983;2(3):428-433. No prevalence 

or incidence reported 

Auricchio S, Greco L, Troncone R. Gluten-sensitive 

enteropathy in childhood. Pediatr Clin North Am 

1988;35(1):157-187. No prevalence or incidence 

reported 

Auricchio S, Greco L, Troncone R. What is the true 

prevalence of coeliac disease?. Gastroenterol Int 

1990;3(3):140-142. Review article 

A-502
Auricchio S, Mazzacca G, Tosi R et al. Coeliac

disease as a familial condition: Identification of

asymptomatic coeliac patients within family groups.

Gastroenterol Int 1988;1(1):25-31. Serology screen 

<1990 

Austin A S, Logan R F A, Thomason K et al. Cigarette 

smoking and adult coeliac disease. Scand J

Gastroenterol 2002;37(8):978-982. No prevalence or 

incidence reported 

Axmacher B, Hed J, Ottoson E et al. Celiac disease 

and organic dust toxic syndrome. Am J Ind Med 

1990;17(1):94-95. No prevalence or incidence 

reported 

Ayres J G. Classification and management of brittle 

asthma. Br J Hosp Med 1997;57(8):387-389. No 

prevalence or incidence reported

Bagdi E, Diss T C, Munson P et al. Mucosal intraepithelial lymphocytes in enteropathy-associated Tcell lymphoma, ulcerative jejunitis, and refractory

celiac disease constitute a neoplastic population. 

Blood 1999;94(1):260-264. No prevalence or

incidence reported 

Bagnasco M, Montagna P, De Alessandri A et al. IgA 

antiendomysium antibodies in human umbilical cord 

sections as a screening test in relatives of patients with 

celiac disease. Allergy 1997;52(10):1017-1021. No

prevalence or incidence reported

Bahia M, Rabello A, Brasileiro Filho G et al. Serum 

antigliadin antibody levels as a screening criterion 

before jejunal biopsy indication for celiac disease in a

developing country. Brazilian Journal of Medical and 

Biological Research = Revista Brasileira De Pesquisas 

Medicas E Biologicas / Sociedade Brasileira De

Biofisica ...Et Al 2001;34(11):1415-1420. No 

prevalence or incidence reported

Bahna S L, Tateno K, Heiner D C. Elevated IgD 

antibodies to wheat in celiac disease. Ann Allergy 

1980;44(3):146-151. No prevalence or incidence 

reported 

Bai J C, Andrush A, Matelo G et al. Fecal fat 

concentration in the differential diagnosis of 

steatorrhea. Am J Gastroenterol 1989;84(1):27-30. No 

prevalence or incidence reported

Bai J C, Maurino E, Martinez C et al. Abnormal 

colonic transit time in untreated celiac sprue. Acta

Gastroenterol Latinoam 1995;25(5):277-284. No

prevalence or incidence reported

Bai J C. Malabsorption syndromes. Digestion 

1998;59(5):530-546. No prevalence or incidence 

reported 

Bai J, Moran C, Martinez C et al. Celiac sprue after 

surgery of the upper gastrointestinal tract. Report of 

10 patients with special attention to diagnosis, clinical 

behavior, and follow-up. J Clin Gastroenterol 

1991;13(5):521-524. No prevalence or incidence 

reported 

Baird I M, Walters R L, Sutton D R. Absorption of 

slow-release iron and effects of ascorbic acid in 

normal subjects and after partial gastrectomy. Br Med 

J 1974;4(5943):505-508. No prevalence or incidence 

reported 

Baker J, Sandhu B K. Nutrition, eating and

gastrointestinal conditions in adolescence. J R Coll

Phys London 2000;34(2):137-140. No prevalence or 

incidence reported 

Balakrishnan V. Management of chronic pancreatitis.

Tropical Gastroenterology - Official Journal of the 

Digestive Diseases Foundation 1986;7(4):141-146. No 

prevalence or incidence reported

Balas A, Vicario J L, Zambrano A et al. Absolute 

linkage of celiac disease and dermatitis herpetiformis 

to HLA-DQ. Tissue Antigens 1997;50(1):52-56. No 

prevalence or incidence reported

Balducci-Silano P L, Layrisse Z E. HLA-DP and 

susceptibility to insulin-dependent diabetes mellitus in 

an ethnically mixed population. Associations with 

other HLA-alleles. J Autoimmun 1995;8(3):425-437. 

No prevalence or incidence reported 

Banerji N K, Hurwitz L J. Nervous system

manifestations after gastric surgery. Acta Neurol 

Scand 1971;47(4):485-513. No prevalence or

incidence reported 

Bansi D S, Chapman R W, Fleming K A. Prevalence 

and diagnostic role of antineutrophil cytoplasmic 

antibodies in inflammatory bowel disease. Eur J 

Gastroenterol Hepatol 1996;8(9):881-885. No

prevalence or incidence reported

Bansi D S, Fleming K A, Chapman R W. Importance 

of antineutrophil cytoplasmic antibodies in primary

sclerosing cholangitis and ulcerative colitis:

prevalence, titre, and IgG subclass. Gut 

1996;38(3):384-389. No prevalence or incidence 

reported 

Banwell J G, Hutt M R, Leonard P J et al. Exocrine

pancreatic disease and the malabsorption syndrome in

tropical Africa. Gut 1967;8(4):388-401. No prevalence 

or incidence reported 

Banwell J G, Marsden P D, Blackman V et al. 

Hookworm infection and intestinal absorption

amongst Africans in Uganda. Am J Trop Med Hyg 

1967;16(3):304-308. No prevalence or incidence 

reported 

A-503
Barakat M H, Ali S M, Badawi A R et al. Peroral

endoscopic duodenal biopsy in infants and children. 

Acta Paediatr Scand 1983;72(4):563-569. No 

prevalence or incidence reported

Barbato M, Miglietta M R, Viola F et al. Impact of

modification of diagnostic techniques and criteria on 

the presentation of celiac disease in the last 16 years.

Observation in Rome. Minerva Pediatr

1996;48(9):359-363. No prevalence or incidence 

reported 

Bardella M T, Fraquelli M, Quatrini M et al. 

Prevalence of hypertransaminasemia in adult celiac 

patients and effect of gluten-free diet. Hepatology

1995;22(3):833-836. No prevalence or incidence 

reported 

Bardella M T, Fredella C, Prampolini L et al. Body

composition and dietary intakes in adult celiac disease 

patients consuming a strict gluten-free diet. Am J Clin 

Nutr 2000;72(4):937-939. No prevalence or incidence 

reported 

Bardella M T, Fredella C, Prampolini L et al. Gluten 

sensitivity in monozygous twins: A long-term followup of five pairs. Am J Gastroenterol 2000;95(6):1503-

1505. No prevalence or incidence reported 

Bardella M T, Minoli G, Radaelli F et al. Reevaluation

of duodenal endoscopic markers in the diagnosis of 

celiac disease. Gastroenterol Int 2000;51(6):714-716. 

No prevalence or incidence reported 

Bardella M T, Minoli G, Ravizza D et al. Increased 

prevalence of celiac disease in patients with dyspepsia. 

Arch Intern Med 2000;160(10):1489-1491. Not a 

relevant screening group 

Bardella M T, Molteni N, Prampolini L et al. Need for 

follow up in coeliac disease. Arch Dis Child

1994;70(3):211-213. No prevalence or incidence 

reported 

Bardella M T, Molteni N, Quatrini M et al. Clinical, 

biochemical and histological abnormalities in adult 

celiac patients on gluten-free diet. Gastroenterol Clin 

Biol 1985;9(11):787-789. No prevalence or incidence 

reported 

Bardella M T, Vecchi M, Conte D et al. Chronic 

unexplained hypertransaminasemia may be caused by

occult celiac disease. Hepatology 1999;29(3):654-657. 

Not a relevant screening group 

Barera G, Mora S, Brambilla P et al. Body

composition in children with celiac disease and the 

effects of a gluten-free diet: a prospective case-control 

study. Am J Clin Nutr 2000;72(1):71-75. No

prevalence or incidence reported

Barlow J M, Johnson C D, Stephens D H. Celiac 

disease: how common is jejunoileal fold pattern

reversal found at small-bowel follow-through?.

Ajr.American Journal of Roentgenology

1996;166(3):575-577. No prevalence or incidence 

reported 

Baroncelli G I, Federico G, Bertelloni S et al. 

Assessment of bone quality by quantitative ultrasound 

of proximal phalanges of the hand and fracture rate in 

children and adolescents with bone and mineral 

disorders. Pediatr Res 2003;54(1):125-136. No

prevalence or incidence reported

Barr G D, Grehan M J. Coeliac disease. Med J Aust

1998;169(2):109-114. No prevalence or incidence 

reported 

Barr G, Cameron D, King S et al. Current status and 

management of coeliac disease. Med Today

2003;4(6):30-39. No prevalence or incidence reported 

Barry R E, Baker P, Read A E. Coeliac disease. The 

clinical presentation. Clin Gastroenterol 1974;3(1):55-

69. No prevalence or incidence reported 

Barry R E, Morris J S, Kenwright S et al. Coeliac 

disease and malignancy. The possible importance of 

familial involvement. Scand J Gastroenterol 

1971;6(3):205-207. No prevalence or incidence 

reported 

Barta L, Kosnai I, Molnar M et al. Simultaneous

occurrence of diabetes mellitus and coeliac disease. 

Acta Paediatr Hung 1985;26(4):303-306. No 

prevalence or incidence reported

Barton D M, Baskar V, Kamalakannan D et al. An 

assessment of care of paediatric and adolescent

patients with diabetes in a large district general 

hospital. Diabetic Medicine - a Journal of the British 

Diabetic Association 2003;20(5):394-398. No 

prevalence or incidence reported

Bateson M C, Hopwood D, MacGillivray J B. Jejunal 

morphology in multiple sclerosis. Lancet 

1979;1(8126):1108-1110. No prevalence or incidence 

reported 

Beaumont D M, Mian M S. Coeliac disease in old age:

'A catch in the rye'. Age Ageing 1998;27(4):535-538. 

No prevalence or incidence reported 

Becker C. Clinical evaluation for osteoporosis. Clin 

Geriatr Med 2003;19(2):299-320. No prevalence or

incidence reported 

Beckett C G, Ciclitira P J. Celiac disase. Curr Opin 

Gastroenterol 1997;13(2):107-111. No prevalence or 

incidence reported 

A-504
Beckett C. A gut issue. Nurs Times 1999;95(8):65-6, 

69. No prevalence or incidence reported 

Behne D. Selenium. Ann Nestle 1994;52(3):107-117. 

No prevalence or incidence reported 

Bell I R, Schwartz G E, Peterson J M et al. Possible 

time-dependent sensitization to xenobiotics: selfreported illness from chemical odors, foods, and 

opiate drugs in an older adult population. Arch 

Environ Health 1993;48(5):315-327. No prevalence or

incidence reported 

Bell I R, Schwartz G E, Peterson J M et al. Symptom 

and personality profiles of young adults from a college

student population with self-reported illness from

foods and chemicals. J Am Coll Nutr 1993;12(6):693-

702. No prevalence or incidence reported 

Bell J I. The major histocompatibility complex and 

disease. Curr Opin Immunol 1989;2(1):114-116. No 

prevalence or incidence reported

Bell J, Rassenti L, Smoot S et al. HLA-DQ beta-chain 

polymorphism linked to myasthenia gravis. Lancet 

1986;1(8489):1058-1060. No prevalence or incidence 

reported 

Bell S, Green P H R, Kagnoff M F. American 

gastroenterological association medical position

statement: Celiac sprue. Gastroenterology

2001;120(6):1522-1525. No prevalence or incidence 

reported 

Belloni Cesare, Avanzini Maria A, De Silvestri et al.

No evidence of autoimmunity in 6-year-old children 

immunized at birth with recombinant hepatitis B 

vaccine. Pediatrics 2002;110(1 Pt 1):E4No prevalence 

or incidence reported 

Berg N O, Lindberg T. Incidence of coeliac disease 

and transient gluten intolerance in children in a 

Swedish urban community. Acta Paediatr Scand 

1979;68(3):397-400. Not a relevant screening 

geography

Bernardini R, Novembre E, Ingargiola A et al. 

Prevalence and risk factors of latex sensitization in an 

unselected pediatric population. J Allergy Clin

Immunol 1998;101(5):621-625. No prevalence or

incidence reported 

Bernstein Charles N, Leslie William D, Leboff Meryl

S. AGA technical review on osteoporosis in 

gastrointestinal diseases. Gastroenterology

2003;124(3):795-841. No prevalence or incidence 

reported 

Bernstein Charles N, Leslie William D. The

pathophysiology of bone disease in gastrointestinal 

disease. Eur J Gastroenterol Hepatol 2003;15(8):857-

864. No prevalence or incidence reported 

Berrill W T, Eade O E, Fitzpatrick P F. Bird Fancier's 

lung and jejunal villous atrophy. Lancet 

1975;2(7943):1006-1008. No prevalence or incidence 

reported 

Berti I, Trevisiol C, Tommasini A et al. Usefulness of 

screening program for celiac disease in autoimmune 

thyroiditis. Dig Dis Sci 2000;45(2):403-406. No

prevalence or incidence reported

Betuel H, Gebuhrer L, Descos L et al. Adult celiac 

disease associated with HLA-DRw3 and -DRw7.

Tissue Antigens 1980;15(3):231-238. No prevalence 

or incidence reported 

Bevan S, Popat S, Braegger C P et al. Contribution of 

the MHC region to the familial risk of coeliac disease.

J Med Genet 1999;36(9):687-690. No prevalence or 

incidence reported 

Bevan S, Popat S, Houlston R S. Relative power of 

linkage and transmission disequilibrium test strategies 

to detect non-HLA linked coeliac disease 

susceptibility genes. Gut 1999;45(5):668-671. No 

prevalence or incidence reported

Bhatnagar S, Bhan M K. Serological diagnosis of 

celiac disease. Indian J Pediatr 1999;66(1 Suppl):S26-

S31. No prevalence or incidence reported 

Biagi F, Corazza G R. Gene and gliadin/gut and

kidney. Am J Gastroenterol 2002;97(10):2486-2488. 

No prevalence or incidence reported 

Biagi F, Corazza G R. Tissue transglutaminase

antibodies: Is sensitivity more important than 

specificity?. Digestive and Liver Disease - Official

Journal of the Italian Society of Gastroenterology and 

the Italian Association for the Study of the Liver 

2001;33(5):401-402. No prevalence or incidence 

reported 

Biagi F, Ellis H J, Parnell N D et al. A non-toxic 

analogue of a coeliac-activating gliadin peptide: a 

basis for immunomodulation?. Aliment Pharmacol 

Ther 1999;13(7):945-950. No prevalence or incidence 

reported 

Bianchi M L, Bardella M T. Bone and celiac disease. 

Calcif Tissue Int 2002;71(6):465-471. No prevalence 

or incidence reported 

Biemond I, Pena A S, Groenland F et al. Coeliac 

disease in The Netherlands: demographic data of a 

patient survey among the members of the Dutch 

Coeliac Society. Neth J Med 1987;31(5-6):263-268. 

No prevalence or incidence reported 

Bilbao J R, Martin-Pagola A, Vitoria J C et al. HLADRB1 and MHC class 1 chain-related A haplotypes in 

Basque families with celiac disease. Tissue Antigens

A-505
2002;60(1):71-76. No prevalence or incidence 

reported 

Bilbao J, Ramon Vitoria, Juan C et al. 

Immunoglobulin G autoantibodies against tissuetransglutaminase. A sensitive, cost-effective assay for 

the screening of celiac disease. Autoimmunity

2002;35(4):255-259. No prevalence or incidence 

reported 

Bini E J. Helicobacter pylori and iron deficiency

anemia: Guilty as charged?. Am J Med 

2001;111(6):495-497. No prevalence or incidence 

reported 

Birkbeck J A. Coeliac disease in a diabetic child.

Lancet 1969;2(7618):496No prevalence or incidence 

reported 

Bischoff S C, Mayer J H, Manns M P. Allergy and the 

gut. Int Arch Allergy Immunol 2000;121(4):270-283. 

No prevalence or incidence reported 

Bischoff S C, Mayer J, Wedemeyer J et al. 

Colonoscopic allergen provocation (COLAP): a new 

diagnostic approach for gastrointestinal food allergy.

Gut 1997;40(6):745-753. No prevalence or incidence 

reported 

Bischoff S C. Mucosal allergy: role of mast cells and 

eosinophil granulocytes in the gut. Bailliere's Clinical 

Gastroenterology 1996;10(3):443-459. No prevalence 

or incidence reported 

Bizzaro N, Villalta D, Tonutti E et al. Association of 

celiac disease with connective tissue diseases and 

autoimmune diseases of the digestive tract.

Autoimmun Rev 2003;2(6):358-363. No prevalence or

incidence reported 

Bjorksten B. Allergy priming early in life. Lancet

1999;353(9148):167-168. No prevalence or incidence 

reported 

Bjorksten B. The role of the gastrointestinal tract in 

the development of respiratory hypersensitivities.

Toxicol Lett 1996;86(2-3):85-88. No prevalence or

incidence reported 

Bjorksten F, Backman A, Jarvinen K A et al. 

Immunoglobulin E specific to wheat and rye flour

proteins. Clin Allergy 1977;7(5):473-483. No 

prevalence or incidence reported

Bjornsson E, Janson C, Plaschke P et al. Prevalence of

sensitization to food allergens in adult Swedes. Annals 

of Allergy, Asthma & Immunology - Official 

Publication of the American College of Allergy,

Asthma, & Immunology 1996;77(4):327-332. No 

prevalence or incidence reported

Black Corri, Kaye James A, Jick Hershel. Relation of 

childhood gastrointestinal disorders to autism: nested 

case-control study using data from the UK General 

Practice Research Database. BMJ

2002;325(7361):419-421. No prevalence or incidence 

reported 

Blanco A, Garrote J A, Alonso M et al. Soluble CD4 

antigen is increased in active coeliac disease. Adv Exp 

Med Biol 1995;371b1355-1358. No prevalence or

incidence reported 

Blomme B, Gerlo E, Hauser B et al. Disaccharidase 

activities in Belgian children: Reference intervals and 

comparison with non-Belgian Caucasian children. 

Acta Paediatr Int J Paediatr 2003;92(7):806-810. No 

prevalence or incidence reported

Bode S, Gudmand-Hoyer E. Incidence and clinical 

significance of lactose malabsorption in adult coeliac 

disease. Scand J Gastroenterol 1988;23(4):484-488. 

No prevalence or incidence reported 

Bode S, Gudmand-Hoyer E. Symptoms and 

haematologic features in consecutive adult coeliac 

patients. Scand J Gastroenterol 1996;31(1):54-60. No 

prevalence or incidence reported

Bodmer W F. The HLA system and disease. The

Oliver Sharpey Lecture 1979. J R Coll Physicians

Lond 1980;14(1):43-50. No prevalence or incidence 

reported 

Boehm P, Nassimbeni G, Ventura A. Chronic nonspecific diarrhoea in childhood: How often is it 

iatrogenic?. Acta Paediatr Int J Paediatr 

1998;87(3):268-271. No prevalence or incidence 

reported 

Boersma B, Houwen R H J, Blum W F et al. Catch-up 

growth and endocrine changes in childhood celiac 

disease. Endocrine changes during catch-up growth. 

Horm Res 2002;58(Suppl 1):57-65. No prevalence or

incidence reported 

Bognetti E, Riva M C, Bonfanti R et al. Growth

changes in children and adolescents with short-term

diabetes. Diabetes Care 1998;21(8):1226-1229. No 

prevalence or incidence reported

Bolognesi E, Karell K, Percopo S et al. Additional 

factor in some HLA DR3/DQ2 haplotypes confers a 

fourfold increased genetic risk of celiac disease.

Tissue Antigens 2003;61(4):308-316. No prevalence 

or incidence reported 

Bolsover W J, Hall M A, Vaughan R W et al. A 

family study confirms that the HLA-DP associations

with celiac disease are the result of an extended HLADR3 haplotype. Hum Immunol 1991;31(2):100-108. 

No prevalence or incidence reported 

Bonamico M, Ballati G, Mariani P et al. Screening for 

coeliac disease: the meaning of low titers of antigliadin antibodies (AGA) in non-coeliac children. Eur 

A-506
J Epidemiol 1997;13(1):55-59. No prevalence or 

incidence reported 

Bonamico M, Bottaro G, Pasquino A M et al. Celiac 

disease and turner syndrome. J Pediatr Gastroenterol 

Nutr 1998;26(5):496-499. No prevalence or incidence 

reported 

Bonamico M, Mariani P, Danesi H M et al. Prevalence

and clinical picture of celiac disease in italian down 

syndrome patients: a multicenter study. J Pediatr

Gastroenterol Nutr 2001;33(2):139-143. Not a relevant

screening group

Bonamico M, Mariani P, Mazzilli M C et al.

Frequency and clinical pattern of celiac disease among 

siblings of celiac children. J Pediatr Gastroenterol

Nutr 1996;23(2):159-163. Not a relevant screening 

group 

Bonamico M, Mariani P, Mazzilli M C et al.

Frequency and clinical pattern of celiac disease among 

siblings of celiac children. J Pediatr Gastroenterol

Nutr 1996;23(2):159-163. Not a relevant screening 

group 

Bonamico M, Morellini M, Mariani P et al. HLA

antigens and antigliadin antibodies in coeliac disease. 

Dis Markers 1991;9(6):313-317. No prevalence or

incidence reported 

Bonamico M, Rasore-Quartino A, Mariani P et al.

Down syndrome and coeliac disease: Usefulness of 

antigliadin and antiendomysium antibodies. Acta 

Paediatr Int J Paediatr 1996;85(12):1503-1505. No

prevalence or incidence reported

Bonamico M, Scire G, Mariani P et al. Short stature as

the primary manifestation of monosymptomatic celiac 

disease. J Pediatr Gastroenterol Nutr 1992;14(1):12-

16. No prevalence or incidence reported 

Bonamico M, Vania A, Monti S et al. Iron deficiency

in children with celiac disease. J Pediatr Gastroenterol

Nutr 1987;6(5):702-706. No prevalence or incidence 

reported 

Bonamico Margherita, Pasquino Anna M, Mariani 

Paolo et al. Prevalence and clinical picture of celiac 

disease in Turner syndrome. J Clin Endocrinol Metab

2002;87(12):5495-5498. Not a relevant screening

group 

Bonifacio E, Ziegler A G, Hummel M et al. Gluten: is 

it also a determinant of islet autoimmunity?. Diabetes 

Metab Rev 1998;14(3):258-259. No prevalence or

incidence reported 

Boniotto Michele, Braida Laura, Spano Andrea et al. 

Variant mannose-binding lectin alleles are associated 

with celiac disease. Immunogenetics 2002;54(8):596-

598. No prevalence or incidence reported 

Bontems P, Deprettere A, Cadranel S et al. The

coeliac iceberg: a consensus in paediatrics. Acta

Gastroenterol Belg 2000;63(2):157-162. No 

prevalence or incidence reported

Book L, Hart A, Black J et al. Prevalence and clinical 

characteristics of celiac disease in Downs syndrome in 

a US study. Am J Med Genet 2001;98(1):70-74. Not a 

relevant screening group 

Book Linda S. Diagnosing celiac disease in 2002: 

who, why, and how?. Pediatrics 2002;109(5):952-954. 

No prevalence or incidence reported 

Bottaro G, Cataldo F, Rotolo N et al. The clinical

pattern of subclinical/silent celiac disease: an analysis

on 1026 consecutive cases. Am J Gastroenterol 

1999;94(3):691-696. Not a relevant screening group 

Bottaro G, Failla P, Rotolo N et al. Changes in coeliac 

disease behaviour over the years. Acta Paediatr 

1993;82(6-7):566-568. Not a relevant screening test 

Boudraa G, Hachelaf W, Benbouabdellah M et al. 

Prevalence of coeliac disease in diabetic children and 

their first- degree relatives in west Algeria: screening 

with serological markers. Acta Paediatr 

1996;412(Suppl):58-60. Not a relevant screening 

geography

Bouguerra F, Babron M C, Eliaou J F et al. 

Synergistic effect of two HLA heterodimers in the

susceptibility to celiac disease in Tunisia. Genet 

Epidemiol 1997;14(4):413-422. No prevalence or

incidence reported 

Bouguerra F, Dugoujon J M, Babron M C et al. 

Susceptibility to coeliac disease in Tunisian children 

and GM immunoglobulin allotypes. European Journal 

of Immunogenetics - Official Journal of the British 

Society for Histocompatibility and Immunogenetics 

1999;26(4):293-297. No prevalence or incidence 

reported 

Bourgain C, Genin E, Holopainen P et al. Use of 

closely related affected individuals for the genetic 

study of complex diseases in founder populations. Am 

J Hum Genet 2001;68(1):154-159. No prevalence or 

incidence reported 

Bourke M, O'Donovan M, Stevens F M et al. Alpha 1-

antitrypsin phenotypes in coeliac patients and a 

control population in the west of Ireland. Ir J Med Sci 

1993;162(5):171-172. No prevalence or incidence 

reported 

Bourke S, Murphy B, Stafford F et al. Population

differences in intestinal permeability to chromium

EDTA. 1988;157(9):287-289. No prevalence or 

incidence reported 

A-507
Boy M F, La Nasa G, Balestrieri A et al. Distribution 

of HLA-DPB1, -DQB1 -DQA1 alleles among 

Sardinian celiac patients. Dis Markers 

1995;12(3):199-204. No prevalence or incidence 

reported 

Boyd S, Collins B J, Bell P M et al. Clinical 

presentation of coeliac disease in adult

gastroenterological practice. Ulster Med J

1985;54(2):140-147. No prevalence or incidence 

reported 

Brady M S, Rickard K, Yu P L et al. Effectiveness and 

safety of small vs. large doses of enteric coated

pancreatic enzymes in reducing steatorrhea in children

with cystic fibrosis: a prospective randomized study.

Pediatr Pulmonol 1991;10(2):79-85. No prevalence or

incidence reported 

Braegger C P, MacDonald T T. The immunologic 

basis for celiac disease and related disorders. Semin 

Gastrointest Dis 1996;7(3):124-133. No prevalence or

incidence reported 

Braga M, Zerbi A, Dal Cin S et al. Postoperative

management of patients with total exocrine pancreatic 

insufficiency. Br J Surg 1990;77(6):669-672. No

prevalence or incidence reported

Bragelmann R, Armbrecht U, Rosemeyer D et al. The 

effect of pancreatic enzyme supplementation in

patients with steatorrhoea after total gastrectomy. Eur

J Gastroenterol Hepatol 1999;11(3):231-237. No 

prevalence or incidence reported

Brai M, Accardo P, Bellavia D. Polymorphism of the 

complement components in human pathology. Annali 

Italiani Di Medicina Interna - Organo Ufficiale Della 

Societa Italiana Di Medicina Interna 1994;9(3):167-

172. No prevalence or incidence reported 

Brandt L J, Locke G R, Olden K et al. An evidencebased approach to the management of irritable bowel 

syndrome in North America. Am J Gastroenterol 

2002;97(11 SUPPL.):S1-S26. No prevalence or 

incidence reported 

Brandtzaeg P, Baklien K. Characterization of the IgA 

immunocyte population and its product with excessive 

intestinal formation of IgA. Clin Exp Immunol 

1977;30(1):77-88. No prevalence or incidence 

reported 

Branski D, Troncone R. Celiac disease: A reappraisal.

Eur J Pediatr 1998;133(2):181-187. No prevalence or

incidence reported 

Brautbar C, Freier S, Ashkenazi A et al. 

Histocompatibility determinants in Israeli Jewish 

patients with coeliac disease: population and family

study. Tissue Antigens 1981;17(3):313-322. No

prevalence or incidence reported

Brautbar C, Zlotogora J, Laufer N et al. Do identical 

HLA-DR3 genes convey susceptibility to celiac 

disease and insulin dependent diabetes mellitus?.

Tissue Antigens 1984;23(1):58-60. No prevalence or 

incidence reported 

Braverman D Z. Gallbladder contraction in patients 

with irritable bowel syndrome. Isr J Med Sci

1987;23(3):181-184. No prevalence or incidence 

reported 

Brett P M, Yiannakou J Y, Morris M A et al. A 

pedigree-based linkage study of coeliac disease:

failure to replicate previous positive findings. Ann 

Hum Genet 1998;62(Pt 1):25-32. No prevalence or 

incidence reported 

Brett P M, Yiannakou J Y, Morris M A et al. Common 

HLA alleles, rather than rare mutants, confer 

susceptibility to coeliac disease. Ann Hum Genet

1999;63(Pt 3):217-225. No prevalence or incidence 

reported 

Brigden M L. A systematic approach to macrocytosis: 

Sorting out the causes. Postgrad Med 1995;97(5):171-

172+175. No prevalence or incidence reported 

Brink S J. Pediatric, adolescent, and young-adult 

nutrition issues in IDDM. Diabetes Care

1988;11(2):192-200. No prevalence or incidence 

reported 

Brocchi E, Tomassetti P, Misitano B et al. Endoscopic 

markers in adult coeliac disease. Digestive and Liver 

Disease - Official Journal of the Italian Society of 

Gastroenterology and the Italian Association for the 

Study of the Liver 2002;34(3):177-182. No prevalence 

or incidence reported 

Brooklyn Trevor N, Di Mambro, Alexandra J et al. 

Patients over 45 years with iron deficiency require 

investigation. Eur J Gastroenterol Hepatol 

2003;15(5):535-538. No prevalence or incidence 

reported 

Brown J C, EDITOR S, Matsuo Y et al. The 

regulation of insulin secretion by gastrointestinal

hormones. Gastrointestinal Function Regulation and 

Disturbances: Proceedings of the Seventh Symposium

on the Regulation and Disturbances of Gastrointestinal

Function Ic 1989;3-20. No prevalence or incidence 

reported 

Brown M R, Lillibridge C B. When to think of celiac 

disease: the classical features of gluten sensitive 

enteropathy are absent. Clin Pediatr (Phila)

1975;14(1):76-82. No prevalence or incidence 

reported 

Bruno G, Cantani A, Ragno V et al. Natural history of 

IgE antibodies in children at risk for atopy. Annals of 

Allergy, Asthma & Immunology - Official Publication

A-508
of the American College of Allergy, Asthma, & 

Immunology 1995;74(5):431-436. No prevalence or 

incidence reported 

Brusco G, Di Stefano M, Corazza G R. Increased red 

cell distribution width and coeliac disease. Digestive 

and Liver Disease - Official Journal of the Italian

Society of Gastroenterology and the Italian

Association for the Study of the Liver 2000;32(2):128-

130. No prevalence or incidence reported 

Brusco G, Izzi L, Corazza G R. Tissue 

transglutaminase antibodies for coeliac disease 

screening. Ital J Gastroenterol Hepatol 

1998;30(5):496-497. No prevalence or incidence 

reported 

Bryant D A, Mintz E D, Puhr N D et al. Colonic 

epithelial lymphocytosis associated with an epidemic 

of chronic diarrhea. Am J Surg Pathol 

1996;20(9):1102-1109. No prevalence or incidence 

reported 

Budiarso A, Sunoto S, Hendardji H et al. Incidence of

steatorrhoea in Indonesian infants. Paediatr Indones 

1977;17(1-2):6-9. No prevalence or incidence reported 

Burgin-Wolff A, Bertele R M, Berger R et al. A

reliable screening test for childhood celiac disease:

fluorescent immunosorbent test for gliadin antibodies. 

A prospective multicenter study. Eur J Pediatr

1983;102(5):655-660. No prevalence or incidence 

reported 

Burgin-Wolff A, Dahlbom I, Hadziselimovic F et al.

Antibodies against human tissue transglutaminase and 

endomysium in diagnosing and monitoring coeliac 

disease. Scand J Gastroenterol 2002;37(6):685-691. 

No prevalence or incidence reported 

Burks A W, Sampson H. Food allergies in children. 

Curr Probl Pediatr 1993;23(6):230-252. No prevalence 

or incidence reported 

Burrows R, Leiva L, Burgueno M et al. Bone mineral

density (BMD) in children with celiac disease (CD): 

Its relation to puberty and calcium intake. Nutr Res 

1999;19(4):493-499. No prevalence or incidence 

reported 

Bushara K O, Goebel S U, Shill H et al. Gluten 

sensitivity in sporadic and hereditary cerebellar ataxia. 

Ann Neurol 2001;49(4):540-543. No prevalence or

incidence reported 

Businco L, Ziruolo M G, Ferrara M et al. Natural 

history of atopic dermatitis in childhood: an updated 

review and personal experience of a five-year followup. Allergy 1989;44(Suppl 9):70-78. No prevalence or

incidence reported 

Buts J P, Morin C L, Roy C C et al. One-hour blood 

xylose test: a reliable index of small bowel function. 

Eur J Pediatr 1978;92(5):729-733. No prevalence or 

incidence reported 

Butterworth Jeffrey R, Cooper Brian T, Rosenberg

William M C et al. The role of hemochromatosis 

susceptibility gene mutations in protecting against iron 

deficiency in celiac disease. Gastroenterology

2002;123(2):444-449. No prevalence or incidence 

reported 

Buysschaert M. Coeliac disease in patients with type 1 

diabetes mellitus and auto-immune thyroid disorders. 

Acta Gastro-Enterol Belg 2003;66(3):237-240. 

Review article 

Cacciari E, Salardi S, Lazzari R et al. Short stature and

celiac disease: a relationship to consider even in 

patients with no gastrointestinal tract symptoms. Eur J 

Pediatr 1983;103(5):708-711. No prevalence or 

incidence reported 

Cacciari E, Salardi S, Volta U et al. Antigliadin 

antibodies in coeliac children with short stature. 

Lancet 1985;2(8469-8470):1434No prevalence or

incidence reported 

Cacciari E, Salardi S, Volta U et al. Can antigliadin 

antibody detect symptomless coeliac disease in

children with short stature?. Lancet

1985;1(8444):1469-1471. No prevalence or incidence 

reported 

Cacciari E, Salardi S, Volta U et al. Prevalence and 

characteristics of coeliac disease in type 1 diabetes

mellitus. Acta Paediatr Scand 1987;76(4):671-672. 

Serology screen <1990 

Caffarelli C, Romanini E, Caruana P et al. Clinical 

food hypersensitivity: the relevance of duodenal 

immunoglobulin E-positive cells. Pediatr Res 

1998;44(4):485-490. No prevalence or incidence 

reported 

Caffrey C, Hitman G A, Niven M J et al. HLA-DP and 

coeliac disease: family and population studies. Gut 

1990;31(6):663-667. No prevalence or incidence 

reported 

Callender J E, Grantham-McGregor S M, Walker S P

et al. Treatment effects in Trichuris dysentery 

syndrome. Acta Paediatr 1994;83(11):1182-1187. No 

prevalence or incidence reported

Callender S T, Warner G T. Iron absorption from 

bread. Am J Clin Nutr 1968;21(10):1170-1174. No 

prevalence or incidence reported

Calsbeek Hiske, Rijken Mieke, Bekkers Marc J T M et 

al. Social position of adolescents with chronic

digestive disorders. Eur J Gastroenterol Hepatol 

A-509
2002;14(5):543-549. No prevalence or incidence 

reported 

Cameron A J, Hoffman H N. Zollinger-Ellison 

syndrome. Clinical features and long-term follow-up. 

Mayo Clin Proc 1974;49(1):44-51. No prevalence or 

incidence reported 

Campbell C B, Roberts R K, Cowen A E. The 

changing clinical presentation of coeliac disease in

adults. Med J Aust 1977;1(4):89-93. No prevalence or

incidence reported 

Candy D C, Howard F M, McNeish A S. Familial 

inherited abnormalities: miscellaneous disorders. Clin 

Gastroenterol 1982;11(1):207-229. No prevalence or 

incidence reported 

Capristo E, Addolorato G, Mingrone G et al. Changes 

in body composition, substrate oxidation, and resting 

metabolic rate in adult celiac disease patients after a 1-

y gluten-free diet treatment. Am J Clin Nutr

2000;72(1):76-81. No prevalence or incidence 

reported 

Carlsson A, Axelsson I, Borulf S et al. Prevalence of 

IgA-antigliadin antibodies and IgA-antiendomysium 

antibodies related to celiac disease in children with 

Down syndrome. Pediatrics 1998;101(2):272-275. Not 

a relevant screening group 

Carlsson A. Coeliac disease in different child 

populations. Scand J Nutr Naringsforsk 

2001;45(4):186-187. Review article 

Carlsson Annelie K, Lindberg Bengt A, Bredberg

Anders C A et al. Enterovirus infection during

pregnancy is not a risk factor for celiac disease in the 

offspring. J Pediatr Gastroenterol Nutr 

2002;35(5):649-652. No prevalence or incidence 

reported 

Carnicer J, Farre C, Varea V et al. Prevalence of 

coeliac disease in Down Syndrome. Eur J

Gastroenterol Hepatol 2001;13(3):263-267. Not a 

relevant screening group 

Carpenter C B. Autoimmunity and HLA. J Clin 

Immunol 1982;2(3):157-165. No prevalence or

incidence reported 

Carratu R, Secondulfo M, de Magistris L et al. Altered

intestinal permeability to mannitol in diabetes mellitus 

type I. J Pediatr Gastroenterol Nutr 1999;28(3):264-

269. No prevalence or incidence reported 

Carrington J M, Hewitt C J, Dowsett L R et al. The 

prevalence of coeliac disease in Otago. N Z Med J

1987;100(828):460-462. Serology screen <1990 

Carrington J M. Coeliac disease: an analysis of

Coeliac Society membership records. N Z Med J 

1986;99(800):279-281. No prevalence or incidence 

reported 

Carroccio A, Fontana M, Spagnuolo M I et al. 

Pancreatic dysfunction and its association with fat 

malabsorption in HIV infected children. Gut

1998;43(4):558-563. No prevalence or incidence 

reported 

Carroccio A, Iacono G, Montalto G et al. Pancreatic 

enzyme therapy in childhood celiac disease. A doubleblind prospective randomized study. Dig Dis Sci 

1995;40(12):2555-2560. No prevalence or incidence 

reported 

Carroccio A, Iacono G, Montalto G et al. Pancreatic 

insufficiency in celiac disease is not dependent on

nutritional status. Dig Dis Sci 1994;39(10):2235-2242. 

No prevalence or incidence reported 

Carroccio A, Iannitto E, Cavataio F et al. Sideropenic 

anemia and celiac disease: one study, two points of 

view. Dig Dis Sci 1998;43(3):673-678. No prevalence 

or incidence reported 

Carroccio A, Pardo F, Montalto G et al. Use of

famotidine in severe exocrine pancreatic insufficiency

with persistent maldigestion on enzymatic 

replacement therapy. A long-term study in cystic 

fibrosis. Dig Dis Sci 1992;37(9):1441-1446. No 

prevalence or incidence reported

Carroccio Antonio, Iannitto Emilio, Di Prima et al. 

Screening for celiac disease in non-Hodgkin's 

lymphoma patients: a serum anti-transglutaminasebased approach. Dig Dis Sci 2003;48(8):1530-1536. 

No prevalence or incidence reported 

Carswell F, Gibson A A, McAllister T A. Giardiasis 

and coeliac disease. Arch Dis Child 1973;48(6):414-

418. No prevalence or incidence reported 

Carta Mauro, Giovanni Hardoy, Maria Carolina et al. 

Association between panic disorder, major depressive 

disorder and celiac disease: a possible role of thyroid 

autoimmunity. J Psychosom Res 2002;53(3):789-793. 

No prevalence or incidence reported 

Casellas F, Chicharro L, Malagelada J R. Potential 

usefulness of hydrogen breath test with D-xylose in 

clinical management of intestinal malabsorption. Dig 

Dis Sci 1993;38(2):321-327. No prevalence or

incidence reported 

Casellas F, Sardi J, De Torres I et al. Hydrogen breath

test with D-xylose for celiac disease screening is as

useful in the elderly as in other age groups. Dig Dis 

Sci 2001;46(10):2201-2205. No prevalence or

incidence reported 

A-510
Caspary W F, Stein J. Diseases of the small intestine.

Eur J Gastroenterol Hepatol 1999;11(1):21-25. No

prevalence or incidence reported

Castellino F, Scaglione N, Grosso S B et al. A novel 

method for detecting IgA endomysial antibodies by

using human umbilical vein endothelial cells. Eur J 

Gastroenterol Hepatol 2000;12(1):45-49. No

prevalence or incidence reported

Castro M, Crino A, Papadatou B et al. Down 

Syndrome and celiac disease: the prevalence of high 

IgA-antigliadin antibodies and HLA-DR and DQ 

antigens in trisomy 21. J Pediatr Gastroenterol Nutr 

1993;16(3):265-268. Not a relevant screening group 

Cataldo F, Lio D, Marino V et al. Cytokine

genotyping (TNF and IL-10) in patients with celiac

disease and selective IgA deficiency. Am J

Gastroenterol 2003;98(4):850-856. No prevalence or 

incidence reported 

Cataldo F, Lio D, Marino V et al. IgG(1) 

antiendomysium and IgG antitissue transglutaminase 

(anti-tTG) antibodies in coeliac patients with selective 

IgA deficiency. Working Groups on Celiac Disease of 

SIGEP and Club del Tenue. Gut 2000;47(3):366-369. 

No prevalence or incidence reported 

Cataldo F, Marino V, Bottaro G et al. Celiac disease 

and selective immunoglobulin A deficiency. Eur J 

Pediatr 1997;131(2):306-308. No prevalence or 

incidence reported 

Cataldo F, Marino V, Di Stefano P. Celiac disease and

risk of atopy in childhood. Pediatr Asthma Allergy

Immunol 2001;15(2):77-80. No prevalence or

incidence reported 

Cataldo F, Marino V, Ventura A et al. Prevalence and

clinical features of selective immunoglobulin A 

deficiency in coeliac disease: an Italian multicentre 

study. Italian Society of Paediatric Gastroenterology

and Hepatology (SIGEP) and "Club del Tenue" 

Working Groups on Coeliac Disease. Gut 

1998;42(3):362-365. No prevalence or incidence 

reported 

Cataldo F, Ventura A, Lazzari R et al.

Antiendomysium antibodies and coeliac disease: 

solved and unsolved questions. An Italian multicentre 

study. Acta Paediatr 1995;84(10):1125-1131. No 

prevalence or incidence reported

Cataldo Francesco, Marino Vincenzo. Increased

prevalence of autoimmune diseases in first-degree

relatives of patients with celiac disease. J Pediatr 

Gastroenterol Nutr 2003;36(4):470-473. No 

prevalence or incidence reported

Catassi C, Doloretta Macis M, Ratsch I M et al. The

distribution of DQ genes in the Saharawi population 

provides only a partial explanation for the high celiac 

disease prevalence. Tissue Antigens 2001;58(6):402-

406. No prevalence or incidence reported 

Catassi C, Fabiani E, Ratsch I M et al. Celiac disease 

in the general population: should we treat 

asymptomatic cases?. J Pediatr Gastroenterol Nutr

1997;24(5):S10-S12. No prevalence or incidence 

reported 

Catassi C, Fabiani E. The spectrum of coeliac disease 

in children. Bailliere's Clinical Gastroenterology

1997;11(3):485-507. No prevalence or incidence 

reported 

Catassi C, Fornaroli F, Fasano A. Celiac disease:

From basic immunology to bedside practice. Clin

Appl Immunol Rev 2002;3(1-2):61-71. No prevalence 

or incidence reported 

Catassi C, Guerrieri A, Bartolotta E. Antigliadin 

antibodies at onset of diabetes in children. Lancet 

1987;2(8551):158No prevalence or incidence reported 

Catassi C, Ratsch I-M, Gandolfi L et al. Why is 

coeliac disease endemic in the people of the Sahara?.

Lancet 1999;354(9179):647-648. No prevalence or

incidence reported 

Catassi Carlo, Fabiani Elisabetta, Corrao Giovanni et

al. Risk of non-Hodgkin lymphoma in celiac disease. 

Jama - the Journal of the American Medical

Association 2002;287(11):1413-1419. No prevalence 

or incidence reported 

Catino M, Tumini S, Mezzetti A et al. Coeliac disease 

and diabetes mellitus in children: A non casual 

association. Diabetes Nutr Metab Clin Exp

1998;11(5):296-302. No prevalence or incidence 

reported 

Cavell B, Stenhammar L, Ascher H et al. Increasing 

incidence of childhood coeliac disease in Sweden. 

Results of a national study. Acta Paediatr 

1992;81(8):589-592. Serology screen <1990 

Ceccarelli M, Caiulo V A, Ughi C. Changing pattern 

of coeliac disease in western Toscana. Acta Paediatr 

Scand 1991;80(5):547-548. No prevalence or

incidence reported 

Cellier C, Cervoni J P, Patey N et al. Gluten-free diet

induces regression of T-cell activation in the rectal 

mucosa of patients with celiac disease. Am J

Gastroenterol 1998;93(9):1527-1530. No prevalence 

or incidence reported 

Cellier C, Cuillerier E, Patey-Mariaud de et al. Push 

enteroscopy in celiac sprue and refractory sprue.

Gastroenterol Int 1999;50(5):613-617. No prevalence 

or incidence reported 

A-511
Cellier C, Delabesse E, Helmer C et al. Refractory 

sprue, coeliac disease, and enteropathy-associated Tcell lymphoma. French Coeliac Disease Study Group. 

Lancet 2000;356(9225):203-208. No prevalence or

incidence reported 

Cervetto J L, Ramonet M, Nahmod L H et al. 

Giardiasis. Functional, immunological and histological 

study of the small bowel. Therapeutic trial with a

single dose of tinidazole. Arq Gastroenterol 

1987;24(2):102-112. No prevalence or incidence 

reported 

Challacombe D N, Mecrow I K, Elliott K et al.

Changing infant feeding practices and declining

incidence of coeliac disease in West Somerset. Arch 

Dis Child 1997;77(3):206-209. No prevalence or

incidence reported 

Challacombe D N. The incidence of coeliac disease 

and early weaning. Arch Dis Child 1983;58(5):326No 

prevalence or incidence reported

Chambers T L. Coexistent coeliac disease, diabetes

mellitus, and hyperthyroidism. Arch Dis Child

1975;50(2):162-164. No prevalence or incidence 

reported 

Chapman R W, Laidlow J M, Colin-Jones D et al.

Increased prevalence of epilepsy in coeliac disease. Br

Med J 1978;2(6132):250-251. No prevalence or 

incidence reported 

Chari S T, Mohan V, Jayanthi V et al. Comparative 

study of the clinical profiles of alcoholic chronic 

pancreatitis and tropical chronic pancreatitis in Tamil 

Nadu, south India. Pancreas 1992;7(1):52-58. No 

prevalence or incidence reported

Charron D. HLA class II disease associations: 

Molecular basis. J Autoimmun 1992;5(Suppl A):45-

53. No prevalence or incidence reported 

Charron D. Molecular basis of human leukocyte 

antigen class II disease associations. Adv Immunol 

1990;48(-):107-159. No prevalence or incidence 

reported 

Chartrand L J, Russo P A, Duhaime A G et al. Wheat

starch intolerance in patients with celiac disease. J Am

Diet Assoc 1997;97(6):612-618. No prevalence or

incidence reported 

Chatzicostas Costantinos, Roussomoustakaki Maria, 

Drygiannakis Dimitrios et al. Primary biliary cirrhosis 

and autoimmune cholangitis are not associated with 

coeliac disease in Crete. Bmc Gastroenterology

Electronic Resource 2002;2(1):5No prevalence or

incidence reported 

Chernavsky Alejandra C, Rubio Andrea E, Vanzulli 

Silvia et al. Evidences of the involvement of Bak, a 

member of the Bcl-2 family of proteins, in active 

coeliac disease. Autoimmunity 2002;35(1):29-37. No 

prevalence or incidence reported

Chiechi L M, Valerio T, Loizzi P. Postmenopausal 

osteoporosis and celiac disease. Clin Exp Obstet 

Gynecol 2002;29(3):187-188. No prevalence or 

incidence reported 

Chimenti C, Pieroni M, Frustaci A. Celiac disease in

idiopathic dilated cardiomyopathy. Ital Heart J 

2001;2(9):658-659. No prevalence or incidence 

reported 

Chin R L, Sander H W, Brannagan T H et al. Celiac 

neuropathy. Neurology 2003;60(10):1581-1585. No 

prevalence or incidence reported

Chinen J, Shearer W T. Basic and clinical

immunology. J Allergy Clin Immunol 2003;111(Suppl 

3):S813-S818. No prevalence or incidence reported 

Chitturi S, Farrell G C. Etiopathogenesis of 

nonalcoholic steatohepatitis. Semin Liver Dis 

2001;21(1):27-41. No prevalence or incidence 

reported 

Chorzelski T P, Olszewska M, Jarzabek-Chorzelska M

et al. Is chronic ulcerative stomatitis an entity?

Clinical and immunological findings in 18 cases. Eur J 

Dermatol 1998;8(4):261-265. No prevalence or

incidence reported 

Ciacci C, Cavallaro R, Romano R et al. Increased risk

of surgery in undiagnosed celiac disease. Dig Dis Sci 

2001;46(10):2206-2208. No prevalence or incidence 

reported 

Ciacci C, Cirillo M, Auriemma G et al. Celiac disease 

and pregnancy outcome. Am J Gastroenterol 

1996;91(4):718-722. No prevalence or incidence 

reported 

Ciacci C, Cirillo M, Giorgetti G et al. Low plasma

cholesterol: a correlate of nondiagnosed celiac disease 

in adults with hypochromic anemia. Am J 

Gastroenterol 1999;94(7):1888-1891. No prevalence 

or incidence reported 

Ciacci C, Cirillo M, Mellone M et al. Hypocalciuria in 

overt and subclinical celiac disease. Am J

Gastroenterol 1995;90(9):1480-1484. No prevalence 

or incidence reported 

Ciacci C, Cirillo M, Sollazzo R et al. Gender and

clinical presentation in adult celiac disease. Scand J

Gastroenterol 1995;30(11):1077-1081. No prevalence 

or incidence reported 

Ciacci C, De Rosa A, de Michele G et al. Sexual

behaviour in untreated and treated coeliac patients. 

Eur J Gastroenterol Hepatol 1998;10(8):649-651. No 

prevalence or incidence reported

A-512
Ciacci C, Di Vizio D, Seth R et al. Selective reduction

of intestinal trefoil factor in untreated coeliac disease.

Clin Exp Immunol 2002;130(3):526-531. No 

prevalence or incidence reported

Ciacci C, Maurelli L, Klain M et al. Effects of dietary 

treatment on bone mineral density in adults with celiac

disease: factors predicting response. Am J

Gastroenterol 1997;92(6):992-996. No prevalence or 

incidence reported 

Ciacci C, Squillante A, Rendina D et al. Helicobacter

pylori infection and peptic disease in coeliac disease. 

Eur J Gastroenterol Hepatol 2000;12(12):1283-1287. 

No prevalence or incidence reported 

Ciacci Carolina, Cirillo Massimo, Cavallaro

Raimondo et al. Long-term follow-up of celiac adults 

on gluten-free diet: prevalence and correlates of

intestinal damage. Digestion 2002;66(3):178-185. No 

prevalence or incidence reported

Ciacci Carolina, Iavarone Alessandro, Siniscalchi 

Monica et al. Psychological dimensions of celiac 

disease: toward an integrated approach. Dig Dis Sci 

2002;47(9):2082-2087. No prevalence or incidence 

reported 

Ciampolini M, Bini S. Serum lipids in celiac children. 

J Pediatr Gastroenterol Nutr 1991;12(4):459-460. No 

prevalence or incidence reported

Ciclitira P J, Hall M A. Coeliac disease. Bailliere's

Clin Gastroenterol 1990;4(1):43-59. No prevalence or

incidence reported 

Ciclitira P J, Sturgess R. Clinicopathologic 

mechanisms in celiac disease. Curr Opin Gastroenterol

1992;8(2):262-267. No prevalence or incidence 

reported 

Ciclitira P J. Coeliac disease: foreword. Digestive and

Liver Disease - Official Journal of the Italian Society

of Gastroenterology and the Italian Association for the

Study of the Liver 2002;34(3):214-215. No prevalence 

or incidence reported 

Ciclitira P J. Recent advances in coeliac disease. Clin 

Med 2003;3(2):166-169. No prevalence or incidence 

reported 

Clemente M G, Musu M P, Frau F et al. Immune 

reaction against the cytoskeleton in coeliac disease. 

Gut 2000;47(4):520-526. No prevalence or incidence 

reported 

Clemente Maria, Grazia Musu, Maria Paola et al. 

Antitissue transglutaminase antibodies outside celiac

disease. J Pediatr Gastroenterol Nutr 2002;34(1):31-

34. No prevalence or incidence reported 

Clements M R, Davies M, Hayes M E et al. The role 

of 1,25-dihydroxyvitamin D in the mechanism of 

acquired vitamin D deficiency. Clin Endocrinol (Oxf) 

1992;37(1):17-27. No prevalence or incidence 

reported 

Clerget-Darpoux F, Bouguerra F, Kastally R et al. 

High risk genotypes for celiac disease. Comptes

Rendus De L'academie Des Sciences.Serie Iii, 

Sciences De La Vie 1994;317(10):931-936. No

prevalence or incidence reported

Clot F, Babron M C, Percopo S et al. Study of two 

ectopeptidases in the susceptibility to celiac disease:

two newly identified polymorphisms of 

dipeptidylpeptidase IV. J Pediatr Gastroenterol Nutr 

2000;30(4):464-466. No prevalence or incidence 

reported 

Clot F, Fulchignoni-Lataud M C, Renoux C et al. 

Linkage and association study of the CTLA-4 region 

in coeliac disease for Italian and Tunisian populations. 

Tissue Antigens 1999;54(5):527-530. No prevalence 

or incidence reported 

Clot F, Gianfrani C, Babron M C et al. HLA-DR53 

molecules are associated with susceptibility to celiac 

disease and selectively bind gliadin-derived peptides. 

Immunogenetics 1999;49(9):800-807. No prevalence 

or incidence reported 

Cockel R, Anderson C M, Hill E E et al. Familial 

steatorrhoea with calcification of the basal ganglia and

mental retardation. Gut 1970;11(12):1064No 

prevalence or incidence reported

Cockel R, Hill E E, Rushton D I et al. Familial

steatorrhoea with calcification of the basal ganglia and

mental retardation. Q J Med 1973;42(168):771-783. 

No prevalence or incidence reported 

Cogulu O, Ozkinay F, Gunduz C et al. Celiac disease 

in children with down syndrome: Importance of

follow-up and serologic screening. Pediatr Int 

2003;45(4):395-399. No prevalence or incidence 

reported 

Colaco J, Egan-Mitchell B, Stevens F M et al.

Compliance with gluten free diet in coeliac disease. 

Arch Dis Child 1987;62(7):706-708. No prevalence or

incidence reported 

Cole S G, Kagnoff M F. Celiac disease. Annu Rev 

Nutr 1985;5241-266. No prevalence or incidence 

reported 

Coleman M D. Dapsone-mediated agranulocytosis: 

Risks, possible mechanisms and prevention.

Toxicology 2001;162(1):53-60. No prevalence or

incidence reported 

A-513
Colle I, Van Vlierberghe H. Diagnosis and therapeutic 

problems of primary sclerosing cholangitis. Acta

Gastro-Enterol Belg 2003;66(2):155-159. No

prevalence or incidence reported

Collin P, Hallstrom O, Maki M et al. Atypical coeliac 

disease found with serologic screening. Scand J 

Gastroenterol 1990;25(3):245-250. No prevalence or 

incidence reported 

Collin P, Helin H, Maki M et al. Follow-up of patients

positive in reticulin and gliadin antibody tests with

normal small-bowel biopsy findings. Scand J 

Gastroenterol 1993;28(7):595-598. No prevalence or 

incidence reported 

Collin P, Kaukinen K, Maki M. Clinical features of 

celiac disease today. Dig Dis 1999;17(2):100-106. No 

prevalence or incidence reported

Collin P, Korpela M, Hallstrom O et al. Rheumatic 

complaints as a presenting symptom in patients with 

coeliac disease. Scand J Rheumatol 1992;21(1):20-23. 

No prevalence or incidence reported 

Collin P, Pukkala E, Reunala T. Malignancy and 

survival in dermatitis herpetiformis: a comparison 

with coeliac disease. Gut 1996;38(4):528-530. No 

prevalence or incidence reported

Collin P, Reunala T, Pukkala E et al. Coeliac disease--

associated disorders and survival. Gut

1994;35(9):1215-1218. No prevalence or incidence 

reported 

Collin P, Reunala T. Recognition and management of 

the cutaneous manifestations of celiac disease: A 

guide for dermatologists. Am J Clin Dermatol 

2003;4(1):13-20. No prevalence or incidence reported 

Collin P, Salmi J, Hallstrom O et al. Autoimmune 

thyroid disorders and coeliac disease. Eur J Endocrinol 

1994;130(2):137-140. No prevalence or incidence 

reported 

Collin P, Salmi J, Hallstrom O et al. High frequency 

of coeliac disease in adult patients with type-I 

diabetes. Scand J Gastroenterol 1989;24(1):81-84. Not 

a relevant screening geography

Collin P, Vilska S, Heinonen P K et al. Infertility and 

coeliac disease. Gut 1996;39(3):382-384. No 

prevalence or incidence reported

Collin Pekka, Kaukinen Katri, Valimaki Matti et al.

Endocrinological disorders and celiac disease. Endocr 

Rev 2002;23(4):464-483. No prevalence or incidence 

reported 

Collin Pekka, Syrjanen Jaana, Partanen Jukka et al. 

Celiac disease and HLA DQ in patients with IgA 

nephropathy. Am J Gastroenterol 2002;97(10):2572-

2576. Not a relevant screening group 

Collins B J, Bell P M, Boyd S et al. Endocrine and 

exocrine pancreatic function in treated coeliac disease.

Pancreas 1986;1(2):143-147. No prevalence or

incidence reported 

Colomina M J, Puig L, Godet C et al. Prevalence of 

asymptomatic cardiac valve anomalies in idiopathic 

scoliosis. Pediatr Cardiol 2002;23(4):426-429. No 

prevalence or incidence reported

Colonna M, Bresnahan M, Bahram S et al. Allelic 

variants of the human putative peptide transporter 

involved in antigen processing. Proc Natl Acad Sci U 

S A 1992;89(9):3932-3936. No prevalence or

incidence reported 

Combarros O, Infante J, Lopez-Hoyos M et al. Celiac 

disease and idiopathic cerebellar ataxia. Neurology

2000;54(12):2346No prevalence or incidence reported 

Compston J. Is fracture risk increased in patients with 

coeliac disease?. Gut 2003;52(4):459-460. No 

prevalence or incidence reported

Congia M, Cucca F, Frau F et al. A gene dosage effect 

of the DQA1*0501/DQB1*0201 allelic combination 

influences the clinical heterogeneity of celiac disease.

Hum Immunol 1994;40(2):138-142. No prevalence or

incidence reported 

Congia M, Frau F, Lampis R et al. A high frequency

of the A30, B18, DR3, DRw52, DQw2 extended 

haplotype in Sardinian celiac disease patients: further 

evidence that disease susceptibility is conferred by DQ 

A1*0501, B1*0201. Tissue Antigens 1992;39(2):78-

83. No prevalence or incidence reported 

Cook H B, Burt M J, Collett J A et al. Adult coeliac 

disease: prevalence and clinical significance. J

Gastroenterol Hepatol 2000;15(9):1032-1036. Not a 

relevant screening geography

Cooke W T. Symposium. Crohn's disease: medical 

management. Dis Colon Rectum 1975;18(3):194-197. 

No prevalence or incidence reported 

Cooper A, Brew S, De Lusignan S. The effectiveness 

of blood tests in detecting secondary osteoporosis or 

mimicking conditions in postmenopausal women. Br J 

Gen Pract 2002;52(477):311-313. No prevalence or 

incidence reported 

Cooper B T, Holmes G K, FPERGUSON R et al. 

Proceedings: Chronic diarrhoea and gluten sensitivity.

Gut 1976;17(5):398No prevalence or incidence 

reported 

Corazza G R, Biagi F, Volta U et al. Autoimmune 

enteropathy and villous atrophy in adults. Lancet 

1997;350(9071):106-109. No prevalence or incidence 

reported 

A-514
Corazza G R, Caletti G C, Lazzari R et al. Scalloped 

duodenal folds in childhood celiac disease. 

Gastroenterol Int 1993;39(4):543-545. No prevalence 

or incidence reported 

Corazza G R, Di Sario A, Cecchetti L et al. Bone mass 

and metabolism in patients with celiac disease.

Gastroenterology 1995;109(1):122-128. No 

prevalence or incidence reported

Corazza G R, Di Sario A, Sacco G et al. Subclinical

coeliac disease: an anthropometric assessment. J 

Intern Med 1994;236(2):183-187. No prevalence or

incidence reported 

Corazza G R, Di Stefano M, Jorizzo R A et al.

Propeptide of type I procollagen is predictive of

posttreatment bone mass gain in adult celiac disease. 

Gastroenterology 1997;113(1):67-71. No prevalence 

or incidence reported 

Corazza G R, Frisoni M, Filipponi C et al. 

Investigation of QT interval in adult coeliac disease. 

Br Med J 1992;304(6837):1285No prevalence or 

incidence reported 

Corazza G R, Frisoni M, Treggiari E A et al.

Subclinical celiac sprue. Increasing occurrence and 

clues to its diagnosis. J Clin Gastroenterol 

1993;16(1):16-21. Not a relevant screening test 

Corazza G R, Gasbarrini G. Coeliac disease in adults. 

Bailliere's Clinical Gastroenterology 1995;9(2):329-

350. No prevalence or incidence reported 

Corazza G R, Zoli G, Di Sabatino A et al. A 

reassessment of splenic hypofunction in celiac disease.

Am J Gastroenterol 1999;94(2):391-397. No 

prevalence or incidence reported

Cornes J S. Hodgkin's disease of the gastrointestinal 

tract. Proc R Soc Med 1967;60(8):732-733. No

prevalence or incidence reported

Corrao G, Corazza G R, Andreani M L et al.

Serological screening of coeliac disease: choosing the 

optimal procedure according to various prevalence

values. Gut 1994;35(6):771-775. No prevalence or

incidence reported 

Corrao G, Corazza G R, Bagnardi V et al. Mortality in

patients with coeliac disease and their relatives: a

cohort study. Lancet 2001;358(9279):356-361. No

prevalence or incidence reported

Cottone M, Marrone C, Casa A et al. Familial

occurrence of inflammatory bowel disease in celiac 

disease. Inflamm Bowel Dis 2003;9(5):321-323. No 

prevalence or incidence reported

Cottone M, Termini A, Oliva L et al. Mortality and 

causes of death in celiac disease in a Mediterranean

area. Dig Dis Sci 1999;44(12):2538-2541. No 

prevalence or incidence reported

Cottrill C, Glueck C J, Leuba V et al. Familial 

homozygous hypobetalipoproteinemia. MetabolismClinical and Experimental 1974;23(8):779-791. No 

prevalence or incidence reported

Cowan B, Satija V K, Malvea B P. Steatorrhoea in the

Punjab: the results of a village survey. Am J Trop Med 

Hyg 1971;74(6):137-140. No prevalence or incidence 

reported 

Cowan B. Malnutrition and malabsorption: studies in 

the Punjab. Am J Clin Nutr 1972;25(11):1234-1235. 

No prevalence or incidence reported 

Cox M A, Iqbal T H, Cooper B T et al. An analytical 

method for the quantitation of mannitol and

disaccharides in serum: a potentially useful technique 

in measuring small intestinal permeability in vivo. 

Clin Chim Acta 1997;263(2):197-205. No prevalence 

or incidence reported 

Crandall C. Laboratory workup for osteoporosis: 

Which tests are most cost-effective?. Postgrad Med 

2003;114(3):35-44. No prevalence or incidence 

reported 

Cremata J A, Sorell L, Montesino R et al.

Hypogalactosylation of serum IgG in patients with 

coeliac disease. Clin Exp Immunol 2003;133(3):422-

429. No prevalence or incidence reported 

Crenn Pascal, Vahedi Kouroche, Lavergne-Slove

Anne et al. Plasma citrulline: A marker of enterocyte

mass in villous atrophy-associated small bowel 

disease. Gastroenterology 2003;124(5):1210-1219. No 

prevalence or incidence reported

Croft D N. Body iron loss and cell loss from epithelia.

Proc R Soc Med 1970;63(12):1221-1224. No 

prevalence or incidence reported

Cronin C C, Jackson L M, Feighery C et al. Coeliac 

disease and epilepsy. Qjm - Monthly Journal of the 

Association of Physicians 1998;91(4):303-308. No 

prevalence or incidence reported

Cronin C C, Shanahan F. Exploring the iceberg - The 

spectrum of celiac disease. Am J Gastroenterol

2003;98(3):518-520. No prevalence or incidence 

reported 

Cronin C C, Shanahan F. Insulin-dependent diabetes

mellitus and coeliac disease. Lancet

1997;349(9058):1096-1097. No prevalence or

incidence reported 

A-515
Cronin C C, Shanahan F. Why is celiac disease so

common in Ireland?. Perspect Biol Med 

2001;44(3):342-352. No prevalence or incidence 

reported 

Crowe J P, Falini N P. Gluten in pharmaceutical 

products. Am J Health-Syst Pharm 2001;58(5):396-

401. No prevalence or incidence reported 

Csizmadia C G, Mearin M L, Oren A et al. Accuracy

and cost-effectiveness of a new strategy to screen for 

celiac disease in children with Down syndrome. Eur J

Pediatr 2000;137(6):756-761. Not a relevant screening 

group 

Cudworth A G, Woodrow J C. HL-A system and 

diabetes mellitus. Diabetes 1975;24(4):345-349. No 

prevalence or incidence reported

Cummins A G, Thompson F M, Butler R N et al. 

Improvement in intestinal permeability precedes

morphometric recovery of the small intestine in

coeliac disease. Clinical Science (London, England - 

1979) 2001;100(4):379-386. No prevalence or

incidence reported 

Cunningham A S, Jelliffe D B, Jelliffe E F. Breastfeeding and health in the 1980s: a global 

epidemiologic review. Eur J Pediatr 1991;118(5):659-

666. No prevalence or incidence reported 

Cuoco L, Cammarota G, Jorizzo R A et al. Link

between Helicobacter pylori infection and irondeficiency anaemia in patients with coeliac disease. 

Scand J Gastroenterol 2001;36(12):1284-1288. No

prevalence or incidence reported

Cuoco L, Cammarota G, Tursi A et al. Disappearance 

of gastric mucosa-associated lymphoid tissue in

coeliac patients after gluten withdrawal. Scand J

Gastroenterol 1998;33(4):401-405. No prevalence or 

incidence reported 

Cuoco L, Certo M, Jorizzo R A et al. Prevalence and 

early diagnosis of coeliac disease in autoimmune 

thyroid disorders. Ital J Gastroenterol Hepatol 

1999;31(4):283-287. No prevalence or incidence 

reported 

Cuomo A, Romano M, Rocco A et al. Reflux 

oesophagitis in adult coeliac disease: beneficial effect

of a gluten free diet. Gut 2003;52(4):514-517. No 

prevalence or incidence reported

Curione M, Barbato M, De Biase L et al. Prevalence 

of coeliac disease in idiopathic dilated 

cardiomyopathy. Lancet 1999;354(9174):222-223. No 

prevalence or incidence reported

Czaja A J. Autoimmune liver disease. Curr Opin

Gastroenterol 1999;15(3):240-248. No prevalence or 

incidence reported 

Czaja A J. Autoimmune liver disease. Curr Opin

Gastroenterol 2003;19(3):232-242. No prevalence or 

incidence reported 

Dahan S, Slater P E, Cooper M et al. Coeliac disease 

in the Rehovot-Ashdod region of Israel: incidence and

ethnic distribution. J Epidemiol Community Health 

1984;38(1):58-60. Not a relevant screening geography

Dahele A V, Aldhous M C, Humphreys K et al. Serum 

IgA tissue transglutaminase antibodies in coeliac

disease and other gastrointestinal diseases. Qjm - 

Monthly Journal of the Association of Physicians 

2001;94(4):195-205. No prevalence or incidence 

reported 

Dahele A, Ghosh S. Vitamin B12 deficiency in 

untreated celiac disease. Am J Gastroenterol 

2001;96(3):745-750. No prevalence or incidence 

reported 

Dahele A, Kingstone K, Bode J et al. Anti-endomysial 

antibody negative celiac disease: does additional 

serological testing help?. Dig Dis Sci 2001;46(1):214-

221. No prevalence or incidence reported 

Dahlqvist G. Celiac disease and insulin-dependent

diabetes mellitus--no proof for a causal association. 

Acta Paediatr 1995;84(12):1337-1338. No prevalence 

or incidence reported 

Damen G M, Boersma B, Wit J M et al. Catch-up 

growth in 60 children with celiac disease. J Pediatr 

Gastroenterol Nutr 1994;19(4):394-400. No 

prevalence or incidence reported

Damoiseaux Jan G M C, Bouten Bas, Linders Annick 

M L W et al. Diagnostic value of anti-Saccharomyces 

cerevisiae and antineutrophil cytoplasmic antibodies 

for inflammatory bowel disease: high prevalence in 

patients with celiac disease. J Clin Immunol 

2002;22(5):281-288. No prevalence or incidence 

reported 

Danne T. Current issues in paediatric diabetology:

Introduction to meet-the-expert sessions. Horm Res 

2002;57(Suppl 1):91-92. No prevalence or incidence 

reported 

Dausset J. Biologic role of the HLA system. HLA 

complex in human biology in the light of associations 

with disease. Transplant Proc 1977;9(1):523-529. No 

prevalence or incidence reported

David T J, Ajdukiewicz A B. A family study of

coeliac disease. J Med Genet 1975;12(1):79-82. 

Serology screen <1990 

Davis M K. Breastfeeding and chronic disease in

childhood and adolescence. Pediatr Clin North Am

A-516
2001;48(1):125-41, Ix. No prevalence or incidence 

reported 

Davison S. Coeliac disease and liver dysfunction. 

Arch Dis Child 2002;87(4):293-296. No prevalence or

incidence reported 

Dawood F H, Jabbar A A, Al Mudaris A F et al. 

Association of HLA antigens with coeliac disease

among Iraqi children. Tissue Antigens 1981;18(1):35-

39. No prevalence or incidence reported 

Dawson A M. Nutritional disturbances in Crohn's 

disease. Br J Surg 1972;59(10):817-819. No 

prevalence or incidence reported

Dawson A M. Nutritional disturbances in Crohn's 

disease. Proc R Soc Med 1971;64(2):166-170. No 

prevalence or incidence reported

de Francischi M L, Salgado J M, da Costa C P. 

Immunological analysis of serum for buckwheat fed 

celiac patients. Plant Foods Hum Nutr 

1994;46(3):207-211. No prevalence or incidence 

reported 

de Freitas I, Sipahi Aytan, Miranda Damiao et al.

Celiac disease in Brazilian adults. J Clin Gastroenterol 

2002;34(4):430-434. No prevalence or incidence 

reported 

De Giacomo C, Gianatti A, Negrini R et al.

Lymphocytic gastritis: a positive relationship with

celiac disease. Eur J Pediatr 1994;124(1):57-62. No

prevalence or incidence reported

de la, Concha E G, Fernandez-Arquero M et al. Celiac 

disease and TNF promoter polymorphisms. Hum 

Immunol 2000;61(5):513-517. No prevalence or 

incidence reported 

de la, Paz Bettinotti M, Kolek A et al. Polymorphism

of the 5' flanking region of the HLA-DQA1 gene in 

coeliac disease. European Journal of Immunogenetics 

- Official Journal of the British Society for

Histocompatibility and Immunogenetics 

1993;20(5):399-407. No prevalence or incidence 

reported 

de Lecea A, Ribes-Koninckx C, Polanco I et al. 

Serological screening (antigliadin and 

antiendomysium antibodies) for non-overt coeliac 

disease in children of short stature. Acta Paediatr

1996;412(Suppl):54-55. No prevalence or incidence 

reported 

de Vizia B, Poggi V, Conenna R et al. Iron absorption 

and iron deficiency in infants and children with 

gastrointestinal diseases. J Pediatr Gastroenterol Nutr 

1992;14(1):21-26. No prevalence or incidence 

reported 

Dean G, Hanniffy L, Stevens F et al. Schizophrenia 

and coeliac disease. Ir Med J 1975;68(21):545-546. 

No prevalence or incidence reported 

Del Rosario M A, Fitzgerald J F, Chong S K et al. 

Further studies of anti-endomysium and anti-gliadin 

antibodies in patients with suspected celiac disease. J 

Pediatr Gastroenterol Nutr 1998;27(2):191-195. No 

prevalence or incidence reported

Delco F, El Serag H B, Sonnenberg A. Celiac sprue 

among US military veterans: associated disorders and 

clinical manifestations. Dig Dis Sci 1999;44(5):966-

972. No prevalence or incidence reported 

DeMarchi M, Borelli I, Olivetti E et al. Two HLA-D 

and DR alleles are associated with coeliac disease.

Tissue Antigens 1979;14(4):309-316. No prevalence 

or incidence reported 

DeMarchi M, Carbonara A, Ansaldi N et al. HLADR3 and DR7 in coeliac disease: immunogenetic and 

clinical aspects. Gut 1983;24(8):706-712. No 

prevalence or incidence reported

Demir H, Yuce A, Kocak N et al. Celiac disease in

Turkish children: presentation of 104 cases. Pediatrics 

International - Official Journal of the Japan Pediatric 

Society 2000;42(5):483-487. No prevalence or

incidence reported 

Dennis N R, Stokes C R. Risk of coeliac disease in

children of patients and effect of HLA genotype. J 

Med Genet 1978;15(1):20-22. No prevalence or 

incidence reported 

Deprez Pierre H, Sempoux Christine, De Saeger et al. 

Expression of cholecystokinin in the duodenum of

patients with coeliac disease: respective role of 

atrophy and lymphocytic infiltration. Clinical Science 

(London, England - 1979) 2002;103(2):171-177. No 

prevalence or incidence reported

der Ohe M R. Diarrhoea in patients with diabetes 

mellitus. Eur J Gastroenterol Hepatol 1995;7(8):730-

736. No prevalence or incidence reported 

Desjeux Ariadne, Barthet Marc, Barthellemy Sandrine 

et al. Serum measurements of pancreatitis associated 

protein in active Crohn's disease with ileal location. 

Gastroenterol Clin Biol 2002;26(1):23-28. No

prevalence or incidence reported

Devi Rampertab S, Fleischauer A, Neugut A I et al. 

Risk of duodenal adenoma in celiac disease. Scand J 

Gastroenterol 2003;38(8):831-833. No prevalence or 

incidence reported 

Dewar D, Pereira S P, Ciclitira P J. The pathogenesis 

of coeliac disease. Int J Biochem Cell Biol

2004;36(1):17-24. No prevalence or incidence 

reported 

A-517
Dezi R, Niveloni S, Sugai E et al. Gluten sensitivity in

the rectal mucosa of first-degree relatives of celiac

disease patients. Am J Gastroenterol 1997;92(8):1326-

1330. No prevalence or incidence reported 

Dhesi I, Marsh M N, Kelly C et al. Morphometric 

analysis of small intestinal mucosa. II. Determination 

of lamina propria volumes; plasma cell and neutrophil 

populations within control and coeliac disease 

mucosae. Virchows Archiv.A, Pathological Anatomy 

and Histopathology 1984;403(2):173-180. No

prevalence or incidence reported

Di Mario U, Anastasi E, Mariani P et al. Diabetesrelated autoantibodies do appear in children with 

coeliac disease. Acta Paediatr 1992;81(8):593-597. No 

prevalence or incidence reported

Di Sabatino A, Bertrandi E, Casadei Maldini M et al. 

Phenotyping of peripheral blood lymphocytes in adult 

coeliac disease. Immunology 1998;95(4):572-576. No 

prevalence or incidence reported

Di Sabatino A, Ciccocioppo R, D'Alo S et al. 

Intraepithelial and lamina propria lymphocytes show 

distinct patterns of apoptosis whereas both populations 

are active in Fas based cytotoxicity in coeliac disease. 

Gut 2001;49(3):380-386. No prevalence or incidence 

reported 

Di Stefano M, Jorizzo R A, Veneto G et al. Bone mass

and metabolism in dermatitis herpetiformis. Dig Dis 

Sci 1999;44(10):2139-2143. No prevalence or

incidence reported 

Di Stefano M, Veneto G, Corrao G et al. Role of

lifestyle factors in the pathogenesis of osteopenia in 

adult coeliac disease: a multivariate analysis. Eur J 

Gastroenterol Hepatol 2000;12(11):1195-1199. No

prevalence or incidence reported

Di Stefano, Michele Miceli, Emanuela Malservisi et

al. Mixing of the intestinal content and variations of 

fermentation capacity do not affect the results of

hydrogen breath test. Am J Gastroenterol 

2003;98(7):1584-1587. No prevalence or incidence 

reported 

Diamanti A, Maino C, Niveloni S et al.

Characterization of gastric mucosal lesions in patients 

with celiac disease: a prospective controlled study. 

Am J Gastroenterol 1999;94(5):1313-1319. No 

prevalence or incidence reported

Dickey W, Bodkin S. Prospective study of body mass 

index in patients with coeliac disease. BMJ 

1998;317(7168):1290No prevalence or incidence 

reported 

Dickey W, Hughes D F, McMillan S A. 

Disappearance of endomysial antibodies in treated 

celiac disease does not indicate histological recovery. 

Am J Gastroenterol 2000;95(3):712-714. No 

prevalence or incidence reported

Dickey W, Hughes D F, McMillan S A. Reliance on 

serum endomysial antibody testing underestimates the 

true prevalence of coeliac disease by one fifth. Scand J

Gastroenterol 2000;35(2):181-183. No prevalence or 

incidence reported 

Dickey W, Hughes D. Disappointing sensitivity of

endoscopic markers for villous atrophy in a high-risk 

population: implications for celiac disease diagnosis 

during routine endoscopy. Am J Gastroenterol 

2001;96(7):2126-2128. No prevalence or incidence 

reported 

Dickey W, Hughes D. Prevalence of celiac disease and 

its endoscopic markers among patients having routine 

upper gastrointestinal endoscopy. Am J Gastroenterol 

1999;94(8):2182-2186. No prevalence or incidence 

reported 

Dickey W, McConnell J B. How many hospital visits 

does it take before celiac sprue is diagnosed?. J Clin 

Gastroenterol 1996;23(1):21-23. No prevalence or

incidence reported 

Dickey W, McMillan S A, Callender M E. High 

prevalence of celiac sprue among patients with 

primary biliary cirrhosis. J Clin Gastroenterol 

1997;25(1):328-329. No prevalence or incidence 

reported 

Dickey W, McMillan S A, Collins J S et al. Liver 

abnormalities associated with celiac sprue. How 

common are they, what is their significance, and what 

do we do about them?. J Clin Gastroenterol 

1995;20(4):290-292. No prevalence or incidence 

reported 

Dickey W, McMillan S A, Hughes D F. Identification 

of coeliac disease in primary care. Scand J

Gastroenterol 1998;33(5):491-493. No prevalence or 

incidence reported 

Dickey W, McMillan S A, Hughes D F. Sensitivity of 

serum tissue transglutaminase antibodies for

endomysial antibody positive and negative coeliac 

disease. Scand J Gastroenterol 2001;36(5):511-514. 

No prevalence or incidence reported 

Dickey W, McMillan S A, McCrum E E et al.

Association between serum levels of total IgA and IgA 

class endomysial and antigliadin antibodies: 

implications for coeliac disease screening. Eur J

Gastroenterol Hepatol 1997;9(6):559-562. No

prevalence or incidence reported

A-518
Dickey W. Colon neoplasia co-existing with coeliac

disease in older patients: coincidental, probably;

important, certainly. Scand J Gastroenterol 

2002;37(9):1054-1056. No prevalence or incidence 

reported 

Dickey W. Diagnosis of coeliac disease at open-access

endoscopy. Scand J Gastroenterol 1998;33(6):612-

615. No prevalence or incidence reported 

Dickey W. Low serum vitamin B12 is common in

coeliac disease and is not due to autoimmune gastritis.

Eur J Gastroenterol Hepatol 2002;14(4):425-427. No 

prevalence or incidence reported

Dieterich W, Ehnis T, Bauer M et al. Identification of 

tissue transglutaminase as the autoantigen of celiac 

disease. Nat Med 1997;3(7):797-801. No prevalence 

or incidence reported 

Dissanayake A S, Truelove S C, Whitehead R. Jejunal 

mucosal recovery in coeliac disease in relation to the

degree of adherence to a gluten-free diet. Q J Med 

1974;43(170):161-185. No prevalence or incidence 

reported 

Djilali-Saiah I, Benini V, Schmitz J et al. Absence of 

primary association between DM gene polymorphism 

and insulin-dependent diabetes mellitus or celiac 

disease. Hum Immunol 1996;49(1):22-27. No

prevalence or incidence reported

Djilali-Saiah I, Caillat-Zucman S, Schmitz J et al. 

Polymorphism of antigen processing (TAP, LMP) and 

HLA class II genes in celiac disease. Hum Immunol 

1994;40(1):8-16. No prevalence or incidence reported 

Djilali-Saiah I, Schmitz J, Harfouch-Hammoud E et al. 

CTLA-4 gene polymorphism is associated with

predisposition to coeliac disease. Gut 1998;43(2):187-

189. No prevalence or incidence reported 

Dobru D, Pascu O, Tant cedil et al. The prevalence of

coeliac disease at endoscopy units in Romania: 

Routine biopsies during gastroscopy are mandatory (A 

multicentre study). Rom J Gastroenterol 

2003;12(2):97-100. Not a relevant screening

geography

Dohan F C, Harper E H, Clark M H et al. Is

schizophrenia rare if grain is rare?. Biol Psychiatry

1984;19(3):385-399. No prevalence or incidence 

reported 

Dohan F C. Cereals and schizophrenia data and 

hypothesis. Acta Psychiatr Scand 1966;42(2):125-152. 

No prevalence or incidence reported 

Dohan F C. The possible pathogenic effect of cereal 

grains in schizophrenia. Celiac disease as a model.

Acta Neurol (Napoli) 1976;31(2):195-205. No

prevalence or incidence reported

Driessen A, Ectors N. Lymphomas of the gastrointestinal tract: Uncommon types: LYMPHOMES DU 

TRACTUS GASTRO-INTESTINAL: TYPES

RARES. Acta Endoscopica 2003;33(3):327-345. No 

prevalence or incidence reported

Drury M I, Keelan D M, Timoney F J et al. Juvenile 

familial endocrinopathy. Clin Exp Immunol 

1970;7(1):125-132. No prevalence or incidence 

reported 

Dugoujon J M, Cambon-Thomsen A. Immunoglobulin 

allotypes (GM and KM) and their interactions with 

HLA antigens in autoimmune diseases: A review.

Autoimmunity 1995;22(4):245-260. No prevalence or

incidence reported 

Dugoujon J M, Guitard E, Senegas M T. Gm and Km 

allotypes in autoimmune diseases. G Ital Cardiol 

1992;22(1):85-95. No prevalence or incidence 

reported 

Duncan A, Park R P, Lee F D et al. A retrospective 

assessment of the clinical value of jejunal

disaccharidase analysis. Scand J Gastroenterol 

1994;29(12):1111-1116. No prevalence or incidence 

reported 

Dunger David, Ahmed Lynn, Ong Ken. Growth and 

body composition in type 1 diabetes mellitus. Horm

Res 2002;58(Suppl 1):66-71. No prevalence or 

incidence reported 

Dyer N H, Rutherford C, Visick J H et al. The

incidence and reliability of individual radiographic 

signs in the small intestine in Crohn's disease. Br J 

Radiol 1970;43(510):401-408. No prevalence or 

incidence reported 

Eastell Richard. Management of osteoporosis due to 

ovarian failure. Med Pediatr Oncol 2003;41(3):222-

227. No prevalence or incidence reported 

Ebisawa M, Ikematsu K, Imai T et al. Food Allergy in 

Japan. Allergy Clin Immunol Int 2003;15(5):214-217. 

No prevalence or incidence reported 

Ebo D G, Stevens W J. IgE-mediated food allergy - 

Extensive review of the literature. Acta Clin Belg

2001;56(4):234-247. No prevalence or incidence 

reported 

Ectors N. Infectious disorders of the duodenum: 

MALADIES INFECTIEUSES DU DUODENUM.

Acta Endoscopica 2002;32(2):133-156. No prevalence 

or incidence reported 

Egan C A, O'Loughlin S, Gormally S et al. Dermatitis

Herpetiformis: a review of fifty-four patients. Ir J Med 

Sci 1997;166(4):241-244. No prevalence or incidence 

reported 

A-519
Egan L J, Walsh S V, Stevens F M et al. Celiacassociated lymphoma. A single institution experience

of 30 cases in the combination chemotherapy era. J 

Clin Gastroenterol 1995;21(2):123-129. No 

prevalence or incidence reported

Ehrlich R M. Diabetes mellitus in childhood. Pediatr

Clin North Am 1974;21(4):871-884. No prevalence or

incidence reported 

Eichler I, Frisch H, Granditsch G. Growth failure and 

insulin-like growth factor (IGF-I) in childhood celiac 

disease. Klin Wochenschr 1991;69(18):825-829. No 

prevalence or incidence reported

Eiermann T H, Vejbaesya S, Prestel H et al. 

Association and linkage of human leukocyte antigens 

with psoriasis - Revisited. Infusther Transfusionsmed 

2002;29(6):326-330. No prevalence or incidence 

reported 

Eigenmann P A, Calza A-M. Diagnosis of IgEmediated food allergy among Swiss children with

atopic dermatitis. Pediatr Allergy Immunol 

2000;11(2):95-100. No prevalence or incidence 

reported 

Eigenmann P A, Sampson H A. Interpreting skin prick 

tests in the evaluation of food allergy in children.

Pediatric Allergy and Immunology - Official 

Publication of the European Society of Pediatric 

Allergy and Immunology 1998;9(4):186-191. No 

prevalence or incidence reported

Eigenmann P A, Sicherer S H, Borkowski T A et al.

Prevalence of IgE-mediated food allergy among 

children with atopic dermatitis. Pediatrics 

1998;101(3):E8No prevalence or incidence reported 

Ek B. On the familiar incidence of idiopathic sprue 

and the significance of pregnancy and partial 

gastrectomy for the manifestation of the symptoms. 

Preliminary report. Acta Med Scand 1967;181(1):125-

126. No prevalence or incidence reported 

Ek B. Studies on idiopathic non-tropical sprue. The 

familial occurrence of sprue. Relationship between

sprue and megaloblastic anaemia of pregnancy and 

puerperium. The significance of partial gastrectomy

for manifestation of symptoms. Acta Med Scand

1970;508(Suppl):1-72. No prevalence or incidence 

reported 

Ekbom A, Adami H-O. The epidemiology of

inflammatory bowel disease. Curr Opin Gastroenterol 

1991;7(4):649-653. No prevalence or incidence 

reported 

El Salhy M, Suhr O, Danielsson A. Peptide YY in 

gastrointestinal disorders. Peptides 2002;23(2):397-

402. No prevalence or incidence reported 

Eliakim R, Sherer D M. Celiac disease: fertility and 

pregnancy. Gynecol Obstet Invest 2001;51(1):3-7. No 

prevalence or incidence reported

Ellis A, Taylor C J, Dillon-Remmy M et al. HLA-DR 

typing in coeliac disease: evidence for genetic

heterogeneity. Br Med J (Clin Res Ed) 

1984;289(6458):1571-1573. No prevalence or

incidence reported 

Ellis A. The genetic epidemiology of coeliac disease. 

Genet Epidemiol 1986;1(Suppl):267-269. No 

prevalence or incidence reported

Ellman L K, Chatchatee P, Sicherer S H et al. Food 

hypersensitivity in two groups of children and young 

adults with atopic dermatitis evaluated a decade apart.

Pediatr Allergy Immunol 2002;13(4):295-298. No 

prevalence or incidence reported

Elmes M E, Jones J G, Stanton M R. Changes in the 

Paneth cell population of human small intestine 

assessed by image analysis of the secretory granule 

area. J Clin Pathol 1983;36(8):867-872. No prevalence 

or incidence reported 

Elsborg L, Mosbech J. Sprue: a follow-up study of an 

old series. Dan Med Bull 1978;25(5):205-206. No 

prevalence or incidence reported

Endres W, Wuttge B. Occurrence of secondary

cystathioninuria in children with inherited metabolic 

disorders, liver diseases, neoplasms, cystic fibrosis 

and celiac disease. Eur J Pediatr 1978;129(1):29-35. 

No prevalence or incidence reported 

Engstrom J, Hellstrom K, Lundh G et al. Microflora of

small intestine, incidence of steatorrhoea and 

indicanuria before and after conversion of billroth II to

billroth I type of gastric resection. Acta Chir Scand 

1973;139(6):546-550. No prevalence or incidence 

reported 

Engstrom J, Hellstrom K. Microflora of the small 

intestine and the incidence of liver disease,

steatorrhoea, and indicanuria in patients subjected to 

partial gastrectomy. Acta Chir Scand 

1973;139(6):539-545. No prevalence or incidence 

reported 

Ensari A, Marsh M N, Loft D E et al. Morphometric 

analysis of intestinal mucosa. V. Quantitative 

histological and immunocytochemical studies of rectal 

mucosae in gluten sensitivity. Gut 1993;34(9):1225-

1229. No prevalence or incidence reported 

Ensari A, Marsh M N, Morgan S et al. Diagnosing 

coeliac disease by rectal gluten challenge: a

prospective study based on immunopathology,

computerized image analysis and logistic regression 

analysis. Clinical Science (London, England - 1979) 

A-520
2001;101(2):199-207. No prevalence or incidence 

reported 

Erkan T, Kutlu T, Yilmaz E et al. Human leukocyte 

antigens in Turkish pediatric celiac patients. Turk J

Pediatr 1999;41(2):181-188. No prevalence or

incidence reported 

Evans W B, Wollaeger E E. Incidence and severity of 

nutritional deficiency states in chronic exocrine 

pancreatic insufficency: comparison with nontropical 

sprue. Am J Dig Dis 1966;11(8):594-606. No 

prevalence or incidence reported

Everts B, Stotzer P, Olsson M et al. Increased luminal 

nitric oxide concentrations in the small intestine of

patients with coeliac disease. Eur J Clin Invest 

1999;29(8):692-696. No prevalence or incidence 

reported 

Exner G U, Sacher M, Shmerling D H et al. Growth 

retardation and bone mineral status in children with 

coeliac disease recognized after the age of 3 years.

Helv Paediatr Acta 1978;33(6):497-507. No 

prevalence or incidence reported

Eysink P E D, Bindels P J E, Stapel S O et al. Do 

levels of immunoglobulin G antibodies to foods 

predict the development of immunoglobulin E 

antibodies to cat, dog and/or mite?. Clin Exp Allergy

2002;32(4):556-562. No prevalence or incidence 

reported 

Eysink P E, De Jong M H, Bindels P J et al. Relation 

between IgG antibodies to foods and IgE antibodies to 

milk, egg, cat, dog and/or mite in a cross-sectional 

study. Clinical and Experimental Allergy - Journal of 

the British Society for Allergy and Clinical

Immunology 1999;29(5):604-610. No prevalence or 

incidence reported 

Fabiani E, Catassi C, Villari A et al. Dietary 

compliance in screening-detected coeliac disease

adolescents. Acta Paediatr 1996;412(Suppl):65-67. No 

prevalence or incidence reported

Fabiani E, Taccari L M, Ratsch I M et al. Compliance 

with gluten-free diet in adolescents with screeningdetected celiac disease: a 5-year follow-up study. Eur 

J Pediatr 2000;136(6):841-843. No prevalence or

incidence reported 

Failla P, Ruberto C, Pagano M C et al. Celiac disease 

in Down Syndrome with HLA serological and 

molecular studies. J Pediatr Gastroenterol Nutr

1996;23(3):303-306. No prevalence or incidence 

reported 

Fakhri Z I. Causes of hypersensitivity reactions in

flour mill workers in Sudan. Occup Med 

1992;42(3):149-154. No prevalence or incidence 

reported 

Falchuk Z M, Katz A J, Shwachman H et al. Glutensensitive enteropathy: genetic analysis and organ 

culture study in 35 families. Scand J Gastroenterol 

1978;13(7):839-843. No prevalence or incidence 

reported 

Falk M C, NG G, Zhang G Y et al. Predominance of T 

cell receptor V delta 3 in small bowel biopsies from

coeliac disease patients. Clin Exp Immunol 

1994;98(1):78-82. No prevalence or incidence 

reported 

Faloon W W, Flood M S, Aroesty S et al. Assessment 

of jejunoileostomy for obesity--some observations 

since 1976. Am J Clin Nutr 1980;33(2 Suppl):431-

439. No prevalence or incidence reported 

Falth-Magnusson K, Franzen L, Jansson G et al. Infant 

feeding history shows distinct differences between 

Swedish celiac and reference children. Pediatric

Allergy and Immunology - Official Publication of the 

European Society of Pediatric Allergy and 

Immunology 1996;7(1):1-5. No prevalence or

incidence reported 

Falzon L. Topic: Gluten-free diet of coeliac disease. J

Clin Excellence 2001;3(4):209-211. No prevalence or

incidence reported 

Farre C, Esteve M, Curcoy A et al. 

Hypertransaminasemia in pediatric celiac disease

patients and its prevalence as a diagnostic clue. Am J 

Gastroenterol 2002;97(12):3176-3181. No prevalence 

or incidence reported 

Farrell R J, Kelly C P. Diagnosis of celiac sprue. Am J 

Gastroenterol 2001;96(12):3237-3246. Review article 

Farrell Richard J, Kelly Ciaran P. Celiac sprue. N Engl 

J Med 2002;346(3):180-188. No prevalence or

incidence reported 

Fasano A, Catassi C. Current approaches to diagnosis

and treatment of celiac disease: an evolving spectrum. 

Gastroenterology 2001;120(3):636-651. No 

prevalence or incidence reported

Fasano A. European and North American populations 

should be screened for coeliac disease. Gut 

2003;52(2):168-169. No prevalence or incidence 

reported 

Fasano A. Where have all the American celiacs gone?.

Acta Paediatr 1996;412(Suppl):20-24. No prevalence 

or incidence reported 

Fasano Alessio. Celiac disease--how to handle a 

clinical chameleon. N Engl J Med 2003;348(25):2568-

2570. No prevalence or incidence reported 

A-521
Fdez-Morera J L, Rodrigo L, Lopez-Vazquez A et al. 

MHC class I chain-related gene a transmembrane 

polymorphism modulates the extension of ulcerative 

colitis. Hum Immunol 2003;64(8):816-822. No

prevalence or incidence reported

Fedrick J A, Pandey J P, Verkasalo M et al. 

Immunoglobulin allotypes and the immune response 

to wheat gliadin in a Finnish population with celiac 

disease. Exp Clin Immunogenet 1985;2(4):185-190. 

No prevalence or incidence reported 

Feighery C. Coeliac disease. Br Med J 

1999;319(7204):236-239. No prevalence or incidence 

reported 

Feltkamp T E, Aarden L A, Lucas C J et al. Genetic 

risk factors for autoimmune diseases. Immunol Today

1999;20(1):10-12. No prevalence or incidence 

reported 

Ferfoglia G, Pulitano R, Sategna-Guidetti C. Do 

dietary antibodies still play a role in the diagnosis and 

follow-up of coeliac disease? A comparison among 

different serological tests. Panminerva Med 

1995;37(2):55-59. No prevalence or incidence 

reported 

Ferguson A, Denton-Miller P, Lai C L. Coeliac 

disease--objectives of life-long follow-up. Health Bull 

(Edinb) 1977;35(2):78-80. No prevalence or incidence 

reported 

Ferguson A, Hutton M M, Maxwell J D et al. Adult 

coeliac disease in hyposplenic patients. Lancet

1970;1(7639):163-164. No prevalence or incidence 

reported 

Ferguson A, Kingstone K. Coeliac disease and 

malignancies. Acta Paediatr 1996;412(Suppl):78-81. 

No prevalence or incidence reported 

Ferguson A, Ziegler K, Strobel S. Gluten intolerance 

(coeliac disease). Ann Allergy 1984;53(6 Pt 2):637-

642. No prevalence or incidence reported 

Ferguson A. Celiac disease, an eminently treatable 

condition, may be underdiagnosed in the United

States. Am J Gastroenterol 1997;92(8):1252-1254. 

Review article 

Ferguson A. Coeliac disease (gluten hypersensitivity).

J Hum Nutr 1976;30(3):193-201. No prevalence or

incidence reported 

Ferguson A. Coeliac disease. Prescr J 1997;37(4):206-

212. No prevalence or incidence reported 

Ferguson A. Immunological functions of the gut in 

relation to nutritional state and mode of delivery of

nutrients. Gut 1994;35(1 Suppl):S10-S12. No 

prevalence or incidence reported

Fernandez L, Fernandez-Arquero M, Gual L et al.

Triplet repeat polymorphism in the transmembrane 

region of the MICA gene in celiac disease. Tissue

Antigens 2002;59(3):219-222. No prevalence or 

incidence reported 

Fernandez N, Hitman G A, Festenstein H et al. Novel 

HLA class II-associated structural patterns in coeliac

disease and type I diabetes. Clin Exp Immunol 

1988;72(3):362-366. No prevalence or incidence 

reported 

Fernandez-Arquero M, Caldes T, Casado E et al. 

Polymorphism within the HLA-DQB1*02 promoter 

associated with susceptibility to coeliac disease.

European Journal of Immunogenetics - Official 

Journal of the British Society for Histocompatibility

and Immunogenetics 1998;25(1):1-3. No prevalence 

or incidence reported 

Fernandez-Arquero M, Figueredo M A, Maluenda C 

et al. HLA-linked genes acting as additive

susceptibility factors in celiac disease. Hum Immunol 

1995;42(4):295-300. No prevalence or incidence 

reported 

Fernandez-Arquero M, Polanco I, Escobar H et al. 

HLA-DQ alleles and susceptibility to celiac disease in

Spanish children. Tissue Antigens 1995;45(2):145-

147. No prevalence or incidence reported 

Ferrante P, Petronzelli F, Mariani P et al. Oligotyping 

of Italian celiac patients with the 11th International 

Histocompatibility Workshop reagents. Tissue

Antigens 1992;39(1):38-39. No prevalence or

incidence reported 

Festenstein H, Nyulassy S. Workshop on HLA and 

disease. Transplant Proc 1979;11(1):1183-1185. No 

prevalence or incidence reported

Fickling W E, McFarlane X A, Bhalla A K et al. The 

clinical impact of metabolic bone disease in coeliac 

disease. Postgrad Med J 2001;77(903):33-36. No 

prevalence or incidence reported

Fine K D, Do K, Schulte K et al. High prevalence of 

celiac sprue-like HLA-DQ genes and enteropathy in 

patients with the microscopic colitis syndrome. Am J 

Gastroenterol 2000;95(8):1974-1982. Not a relevant 

screening group

Fine K D, Lee E L, Meyer R L. Colonic 

histopathology in untreated celiac sprue or refractory

sprue: is it lymphocytic colitis or colonic

lymphocytosis?. Hum Pathol 1998;29(12):1433-1440. 

No prevalence or incidence reported 

Fine K D, Meyer R L, Lee E L. The prevalence and 

causes of chronic diarrhea in patients with celiac sprue 

treated with a gluten-free diet. Gastroenterology

A-522
1997;112(6):1830-1838. No prevalence or incidence 

reported 

Fine K D, Ogunji F, Saloum Y et al. Celiac sprue: 

another autoimmune syndrome associated with

hepatitis C. Am J Gastroenterol 2001;96(1):138-145. 

No prevalence or incidence reported 

Fine K D. The prevalence of occult gastrointestinal 

bleeding in celiac sprue. N Engl J Med 

1996;334(18):1163-1167. No prevalence or incidence 

reported 

Finkel M, Gelb A M, Cohen N et al. Long-term 

follow-up study in idiopathic steatorrhea. Am J 

Gastroenterol 1967;47(1):35-40. No prevalence or

incidence reported 

Fischer G F, Mayr W R. Molecular genetics of the 

HLA complex. Wien Klin Wochenschr 2001;113(20-

21):814-824. No prevalence or incidence reported

Flanders G, Graves P, Rewers M. Prevention of type 1 

diabetes from laboratory to public health. 

Autoimmunity 1999;29(3):235-246. No prevalence or

incidence reported 

Fleming A F. Iron deficiency in the tropics. Clin

Haematol 1982;11(2):365-388. No prevalence or

incidence reported 

Floreani A, Betterle C, Baragiotta A et al. Prevalence

of coeliac disease in primary biliary cirrhosis and of 

antimitochondrial antibodies in adult coeliac disease 

patients in Italy. Digestive and Liver Disease - Official 

Journal of the Italian Society of Gastroenterology and 

the Italian Association for the Study of the Liver 

2002;34(4):258-261. No prevalence or incidence 

reported 

Fogg Matthew I, Spergel Jonathan M. Management of 

food allergies. Expert Opin Pharmacother 

2003;4(7):1025-1037. No prevalence or incidence 

reported 

Foldes-Papp Zeno, Demel Ulrike, Berry Desiree et al. 

Tissue transglutaminase antibody determination in

celiac disease. Analysis of diagnostic specificity of 

anti-human IgA-type assays. J Immunoassay

Immunochem 2002;23(2):211-227. No prevalence or 

incidence reported 

Fotoulaki M, Nousia-Arvanitakis S, AugoustidouSavvopoulou P et al. Clinical application of 

immunological markers as monitoring tests in celiac 

disease. Dig Dis Sci 1999;44(10):2133-2138. No 

prevalence or incidence reported

Fox L A. Diabetes therapy in children: Setting ageappropriate goals. Drug Benefit Trends 2002;14(Suppl 

D):30-35+44. No prevalence or incidence reported 

Francis James, Carty John E, Scott Brian B. The 

prevalence of coeliac disease in rheumatoid arthritis. 

Eur J Gastroenterol Hepatol 2002;14(12):1355-1356. 

No prevalence or incidence reported 

Frank L, Marian A, Visser M et al. Exposure to

peanuts in utero and in infancy and the development 

of sensitization to peanut allergens in young children. 

Pediatr Allergy Immunol 1999;10(1):27-32. No

prevalence or incidence reported

Franklin J L, Asquith P, Rosenberg I H. The 

occurrence of cystic fibrosis and celiac sprue within a

single sibship. Am J Dig Dis 1974;19(2):149-155. No 

prevalence or incidence reported

Fraser J S, Ciclitira P J. Pathogenesis of coeliac

disease: Implications for treatment. World J

Gastroenterol 2001;7(6):772-776. No prevalence or

incidence reported 

Fraser J S, Woodhouse N J, El Shafie O T et al. Occult 

celiac disease in adult Omanis with unexplained iron 

deficiency anemia. Saudi Med J 2003;24(7):791No 

prevalence or incidence reported

Fraser N G, Ferguson A, Murray D. Dermatitis 

herpetiformis in two patients with idiopathic

steatorrhoea (adult coeliac disease). Br Med J

1968;3(622):30-31. No prevalence or incidence 

reported 

Freeman H J. Biopsy-defined adult celiac disease in 

Asian-Canadians. Can J Gastroenterol 

2003;17(7):433-436. No prevalence or incidence 

reported 

Freeman H J. Failure of added dietary gluten to induce 

small intestinal histopathological changes in patients 

with watery diarrhea and lymphocytic colitis. Can J

Gastroenterol 1996;10(7):436-439. No prevalence or 

incidence reported 

Freeman H J. Free perforation due to intestinal 

lymphoma in biopsy-defined or suspected celiac 

disease. J Clin Gastroenterol 2003;37(4):299-302. No 

prevalence or incidence reported

Freeman H J. Hepatobiliary tract and pancreatic

disorders in celiac disease. Can J Gastroenterol

1997;11(1):77-81. No prevalence or incidence 

reported 

Freeman H J. Neoplastic disorders in 100 patients with 

adult celiac disease. Can J Gastroenterol 

1996;10(3):163-166. No prevalence or incidence 

reported 

Freeman H J. Solid-phase ELISA for tissue

transglutaminase, an endomysial target for possible 

serological diagnosis of celiac disease. Can J

A-523
Gastroenterol 1998;12(5):323-324. No prevalence or 

incidence reported 

Freeman H J. Survey of gastroenterologists on the 

diagnosis and treatment of adult patients with celiac 

disease in British Columbia. Can J Gastroenterol

1998;12(2):149-152. No prevalence or incidence 

reported 

Freemark M, Levitsky L L. Screening for celiac

disease in children with type 1 diabetes: Two views of 

the controversy. Diabetes Care 2003;26(6):1932-1939. 

No prevalence or incidence reported 

Freier S. Paediatric gastrointestinal allergy. Clin

Allergy 1973;3(Suppl):597-618. No prevalence or

incidence reported 

Frezal J, Rey J. Genetics of disorders of intestinal

digestion and absorption. Adv Hum Genet 1970;1275-

336. No prevalence or incidence reported 

Fric P, Lojda Z, Jodl J et al. Analysis of peroral jejunal

biopsies in clinically asymptomatic parents of children 

with celiac sprue. Digestion 1969;2(1):35-42. Not a 

relevant screening geography

Fried M W. Side effects of therapy of hepatitis C and 

their management. J Gastroenterol Hepatol 2002;36(5 

I):S237-S244. No prevalence or incidence reported 

Friis S U, Gudmand-Hoyer E. Screening for coeliac 

disease in adults by simultaneous determination of

IgA and IgG gliadin antibodies. Scand J Gastroenterol 

1986;21(9):1058-1062. No prevalence or incidence 

reported 

Frisoni G B, Carabellese N, Longhi M et al. Is celiac 

disease associated with Alzheimer's disease?. Acta

Neurol Scand 1997;95(3):147-151. No prevalence or 

incidence reported 

Frustaci Andrea, Cuoco Lucio, Chimenti Cristina et al. 

Celiac disease associated with autoimmune 

myocarditis. Circulation 2002;105(22):2611-2618. No 

prevalence or incidence reported

Fry L, Seah P P, Hoffbrand A V. Dermatitis 

herpetiformis. Clin Gastroenterol 1974;3(1):145-157. 

No prevalence or incidence reported 

Fry L, Seah P P, Riches D J et al. Clearance of skin 

lesions in dermatitis herpetiformis after gluten 

withdrawal. Lancet 1973;1(7798):288-291. No

prevalence or incidence reported

Fry L. Dermatitis herpetiformis. Bailliere's Clin

Gastroenterol 1995;9(2):371-393. No prevalence or

incidence reported 

Fry Lionel. Dermatitis herpetiformis: problems, 

progress and prospects. European Journal of

Dermatology - Ejd 2002;12(6):523-531. No 

prevalence or incidence reported

Fundia A F, Gonzalez Cid M B, Bai J et al. 

Chromosome instability in lymphocytes from patients 

with celiac disease. Clin Genet 1994;45(2):57-61. No 

prevalence or incidence reported

Fundia A, Gomez J C, Maurino E et al. Chromosome 

instability in untreated adult celiac disease patients. 

Acta Paediatr 1996;412(Suppl):82-84. No prevalence 

or incidence reported 

Gabrielli Maurizio, Cremonini Filippo, Fiore 

Giuseppe et al. Association between migraine and 

Celiac disease: results from a preliminary case-control 

and therapeutic study. Am J Gastroenterol 

2003;98(3):625-629. No prevalence or incidence 

reported 

Gale J, Simmonds P D, Mead G M et al. Enteropathytype intestinal T-cell lymphoma: clinical features and 

treatment of 31 patients in a single center. Journal of 

Clinical Oncology - Official Journal of the American

Society of Clinical Oncology 2000;18(4):795-803. No 

prevalence or incidence reported

Gale L, Wimalaratna H, Brotodiharjo A et al. Down 

Syndrome is strongly associated with coeliac disease. 

Gut 1997;40(4):492-496. Not a relevant screening 

group 

Galli-Tsinopoulou A, Nousia-Arvanitakis S, 

Dracoulacos D et al. Autoantibodies predicting 

diabetes mellitus type I in celiac disease. Horm Res

1999;52(3):119-124. No prevalence or incidence 

reported 

Gandolfi L, Pratesi R, Cordoba J C et al. Prevalence of

celiac disease among blood donors in Brazil. Am J 

Gastroenterol 2000;95(3):689-692. Not a relevant 

screening geography

Gans R O B, Ueda Y, Ito S et al. The occurrence of 

IgA-nephropathy in patients with diabetes mellitus 

may not be coincidental: A report of five cases. Am J 

Kidney Dis 1992;20(3):255-260. No prevalence or

incidence reported 

Garces M C, Gomez-Cerezo J, Codoceo R et al.

Postprandial cholecystokinin response in patients with 

chronic pancreatitis in treatment with oral substitutive

pancreatic enzymes. Dig Dis Sci 1998;43(3):562-566. 

No prevalence or incidence reported 

Garcia Vilela E, De Lourdes, de Abreu et al. 

Agreement between pathologists concerning 

assessment of intestinal biopsies from adult celiac

disease patients. Gastroenterol Int 2002;15(1-2):1-8. 

No prevalence or incidence reported 

A-524
Gardiner A J, Mutton K J, Walker-Smith J A. A 

family study of coeliac disease. Aust Paediatr J

1973;9(1):18-24. Not a relevant screening geography

Gardiner A, Porteous N, Walker-Smith J A. The effect

of coeliac disease on the mother-child relationship. 

Aust Paediatr J 1972;8(1):39-43. No prevalence or

incidence reported 

Garioch J J, Lewis H M, Sargent S A et al. 25 years'

experience of a gluten-free diet in the treatment of

dermatitis herpetiformis. Br J Dermatol 

1994;131(4):541-545. No prevalence or incidence 

reported 

Garioch J J. Dermatitis herpetiformis and its

management. Prescr J 1996;36(3):141-145. No

prevalence or incidence reported

Garn S M, Poznanski A K, Nagy J M. Bone 

measurement in the differential diagnosis of 

osteopenia and osteoporosis. Radiology

1971;100(3):509-518. No prevalence or incidence 

reported 

Garrote J A, Sorell L, Alfonso P et al. A novel visual 

immunoassay for coeliac disease screening. Eur J Clin 

Invest 1999;29(8):697-699. No prevalence or

incidence reported 

Garrote Jose A, Arranz Eduardo, Telleria Juan J et al. 

TNF alpha and LT alpha gene polymorphisms as 

additional markers of celiac disease susceptibility in a

DQ2-positive population. Immunogenetics 

2002;54(8):551-555. No prevalence or incidence 

reported 

Gasbarrini A, Ojetti V, Cuoco L et al. Lack of 

endoscopic visualization of intestinal villi with the 

"immersion technique" in overt atrophic celiac 

disease. Gastrointest Endosc 2003;57(3):348-351. No 

prevalence or incidence reported

Gasbarrini G, Ciccocioppo R, De Vitis I et al. Coeliac 

Disease in the Elderly. A multicentre Italian study. 

Gerontology 2001;47(6):306-310. No prevalence or

incidence reported 

Gastard J, Joubaud F, Farbos T et al. Etiology and 

course of primary chronic pancreatitis in Western 

France. Digestion 1973;9(5):416-428. No prevalence 

or incidence reported 

Gautrin D, Ghezzo H, Infante-Rivard C et al. 

Incidence and host determinants of work-related 

rhinoconjunctivitis in apprentice pastry-makers.

Allergy Eur J Allergy Clin Immunol 2002;57(10):913-

918. No prevalence or incidence reported 

Gawkrodger D J, Blackwell J N, Gilmour H M et al. 

Dermatitis herpetiformis: diagnosis, diet and 

demography. Gut 1984;25(2):151-157. No prevalence 

or incidence reported 

Gay G J, Delmotte J S. Enteroscopy in small intestinal

inflammatory diseases. Gastrointest Endosc Clin N 

Am 1999;9(1):115-123. No prevalence or incidence 

reported 

Gayer G, Apter S, Hofmann C et al. Intussusception in 

adults: CT diagnosis. Clin Radiol 1998;53(1):53-57. 

No prevalence or incidence reported 

Gazet J C, Pilkington T R, Kalucy R S et al. Treatment 

of gross obesity by jejunal bypass. Br Med J 

1974;4(5940):311-314. No prevalence or incidence 

reported 

Gazit E, Avigad S, Zfat Z et al. The association of HLA-B8 and childhood celiac disease in an Israeli 

population. Isr J Med Sci 1977;13(4):400-404. No 

prevalence or incidence reported

Gebhard R L, Katz S I, Marks J et al. HL-A antigen 

type and small-intestinal disease in dermatitis

herpetiformis. Lancet 1973;2(7832):760-762. No

prevalence or incidence reported

Gemme G, Vignolo M, Naselli A et al. Linear growth 

and skeletal maturation in subjects with treated celiac 

disease. J Pediatr Gastroenterol Nutr 1999;29(3):339-

342. No prevalence or incidence reported 

George E K, Hertzberger-ten Cate R, Suijlekom-Smit 

L W et al. Juvenile chronic arthritis and coeliac

disease in The Netherlands. Clin Exp Rheumatol 

1996;14(5):571-575. No prevalence or incidence 

reported 

George E K, Jansen T L, Mearin M L et al. 

Epidemiology of celiac disease in The Netherlands. J 

Pediatr Gastroenterol Nutr 1997;24(5):S7-S9. Not a 

relevant screening test 

George E K, Mearin M L, Bouquet J et al. High

frequency of celiac disease in Down syndrome. Eur J 

Pediatr 1996;128(4):555-557. No prevalence or 

incidence reported 

George E K, Mearin M L, Bouquet J et al. Screening 

for coeliac disease in Dutch children with associated 

diseases. Acta Paediatr 1996;412(Suppl):52-53. No 

prevalence or incidence reported

George E K, Mearin M L, Franken H C et al. Twenty

years of childhood coeliac disease in The Netherlands: 

a rapidly increasing incidence?. Gut 1997;40(1):61-66. 

Serology screen <1990 

George E K, Mearin M L, van der V et al. Low 

incidence of childhood celiac disease in The 

Netherlands. Pediatr Res 1995;37(2):213-218. 

Serology screen <1990 

A-525
Gheorghe L, Gheorghe C, Aposteanu G et al. Clinical 

spectrum of adult celiac disease in a referral center for 

Southern Romania. Associated disorders and shortterm survival. Rom J Gastroenterol 1996;5(4):223-

228. No prevalence or incidence reported 

Ghezzi A, Zaffaroni M. Neurological manifestations

of gastrointestinal disorders, with particular reference 

to the differential diagnosis of multiple sclerosis. 

Neurol Sci 2002;22(Suppl 2):S117-S122. No 

prevalence or incidence reported

Ghosh S K, Littlewood J M, Goddard D et al. Stool 

microscopy in screening for steatorrhoea. J Clin Pathol

1977;30(8):749-753. No prevalence or incidence 

reported 

Giampietro P G, Ragno V, Daniele S et al. Soy

hypersensitivity in children with food allergy. Ann 

Allergy 1992;69(2):143-146. No prevalence or

incidence reported 

Giannotti A, Tiberio G, Castro M et al. Coeliac 

disease in Williams syndrome. J Med Genet 

2001;38(11):767-768. No prevalence or incidence 

reported 

Giardiello F M, Lazenby A J. The atypical colitides. 

Gastroenterol Clin North Am 1999;28(2):479-490. No 

prevalence or incidence reported

Gilett H R, Freeman H J. Prevalence of celiac disease 

in collagenous and lymphocytic colitis. Can J 

Gastroenterol 2000;14(11):919-921. No prevalence or

incidence reported 

Gilett P M, Gilett H R, Israel D M et al. Increased 

prevalence of celiac disease in girls with Turner

syndrome detected using antibodies to endomysium 

and tissue transglutaminase. Can J Gastroenterol 

2000;14(11):915-918. No prevalence or incidence 

reported 

Gill S S, Heuman D M, Mihas A A. Small intestinal 

neoplasms. J Clin Gastroenterol 2001;33(4):267-282. 

No prevalence or incidence reported 

Gillberg R, Ahren C. Coeliac disease diagnosed by

means of duodenoscopy and endoscopic duodenal 

biopsy. Scand J Gastroenterol 1977;12(8):911-916. No 

prevalence or incidence reported

Gillet H, Ferguson A, Frier B. Coeliac disease often 

co-exists with Type 1 diabetes mellitus. Pract Diabetes

Int 1998;15(4):117-120. No prevalence or incidence 

reported 

Gillett H R, Cauch-Dudek K, Jenny E et al. Prevalence

of IgA antibodies to endomysium and tissue 

transglutaminase in primary biliary cirrhosis. Can J 

Gastroenterol 2000;14(8):672-675. No prevalence or 

incidence reported 

Gillett H R, Freeman H J. Comparison of IgA 

endomysium antibody and IgA tissue transglutaminase 

antibody in celiac disease. Can J Gastroenterol 

2000;14(8):668-671. No prevalence or incidence 

reported 

Gillett H R, Freeman H J. Prevalence of celiac disease 

in collagenous and lymphocytic colitis. Can J 

Gastroenterol 2000;14(11):919-921. No prevalence or

incidence reported 

Gillett H R, Freeman H J. Serological testing in 

screening for adult celiac disease. Can J Gastroenterol

1999;13(3):265-269. No prevalence or incidence 

reported 

Gillett P M, Gillett H R, Israel D M et al. Increased 

prevalence of celiac disease in girls with Turner

syndrome detected using antibodies to endomysium 

and tissue transglutaminase. Can J Gastroenterol 

2000;14(11):915-918. No prevalence or incidence 

reported 

Ginzberg H, Shin J, Ellis L et al. Shwachman 

syndrome: phenotypic manifestations of sibling sets 

and isolated cases in a large patient cohort are similar.

Eur J Pediatr 1999;135(1):81-88. No prevalence or

incidence reported 

Giordano M, Bolognesi E, D'Alfonso S et al. Linkage 

disequilibrium between intra-locus variants in the

aminopeptidase n gene and test of their association 

with coeliac disease. Ann Hum Genet 1999;63(Pt 

3):207-215. No prevalence or incidence reported

Giovagnorio F, Picarelli A, Di Giovambattista F et al. 

Evaluation with Doppler sonography of mesenteric 

blood flow in celiac disease. Ajr.American Journal of

Roentgenology 1998;171(3):629-632. No prevalence 

or incidence reported 

Giusti Judy. What you should know about celiac 

disease. Diabetes Self Manag 2003;20(1):66, 68-69, 

71. No prevalence or incidence reported 

Gobbi G, Bouquet F, Greco L et al. Coeliac disease, 

epilepsy, and cerebral calcifications. The Italian 

Working Group on Coeliac Disease and Epilepsy. 

Lancet 1992;340(8817):439-443. No prevalence or

incidence reported 

Godkin A, Friede T, Davenport M et al. Use of eluted

peptide sequence data to identify the binding

characteristics of peptides to the insulin-dependent

diabetes susceptibility allele HLA-DQ8 (DQ 3.2). Int

Immunol 1997;9(6):905-911. No prevalence or

incidence reported 

Goggins M, Kelleher D. Celiac disease and other 

nutrient related injuries to the gastrointestinal tract.

A-526
Am J Gastroenterol 1994;89(8 Suppl):S2-17. No

prevalence or incidence reported

Goldberg D P. A one-year survey of the prevalence of 

psychiatric illness in patients with disease of the small 

intestine. Gut 1968;9(6):725No prevalence or

incidence reported 

Goldberg D. A psychiatric study of patients with 

diseases of the small intestine. Gut 1970;11(6):459-

465. No prevalence or incidence reported 

Golden M H. Is complete catch-up possible for stunted

malnourished children?. Eur J Clin Nutr 

1994;48(Suppl 1):s58-s70; Discussion S71. No 

prevalence or incidence reported

Gomez J C, Selvaggio G S, Viola M et al. Prevalence 

of celiac disease in Argentina: screening of an adult 

population in the La Plata area. Am J Gastroenterol 

2001;96(9):2700-2704. Not a relevant screening 

geography

Gomez Juan C, Selvaggio Gisella, Pizarro Bibiana et

al. Value of a screening algorithm for celiac disease 

using tissue transglutaminase antibodies as first level 

in a population-based study. Am J Gastroenterol 

2002;97(11):2785-2790. Not a relevant screening

geography

Gonzalez D, Mazure R, Mautalen C et al. Body

composition and bone mineral density in untreated and 

treated patients with celiac disease. Bone

1995;16(2):231-234. No prevalence or incidence 

reported 

Goodchild M C, Nelson R, Anderson C M. Cystic 

fibrosis and coeliac disease: coexistence in two 

children. Arch Dis Child 1973;48(9):684-691. No 

prevalence or incidence reported

Goodwin M S, Goodwin T C. In a dark mirror. Ment 

Hyg 1969;53(4):550-563. No prevalence or incidence 

reported 

Gordon N. Cerebellar ataxia and gluten sensitivity: a 

rare but possible cause of ataxia, even in childhood. 

Dev Med Child Neurol 2000;42(4):283-286. No

prevalence or incidence reported

Gorski J, Niven M J, Sachs J A et al. HLA-DR alpha, -

DX alpha, and DR beta III gene association studies in 

DR3 individuals. Hum Immunol 1987;20(4):273-278. 

No prevalence or incidence reported 

Goswami R, Tandon R K, Dudha A et al. Prevalence 

and significance of steatorrhea in patients with active 

Graves' disease. Am J Gastroenterol 1998;93(7):1122-

1125. No prevalence or incidence reported 

Goulet O, Kedinger M, Brousse N et al. Intractable 

diarrhea of infancy with epithelial and basement

membrane abnormalities. Eur J Pediatr 

1995;127(2):212-219. No prevalence or incidence 

reported 

Gourtsoyiannis N C, Nolan D J. Lymphoma of the 

small intestine: radiological appearances. Clin Radiol 

1988;39(6):639-645. No prevalence or incidence 

reported 

Granot E, Korman S M, Sallon S et al. "Early" vs.

"late" diagnosis of celiac disease in two ethnic groups 

living in the same geographic area. Isr J Med Sci 

1994;30(4):271-275. No prevalence or incidence 

reported 

Greco L, Auricchio S, Mayer M et al. Case control 

study on nutritional risk factors in celiac disease. J 

Pediatr Gastroenterol Nutr 1988;7(3):395-399. No 

prevalence or incidence reported

Greco L, Babron M C, Corazza G R et al. Existence of 

a genetic risk factor on chromosome 5q in Italian

coeliac disease families. Ann Hum Genet 2001;65(Pt 

1):35-41. No prevalence or incidence reported 

Greco L, Corazza G, Babron M C et al. Genome 

search in celiac disease. Am J Hum Genet 

1998;62(3):669-675. No prevalence or incidence 

reported 

Greco L, De Seta L, D'Adamo G et al. Atopy and

coeliac disease: bias or true relation?. Acta Paediatr 

Scand 1990;79(6-7):670-674. No prevalence or

incidence reported 

Greco L, Mayer M, Ciccarelli G et al. Compliance to a

gluten-free diet in adolescents, or "what do 300 

coeliac adolescents eat every day?". Ital J

Gastroenterol Hepatol 1997;29(4):305-310. No

prevalence or incidence reported

Greco L, Percopo S, Clot F et al. Lack of correlation 

between genotype and phenotype in celiac disease. J

Pediatr Gastroenterol Nutr 1998;26(3):286-290. No 

prevalence or incidence reported

Greco L, Percopo S. The coeliac disease task force " 

Free from Gluten," " Improved knowledge to cure

coeliac disease". Acta Paediatr 1996;412(Suppl):25-

28. No prevalence or incidence reported 

Greco L, Romino R, Coto I et al. The first large 

population based twin study of coeliac disease. Gut 

2002;50(5):624-628. No prevalence or incidence 

reported 

Greco L, Tipo V, Di Donato F et al. Pulsatile growth 

pattern during catch-up growth in childhood coeliac 

disease. Acta Paediatr 1994;83(7):724-729. No

prevalence or incidence reported

A-527
Greco L, Tozzi A E, Mayer M et al. Unchanging

clinical picture of coeliac disease presentation in 

Campania, Italy. Eur J Pediatr 1989;148(7):610-613. 

No prevalence or incidence reported 

Greco L, Troncone R. Coeliac families. Acta Paediatr

2002;91(1):16-17. No prevalence or incidence 

reported 

Green P H R, Jabri B. Celiac disease and other

precursors to small-bowel malignancy. Gastroenterol 

Clin North Am 2002;31(2):625-639. No prevalence or

incidence reported 

Green P H R, Stavropoulos S N, Panagi S G et al. 

Characteristics of adult celiac disease in the USA:

results of a national survey. Am J Gastroenterol

2001;96(1):126-131. No prevalence or incidence 

reported 

Green Peter H R, Fleischauer Aaron T, Bhagat Govind 

et al. Risk of malignancy in patients with celiac 

disease. Am J Med 2003;115(3):191-195. No 

prevalence or incidence reported

Green Peter H R, Jabri Bana. Coeliac disease. Lancet

2003;362(9381):383-391. No prevalence or incidence 

reported 

Green R, Luyt D. Clinical characteristics of childhood 

asthmatics in Johannesburg. S Afr Med J 

1997;87(7):878-882. No prevalence or incidence 

reported 

Greenberg D A, Hodge S E, Rotter J I. Evidence for 

recessive and against dominant inheritance at the 

HLA-"linked" locus in coeliac disease. Am J Hum

Genet 1982;34(2):263-277. No prevalence or

incidence reported 

Greenberg D A, Rotter J I. Two locus models for 

gluten sensitive enteropathy: population genetic 

considerations. Am J Med Genet 1981;8(2):205-214. 

No prevalence or incidence reported 

Greenberger N J. Update in gastroenterology. Ann 

Intern Med 1999;131(6):445-452. No prevalence or

incidence reported 

Grigg A P, Angus P W, Hoyt R et al. The incidence,

pathogenesis and natural history of steatorrhea after 

bone marrow transplantation. Bone Marrow 

Transplant 2003;31(8):701-703. No prevalence or

incidence reported 

Grillo R, Petronzelli F, Mora B et al. Search for

coeliac disease susceptibility loci on 7q11.23 

candidate region: absence of association with the 

ELN17 microsatellite marker. Hum Hered 

2000;50(3):180-183. No prevalence or incidence 

reported 

Grodzinsky E, Hed J, Skogh T. IgA antiendomysium 

antibodies have a high positive predictive value for 

celiac disease in asymptomatic patients. Allergy 

1994;49(8):593-597. No prevalence or incidence 

reported 

Groisman G M, Amar M, Livne E. CD10: A valuable 

tool for the light microscopic diagnosis of 

microvillous inclusion disease (familial microvillous 

atrophy). Am J Surg Pathol 2002;26(7):902-907. No 

prevalence or incidence reported

Groll A, Candy D C, Preece M A et al. Short stature as

the primary manifestation of coeliac disease. Lancet 

1980;2(8204):1097-1099. No prevalence or incidence 

reported 

Gruskay F L. Comparison of breast, cow, and soy

feedings in the prevention of onset of allergic disease.

A 15-year prospective study. Clin Pediatr 

1982;21(8):486-491. No prevalence or incidence 

reported 

Guandalini S. Celiac disease in the new world. J 

Pediatr Gastroenterol Nutr 2000;31(4):362-364. No 

prevalence or incidence reported

Guandalini Stefano. Celiac disease. School Nurse

News 2003;20(2):24-27. No prevalence or incidence 

reported 

Guarino A, Spagnuolo M I, Russo S et al. Etiology

and risk factors of severe and protracted diarrhea. J 

Pediatr Gastroenterol Nutr 1995;20(2):173-178. No 

prevalence or incidence reported

Gudmand-Hoyer E. The clinical significance of

disaccharide maldigestion. Am J Clin Nutr 1994;59(3 

Suppl):735s-741s. No prevalence or incidence 

reported 

Guglielmino C R, De Silvestri A, Martinetti M. HLA 

class I and II genes in relation to the genetic structure 

and epidemiology of an Italian province. Exp Clin

Immunogenet 1997;14(2):149-159. No prevalence or 

incidence reported 

Gumaa S N, McNicholl B, Egan-Mitchell B et al.

Coeliac disease in Galway, Ireland 1971-1990. Ir Med 

J 1997;90(2):60-61. Serology screen <1990 

Gupte S. Changing concepts in celiac disease. Jk

Science 2001;3(3):103-104. No prevalence or

incidence reported 

Gutteridge D H, Robinson C J, Joplin G F. Delayed 

strontium absorption in post-menopausal osteoporosis 

and osteomalacia. Clin Sci 1968;34(2):351-363. No 

prevalence or incidence reported

Guvenc cedil, Kaymakog caron, Gurel N et al. The 

prevalence of manifest and latent celiac disease in type

A-528
1 diabetes mellitus. Turk J Gastroenterol 

2002;13(2):103-107. Not a relevant screening 

geography

Haaber A B, Rosenfalck A M, Hansen B et al. Bone 

mineral metabolism, bone mineral density, and body

composition in patients with chronic pancreatitis and 

pancreatic exocrine insufficiency. International 

Journal of Pancreatology - Official Journal of the 

International Association of Pancreatology 

2000;27(1):21-27. No prevalence or incidence 

reported 

Habior Andrzej, Lewartowska Aleksandra, Orlowska 

Janina et al. Association of coeliac disease with

primary biliary cirrhosis in Poland. Eur J 

Gastroenterol Hepatol 2003;15(2):159-164. No

prevalence or incidence reported

Hadjivassiliou M, Davies-Jones G A B, Sanders D S 

et al. Dietary treatment of gluten ataxia. J Neurol

Neurosurg Psychiatry 2003;74(9):1221-1224. No

prevalence or incidence reported

Hadjivassiliou M, Gibson A, Davies-Jones G A et al. 

Does cryptic gluten sensitivity play a part in

neurological illness?. Lancet 1996;347(8998):369-

371. No prevalence or incidence reported 

Hadjivassiliou M, Grunewald R A, Chattopadhyay A 

K et al. Clinical, radiological, neurophysiological, and 

neuropathological characteristics of gluten ataxia.

Lancet 1998;352(9140):1582-1585. No prevalence or 

incidence reported 

Hadjivassiliou M, Grunewald R A, Davies-Jones G A 

B. Gluten sensitivity as a neurological illness. J Neurol 

Neurosurg Psychiatry 2002;72(5):560-563. No

prevalence or incidence reported

Hadjivassiliou Marios, Grunewald Richard, Sharrack 

Basil et al. Gluten ataxia in perspective: epidemiology, 

genetic susceptibility and clinical characteristics.

Brain Dev 2003;126(Pt 3):685-691. No prevalence or

incidence reported 

Hadziselimovic F, Emmons L R, Schaub U et al. 

Occurrence of large granular lymphocytes and natural 

killer cells in the epithelium of the gut distinguishes 

two different coeliac diseases. Gut 1992;33(6):767-

772. No prevalence or incidence reported 

Haeney M R, Goodwin B J, Barratt M E et al. Soya

protein antibodies in man: their occurrence and

possible relevance in coeliac disease. J Clin Pathol 

1982;35(3):319-322. No prevalence or incidence 

reported 

Hagan L L, Goetz D W, Revercomb C H et al. Sudden 

infant death syndrome: A search for allergen

hypersensitivity. Ann Allergy Asthma Immunol 

1998;80(3):227-231. No prevalence or incidence 

reported 

Hakanen M, Luotola K, Salmi J et al. Clinical and

subclinical autoimmune thyroid disease in adult celiac

disease. Dig Dis Sci 2001;46(12):2631-2635. No 

prevalence or incidence reported

Hakeem V, Fifield R, al Bayaty H F et al. Salivary 

IgA antigliadin antibody as a marker for coeliac 

disease. Arch Dis Child 1992;67(6):724-727. No

prevalence or incidence reported

Hall R P, Clark R E, Ward F E. Dermatitis 

herpetiformis in two American blacks: HLA type and 

clinical characteristics. J Am Acad Dermatol

1990;22(3):436-439. No prevalence or incidence 

reported 

Hall R P, Owen S, Smith A et al. TCR Vbeta 

expression in the small bowel of patients with

dermatitis herpetiformis and gluten sensitive 

enteropathy. Limited expression in dermatitis 

herpetiformis and treated asymptomatic gluten

sensitive enteropathy. Exp Dermatol 2000;9(4):275-

282. No prevalence or incidence reported 

Hall R P, Ward F E, Wenstrup R J. An HLA class II 

region restriction fragment length polymorphism 

(RFLP) in patients with dermatitis herpetiformis: 

association with HLA-DP phenotype. J Invest 

Dermatol 1990;95(2):172-177. No prevalence or 

incidence reported 

Hallert C, Astrom J. Intellectual ability of adults after

lifelong intestinal malabsorption due to coeliac 

disease. J Neurol Neurosurg Psychiatry

1983;46(1):87-89. No prevalence or incidence 

reported 

Hallert C, Gotthard R, Jansson G et al. Similar 

prevalence of coeliac disease in children and middleaged adults in a district of Sweden. Gut

1983;24(5):389-391. No prevalence or incidence 

reported 

Hallert C, Gotthard R, Norrby K et al. On the 

prevalence of adult coeliac disease in Sweden. Scand J

Gastroenterol 1981;16(2):257-261. Serology screen 

<1990 

Hallert C, Granno C, Grant C et al. Quality of life of 

adult coeliac patients treated for 10 years. Scand J

Gastroenterol 1998;33(9):933-938. No prevalence or 

incidence reported 

Hallert C, Granno C, Hulten S et al. Living with 

coeliac disease: controlled study of the burden of 

illness. Scand J Gastroenterol 2002;37(1):39-42. No 

prevalence or incidence reported

Hallert C, Grant C, Grehn S et al. Evidence of poor 

vitamin status in coeliac patients on a gluten-free diet 

for 10 years. Aliment Pharmacol Ther 

A-529
2002;16(7):1333-1339. No prevalence or incidence 

reported 

Hallert C, Lohiniemi S. Quality of life of celiac

patients living on a gluten-free diet. Nutrition

1999;15(10):795-797. No prevalence or incidence 

reported 

Halme L, Mecklin J P, Juhola M et al. Primary

gastrointestinal non-Hodgkin's lymphoma. A 

population based study in central Finland in 1975-

1993. Acta Oncol 1997;36(1):69-74. No prevalence or

incidence reported 

Halsted C H, Rowe J W. Occurrence of celiac sprue in

a patient with Fabry's disease. Ann Intern Med 

1975;83(4):524-525. No prevalence or incidence 

reported 

Hamilton J R, McNeill L K. Childhood celiac disease: 

response of treated patients to a small uniform daily

dose of wheat gluten. Eur J Pediatr 1972;81(5):885-

893. No prevalence or incidence reported 

Hansen T, Ronningen K S, Ploski R et al. Coding

region polymorphisms of human T-cell receptor

Vbeta6.9 and Vbeta21.4. Scand J Immunol 

1992;36(2):285-290. No prevalence or incidence 

reported 

Hanson L A, Korotkova M, Haversen L et al. Breastfeeding, a complex support system for the offspring. 

Pediatr Int 2002;44(4):347-352. No prevalence or

incidence reported 

Hanson L A. Human milk and host defence: 

immediate and long-term effects. Acta Paediatrica 

(Oslo, Norway - 1992).Supplement 1999;88(430):42-

46. No prevalence or incidence reported 

Hansson T, Anneren G, Sjoberg O et al. Celiac disease 

in relation to immunologic serum markers, trace 

elements, and HLA-DR and DQ antigens in Swedish 

children with Down syndrome. J Pediatr Gastroenterol 

Nutr 1999;29(3):286-292. No prevalence or incidence 

reported 

Hansson T, Dahlbom I, Hall J et al. Antibody 

reactivity against human and guinea pig tissue 

transglutaminase in children with celiac disease. J

Pediatr Gastroenterol Nutr 2000;30(4):379-384. No 

prevalence or incidence reported

Hansson T, Dannaeus A, Kraaz W et al. Production of 

antibodies to gliadin by peripheral blood lymphocytes 

in children with celiac disease: the use of an enzymelinked immunospot technique for screening and 

follow-up. Pediatr Res 1997;41(4 Pt 1):554-559. No 

prevalence or incidence reported

Hansson T, Ulfgren A-K, Lindroos E et al. 

Transforming growth factor-beta (TGF-beta) and

tissue transglutaminase expression in the small 

intestine in children with coeliac disease. Scand J

Immunol 2002;56(5):530-537. No prevalence or 

incidence reported 

Hansson Tony, Dahlbom Ingrid, Rogberg Siv et al. 

Recombinant human tissue transglutaminase for 

diagnosis and follow-up of childhood coeliac disease. 

Pediatr Res 2002;51(6):700-705. No prevalence or

incidence reported 

Hanukoglu A, Mizrachi A, Dalal I et al. 

Extrapancreatic autoimmune manifestations in type 1 

diabetes patients and their first-degree relatives: A 

multicenter study. Diabetes Care 2003;26(4):1235-

1240. No prevalence or incidence reported 

Harris O D, Cooke W T, Thompson H et al. 

Malignancy in adult coeliac disease and idiopathic

steatorrhoea. Am J Med 1967;42(6):899-912. No 

prevalence or incidence reported

Harris O D, Warner M, Cooke W T. Serum alkaline 

phosphatase in adult coeliac disease. Gut 

1969;10(11):951No prevalence or incidence reported 

Harrison J E, McNeill K G, Wilson D R et al. An 

evaluation of isotopic calcium absorption tests. Clin 

Biochem 1973;6(4):237-245. No prevalence or

incidence reported 

Harrison L C, Honeyman M C. Cow's milk and type 1 

diabetes: The real debate is about mucosal immune 

function. Diabetes 1999;48(8):1501-1507. No 

prevalence or incidence reported

Hartman C, Hochberg Z, Shamir R. Osteoporosis in 

pediatrics. Isr Med Assoc J 2003;5(7):509-515. No 

prevalence or incidence reported

Haslam N, Lock R J, Unsworth D J. Coeliac disease,

anaemia and pregnancy. Clin Lab 2001;47(9-10):467-

469. No prevalence or incidence reported 

Haslam N, Probert C S. An audit of the investigation 

and treatment of folic acid deficiency. J R Soc Med 

1998;91(2):72-73. No prevalence or incidence 

reported 

Hasler William L. Celiac sprue as a possible cause of 

symptoms in presumed irritable bowel syndrome. 

Gastroenterology 2002;122(7):2086-2087. No 

prevalence or incidence reported

Hattevig G, Kjellman B, Fallstrom S P. Congenital 

permanent diabetes mellitus and celiac disease. Eur J

Pediatr 1982;101(6):955-957. No prevalence or 

incidence reported 

Haugen M A, Kjeldsen-Kragh J, Forre O. A pilot 

study of the effect of an elemental diet in the

management of rheumatoid arthritis. Clin Exp 

A-530
Rheumatol 1994;12(3):275-279. No prevalence or

incidence reported 

Healy D A, Neumyer M M, Atnip R G et al.

Evaluation of celiac and mesenteric vascular disease 

with duplex ultrasonography. Journal of Ultrasound in 

Medicine - Official Journal of the American Institute 

of Ultrasound in Medicine 1992;11(9):481-485. No 

prevalence or incidence reported

Heederik D, Houba R. An exploratory quantitative 

risk assessment for high molecular weight sensitizers: 

Wheat flour. Ann Occup Hyg 2001;45(3):175-185. No 

prevalence or incidence reported

Heederik D, Thorne P S, Doekes G. Health-based

occupational exposure limits for high molecular

weight sensitizers: How long is the road we must 

travel?. Ann Occup Hyg 2002;46(5):439-446. No 

prevalence or incidence reported

Heikkinen M, Janatuinen E, Mayo K et al. Usefulness 

of anti-Helicobacter pylori and anti-CagA antibodies

in the selection of patients for gastroscopy. Am J 

Gastroenterol 1997;92(12):2225-2229. No prevalence 

or incidence reported 

Heikkinen M, Pikkarainen P, Takala J et al. Etiology

of dyspepsia: four hundred unselected consecutive

patients in general practice. Scand J Gastroenterol 

1995;30(6):519-523. No prevalence or incidence 

reported 

Heinersdorff N, Taylor T G. Concentration of zinc in

the hair of schoolchildren. Arch Dis Child 

1979;54(12):958-960. No prevalence or incidence 

reported 

Hendrikse W H, Reilly J J, Weaver L T. Malnutrition 

in a children's hospital. Clin Nutr 1997;16(1):13-18. 

No prevalence or incidence reported 

Heneghan M A, Stevens F M, Cryan E M et al. Celiac 

sprue and immunodeficiency states: a 25-year review. 

J Clin Gastroenterol 1997;25(2):421-425. No 

prevalence or incidence reported

Herlinger H, Maglinte D D. Jejunal fold separation in 

adult celiac disease: relevance of enteroclysis. 

Radiology 1986;158(3):605-611. No prevalence or

incidence reported 

Hernandez J L, Michalski J P, McCombs C C et al. 

Evidence for a dominant gene mechanism underlying

coeliac disease in the west of Ireland. Genet 

Epidemiol 1991;8(1):13-27. No prevalence or

incidence reported 

Hernandez M A, Colina G, Ortigosa L. Epilepsy,

cerebral calcifications and clinical or subclinical

coeliac disease. Course and follow up with gluten-free 

diet. Seizure - the Journal of the British Epilepsy

Association 1998;7(1):49-54. No prevalence or 

incidence reported 

Hernell O, Ivarsson A, Persson L A. Coeliac disease:

Effect of early feeding on the incidence of the disease. 

Early Hum Dev 2001;65(Suppl 2):S153-S160. No 

prevalence or incidence reported

Herrera M, Chertkoff L, Palavecino E et al. 

Restriction fragment length polymorphism in HLA 

class II genes of Latin-American Caucasian celiac

disease patients. Hum Immunol 1989;26(4):272-280. 

No prevalence or incidence reported 

Herrera M, Theiler G, Augustovski F et al. Molecular 

characterization of HLA class II genes in celiac

disease patients of Latin American Caucasian origin. 

Tissue Antigens 1994;43(2):83-87. No prevalence or 

incidence reported 

Hertervig E, Wieslander J, Johansson C et al. Antineutrophil cytoplasmic antibodies in chronic 

inflammatory bowel disease. Prevalence and 

diagnostic role. Scand J Gastroenterol 1995;30(7):693-

698. No prevalence or incidence reported 

Hervonen K, Hakanen M, Kaukinen K et al. Firstdegree relatives are frequently affected in coeliac

disease and dermatitis herpetiformis. Scand J 

Gastroenterol 2002;37(1):51-55. Not a relevant 

screening test 

Hetzel P A S, LaBrooy J T, Bellon M. The sup 5sup 

1Cr EDTA absorption test in coeliac patients treated 

with a gluten free diet. Ircs Med Sci 

1986;14(12):1183-1184. No prevalence or incidence 

reported 

Hetzel P A, Bennett G D, Sheldon A B et al. Genetic 

markers in Australian Caucasian subjects with coeliac 

disease. Tissue Antigens 1987;30(1):18-22. No

prevalence or incidence reported

Hilhorst M I, Brink M, Wauters E A K et al. Down 

syndrome and coeliac disease: Five new cases with a

review of the literature. Eur J Pediatr

1993;152(11):884-887. No prevalence or incidence 

reported 

Hill A V S. Immunogenetics and genomics. Lancet 

2001;357(9273):2037-2041. No prevalence or

incidence reported 

Hill D J, Hosking C S, Zhie C Y et al. The frequency 

of food allergy in Australia and Asia. Environ Toxicol 

Pharmacol 1997;4(1-2):101-110. No prevalence or

incidence reported 

Hill D J, Hudson I L, Sheffield L J et al. A low 

allergen diet is a significant intervention in infantile

colic: results of a community-based study. J Allergy 

A-531
Clin Immunol 1995;96(6 Pt 1):886-892. No 

prevalence or incidence reported

Hill I D. Celiac disease - A never-ending story?. Eur J 

Pediatr 2003;143(3):289-291. No prevalence or 

incidence reported 

Hill L E. Hypogammaglobulinaemia in the United 

Kingdom. 3. Clinical features of 

hypogammaglobulinaemia. Special Report 

Series,.Medical Research Council (Great Britain) 

1971;3109-34. No prevalence or incidence reported 

Hillemeier C, Gryboski J. Diabetes and the

gastrointestinal tract in the pediatric patient. Yale J 

Biol Med 1983;56(3):195-201. No prevalence or

incidence reported 

Hitman G A, Niven M J, Festenstein H et al. HLA 

class II alpha chain gene polymorphisms in patients 

with insulin-dependent diabetes mellitus, dermatitis 

herpetiformis, and celiac disease. Eur J Clin Invest

1987;79(2):609-615. No prevalence or incidence 

reported 

Hjelt K, Krasilnikoff P A. The impact of gluten on

haematological status, dietary intakes of haemopoietic 

nutrients and vitamin B12 and folic acid absorption in 

children with coeliac disease. Acta Paediatr Scand 

1990;79(10):911-919. No prevalence or incidence 

reported 

Hobbs J R. Immunoflobulins and malabsorption. Proc 

R Soc Med 1969;62(10):982-985. No prevalence or

incidence reported 

Hodges S, Lobo-Yeo A, Donaldson P et al. 

Autoimmune chronic active hepatitis in a family. Gut 

1991;32(3):299-302. No prevalence or incidence 

reported 

Hoey John. Irritable bowel syndrome: could it be 

celiac disease?. Cmaj - Canadian Medical Association

Journal = Journal De L'association Medicale 

Canadienne 2002;166(4):479-480. No prevalence or 

incidence reported 

Hoffbrand A V. Anaemia in adult coeliac disease. Clin

Gastroenterol 1974;3(1):71-89. No prevalence or 

incidence reported 

Hoffenberg E J, Bao F, Eisenbarth G S et al. 

Transglutaminase antibodies in children with a genetic 

risk for celiac disease. Eur J Pediatr 2000;137(3):356-

360. Not a relevant screening group 

Hoffmann Jorg C, Zeitz Martin. Small bowel disease 

in the elderly: diarrhoea and malabsorption. Best 

Practice & Research.Clinical Gastroenterology

2002;16(1):17-36. No prevalence or incidence 

reported 

Hoffmann M, Vogelsang H, Kletter K et al. 18Ffluoro-deoxy-glucose positron emission tomography

(18F-FDG-PET) for assessment of enteropathy-type T 

cell lymphoma. Gut 2003;52(3):347-351. No 

prevalence or incidence reported

Hogberg L, Nordwall M, Stenhammar L. One 

thousand small-bowel biopsies in children. A singleport versus a double-port capsule. Scand J 

Gastroenterol 2001;36(11):1230-1232. No prevalence 

or incidence reported 

Hoggan R. Considering wheat, rye, and barley

proteins as aids to carcinogens. Med Hypotheses

1997;49(3):285-288. No prevalence or incidence 

reported 

Holden Wendy, Orchard Tim, Wordsworth Paul. 

Enteropathic arthritis. Rheum Dis Clin North Am

2003;29(3):513-30, Viii. No prevalence or incidence 

reported 

Holm K, Maki M, Savilahti E et al. Intraepithelial 

gamma delta T-cell-receptor lymphocytes and genetic 

susceptibility to coeliac disease. Lancet 

1992;339(8808):1500-1503. No prevalence or

incidence reported 

Holmes G K T. Coeliac disease and malignancy. Ann 

Nestle 1993;51(2):66-74. No prevalence or incidence 

reported 

Holmes G K T. Coeliac disease and malignancy.

Digestive and Liver Disease - Official Journal of the 

Italian Society of Gastroenterology and the Italian 

Association for the Study of the Liver 2002;34(3):229-

237. No prevalence or incidence reported 

Holmes G K T. Screening for coeliac disease in type 1 

diabetes. Arch Dis Child 2002;87(6):495-498. No 

prevalence or incidence reported

Holmes G K, Prior P, Lane M R et al. Malignancy in 

coeliac disease--effect of a gluten free diet. Gut

1989;30(3):333-338. No prevalence or incidence 

reported 

Holmes G K, Stokes P L, Sorahan T M et al. Coeliac 

disease, gluten-free diet, and malignancy. Gut

1976;17(8):612-619. No prevalence or incidence 

reported 

Holmes G K. Celiac disease and malignancy. J Pediatr

Gastroenterol Nutr 1997;24(5):S20-S23. No 

prevalence or incidence reported

Holmes G K. Coeliac disease and Type 1 diabetes

mellitus - the case for screening. Diabetic Medicine - a 

Journal of the British Diabetic Association

2001;18(3):169-177. No prevalence or incidence 

reported 

A-532
Holmes G K. Non-malignant complications of coeliac 

disease. Acta Paediatr 1996;412(Suppl):68-75. No

prevalence or incidence reported

Holmgren Peterson K, Falth-Magnusson K, 

Magnusson K-E et al. Children with celiac disease

express inducible nitric oxide synthase in the small 

intestine during gluten challenge. Scand J 

Gastroenterol 1998;33(9):939-943. No prevalence or 

incidence reported 

Holopainen P, Arvas M, Sistonen P et al. 

CD28/CTLA4 gene region on chromosome 2q33 

confers genetic susceptibility to celiac disease. A 

linkage and family-based association study. Tissue

Antigens 1999;53(5):470-475. No prevalence or 

incidence reported 

Holopainen P, Mustalahti K, Uimari P et al. Candidate 

gene regions and genetic heterogeneity in gluten 

sensitivity. Gut 2001;48(5):696-701. No prevalence or

incidence reported 

Holt P R. The small intestine. Clin Gastroenterol

1985;14(4):689-723. No prevalence or incidence 

reported 

Holt Peter R. Gastrointestinal diseases in the elderly. 

Curr Opin Clin Nutr Metab Care 2003;6(1):41-48. No 

prevalence or incidence reported

Holtmeier J, Leuschner U. Medical treatment of

primary biliary cirrhosis and primary sclerosing

cholangitis. Digestion 2001;64(3):137-150. No

prevalence or incidence reported

Hooft C, Devos E, Van Damme J. Coeliac disease in a

diabetic child. Lancet 1969;2(7612):161No prevalence 

or incidence reported 

Hooft C, Roels H, Devos E. Diabetes and coeliac 

disease. Lancet 1969;2(7631):1192No prevalence or 

incidence reported 

Hornell A, Hofvander Y, Kylberg E. Introduction of 

solids and formula to breastfed infants: A longitudinal

prospective study in Uppsala, Sweden. Acta Paediatr

Int J Paediatr 2001;90(5):477-482. No prevalence or 

incidence reported 

Horvath K, Hill I D. Anti-tissue transglutaminase 

antibody as the first line screening for celiac disease: 

Good-bye antigliadin tests?. Am J Gastroenterol 

2002;97(11):2702-2704. No prevalence or incidence 

reported 

Horvath K, Horn G. Tardyferon therapy in 

hyposiderosis of infancy and childhood. Ther Hung 

1992;40(1):40-43. No prevalence or incidence 

reported 

Horvath K, Mehta D I. Celiac disease--a worldwide 

problem. Indian J Pediatr 2000;67(10):757-763. No 

prevalence or incidence reported

Houba R, Heederik D, Doekes G. Wheat sensitization 

and work-related symptoms in the baking industry are 

preventable: An epidemiologic study. Am J Respir

Crit Care Med 1998;158(5 I):1499-1503. No 

prevalence or incidence reported

Houlston R S, Ford D. Genetics of coeliac disease. 

Qjm - Monthly Journal of the Association of

Physicians 1996;89(10):737-743. No prevalence or

incidence reported 

Houlston R S, Tomlinson I P, Ford D et al. Linkage 

analysis of candidate regions for coeliac disease genes.

Hum Mol Genet 1997;6(8):1335-1339. No prevalence 

or incidence reported 

Hourihane J O, Strobel S. Clinical features of food

allergy. Comments Toxicol 2002;8(3):307-319. No

prevalence or incidence reported

Hourihane J O. Prevalence and severity of food 

allergy--need for control. Allergy 1998;53(46 

Suppl):84-88. No prevalence or incidence reported 

Hovdenak N. Prevalence and clinical picture of adult 

gluten-induced enteropathy in a Norwegian 

population. Scand J Gastroenterol 1980; 15(4):401-

404. Unable to obtain full article 

Hovell C J, Collett J A, Vautier G et al. High 

prevalence of coeliac disease in a population-based 

study from Western Australia: a case for screening?. 

Med J Aust 2001;175(5):247-250. Not a relevant 

screening geography

Howard F M, Carter C O, Candy D C et al. A family

study of protracted diarrhoea in infancy. J Med Genet 

1981;18(2):81-86. No prevalence or incidence 

reported 

Howdle P D, Jalal P K, Holmes G K T et al. Primary

small-bowel malignancy in the UK and its association 

with coeliac disease. Qjm - Monthly Journal of the 

Association of Physicians 2003;96(5):345-353. No 

prevalence or incidence reported

Howell W, Martin Calder, Philip C et al. Gene

polymorphisms, inflammatory diseases and cancer. 

Proc Nutr Soc 2002;61(4):447-456. No prevalence or

incidence reported 

Hozyasz K K. Sex ratio variation in offspring of celiac

women - Preliminary report. Pediatr Wspolczesna 

2002;4(3):253-255. No prevalence or incidence 

reported 

Hummel M, Bonifacio E, Stern M et al. Development 

of celiac disease-associated antibodies in offspring of 

A-533
parents with type I diabetes. Diabetologia 

2000;43(8):1005-1011. No prevalence or incidence 

reported 

Hummel M, Ziegler A G, Bonifacio E. Type 1 

diabetes mellitus, celiac disease and their association--

lessons from antibodies. Journal of Pediatric 

Endocrinology & Metabolism - Jpem 2001;14(Suppl 

1):607-610. No prevalence or incidence reported

Hurley T H, Sullivan J R, Hurley J V. Reaction to 

Kveim test material in sarcoidosis and other diseases. 

Lancet 1975;1(7905):494-496. No prevalence or 

incidence reported 

Hussain G, Ali S, Iqbal M M et al. Study of coeliac 

disease in children. J Coll Phys Surg Pak 

1999;9(2):81-84. Not a relevant screening geography

Hyams J S, Treem W R, Justinich C J et al.

Characterization of symptoms in children with

recurrent abdominal pain: resemblance to irritable 

bowel syndrome. J Pediatr Gastroenterol Nutr

1995;20(2):209-214. No prevalence or incidence 

reported 

Hyams J S. Celiac disease: New thoughts an an old 

problem. Curr Opin Pediatr 1997;9(5):487-489. No

prevalence or incidence reported

Hyer W, Cotterill A M, Savage M O. Common causes 

of short stature detectable by a height surveillance 

programme. J Med Screen 1995;2(3):150-153. No 

prevalence or incidence reported

Hylander E, Jarnum S, Kempel K et al. The absorption 

of oxalate, calcium, and fat after jejunoileal bypass. A 

prospective study. Scand J Gastroenterol 

1980;15(3):343-348. No prevalence or incidence 

reported 

Iacono G, Carroccio A, Montalto G et al. Steatocrit 

test: normal range and physiological variations in

preterm and low-birth-weight full-term newborns. 

Acta Paediatr 1992;81(11):933-934. No prevalence or

incidence reported 

Ide A, Eisenbarth G S. Genetic susceptibility in type 1 

diabetes and its associated autoimmune disorders. Rev

Endocr Metab Disord 2003;4(3):243-253. No 

prevalence or incidence reported

Iglesias S, Chapon F, Baron J C. Familial occipital 

calcifications, hemorrhagic strokes,

leukoencephalopathy, dementia, and external carotid 

dysplasia. Neurology 2000;55(11):1661-1667. No

prevalence or incidence reported

Iltanen S, Collin P, Korpela M et al. Celiac disease 

and markers of celiac disease latency in patients with 

primary Sjogren's syndrome. Am J Gastroenterol 

1999;94(4):1042-1046. Not a relevant screening group 

Ilyas M, Niedobitek G, Agathanggelou A et al. NonHodgkin's lymphoma, coeliac disease, and EpsteinBarr virus: a study of 13 cases of enteropathyassociated T- and B-cell lymphoma. Am J Pathol

1995;177(2):115-122. No prevalence or incidence 

reported 

Imai T, Akasawa A, Iikura Y. Nationwide food allergy 

survey. Int Arch Allergy Immunol 2001;124(1-3):312-

314. No prevalence or incidence reported 

Iovino P, Ciacci C, Sabbatini F et al. Esophageal 

impairment in adult celiac disease with steatorrhea.

Am J Gastroenterol 1998;93(8):1243-1249. No 

prevalence or incidence reported

ipetic S, Vlajinac H, Kocev N et al. Family history and 

risk of type 1 diabetes mellitus. Acta Diabetol Lat 

2002;39(3):111-115. No prevalence or incidence 

reported 

Isaacson P G. Gastrointestinal lymphomas of T- and 

B-cell types. Mod Pathol 1999;12(2):151-158. No 

prevalence or incidence reported

Isaksson B, Lindholm B, Sjogren B. A critical 

evaluation of the calcium balance technic. II. Dermal 

calcium losses. Metabolism- Clinical and

Experimental 1967;16(4):303-313. No prevalence or 

incidence reported 

Isbell R G, Carlson H C, Hoffman H N.

Roentgenologic-pathologic correlation in 

malabsorption syndromes. Am J Roentgenol Radium 

Ther Nucl Med 1969;107(1):158-169. No prevalence 

or incidence reported 

Iughetti L, Bulgarelli S, Forese S et al. Endocrine 

aspects of coeliac disease. Journal of Pediatric

Endocrinology & Metabolism - Jpem 2003;16(6):805-

818. No prevalence or incidence reported 

Ivarsson A, Hernell O, Nystrom L et al. Children born 

in the summer have increased risk for coeliac disease.

J Epidemiol Community Health 2003;57(1):36-39. No 

prevalence or incidence reported

Ivarsson A, Hernell O, Stenlund H et al. Breastfeeding protects against celiac disease. Am J Clin Nutr 

2002;75(5):914-921. No prevalence or incidence 

reported 

Ivarsson A, Persson L A, Hernell O. Does breastfeeding affect the risk for coeliac disease?. Adv Exp 

Med Biol 2000;478139-149. No prevalence or

incidence reported 

Ivarsson A. On the multifactorial aetiology of coeliac 

disease. Scand J Nutr Naringsforsk 2001;45(4):184-

185. No prevalence or incidence reported 

A-534
Ivarsson S A, Carlsson A, Bredberg A et al. 

Prevalence of coeliac disease in Turner syndrome. 

Acta Paediatr 1999;88(9):933-936. Not a relevant 

screening group

Iwanczak F, Mozrzymas R, Heimrath Z et al. Clinical 

evaluation of food allergy and food intolerance dietary 

treatment in children. Rocz Akad Med Bialymst

1995;40(3):588-594. No prevalence or incidence 

reported 

Jabbar A A R. HLA and disease associations in Iraq. 

Dis Markers 1993;11(4):161-170. No prevalence or

incidence reported 

Jackson F. The coevolutionary relationship of humans 

and domesticated plants. Am J Phys Anthropol 1996;-

(Suppl 23):161-176. No prevalence or incidence 

reported 

James M W, Scott B B. Coeliac disease: the cause of 

the various associated disorders?. Eur J Gastroenterol 

Hepatol 2001;13(9):1119-1121. No prevalence or

incidence reported 

James M W, Scott B B. Evidence-based clinical 

medicine: Application of a diagnostic test using the 

example of coeliac disease. Cme J Gastroenterol 

Hepatol Nutr 2001;4(1):28-31. No prevalence or 

incidence reported 

James O F W. NASH/NAFLD management. Acta 

Gastro-Enterol Belg 2002;65(4):200-203. No

prevalence or incidence reported

Jameson S. Zinc status in pregnancy: the effect of zinc

therapy on perinatal mortality, prematurity, and 

placental ablation. Ann N Y Acad Sci 1993;678178-

192. No prevalence or incidence reported 

Janatkova I, Malic caron, Fu caron et al. Diagnostic 

asset of assessment of autoantibodies in glutensensitive enteropathy. Epidemiol Mikrobiol Imunol 

2002;51(3):125-130. No prevalence or incidence 

reported 

Janatuinen E K, Kemppainen T A, Julkunen R J K et 

al. No harm from five year ingestion of oats in coeliac 

disease. Gut 2002;50(3):332-335. No prevalence or

incidence reported 

Jansson U, Johansson C. Down syndrome and celiac 

disease. J Pediatr Gastroenterol Nutr 1995;21(4):443-

445. No prevalence or incidence reported 

Jarvinen K-M, Turpeinen M, Suomalainen H. 

Concurrent cereal allergy in children with cow's milk 

allergy manifested with atopic dermatitis. Clin Exp 

Allergy 2003;33(8):1060-1066. No prevalence or

incidence reported 

Jawhari A, Talbot I C. Microscopic, lymphocytic and 

collagenous colitis. Histopathology 1996;29(2):101-

110. No prevalence or incidence reported 

Jaworski Z F. Pathophysiology, diagnosis and

treatment of osteomalacia. Orthop Clin North Am

1972;3(3):623-652. No prevalence or incidence 

reported 

Jeffrey P, Griffin P, Gibson M et al. Small bakeries - 

A cross-sectional study of respiratory symptoms, 

sensitization and dust exposure. Occup Med

1999;49(4):237-241. No prevalence or incidence 

reported 

Jenkins D J A, Taylor R H, Wolever T M S. The 

diabetic diet, dietary carbohydrate and differences in 

digestibility. Diabetologia 1982;23(6):477-484. No 

prevalence or incidence reported

Jenkins D, Goodall A, Scott B B. T-lymphocyte 

populations in normal and coeliac small intestinal 

mucosa defined by monoclonal antibodies. Gut 

1986;27(11):1330-1337. No prevalence or incidence 

reported 

Jenkins D, Goodall A, Scott B. T-cell and plasma cell 

populations in coeliac small intestinal mucosa in

relation to dermatitis herpetiformis. Gut 

1989;30(7):955-958. No prevalence or incidence 

reported 

Jennings J S R, Howdle P D. Celiac disease. Curr

Opin Gastroenterol 2001;17(2):118-126. No 

prevalence or incidence reported

Jevon G P, Dimmick J E, Dohil R et al. Spectrum of 

gastritis in celiac disease in childhood. Pediatric and 

Developmental Pathology - the Official Journal of the 

Society for Pediatric Pathology and the Paediatric

Pathology Society 1999;2(3):221-226. No prevalence 

or incidence reported 

Jewell D P. Celiac disease. Can J Gastroenterol

2000;14(8):665-666. No prevalence or incidence 

reported 

Jiskra J, Limanova Z, Vanic caron et al. IgA and IgG 

antigliadin, IgA anti-tissue transglutaminase and

antiendomysial antibodies in patients with

autoimmune thyroid diseases and their relationship to

thyroidal replacement therapy. Physiol Res 

2003;52(1):79-88. No prevalence or incidence 

reported 

Johanns W, Jakobeit C, Greiner L et al. Ultrasoundguided extracorporeal shock wave lithotripsy of 

pancreatic ductal stones: six years' experience. Can J

Gastroenterol 1996;10(7):471-475. No prevalence or 

incidence reported 

A-535
Johansen B H, Buus S, Vartdal F et al. Binding of

peptides to HLA-DQ molecules: Peptide binding

properties of the disease-associated HLADQ(alpha1(*)0501, beta1(*)0201) molecule. Int 

Immunol 1994;6(3):453-461. No prevalence or

incidence reported 

Johansen B H, Jensen T, Thorpe C J et al. Both alpha 

and beta chain polymorphisms determine the 

specificity of the disease-associated HLA-DQ2 

molecules, with beta chain residues being most 

influential. Immunogenetics 1996;45(2):142-150. No 

prevalence or incidence reported

Johansen B H, Vartdal F, Eriksen J A et al. 

Identification of a putative motif for binding of 

peptides to HLA-DQ2. Int Immunol 1996;8(2):177-

182. No prevalence or incidence reported 

Johnell O, Obrant K J. What is the impact of

osteoporosis?. Bailliere's Clin Rheumatol 

1997;11(3):459-477. No prevalence or incidence 

reported 

Johnson T N, Tanner M S, Taylor C J et al. 

Enterocytic CYP3A4 in a paediatric population: 

developmental changes and the effect of coeliac 

disease and cystic fibrosis. Br J Clin Pharmacol 

2001;51(5):451-460. No prevalence or incidence 

reported 

Johnston S D, Peter Watson R G, McMillan S A. Soda 

bread provocation test for subjects with transient

serology for coeliac disease 3 years after a population 

screening survey. Eur J Gastroenterol Hepatol 

2000;12(9):1013-1015. No prevalence or incidence 

reported 

Johnston S D, Ritchie C, Robinson J. Application of 

red cell distribution width to screening for coeliac

disease in insulin-dependent diabetes mellitus. Ir J 

Med Sci 1999;168(3):167-170. No prevalence or

incidence reported 

Johnston S D, Watson R G P, McMillan S A et al. 

Prevalence of coeliac disease in Northern Ireland.

Lancet 1997;350(9088):1370Not a relevant screening 

test 

Johnston S D, Watson R G P. Small bowel lymphoma 

in unrecognized coeliac disease: A cause for concern?. 

Eur J Gastroenterol Hepatol 2000;12(6):645-648. No 

prevalence or incidence reported

Johnston S D, Watson R G, McMillan S A et al. 

Preliminary results from follow-up of a large-scale 

population survey of antibodies to gliadin, reticulin 

and endomysium. Acta Paediatr 1996;412(Suppl):61-

64. Not a relevant screening test 

Johnston S D, Watson R G, McMillan S A et al. 

Serological markers for coeliac disease: changes with 

time and relationship to enteropathy. Eur J 

Gastroenterol Hepatol 1998;10(3):259-264. No

prevalence or incidence reported

Johnston S D, Watson R G, Middleton D et al. 

Genetic, morphometric and immunohistochemical 

markers of latent coeliac disease. Eur J Gastroenterol 

Hepatol 1999;11(11):1283-1288. No prevalence or

incidence reported 

Johnston Simon D, McMillan Stanley A, Collins John 

S et al. A comparison of antibodies to tissue 

transglutaminase with conventional serological tests in 

the diagnosis of coeliac disease. Eur J Gastroenterol 

Hepatol 2003;15(9):1001-1004. No prevalence or

incidence reported 

Jokinen J, Peters U, Maki M et al. Celiac sprue in 

patients with chronic oral mucosal symptoms. J Clin 

Gastroenterol 1998;26(1):23-26. No prevalence or

incidence reported 

Jones S M, Magnolfi C F, Cooke S K et al. 

Immunologic cross-reactivity among cereal grains and 

grasses in children with food hypersensitivity. J 

Allergy Clin Immunol 1995;96(3):341-351. No

prevalence or incidence reported

Kaczmarski M, Kurzatkowska B. The contribution of 

some constitutional factors to the development of

cow's milk and gluten intolerance in children. Rocz

Akad Med Bialymst 1989;33-34167-176. No 

prevalence or incidence reported

Kaczmarski M, Kurzatkowska B. The contribution of 

some environmental factors to the development of

cow's milk and gluten intolerance in children. Rocz

Akad Med Bialymst 1989;33-34151-165. No 

prevalence or incidence reported

Kaerlev L, Teglbjaerg P S, Sabroe S et al. Medical 

risk factors for small-bowel adenocarcinoma with

focus on Crohn disease: a European population-based 

case-control study. Scand J Gastroenterol 

2001;36(6):641-646. No prevalence or incidence 

reported 

Kagnoff M F, Weiss J B, Brown R J. Immunoglobulin 

allotype markers in gluten-sensitive enteropathy.

Lancet 1983;1(8331):952-953. No prevalence or 

incidence reported 

Kainulainen H, Rantala I, Collin P et al. Blisters in the 

small intestinal mucosa of coeliac patients contain T 

cells positive for cyclooxygenase 2. Gut 

2002;50(1):84-89. No prevalence or incidence 

reported 

Kalapesi Z, Rees J P R. Coeliac disease in 

schoolchildren. Ir Med J 1978;71(6):188-191. No 

prevalence or incidence reported

A-536
Kalayci A G, Kansu A, Girgin N et al. Bone mineral 

density and importance of a gluten-free diet in patients

with celiac disease in childhood. Pediatrics 

2001;108(5):E89No prevalence or incidence reported 

Kallikorm R, Uibo O, Uibo R. Coeliac disease in

spondyloarthropathy: usefulness of serological 

screening. Clin Rheumatol 2000;19(2):118-122. No 

prevalence or incidence reported

Kalra K K, Jain N, Mittal S K. Management of celiac

disease. Indian J Pediatr 1999;66(1 Suppl):S32-S36. 

No prevalence or incidence reported 

Kansu A, Kalayci A G, Altuntas B et al. Autoimmune 

hepatitis in children: A report of ten cases. Turk J Med 

Sci 2000;30(1):55-61. No prevalence or incidence 

reported 

Kanungo A, Samal K C, Sanjeevi C B. Molecular 

mechanisms involved in the etiopathogenesis of 

malnutrition-modulated diabetes mellitus. Ann N Y 

Acad Sci 2002;958138-143. No prevalence or

incidence reported 

Kanungo A, Shtauvere-Brameus A, Samal K C et al. 

Autoantibodies to tissue transglutaminase in patients 

from eastern India with malnutrition-modulated

diabetes mellitus, insulin-dependent diabetes mellitus, 

and non-insulin-dependent diabetes mellitus. Ann N Y 

Acad Sci 2002;958232-234. Not a relevant screening 

geography

Karagiozoglou-Lampoudi T, Nousia-Arvanitaki S, 

Augoustidou-Savopoulou P et al. Insulin secretion 

decline unrelated to jejunal morphology or exocrine 

pancreatic function in children with celiac disease.

Journal of Pediatric Endocrinology & Metabolism - 

Jpem 1996;9(6):585-591. No prevalence or incidence 

reported 

Karczewska K, Lukasik M, Kasner J et al. Familial

occurrence of celiac disease and isolated

immunoglobulin a deficiency. Med Sci Monit 

1998;4(5):836-839. No prevalence or incidence 

reported 

Karell K, Holopainen P, Mustalahti K et al. Not all 

HLA DR3 DQ2 haplotypes confer equal susceptibility 

to coeliac disease: transmission analysis in families. 

Scand J Gastroenterol 2002;37(1):56-61. No

prevalence or incidence reported

Karell K, Korponay-Szabo I, Szalai Zs et al. Genetic

dissection between coeliac disease and dermatitis

herpetiformis in sib pairs. Ann Hum Genet 2002;66(Pt 

5-6):387-392. No prevalence or incidence reported 

Kariv R, Arber N. Malignant tumors of the small 

intestine - New insights into a rare disease. Isr Med 

Assoc J 2003;5(3):188-192. No prevalence or

incidence reported 

Kasperlik-Zal(stroke)uska AA, Czarnocka B, Czech 

W. Autoimmunity as the most frequent cause of

idiopathic secondary adrenal insufficiency: Report of 

111 cases. Autoimmunity 2003;36(3):155-159. No 

prevalence or incidence reported

Kastin D A, Buchman A L. Malnutrition and

gastrointestinal disease. Curr Opin Gastroenterol 

2002;18(2):221-228. No prevalence or incidence 

reported 

Katz A J, Falchuk Z M. Current concepts in gluten

sensitive enteropathy (celiac sprue). Pediatr Clin 

North Am 1975;22(4):767-785. No prevalence or

incidence reported 

Katz K D. Celiac Disease - Current Clinical

Considerations in Treatment and Avoidance of 

Nutritional Deficiencies. Today's Ther Trends

2003;21(4):379-389. No prevalence or incidence 

reported 

Kaukinen K, Collin P, Holm K et al. Small-bowel

mucosal inflammation in reticulin or gliadin antibodypositive patients without villous atrophy. Scand J 

Gastroenterol 1998;33(9):944-949. No prevalence or 

incidence reported 

Kaukinen K, Collin P, Holm K et al. Wheat starchcontaining gluten-free flour products in the treatment 

of coeliac disease and dermatitis herpetiformis. A

long-term follow-up study. Scand J Gastroenterol 

1999;34(2):163-169. No prevalence or incidence 

reported 

Kaukinen K, Maki M, Partanen J et al. Celiac disease 

without villous atrophy: revision of criteria called for. 

Dig Dis Sci 2001;46(4):879-887. No prevalence or

incidence reported 

Kaukinen Katri, Sulkanen Satu, Maki Markku et al. 

IgA-class transglutaminase antibodies in evaluating 

the efficacy of gluten-free diet in coeliac disease. Eur J 

Gastroenterol Hepatol 2002;14(3):311-315. No

prevalence or incidence reported

Kaur Gurvinder, Sarkar N, Bhatnagar S et al. Pediatric 

celiac disease in India is associated with multiple

DR3-DQ2 haplotypes. Hum Immunol 2002;63(8):677-

682. No prevalence or incidence reported 

Kavin H. Adult coeliac disease in South Africa. An 

analysis of 20 cases emphasizing atypical

presentations. South African Medical Journal.SuidAfrikaanse Tydskrif Vir Geneeskunde 

1981;59(18):628-632. No prevalence or incidence 

reported 

Kawasaki E, Eisenbarth G S. High-throughput 

radioassays for autoantibodies to recombinant

A-537
autoantigens. Front Biosci 2000;5e181-e190. No 

prevalence or incidence reported

Kaye P S. Osteoporosis and fracture as a result of

gastrointestinal and hepatic disorders. Pract 

Gastroenterol 1999;23(3):15-34. No prevalence or

incidence reported 

Keaveny A P, Freaney R, McKenna M J et al. Bone 

remodeling indices and secondary

hyperparathyroidism in celiac disease. Am J

Gastroenterol 1996;91(6):1226-1231. No prevalence 

or incidence reported 

Kedzierska A, Turowski G. HLA class I antigens in 

families with coeliac disease. Medical Science

Monitor - International Medical Journal of 

Experimental and Clinical Research 2000;6(5):957-

963. No prevalence or incidence reported 

Kedzierska A, Turowski G. HLA class I haplotypes in 

families of children with coeliac disease. Medical

Science Monitor - International Medical Journal of 

Experimental and Clinical Research 2000;6(2):336-

341. No prevalence or incidence reported 

Keeton G R. Malabsorption in the Bantu. South 

African Medical Journal.Suid-Afrikaanse Tydskrif Vir 

Geneeskunde 1972;46(33):1170-1174. No prevalence 

or incidence reported 

Kellock T D, Pearson J R, Russell R I et al. The 

incidence and clinical significance of faecal hydroxy

fatty acids. Gut 1969;10(12):1055No prevalence or 

incidence reported 

Kelly D A, Phillips A D, Elliott E J et al. Rise and fall

of coeliac disease 1960-85. Arch Dis Child 

1989;64(8):1157-1160. No prevalence or incidence 

reported 

Kelly J, O'Farrelly C, Rees J P et al. Humoral response 

to alpha gliadin as serological screening test for

coeliac disease. Arch Dis Child 1987;62(5):469-473. 

No prevalence or incidence reported 

Kemppainen T A, Kosma V M, Janatuinen E K et al.

Nutritional status of newly diagnosed celiac disease 

patients before and after the institution of a celiac

disease diet--association with the grade of mucosal 

villous atrophy. Am J Clin Nutr 1998;67(3):482-487. 

No prevalence or incidence reported 

Kemppainen T, Kroger H, Janatuinen E et al. Bone 

recovery after a gluten-free diet: a 5-year follow-up 

study. Bone 1999;25(3):355-360. No prevalence or

incidence reported 

Kemppainen T, Kroger H, Janatuinen E et al. 

Osteoporosis in adult patients with celiac disease. 

Bone 1999;24(3):249-255. No prevalence or incidence 

reported 

Kemppainen T, Uusitupa M, Janatuinen E et al.

Intakes of nutrients and nutritional status in coeliac 

patients. Scand J Gastroenterol 1995;30(6):575-579. 

No prevalence or incidence reported 

Kennedy N P, Feighery C. Clinical features of coeliac 

disease today. Biomed Pharmacother 2000;54(7):373-

380. No prevalence or incidence reported 

Kepczyk T, Cremins J E, Long B D et al. A 

prospective, multidisciplinary evaluation of

premenopausal women with iron-deficiency anemia. 

Am J Gastroenterol 1999;94(1):109-115. No 

prevalence or incidence reported

Kero J, Gissler M, Hemminki E et al. Could TH1 and 

TH2 diseases coexist? Evaluation of asthma incidence 

in children with coeliac disease, type 1 diabetes, or

rheumatoid arthritis: a register study. J Allergy Clin 

Immunol 2001;108(5):781-783. No prevalence or

incidence reported 

Kerttula T O, Holm K, Partanen J et al. Circulating T 

lymphocyte subsets in coeliac disease (CoD) patients 

and healthy family members. Clin Exp Immunol 

1998;111(3):536-540. No prevalence or incidence 

reported 

Keuning J J, Pena A S, van Leeuwen A et al. HLADW3 associated with coeliac disease. Lancet

1976;1(7958):506-508. No prevalence or incidence 

reported 

Khoo J, Shek L, Khor E S H et al. Pattern of 

sensitization to common environmental allergens

amongst atopic Singapore children in the first 3 years 

of life. Asian Pac J Allergy Immunol 2001;19(4):225-

229. No prevalence or incidence reported 

Khoshoo V, Bhan M K, Puri S et al. Serum antigliadin antibody profile in childhood protracted 

diarrhoea due to coeliac disease and other causes in a 

developing country. Scand J Gastroenterol 

1989;24(10):1212-1216. No prevalence or incidence 

reported 

Khuffash F A, Barakat M H, Shaltout A A et al. 

Coeliac disease among children in Kuwait: difficulties

in diagnosis and management. Gut 1987;28(12):1595-

1599. No prevalence or incidence reported 

Khulusi S, Rhodes J. Diagnostic dilemmas in colitis. J 

R Coll Phys London 1997;31(6):618-623. No 

prevalence or incidence reported

Kieffer M, Barnetson R S, Blackwell J N. Sequential

studies of gliadin antibodies in patients with dermatitis 

herpetiformis. Arch Dermatol Res 1984;276(2):74-77. 

No prevalence or incidence reported 

A-538
Kieslich M, Errazuriz G, Posselt H G et al. Brain

white-matter lesions in celiac disease: a prospective 

study of 75 diet-treated patients. Pediatrics 

2001;108(2):E21No prevalence or incidence reported 

Kilmartin C, Lynch S, Abuzakouk M et al. Avenin 

fails to induce a Th1 response in coeliac tissue 

following in vitro culture. Gut 2003;52(1):47-52. No 

prevalence or incidence reported

Kilpatrick Z M, Katz J. Occult celiac disease as a

cause of iron deficiency anemia. Jama - the Journal of

the American Medical Association 1969;208(6):999-

1001. No prevalence or incidence reported 

Kim Soo, Youl Jeitner, Thomas M et al. 

Transglutaminases in disease. Neurochem Int 

2002;40(1):85-103. No prevalence or incidence 

reported 

Kimber Ian, Dearman Rebecca J. Factors affecting the

development of food allergy. Proc Nutr Soc 

2002;61(4):435-439. No prevalence or incidence 

reported 

King A L, Ciclitira P J. Celiac disease: strongly

heritable, oligogenic, but genetically complex. Mol 

Genet Metab 2000;71(1-2):70-75. No prevalence or 

incidence reported 

King A L, Fraser J S, Moodie S J et al. Coeliac 

disease: follow-up linkage study provides further

support for existence of a susceptibility locus on

chromosome 11p11. Ann Hum Genet 2001;65(Pt 

4):377-386. No prevalence or incidence reported

King A L, Yiannakou J Y, Brett P M et al. A genomewide family-based linkage study of coeliac disease. 

Ann Hum Genet 2000;64(Pt 6):479-490. No 

prevalence or incidence reported

Kingham J G, Parker D R. The association between 

primary biliary cirrhosis and coeliac disease: a study

of relative prevalences. Gut 1998;42(1):120-122. No 

prevalence or incidence reported

Kinston W, Loader P, Miller L. Emotional health of 

families and their members where a child is obese. J

Psychosom Res 1987;31(5):583-599. No prevalence or

incidence reported 

Kiper N, Gocmen A, Ozcelik U et al. Long-term 

clinical course of patients with idiopathic pulmonary

hemosiderosis (1979-1994): Prolonged survival with 

low-dose corticosteroid therapy. Pediatr Pulmonol 

1999;27(3):180-184. No prevalence or incidence 

reported 

Kitts D, Yuan Y, Joneja J et al. Adverse reactions to 

food constituents: allergy, intolerance, and 

autoimmunity. Can J Physiol Pharmacol 

1997;75(4):241-254. No prevalence or incidence 

reported 

Klasen E C, Polanco I, Biemond I et al. alpha 1-

Antitrypsin and coeliac disease in spain. Gut 

1980;21(11):948-950. No prevalence or incidence 

reported 

Klipstein F A, Beauchamp I, Corcino J J et al.

Nutritional status and intestinal function among rural 

populations of the West Indies. II. Barrio Nuevo,

Puerto Rico. Gastroenterology 1972;63(5):758-767. 

No prevalence or incidence reported 

Knivsberg A M. Urine patterns, peptide levels and

IgA/IgG antibodies to food proteins in children with 

dyslexia. Pediatr Rehabil 1997;1(1):25-33. No

prevalence or incidence reported

Knudtzon J, Fluge G, Aksnes L. Routine 

measurements of gluten antibodies in children of short 

stature. J Pediatr Gastroenterol Nutr 1991;12(2):190-

194. No prevalence or incidence reported 

Kocak N, Varzikoglu M, Yuce A et al. Celiac disease 

in childhood: Analysis of 41 cases. Turk J 

Gastroenterol 1997;8(2):201-205. No prevalence or

incidence reported 

Koch M B, Go V L, DiMagno E P. Can plasma human 

pancreatic polypeptide be used to detect diseases of 

the exocrine pancreas?. Mayo Clin Proc

1985;60(4):259-265. No prevalence or incidence 

reported 

Kocna Petr, Vanickova Zdislava, Perusicova Jindriska 

et al. Tissue transglutaminase-serology markers for 

coeliac disease. Clinical Chemistry and Laboratory 

Medicine - Cclm / Fescc 2002;40(5):485-492. No 

prevalence or incidence reported

Koivisto V A, Kuitunen P, Tiilikainen A et al. HLA 

antigens in patients with juvenile diabetes mellitus, 

coeliac disease and both of the diseases. Diabete 

Metab 1977;3(1):49-53. No prevalence or incidence 

reported 

Koivisto V A, Kuitunen P, Tilikainen A et al. HLA 

antigens, especially B8 and BW15, in patients with

juvenile diabetes mellitus, coeliac disease, and both of 

these diseases [proceedings]. Diabete Metab

1976;2(3):161No prevalence or incidence reported 

Kokkonen J, Holm K, Karttunen T J et al. Children 

with untreated food allergy express a relative 

increment in the density of duodenal 

gammadeltaSUP+ T cells. Scand J Gastroenterol 

2000;35(11):1137-1142. No prevalence or incidence 

reported 

Kokkonen J, Simila S, Vuolukka P. The incidence of

coeliac disease and pyloric stenosis in children in

A-539
Northern Finland. Ann Clin Res 1982;14(3):123-128. 

Serology screen <1990 

Kokkonen J. Lymphonodular hyperplasia on the 

duodenal bulb indicates food allergy in children. 

Endoscopy 1999;31(6):464-467. No prevalence or

incidence reported 

Kolacek S, Petkovic I, Booth I W. Chromosome 

aberrations in coeliac and non-coeliac enteropathies. 

Arch Dis Child 1998;78(5):466-468. No prevalence or

incidence reported 

Kolek A, Vospe caron, Her caron et al. Occurrence of 

coeliac disease in children with Down Syndrome in 

north Moravia, Czech Republic. Eur J Pediatr 

2003;162(3):207-208. No prevalence or incidence 

reported 

Koletzko B. Complementary foods and the 

development of food allergy. Pediatrics 2000;106(5 

II):1285-1286. No prevalence or incidence reported 

Koletzko S, Burgin-Wolff A, Koletzko B et al. 

Prevalence of coeliac disease in diabetic children and 

adolescents. A multicentre study. Eur J Pediatr

1988;148(2):113-117. Not a relevant screening 

geography

Kolho K L, Tiitinen A, Tulppala M et al. Screening 

for coeliac disease in women with a history of

recurrent miscarriage or infertility. Br J Obstet 

Gynaecol 1999;106(2):171-173. No prevalence or

incidence reported 

Kolho K-L, Jusufovic J, Miettinen A et al. Parietal cell

antibodies and Helicobacter pylori in children. J 

Pediatr Gastroenterol Nutr 2000;30(3):265-268. No 

prevalence or incidence reported

Koning F. Celiac disease and malignancy: an 

immunological basis?. J Pediatr Gastroenterol Nutr 

1997;24(5):S18-S19. No prevalence or incidence 

reported 

Kontakou M, Przemioslo R T, Sturgess R P et al. 

Expression of tumour necrosis factor-alpha, 

interleukin-6, and interleukin-2 mRNA in the jejunum 

of patients with coeliac disease. Scand J Gastroenterol

1995;30(5):456-463. No prevalence or incidence 

reported 

Kontiainen S, Schlenzka A, Koskimies S et al.

Autoantibodies and autoimmune diseases in young 

diabetics. Diabetes Res 1990;13(4):151-156. Serology

screen <1990 

Konzen K M, Perrault J, Moir C et al. Long-term 

follow-up of young patients with chronic hereditary or 

idiopathic pancreatitis. Mayo Clin Proc 

1993;68(5):449-453. No prevalence or incidence 

reported 

Korponay-Szabo I R, Dahlbom I, Laurila K et al. 

Elevation of IgG antibodies against tissue 

transglutaminase as a diagnostic tool for coeliac 

disease in selective IgA deficiency. Gut

2003;52(11):1567-1571. No prevalence or incidence 

reported 

Korponay-Szabo I R, Kovacs J B, Czinner A et al. 

High prevalence of silent celiac disease in preschool 

children screened with IgA/IgG antiendomysium 

antibodies. J Pediatr Gastroenterol Nutr 

1999;28(1):26-30. Not a relevant screening geography

Korponay-Szabo I R, Kovacs J B, Lorincz M et al. 

Prospective significance of antiendomysium antibody

positivity in subsequently verified celiac disease. J 

Pediatr Gastroenterol Nutr 1997;25(1):56-63. No 

prevalence or incidence reported

Kosnai I, Kuitunen P, Siimes M A. Iron deficiency in 

children with coeliac disease on treatment with glutenfree diet. Role of intestinal blood loss. Arch Dis Child 

1979;54(5):375-378. No prevalence or incidence 

reported 

Kotaniemi-Syrjanen Anne, Reijonen Tiina M,

Romppanen Jarkko et al. Allergen-specific 

immunoglobulin E antibodies in wheezing infants: the 

risk for asthma in later childhood. Pediatrics 

2003;111(3):E255-E261. No prevalence or incidence 

reported 

Kowalska E, Wasowska-Krolikowska K, ToporowskaKowalska E. Estimation of antithyroid antibodies 

occurrence in children with coeliac disease. Medical

Science Monitor - International Medical Journal of 

Experimental and Clinical Research 2000;6(4):719-

721. No prevalence or incidence reported 

Kowlessar O D, Phillips L D. Celiac disease. Med

Clin North Am 1970;54(3):647-656. No prevalence or

incidence reported 

Kristensen M, Lenz K, Nielsen O V et al. Short bowel 

syndrome following resection for Crohn's disease. 

Scand J Gastroenterol 1974;9(6):559-565. No 

prevalence or incidence reported

Kristiansson B, Karlberg J, Fallstrom S P. Infants with 

low rate of weight gain. I. A study of organic factors 

and growth patterns. Acta Paediatr Scand 

1981;70(5):655-662. No prevalence or incidence 

reported 

Kuc caron, Novakova D, Be caron et al. Gliadin, 

endomysial and thyroid antibodies in patients with 

latent autoimmune diabetes of adults (LADA). Clin 

Exp Immunol 2003;133(1):139-143. No prevalence or

incidence reported 

Kucera P, Novakova D, Behanova M et al. Gliadin, 

endomysial and thyroid antibodies in patients with 

A-540
latent autoimmune diabetes of adults (LADA). Clin 

Exp Immunol 2003;133(1):139-143. No prevalence or

incidence reported 

Kuitunen Mikael, Saukkonen Tero, Ilonen Jorma et al. 

Intestinal permeability to mannitol and lactulose in

children with type 1 diabetes with the HLA-DQB1*02 

allele. Autoimmunity 2002;35(5):365-368. No

prevalence or incidence reported

Kuitunen P, Kosnai I, Savilahti E. Morphometric 

study of the jejunal mucosa in various childhood 

enteropathies with special reference to intraepithelial 

lymphocytes. J Pediatr Gastroenterol Nutr

1982;1(4):525-531. No prevalence or incidence 

reported 

Kulig M, Bergmann R, Niggemann B et al. Prediction

of sensitization to inhalant allergens in childhood: 

evaluating family history, atopic dermatitis and

sensitization to food allergens. The MAS Study

Group. Multicentre Allergy Study. Clinical and

Experimental Allergy - Journal of the British Society 

for Allergy and Clinical Immunology

1998;28(11):1397-1403. No prevalence or incidence 

reported 

Kulig M, Bergmann R, Tacke U et al. Long-lasting 

sensitization to food during the first two years 

precedes allergic airway disease. The MAS Study 

Group, Germany. Pediatric Allergy and Immunology - 

Official Publication of the European Society of

Pediatric Allergy and Immunology 1998;9(2):61-67. 

No prevalence or incidence reported 

Kull K, Uibo O, Salupere R et al. High frequency of 

antigliadin antibodies and absence of antireticulin and 

antiendomysium antibodies in patients with ulcerative 

colitis. J Gastroenterol 1999;34(1):61-65. No

prevalence or incidence reported

Kumar P J, Walker-Smith J, Milla P et al. The teenage

coeliac: follow up study of 102 patients. Arch Dis

Child 1988;63(8):916-920. No prevalence or incidence 

reported 

Kumar P J. European and North American populations 

should be screened for coeliac disease. Gut 

2003;52(2):170-171. No prevalence or incidence 

reported 

Kumar P, Bartram C I. Relevance of the barium 

follow-through examination in the diagnosis of adult 

celiac disease. Gastrointest Radiol 1979;4(3):285-289. 

No prevalence or incidence reported 

Kumar P, Clark M. Primary biliary cirrhosis and 

coeliac disease. Is there an association?. Digestive and 

Liver Disease - Official Journal of the Italian Society

of Gastroenterology and the Italian Association for the

Study of the Liver 2002;34(4):248-250. No prevalence 

or incidence reported 

Kumar R, Lumsden A, Ciclitira P J et al. Human

genome search in celiac disease using gliadin cDNA 

as probe. J Mol Biol 2000;300(5):1155-1167. No

prevalence or incidence reported

Kumar Rajesh, Eastwood Amy L, Brown Milton L et

al. Human genome search in celiac disease: mutated 

gliadin T-cell-like epitope in two human proteins

promotes T-cell activation. J Mol Biol 

2002;319(3):593-602. No prevalence or incidence 

reported 

Kumar V, Lerner A, Valeski J E et al. Endomysial 

antibodies in the diagnosis of celiac disease and the 

effect of gluten on antibody titers. Immunol Invest 

1989;18(1-4):533-544. No prevalence or incidence 

reported 

Kumar V, Rajadhyaksha M, Wortsman J. Celiac

disease-associated autoimmune endocrinopathies. Clin

Diagn Lab Immunol 2001;8(4):678-685. No 

prevalence or incidence reported

Kuscu N K, Akcali S, Kucukmetin N T. Celiac disease 

and polycystic ovary syndrome. International Journal 

of Gynaecology and Obstetrics- the Official Organ of 

the International Federation of Gynaecology and 

Obstetrics 2002;79(2):149-150. No prevalence or

incidence reported 

La Seta F, Salerno G, Buccellato A et al. Radiographic 

indicants of adult celiac disease assessed by doublecontrast small bowel enteroclysis. Eur J Radiol

1992;15(2):157-162. No prevalence or incidence 

reported 

Labate A, Gambardella A, Messina D et al. Silent 

celiac disease in patients with childhood localizationrelated epilepsies. Epilepsia 2001;42(9):1153-1155. 

No prevalence or incidence reported 

Lad R, Jacobson K. The changing face of celiac 

disease. Paediatr Child Health 2001;6(9):644-651. No 

prevalence or incidence reported

Laghi A, Paolantonio P, Catalano C et al. Original

report. MR imaging of the small bowel using 

polyethylene glycol solution as an oral contrast agent 

in adults and children with celiac disease: Preliminary 

observations. Am J Roentgenol 2003;180(1):191-194. 

No prevalence or incidence reported 

Lahat E, Broide E, Leshem M et al. Prevalence of

celiac antibodies in children with neurologic disorders. 

Pediatr Neurol 2000;22(5):393-396. No prevalence or

incidence reported 

Lahdeaho M L, Lehtinen M, Rissa H R et al. 

Antipeptide antibodies to adenovirus E1b protein 

indicate enhanced risk of celiac disease and dermatitis

herpetiformis. Int Arch Allergy Immunol 

A-541
1993;101(3):272-276. No prevalence or incidence 

reported 

Lakatos L, Pandur T, David G et al. Association of 

extraintestinal manifestations of inflammatory bowel 

disease in a province of western Hungary with disease 

phenotype: Results of a 25-year follow-up study.

World J Gastroenterol 2003;9(10):2300-2307. No

prevalence or incidence reported

Lampasona V, Bazzigaluppi E, Barera G et al. Tissue 

transglutaminase and combined screening for coeliac

disease and type 1 diabetes-associated autoantibodies.

Lancet 1998;352(9135):1192-1193. No prevalence or 

incidence reported 

Lancaster Smith M J, Perrin J, Swarbrick E T et al.

Coeliac disease and autoimmunity. Postgrad Med J

1974;50(579):45-48. No prevalence or incidence 

reported 

Langman M J, Banwell J G, Stewart J S et al. ABO 

blood groups, secretor status, and intestinal alkaline 

phosphatase concentrations in patients with celiac 

disease. Gastroenterology 1969;57(1):19-23. No 

prevalence or incidence reported

Langman M J, McConnell T H, Spiegelhalter D J et al. 

Changing patterns of coeliac disease frequency: an 

analysis of Coeliac Society membership records. Gut 

1985;26(2):175-178. No prevalence or incidence 

reported 

Langman M J. Can epidemiology help us prevent 

celiac disease?. Gastroenterology 1986;90(2):489-491. 

No prevalence or incidence reported 

Langman M J. Epidemiology of cancer of the 

oesophagus and stomach. Br J Surg 1971;58(10):792-

793. No prevalence or incidence reported 

Langman M J. Recent changes in the patterns of

chronic digestive disease in the United Kingdom. 

Postgrad Med J 1984;60(709):733-736. No prevalence 

or incidence reported 

Lang-Muritano M, Molinari L, Dommann-Scherrer C

et al. Incidence of enteropathy-associated T-cell 

lymphoma in celiac disease: Implications for children 

and adolescents with type 1 diabetes. Pediatr Diabetes

2002;3(1):42-45. No prevalence or incidence reported 

Lankisch P G, Martinez Schramm A, Petersen F et al.

Diagnostic intervals for recognizing celiac disease. Z 

Gastroenterol 1996;34(8):473-477. No prevalence or 

incidence reported 

Lanning M, Kouvalainen K, Simila S et al. 

Agammaglobulinemia with arthritis and celiac disease 

developing after infectious mononucleosis. Follow up 

study of a case. Scand J Infect Dis 1977;9(2):144-148. 

No prevalence or incidence reported 

Larizza D, Calcaterra V, De Giacomo C et al. Celiac 

disease in children with autoimmune thyroid disease. 

Eur J Pediatr 2001;139(5):738-740. No prevalence or

incidence reported 

Larizza D, Calcaterra V, Luinetti O et al. Evidence for

immunogenetic predisposition in children with celiac 

disease and autoimmune thyroid disease. Int J Med 

Biol Environ 2001;29(2):143-148. No prevalence or 

incidence reported 

Larizza D, Locatelli M, Vitali L et al. Serum liver 

enzymes in Turner syndrome. Eur J Pediatr 

2000;159(3):143-148. No prevalence or incidence 

reported 

Laron Z, Kiess W, Phillip M. Foreword. Journal of 

Pediatric Endocrinology & Metabolism - Jpem 

2001;14(Suppl 1):571No prevalence or incidence 

reported 

Larrick J W. The polymerase chain reaction: A novel 

method for the study of mutation and polymorphism in 

the human population. Clin Ecol 1987;5(4):159-165. 

No prevalence or incidence reported 

Lasch E E, Ramot B, Neumann G. Childhood celiac 

disease in Israel. Epidemiological aspects. Isr J Med 

Sci 1968;4(6):1260-1264. Not a relevant screening 

geography

Laurin P, Falth-Magnusson K, Sundqvist T. Increase 

in nitric oxide urinary products during gluten 

challenge in children with coeliac disease. Scand J

Gastroenterol 2003;38(1):55-60. No prevalence or

incidence reported 

Lawrence J S. Hypogammaglobulinaemia in the 

United Kingdom. IV. Rheumatic disease in 

hypogammaglobulinaemia patients and their relatives. 

Special Report Series,.Medical Research Council 

(Great Britain) 1971;31035-44. No prevalence or

incidence reported 

Le Clainche L, Le Bourgeois M, Fauroux B et al. 

Long-term outcome of idiopathic pulmonary

hemosiderosis in children. Medicine 2000;79(5):318-

326. No prevalence or incidence reported 

Le Quellec A, Clapie M, Callamand P et al. 

Circulating oxyntomodulin-like immunoreactivity in 

healthy children and children with celiac disease. J

Pediatr Gastroenterol Nutr 1998;27(5):513-518. No 

prevalence or incidence reported

Lebenthal E, Branski D. Childhood celiac disease: A 

reappraisal. Eur J Pediatr 1981;98(5):681-690. No 

prevalence or incidence reported

Lebenthal Emanuel, Branski David. Celiac disease: an 

emerging global problem. J Pediatr Gastroenterol Nutr 

A-542
2002;35(4):472-474. No prevalence or incidence 

reported 

Lee F I, Prior J, Murray S M. Celiac disease in 

monozygous twin boys. Asynchronous presentation. 

Dig Dis Sci 1982;27(12):1137-1140. No prevalence or

incidence reported 

Lee J K, Marcos H B, Semelka R C. MR imaging of 

the small bowel using the HASTE sequence. 

Ajr.American Journal of Roentgenology

1998;170(6):1457-1463. No prevalence or incidence 

reported 

Lee M F. The diagnosis of steatorrhoea in outpatients. 

Br J Surg 1970;57(5):387-388. No prevalence or 

incidence reported 

Lee Susie K, Lo Winson, Memeo Lorenzo et al. 

Duodenal histology in patients with celiac disease 

after treatment with a gluten-free diet. Gastroenterol 

Int 2003;57(2):187-191. No prevalence or incidence 

reported 

Leech S. Molecular mimicry in autoimmune disease. 

Arch Dis Child 1998;79(5):448-451. No prevalence or

incidence reported 

Lehto M, Palosuo K, Varjonen E et al. Humoral and 

cellular responses to gliadin in wheat-dependent, 

exercise-induced anaphylaxis. Clinical and

Experimental Allergy - Journal of the British Society 

for Allergy and Clinical Immunology 2003;33(1):90-

95. No prevalence or incidence reported 

Lejarraga H, Caino S, Salvador A et al. Normal

growth velocity before diagnosis of celiac disease. J 

Pediatr Gastroenterol Nutr 2000;30(5):552-556. No 

prevalence or incidence reported

Lembcke B, Schneider H, Lankisch P G. Is the assay 

of disaccharidase activity in small bowel mucosal 

biopsy relevant for clinical gastroenterologists?. Klin 

Wochenschr 1989;67(11):568-575. No prevalence or 

incidence reported 

Lemieux B, Boivin M, Brossard J H et al. Normal 

parathyroid function with decreased bone mineral 

density in treated celiac disease. Can J Gastroenterol 

2001;15(5):302-307. No prevalence or incidence 

reported 

Lenander-Lumikari M, Ihalin R, Lahteenoja H. 

Changes in whole saliva in patients with coeliac 

disease. Arch Oral Biol 2000;45(5):347-354. No

prevalence or incidence reported

Leon F, Camarero C, Pena R et al. Antitransglutaminase IgA ELISA: clinical potential and 

drawbacks in celiac disease diagnosis. Scand J

Gastroenterol 2001;36(8):849-853. No prevalence or 

incidence reported 

Leonard J N, Tucker W F, Fry J S et al. Increased

incidence of malignancy in dermatitis herpetiformis. 

Br Med J (Clin Res Ed) 1983;286(6358):16-18. No 

prevalence or incidence reported

Lepage V, Lamm L U, Charron D. Molecular aspects

of HLA class II and some autoimmune diseases.

European Journal of Immunogenetics - Official 

Journal of the British Society for Histocompatibility

and Immunogenetics 1993;20(3):153-164. No 

prevalence or incidence reported

Lepore L, Martelossi S, Pennesi M et al. Prevalence of

celiac disease in patients with juvenile chronic

arthritis. Eur J Pediatr 1996;129(2):311-313. No

prevalence or incidence reported

Lepore L, Pennesi M, Ventura A et al. Anti-alphagliadin antibodies are not predictive of celiac disease 

in juvenile chronic arthritis. Acta Paediatr 1993;82(6-

7):569-573. No prevalence or incidence reported

Lerner A, Blank M, Lahat N et al. Increased

prevalence of autoantibodies in celiac disease. Dig Dis

Sci 1998;43(4):723-726. No prevalence or incidence 

reported 

Lerner A. Factors affecting the clinical presentation 

and time of diagnosis of celiac disease: the Jerusalem

and the West Bank-Gaza experience. Isr J Med Sci 

1994;30(4):294-295. No prevalence or incidence 

reported 

Leslie D, Lipsky P, Louis Notkins A. Autoantibodies 

as predictors of disease. J Clin Invest 

2001;108(10):1417-1422. No prevalence or incidence 

reported 

Lesort M, Chun W, Johnson G V et al. Tissue 

transglutaminase is increased in Huntington's disease 

brain. J Neurochem 1999;73(5):2018-2027. No 

prevalence or incidence reported

Lesort M, Tucholski J, Miller M L et al. Tissue

transglutaminase: a possible role in neurodegenerative 

diseases. Prog Neurobiol 2000;61(5):439-463. No 

prevalence or incidence reported

Lesort Mathieu, Chun WanJoo, Tucholski Janusz et al. 

Does tissue transglutaminase play a role in

Huntington's disease?. Neurochem Int 2002;40(1):37-

52. No prevalence or incidence reported 

Leth R D, Abrahamsson H, Kilander A et al.

Malabsorption of fat after partial gastric resection. A 

study of pathophysiologic mechanisms. Eur J Surg

1991;157(3):205-208. No prevalence or incidence 

reported 

Levin D C, Baltaxe H A. High incidence of celiac axis

narrowing in asymptomatic individuals. Am J 

A-543
Roentgenol Radium Ther Nucl Med 1972;116(2):426-

429. No prevalence or incidence reported 

Levine A, Bujanover Y, Reif S et al. Comparison of 

assays for anti-endomysial and anti-transglutaminase 

antibodies for diagnosis of pediatric celiac disease. 

Israel Medical Association Journal - Imaj 

2000;2(2):122-125. No prevalence or incidence 

reported 

Levine A, Lahav J, Zahavi I et al. Activated protein C 

resistance in pediatric inflammatory bowel disease. J

Pediatr Gastroenterol Nutr 1998;26(2):172-174. No 

prevalence or incidence reported

Lewis W H, Imber W E. Allergy epidemiology in the 

St. Louis, Missouri, area. V. Cereal ingestants. Ann 

Allergy 1975;35(4):251-254. No prevalence or

incidence reported 

Lie B A, Sollid L M, Ascher H et al. A gene telomeric 

of the HLA class I region is involved in predisposition 

to both type 1 diabetes and coeliac disease. Tissue 

Antigens 1999;54(2):162-168. No prevalence or 

incidence reported 

Lifschitz C H, Polanco I, Lobb K. The urinary

excretion of polyethylene glycol as a test for mucosal 

integrity in children with celiac disease: comparison 

with other noninvasive tests. J Pediatr Gastroenterol 

Nutr 1989;9(1):49-57. No prevalence or incidence 

reported 

Lifshitz F, Tarim O. Nutritional dwarfing. Curr Probl 

Pediatr 1993;23(8):322-336. No prevalence or

incidence reported 

Lightdale C J, Winawer S J. Screening diagnosis and 

staging of esophageal cancer. Semin Oncol 

1984;11(2):101-112. No prevalence or incidence 

reported 

Lim S G, Menzies I S, Lee C A et al. Intestinal

permeability and function in patients infected with

human immunodeficiency virus. A comparison with 

coeliac disease. Scand J Gastroenterol

1993;28(7):573-580. No prevalence or incidence 

reported 

Lin H J, Rotter J I, Conte W J. Use of HLA marker 

associations and HLA haplotype linkage to estimate 

disease risks in families with gluten-sensitive 

enteropathy. Clin Genet 1985;28(3):185-198. No 

prevalence or incidence reported

Lindberg J, Ahren C, Iwarson S. Intestinal villous 

atrophy in chronic active hepatitis. Scand J

Gastroenterol 1979;14(8):1015-1018. No prevalence 

or incidence reported 

Lindblad A, Glaumann H, Strandvik B. Natural 

history of liver disease in cystic fibrosis. Hepatology

1999;30(5):1151-1158. No prevalence or incidence 

reported 

Linder J, Cheruvattath R, Truss C et al. Diagnostic 

yield and clinical implications of push enteroscopy:

Results from a nonspecialized center. J Clin 

Gastroenterol 2002;35(5):383-386. No prevalence or 

incidence reported 

Lindgren S, Sjoberg K, Eriksson S. Unsuspected

coeliac disease in chronic 'cryptogenic' liver disease. 

Scand J Gastroenterol 1994;29(7):661-664. No

prevalence or incidence reported

Lindquist B L, Rogozinski T, Moi H et al. 

Endomysium and gliadin IgA antibodies in children 

with coeliac disease. Scand J Gastroenterol 

1994;29(5):452-456. No prevalence or incidence 

reported 

Lindqvist U, Rudsander A, Bostrom A et al. IgA 

antibodies to gliadin and coeliac disease in psoriatic 

arthritis. Rheumatology (Oxford) 2002;41(1):31-37. 

No prevalence or incidence reported 

Little A-M, Stern P L. Does HLA type predispose 

some individuals to cancer?. Mol Med Today

1999;5(8):337-342. No prevalence or incidence 

reported 

Little T M. Immunoglobulin levels in families with

coeliac disease. Lancet 1972;2(7774):400-401. No

prevalence or incidence reported

Littlewood J M. Coeliac disease in childhood. 

Bailliere's Clinical Gastroenterology 1995;9(2):295-

327. No prevalence or incidence reported 

Liu A H, Murphy J R. Hygiene hypothesis: Fact or

fiction?. J Allergy Clin Immunol 2003;111(3):471-

478. No prevalence or incidence reported 

Liu E, Bao F, Barriga K et al. Fluctuating 

transglutaminase autoantibodies are related to 

histologic features of celiac disease. Clin

Gastroenterol Hepatol 2003;1(5):356-362. No

prevalence or incidence reported

Liu Edwin, Eisenbarth George S. Type 1A diabetes 

mellitus-associated autoimmunity. Endocrinol Metab 

Clin North Am 2002;31(2):391-410, Vii. No

prevalence or incidence reported

Liu Jianjun, Juo Suh, Holopainen Paivi et al. 

Genomewide linkage analysis of celiac disease in 

Finnish families. Am J Hum Genet 2002;70(1):51-59. 

No prevalence or incidence reported 

Ljungman G, Myrdal U. Compliance in teenagers with 

coeliac disease--a Swedish follow-up study. Acta

Paediatr 1993;82(3):235-238. No prevalence or

incidence reported 

A-544
Lloyd J K. Dietary problems associated with the care

of chronically sick children. J Hum Nutr 

1979;33(2):135-139. No prevalence or incidence 

reported 

Lloyd J K. Effects and treatment of malabsorption in 

childhood. Proc Nutr Soc 1972;31(1):61-66. No

prevalence or incidence reported

Lloyd-Still J D, Shwachman H. Duodenal microflora: 

a prospective study in pediatric gastrointestinal

disorders. Am J Dig Dis 1975;20(8):708-715. No 

prevalence or incidence reported

Lloyd-Still J D. Chronic diarrhea of childhood and the 

misuse of elimination diets. Eur J Pediatr 

1979;95(1):10-13. No prevalence or incidence 

reported 

Lloyd-Still J D. Where have all the celiacs gone?.

Pediatrics 1978;61(6):929-930. No prevalence or

incidence reported 

Lo Winson, Sano Kevin, Lebwohl Ben et al. Changing 

presentation of adult celiac disease. Dig Dis Sci

2003;48(2):395-398. No prevalence or incidence 

reported 

Lofgren J, Jarnerot G, Danielsson D et al. Incidence 

and prevalence of primary biliary cirrhosis in a 

defined population in Sweden. Scand J Gastroenterol 

1985;20(5):647-650. No prevalence or incidence 

reported 

Loft D E, Marsh M N, Crowe P T. Rectal gluten 

challenge and diagnosis of coeliac disease. Lancet 

1990;335(8701):1293-1295. No prevalence or

incidence reported 

Loft D E. The epidemiology and diagnosis of coeliac 

disease. Eur J Gastroenterol Hepatol 1993;5(2):69-72. 

No prevalence or incidence reported 

Logan J S. The relation of meat-eating to the incidence

and severity of sprue and the relation of sprue to 

diarrhoea in the United Kingdom. Ulster Med J 

1971;40(2):151-157. No prevalence or incidence 

reported 

Logan R F, Rifkind E A, Busuttil A et al. Prevalence 

and "incidence" of celiac disease in Edinburgh and the 

Lothian region of Scotland. Gastroenterology

1986;90(2):334-342. Serology screen <1990 

Logan R F, Rifkind E A, Turner I D et al. Mortality in

celiac disease. Gastroenterology 1989;97(2):265-271. 

No prevalence or incidence reported 

Logan R F, Tucker G, Rifkind E A et al. Changes in 

clinical features of coeliac disease in adults in

Edinburgh and the Lothians 1960-79. Br Med J (Clin 

Res Ed) 1983;286(6359):95-97. Serology screen 

<1990 

Logan R F. Screening for coeliac disease--has the time 

come for mass screening?. Acta Paediatr 

1996;412(Suppl):15-19. No prevalence or incidence 

reported 

Lohiniemi S, Maki M, Kaukinen K et al. 

Gastrointestinal symptoms rating scale in coeliac

disease patients on wheat starch-based gluten-free

diets. Scand J Gastroenterol 2000;35(9):947-949. No 

prevalence or incidence reported

Lomoschitz F, Schima W, Schober E et al. 

Enteroclysis in adult celiac disease: diagnostic value 

of specific radiographic features. Eur Radiol 

2002;13(4):890-896. No prevalence or incidence 

reported 

Londei M. The external world of gluten and

autoimmunity. Gut 2001;49(4):463-464. No 

prevalence or incidence reported

Long R G, Wills M R. Hepatic osteodystrophy. Br J 

Hosp Med 1978;20(3):312-321. No prevalence or

incidence reported 

Lonnerdal B, Dewey K G. Epidemiology of iron

deficiency in infants and children. Ann Nestle 

1995;53(1):11-17. No prevalence or incidence 

reported 

Lopez-Vazquez A, Rodrigo L, Fuentes D et al. MHC 

class I chain related gene A (MICA) modulates the 

development of coeliac disease in patients with the 

high risk heterodimer DQA1*0501/DQB1*0201. Gut 

2002;50(3):336-340. No prevalence or incidence 

reported 

Lopez-Vazquez Antonio, Rodrigo Luis, Fuentes 

Dolores et al. MICA-A5.1 allele is associated with

atypical forms of celiac disease in HLA-DQ2-negative 

patients. Immunogenetics 2002;53(10-11):989-991. 

No prevalence or incidence reported 

Lorber M, Gershwin M E, Shoenfeld Y. The 

coexistence of systemic lupus erythematosus with 

other autoimmune diseases: The kaleidoscope of 

autoimmunity. Semin Arthritis Rheum 

1994;24(2):105-113. No prevalence or incidence 

reported 

Lorini R, Scaramuzza A, Vitali L et al. Clinical

aspects of coeliac disease in children with insulindependent diabetes mellitus. Journal of Pediatric 

Endocrinology & Metabolism - Jpem 1996;9(Suppl 

1):101-111. No prevalence or incidence reported

Louis E J, Thomson G, Payami H. The affected sib 

method. II. The intermediate model. Ann Hum Genet 

A-545
1983;47(3):225-243. No prevalence or incidence 

reported 

Louka A S, Moodie S J, Karell K et al. A collaborative 

European search for non-DQA1 *05-DQB1 *02 

Celiac disease loci on HLA-Dr3 haplotypes: Analysis

of transmission from homozygous parents. Hum 

Immunol 2003;64(3):350-358. No prevalence or 

incidence reported 

Louka A S, Nilsson S, Olsson M et al. HLA in coeliac 

disease families: a novel test of risk modification by

the 'other' haplotype when at least one DQA1*05-

DQB1*02 haplotype is carried. Tissue Antigens 

2002;60(2):147-154. No prevalence or incidence 

reported 

Louka A S, Stensby E K, Ek J et al. Coeliac disease 

candidate genes: no association with functional 

polymorphisms in matrix metalloproteinase 1 and 3 

gene promoters. Scand J Gastroenterol 

2002;37(8):931-935. No prevalence or incidence 

reported 

Louka A S, Torinsson Naluai A, D'Alfonso S et al. 

The IL12B gene does not confer susceptibility to

coeliac disease. Tissue Antigens 2002;59(1):70-72. No 

prevalence or incidence reported

Lowenstein H, Krasilnikoff P A, Bjerrum O J et al.

Occurrence of specific precipitins against bovine whey

proteins in serum from children with gastrointestinal

disorders. Int Arch Allergy Appl Immunol 1977;55(1-

6):514-525. No prevalence or incidence reported

Lubrano E, Ciacci C, Ames P R J et al. The arthritis of 

coeliac disease: Prevalence and pattern in 200 adult 

patients. Br J Rheumatol 1996;35(12):1314-1318. No 

prevalence or incidence reported

Ludvigsson J F, Falth-Magnusson K, Ludvigsson J. 

Tissue transglutaminase auto-antibodies in cord blood 

from children to become celiacs. Scand J

Gastroenterol 2001;36(12):1279-1283. No prevalence 

or incidence reported 

Ludvigsson J F, Ludvigsson J. Coeliac disease in the 

father affects the newborn. Gut 2001;49(2):169-175. 

No prevalence or incidence reported 

Ludvigsson J F, Ludvigsson J. Stressful life events, 

social support and confidence in the pregnant woman 

and risk of coeliac disease in the offspring. Scand J

Gastroenterol 2003;38(5):516-521. No prevalence or 

incidence reported 

Ludvigsson J F. Effect of gastroenteritis during

pregnancy on neonatal outcome. European Journal of 

Clinical Microbiology & Infectious Diseases - Official 

Publication of the European Society of Clinical 

Microbiology 2001;20(12):843-849. No prevalence or

incidence reported 

Luostarinen L K, Collin P O, Peraaho M J et al. 

Coeliac disease in patients with cerebellar ataxia of 

unknown origin. Ann Med 2001;33(6):445-449. No 

prevalence or incidence reported

Luostarinen L, Dastidar P, Collin P et al. Association

between coeliac disease, epilepsy and brain atrophy.

Eur Neurol 2001;46(4):187-191. No prevalence or

incidence reported 

Luostarinen L, Himanen S-L, Luostarinen M et al. 

Neuromuscular and sensory disturbances in patients 

with well treated coeliac disease. J Neurol Neurosurg 

Psychiatry 2003;74(4):490-494. No prevalence or

incidence reported 

Luostarinen L, Pirttila T, Collin P. Coeliac disease 

presenting with neurological disorders. Eur Neurol 

1999;42(3):132-135. No prevalence or incidence 

reported 

Lutwak L. Symposium on osteoporosis. Nutritional 

aspects of osteoporosis. J Am Geriatr Soc 

1969;17(2):115-119. No prevalence or incidence 

reported 

Luzi Giuseppe, Zullo Angelo, Iebba Filippo et al.

Duodenal pathology and clinical-immunological 

implications in common variable immunodeficiency

patients. Am J Gastroenterol 2003;98(1):118-121. No 

prevalence or incidence reported

Luzza F, Mancuso M, Imeneo M et al. Helicobacter 

pylori infection in children with celiac disease:

prevalence and clinicopathologic features. J Pediatr 

Gastroenterol Nutr 1999;28(2):143-146. No 

prevalence or incidence reported

Lynch H T, Smyrk T C, Lynch P M et al. 

Adenocarcinoma of the small bowel in lynch 

syndrome II. Cancer 1989;64(10):2178-2183. No

prevalence or incidence reported

MacFarlane Amanda J, Burghardt Karolina M, Kelly

John et al. A type 1 diabetes-related protein from 

wheat (Triticum aestivum). cDNA clone of a wheat 

storage globulin, Glb1, linked to islet damage. J Biol 

Chem 2002;278(1):54-63. No prevalence or incidence 

reported 

Mackay I R, Morris P J. Association of autoimmune

active chronic hepatitis with HL-A1,8. Lancet

1972;2(7781):793-795. No prevalence or incidence 

reported 

Mackey J, Treem W R, Worley G et al. Frequency of 

celiac disease in individuals with Down syndrome in 

the United States. Clin Pediatr (Phila) 2001;40(5):249-

252. Not a relevant screening group 

A-546
Mackner L M, McGrath A M, Stark L J. Dietary

recommendations to prevent and manage chronic 

pediatric health conditions: Adherence, intervention, 

and future directions. J Dev Behav Pediatr 

2001;22(2):130-143. No prevalence or incidence 

reported 

Mader R, Adawi M, Schonfeld S. Malabsorption in 

systemic lupus erythematosus. Clin Exp Rheumatol 

1997;15(6):659-661. No prevalence or incidence 

reported 

Madsen C. Prevalence of food allergy/intolerance in 

Europe. Environ Toxicol Pharmacol 1997;4(1-2):163-

167. No prevalence or incidence reported 

Magalotti D, Volta U, Bonfiglioli A et al. Splanchnic 

haemodynamics in patients with coeliac disease:

effects of a gluten-free diet. Digestive and Liver

Disease - Official Journal of the Italian Society of 

Gastroenterology and the Italian Association for the 

Study of the Liver 2003;35(4):262-268. No prevalence 

or incidence reported 

Magnolfi C F, Zani G, Lacava L et al. Soy allergy in 

atopic children. Annals of Allergy, Asthma & 

Immunology - Official Publication of the American 

College of Allergy, Asthma, & Immunology

1996;77(3):197-201. No prevalence or incidence 

reported 

Magrath G, Hartland B V. Dietary recommendations 

for children and adolescents with diabetes: An 

implementation paper. J Hum Nutr Diet 

1993;6(6):491-507. No prevalence or incidence 

reported 

Magrath G, Hartland B V. Dietary recommendations 

for children and adolescents with diabetes: an

implementation paper. British Diabetic Association's

Professional Advisory Committee. Diabetic Medicine

- a Journal of the British Diabetic Association

1993;10(9):874-885. No prevalence or incidence 

reported 

Mahadeva S, Wyatt J I, Howdle P D. Is a raised 

intraepithelial lymphocyte count with normal 

duodenal villous architecture clinically relevant?. J 

Clin Pathol 2002;55(6):424-428. No prevalence or

incidence reported 

Mainardi Elsa, Montanelli Alessandro, Dotti Maria et

al. Thyroid-related autoantibodies and celiac disease: a 

role for a gluten-free diet?. J Clin Gastroenterol 

2002;35(3):245-248. No prevalence or incidence 

reported 

Maki M, Aine L, Lipsanen V et al. Dental enamel

defects in first-degree relatives of coeliac disease

patients. Lancet 1991;337(8744):763-764. No 

prevalence or incidence reported

Maki M, Collin P. Coeliac disease. Lancet

1997;349(9067):1755-1759. No prevalence or

incidence reported 

Maki M, Hallstrom O, Huupponen T et al. Increased 

prevalence of coeliac disease in diabetes. Arch Dis

Child 1984;59(8):739-742. Serology screen <1990 

Maki M, Huupponen T, Holm K et al. Seroconversion 

of reticulin autoantibodies predicts coeliac disease in 

insulin dependent diabetes mellitus. Gut 

1995;36(2):239-242. Not a relevant screening test 

Mallas E G, Williamson N, Cooper B T et al. IgA

class reticulin antibodies in relatives of patients with 

coeliac disease. Gut 1977;18(8):647-650. Serology

screen <1990 

Mallet M. Coeliac disease in the very elderly. Cme J

Geriatr Med 2002;4(2):70-73. Review article 

Maluenda C, Phillips A D, Briddon A et al.

Quantitative analysis of small intestinal mucosa in

cow's milk-sensitive enteropathy. J Pediatr 

Gastroenterol Nutr 1984;3(3):349-356. No prevalence 

or incidence reported 

Mandal A, Mayberry J. How common is celiac disease 

in South America?. Am J Gastroenterol 

2000;95(3):579-580. No prevalence or incidence 

reported 

Mann N S, Mann S K. Celiac sprue and diabetes

mellitus. J Clin Gastroenterol 1993;16(1):4-5. No

prevalence or incidence reported

Mannell A, van Heerden J A, Weiland L H et al. 

Factors influencing survival after resection for ductal 

adenocarcinoma of the pancreas. Ann Surg 

1986;203(4):403-407. No prevalence or incidence 

reported 

Mannion A, Stevens F M, McCarthy C F et al.

Extended major histocompatibility complex

haplotypes in celiac patients in the west of Ireland.

Am J Med Genet 1993;45(3):373-377. No prevalence 

or incidence reported 

Mantovani V, Corazza G R, Bragliani M et al. Asp57-

negative HLA DQ beta chain and DQA1*0501 allele 

are essential for the onset of DQw2-positive and 

DQw2-negative coeliac disease. Clin Exp Immunol 

1993;91(1):153-156. No prevalence or incidence 

reported 

Mantovani V, Corazza G R, Frisoni M et al. HLA-DP 

polymorphism in northern Italian celiac patients.

Tissue Antigens 1992;40(4):182-186. No prevalence 

or incidence reported 

Mariani P, Mazzilli M C, Margutti G et al. Coeliac 

disease, enamel defects and HLA typing. Acta

A-547
Paediatr 1994;83(12):1272-1275. No prevalence or

incidence reported 

Mariani P, Viti M G, Montuori M et al. The glutenfree diet: a nutritional risk factor for adolescents with 

celiac disease?. J Pediatr Gastroenterol Nutr

1998;27(5):519-523. No prevalence or incidence 

reported 

Marin G A, Clark M L, Senior J R. Studies of 

malabsorption occurring in patients with Laennec's

cirrhosis. Gastroenterology 1969;56(4):727-736. No 

prevalence or incidence reported

Marks D R, Marks L M. Food allergy: Manifestations, 

evaluation, and management. Postgrad Med 

1993;93(2):191-196+201. No prevalence or incidence 

reported 

Marks I N, Bank S, Louw J H. Chronic pancreatitis in 

the Western Cape. Digestion 1973;9(5):447-453. No 

prevalence or incidence reported

Marks J, Shuster S. Iron metabolism in skin disease.

Arch Dermatol 1968;98(5):469-475. No prevalence or

incidence reported 

Marks J, Shuster S. Vitamin B12 excretion in patients 

with various skin diseases. Br Med J 1970;3(723):618-

621. No prevalence or incidence reported 

Marn C S, Gore R M, Ghahremani G G. Duodenal 

manifestations of nontropical sprue. Gastrointest 

Radiol 1986;11(1):30-35. No prevalence or incidence 

reported 

Marsh M N, Bjarnason I, Shaw J et al. Studies of

intestinal lymphoid tissue. XIV--HLA status, mucosal 

morphology, permeability and epithelial lymphocyte 

populations in first degree relatives of patients with 

coeliac disease. Gut 1990;31(1):32-36. No prevalence 

or incidence reported 

Marsh M N, Mathan M, Mathan V I. Studies of 

intestinal lymphoid tissue. VII. The secondary nature 

of lymphoid cell "activation" in the jejunal lesion of 

tropical sprue. Am J Pathol 1983;112(3):302-312. No 

prevalence or incidence reported

Marsh M N. Screening for latent gluten sensitivity:

questions many, but answers few. Eur J Gastroenterol 

Hepatol 1996;8(1):3-6. No prevalence or incidence 

reported 

Marsh M N. Studies of intestinal lymphoid tissue. XI--

The immunopathology of cell-mediated reactions in 

gluten sensitivity and other enteropathies. Scanning 

Microsc 1988;2(3):1663-1684. No prevalence or 

incidence reported 

Marsh M N. The immunopathology of the small 

intestinal reaction in gluten-sensitivity. Immunol 

Invest 1989;18(1-4):509-531. No prevalence or

incidence reported 

Marshall C M, Grunow J E. Emesis in infants as a 

consequence of feedings. Semin Pediatr Surg 

1995;4(3):147-151. No prevalence or incidence 

reported 

Martelossi S, Zanatta E, Del Santo E et al. Dental

enamel defects and screening for coeliac disease. Acta 

Paediatr 1996;412(Suppl):47-48. No prevalence or

incidence reported 

Martinelli P, Troncone R, Paparo F et al. Coeliac

disease and unfavourable outcome of pregnancy. Gut 

2000;46(3):332-335. No prevalence or incidence 

reported 

Martinetti M, De Silvestri A, Belloni C et al. Humoral 

response to recombinant hepatitis B virus vaccine at 

birth: Role of HLA and beyond. Clin Immunol 

2000;97(3):234-240. No prevalence or incidence 

reported 

Martini Silvia, Mengozzi Giulio, Aimo Giuseppe et al.

Comparative evaluation of serologic tests for celiac

disease diagnosis and follow-up. Clin Chem 

2002;48(6 Pt 1):960-963. No prevalence or incidence 

reported 

Martin-Villa J M, Lopez-Suarez J C, Perez-Blas M et

al. Coeliac- and enteropathy-associated autoantibodies

in Spanish insulin-dependent diabetes mellitus patients

and their relation to HLA antigens. J Diabetes

Complications 2001;15(1):38-43. No prevalence or

incidence reported 

Martucci S, Biagi F, Di Sabatino A et al. Coeliac

disease. Digestive and Liver Disease - Official Journal 

of the Italian Society of Gastroenterology and the 

Italian Association for the Study of the Liver 

2002;34(Suppl 2):150-153. No prevalence or

incidence reported 

Masala S, Annibale B, Fiori R et al. DXA vs. QCT for 

subclinical celiac disease patients. Acta Diabetol Lat

2003;40(Suppl 1):S174-S176. No prevalence or 

incidence reported 

Masoero G, Andriulli A, Santini B et al. Serum

trypsinlike immunoreactivity in cystic fibrosis. An aid

in assessing progressive involvement of the pancreas. 

Am J Dis Child 1983;137(2):167-170. No prevalence 

or incidence reported 

Matek Z, Jungvirth-Hegedus M, Kolacek S. 

Epidemiology of coeliac disease in children in one

Croatian county: possible factors that could affect the 

incidence of coeliac disease and adherence to a glutenfree diet (Part II). Coll Antropol 2000;24(2):397-404. 

Not a relevant screening geography

A-548
Matek Z, Jungvirth-Hegedus M, Kolacek S. 

Epidemiology of coeliac disease in children in one

Croatian county: the cumulative incidence over tenyear period and the way of clinical presentation (Part 

I). Coll Antropol 1999;23(2):621-628. Not a relevant 

screening geography

Mathan V I, Baker S J. Epidemic tropical sprue and 

other epidemics of diarrhea in South Indian villages. 

Am J Clin Nutr 1968;21(9):1077-1087. No prevalence 

or incidence reported 

Mathus-Vliegen E M H. Lymphoma in coeliac 

disease. J R Soc Med 1995;88(12):672-677. No

prevalence or incidence reported

Mathus-Vliegen E M, Van Halteren H, Tytgat G N.

Malignant lymphoma in coeliac disease: various

manifestations with distinct symptomatology and 

prognosis?. J Intern Med 1994;236(1):43-49. No 

prevalence or incidence reported

Matteoni C A, Goldblum J R, Wang N et al. Celiac

disease is highly prevalent in lymphocytic colitis. J 

Clin Gastroenterol 2001;32(3):225-227. No 

prevalence or incidence reported

Mattera D, Sollazzo R, Sarrantonio G et al. Serum

iron, serum ferritin and oral ion load in coeliac 

patients on a free diet. Ital J Gastroenterol 

1988;20(3):120-124. No prevalence or incidence 

reported 

Matteucci E, Cinapri V, Quilici S et al. Screening for 

coeliac disease in families of adults with Type 1 

diabetes based on serological markers. Diabetes Nutr 

Metab 2001;14(1):37-42. Not a relevant screening 

group 

Maurino E, Capizzano H, Niveloni S et al. Value of 

endoscopic markers in celiac disease. Dig Dis Sci 

1993;38(11):2028-2033. No prevalence or incidence 

reported 

Maurino Eduardo, Niveloni Sonia, Chernavsky

Alejandra et al. Azathioprine in refractory sprue:

results from a prospective, open-label study. Am J 

Gastroenterol 2002;97(10):2595-2602. No prevalence 

or incidence reported 

Mautalen C, Gonzalez D, Mazure R et al. Effect of 

treatment on bone mass, mineral metabolism, and

body composition in untreated celiac disease patients. 

Am J Gastroenterol 1997;92(2):313-318. No 

prevalence or incidence reported

Mautner V, Steinthorsdottir V, Bailey A. Enteric 

adenoviruses. Curr Top Microbiol Immunol 

1995;199(III):229-282. No prevalence or incidence 

reported 

Mayberry J F, Smart H L, Toghill P J. Familial 

association between coeliac disease and ulcerative

colitis: preliminary communication. J R Soc Med

1986;79(4):204-205. No prevalence or incidence 

reported 

Mazure R M, Vazquez H, Gonzalez D et al. Early 

changes of body composition in asymptomatic celiac

disease patients. Am J Gastroenterol 1996;91(4):726-

730. No prevalence or incidence reported 

Mazzacca G. Diet, coeliac disease and gastrointestinal

neoplasm. Adv Exp Med Biol 1993;348133-136. No 

prevalence or incidence reported

Mazzilli M C, Ferrante P, Mariani P et al. A study of 

Italian pediatric celiac disease patients confirms that 

the primary HLA association is to the DQ(alpha 

1*0501, beta 1*0201) heterodimer. Hum Immunol 

1992;33(2):133-139. No prevalence or incidence 

reported 

Mazzola G, Berrino M, Bersanti M et al. 

Immunoglobulin and HLA-DP genes contribute to the 

susceptibility to juvenile dermatitis herpetiformis. 

European Journal of Immunogenetics - Official 

Journal of the British Society for Histocompatibility

and Immunogenetics 1992;19(3):129-139. No 

prevalence or incidence reported

Mc Manus R, Wilson A G, Mansfield J et al. TNF2, a 

polymorphism of the tumour necrosis-alpha gene 

promoter, is a component of the celiac disease major 

histocompatibility complex haplotype. Eur J Immunol 

1996;26(9):2113-2118. No prevalence or incidence 

reported 

McCarthy C F. Coeliac disease: its Irish dimensions. Ir

J Med Sci 1975;144(1):1-13. No prevalence or

incidence reported 

McCarthy C F. The incidence of coeliac disease and 

its familial occurrence. Ir Med J 1974;67(15):420-421. 

No prevalence or incidence reported 

McCarthy D, Manning N, Rees J P et al. 

Hypothyroidism and coeliac disease--a family study. 

Ir J Med Sci 1976;145(7):237-238. No prevalence or 

incidence reported 

McCrae W M, Eastwood M A, Martin M R et al. 

Neglected coeliac disease. Lancet 1975;1(7900):187-

190. No prevalence or incidence reported 

McCrae W M, Sweet E M. Diagnosis of osteoporosis 

in childhood. Br J Radiol 1967;40(470):104-107. No 

prevalence or incidence reported

McCrae W M. Inheritance of coeliac disease. J Med 

Genet 1969;6(2):129-131. No prevalence or incidence 

reported 

A-549
McEvoy A, Dutton J, James O F. Bacterial 

contamination of the small intestine is an important 

cause of occult malabsorption in the elderly. Br Med J 

(Clin Res Ed) 1983;287(6395):789-793. No 

prevalence or incidence reported

McFarlane X A, Bhalla A K, Reeves D E et al. 

Osteoporosis in treated adult coeliac disease. Gut 

1995;36(5):710-714. No prevalence or incidence 

reported 

McFarlane X A, Bhalla A K, Robertson D A. Effect of

a gluten free diet on osteopenia in adults with newly 

diagnosed coeliac disease. Gut 1996;39(2):180-184. 

No prevalence or incidence reported 

McGowan M, Gibney M J. Calcium intakes in 

individuals on diets for the management of cows' milk 

allergy: a case control study. Eur J Clin Nutr 

1993;47(9):609-616. No prevalence or incidence 

reported 

McIntyre A S, Ng D P, Smith J A et al. The 

endoscopic appearance of duodenal folds is predictive 

of untreated adult celiac disease. Gastroenterol Int

1992;38(2):148-151. No prevalence or incidence 

reported 

McKenna R, Stevens F M, McNicholl B et al. Family

and population studies of HLA and coeliac disease in

the West of Ireland. Tissue Antigens 1983;22(3):175-

181. No prevalence or incidence reported 

McKinley M, Leibowitz S, Bronzo R et al. 

Appropriate response to pneumococcal vaccine in 

celiac sprue. J Clin Gastroenterol 1995;20(2):113-116. 

No prevalence or incidence reported 

McLoughlin R, Sebastian S S, Qasim A et al. Coeliac 

disease in Europe. Aliment Pharmacol Ther Suppl 

2003;18(3):45-48. No prevalence or incidence 

reported 

McMillan S A, Dickey W, Douglas J P et al. 

Transthyretin values correlate with mucosal recovery

in patients with coeliac disease taking a gluten free 

diet. J Clin Pathol 2001;54(10):783-786. No 

prevalence or incidence reported

McMillan S A, Johnston S D, Watson R G et al. 

Dietary intake, smoking, and transient anti-gliadin

antibodies. Scand J Gastroenterol 1998;33(5):499-503. 

No prevalence or incidence reported 

McNamee S, McLoughlin R, Stevens F M et al. 

Coeliac disease in the older patient. Rev Clin Gerontol 

2002;12(2):119-126. No prevalence or incidence 

reported 

McNeish A S, Anderson C M. Coeliac disease. The 

disorder in childhood. Clin Gastroenterol 

1974;3(1):127-144. No prevalence or incidence 

reported 

McNeish A S, Harms H K, Rey J et al. The diagnosis 

of coeliac disease. A commentary on the current

practices of members of the European Society for 

Paediatric Gastroenterology and Nutrition (ESPGAN). 

Arch Dis Child 1979;54(10):783-786. No prevalence 

or incidence reported 

McNeish A S, Sweet E M. Lactose intolerance in

childhood coeliac disease. Assessment of its incidence 

and importance. Arch Dis Child 1968;43(230):433-

437. No prevalence or incidence reported 

McNicholl B, Egan-Mitchell B, Stevens F et al.

Mucosal recovery in treated childhood celiac disease 

(gluten-sensitive enteropathy). Eur J Pediatr 

1976;89(3):418-424. No prevalence or incidence 

reported 

McNicholl B. Coeliac disease: ecology, life history 

and management. Human Nutrition.Applied Nutrition 

1986;40(1):55-60. No prevalence or incidence 

reported 

McNicholl B. Management of coeliac disease.

Midwife Health Visit Community Nurse

1986;22(10):361-364. No prevalence or incidence 

reported 

McPherson J R. Jejunal biopsy. Med Clin North Am 

1970;54(4):851-862. No prevalence or incidence 

reported 

McPhillips J. Understanding coeliac disease: 

symptoms and long-term risks. Br J Nurs 

2000;9(8):479-483. No prevalence or incidence 

reported 

Mearin M L, Biemond I, Pena A S et al. HLA-DR

phenotypes in Spanish coeliac children: their

contribution to the understanding of the genetics of the 

disease. Gut 1983;24(6):532-537. No prevalence or

incidence reported 

Mearin M L, Bouquet J, Mourad N et al. HLA-DR

antigens and phenotypes in Dutch coeliac children and 

their families. Clin Genet 1985;27(1):45-50. No

prevalence or incidence reported

Mearin M L, Koninckx C R, Biemond I et al. 

Influence of genetic factors on the serum levels of

antigliadin antibodies in celiac disease. J Pediatr 

Gastroenterol Nutr 1984;3(3):373-377. No prevalence 

or incidence reported 

Mearin M L, Polanco I, Strober W et al. B-cell

antigens recognized by maternal antisera in glutensensitive enteropathy. J Clin Nutr Gastroenterol

1986;1(1):30-36. No prevalence or incidence reported 

Meddeb-Garnaoui A, Zeliszewski D, Mougenot J F et 

al. Reevaluation of the relative risk for susceptibility

A-550
to celiac disease of HLA-DRB1, -DQA1, -DQB1, -

DPB1, and -TAP2 alleles in a French population. Hum 

Immunol 1995;43(3):190-199. No prevalence or 

incidence reported 

Mediene S, Hakem S, Bard J M et al. Serum 

lipoprotein profile in Algerian patients with celiac 

disease. Clin Chim Acta 1995;235(2):189-196. No 

prevalence or incidence reported

Meeuwisse G W. Immunological consideration on

breast vs. formula feeding. Klin Padiatr 

1985;197(4):322-325. No prevalence or incidence 

reported 

Mehra N K, Kaur Gurvinder, Kanga Uma et al. 

Immunogenetics of autoimmune diseases in Asian 

Indians. Ann N Y Acad Sci 2002;858333-336. No 

prevalence or incidence reported

Meini A, Pillan N M, Villanacci V et al. Prevalence 

and diagnosis of celiac disease in IgA-deficient 

children. Annals of Allergy, Asthma & Immunology - 

Official Publication of the American College of

Allergy, Asthma, & Immunology 1996;77(4):333-336. 

Not a relevant screening group 

Meloni G F, Dessole S, Vargiu N et al. The prevalence

of coeliac disease in infertility. Hum Reprod 

1999;14(11):2759-2761. Not a relevant screening

group 

Meloni G F, Tomasi P A, Bertoncelli A et al.

Prevalence of silent celiac disease in patients with

autoimmune thyroiditis from Northern Sardinia. J 

Endocrinol Invest 2001;24(5):298-302. No prevalence 

or incidence reported 

Meloni G, Dore A, Fanciulli G et al. Subclinical

coeliac disease in schoolchildren from northern

Sardinia. Lancet 1999;353(9146):37Not a relevant 

screening geography

Menendez-Corrada R. Current views on tropical sprue 

and a comparison to nontropical sprue. Med Clin

North Am 1968;52(6):1367-1385. No prevalence or 

incidence reported 

Messmann H. Squamous cell cancer of the 

oesophagus. Best Practice & Research.Clinical 

Gastroenterology 2001;15(2):249-265. No prevalence 

or incidence reported 

Metcalf J. Coeliac disease and primary biliary 

cirrhosis: a case for mutual screening. Gut

1998;42(1):9-10. No prevalence or incidence reported 

Metcalfe D D. Food hypersensitivity. J Allergy Clin 

Immunol 1984;73(6):749-762. No prevalence or 

incidence reported 

Metskula K, Grunberg H, Uibo O et al. Antigliadin 

antibodies and autoantibodies among 9, 12 and 15 

year-old schoolchildren. Cent-Eur J Immunol 

1998;23(3-4):197-202. Not a relevant screening 

geography

Meuli R, Pichler W J, Gaze H et al. Genetic difference

in HLA-DR phenotypes between coeliac disease and 

transitory gluten intolerance. Arch Dis Child

1995;72(1):29-32. No prevalence or incidence 

reported 

Meyer D, Stavropolous S, Diamond B et al. 

Osteoporosis in a north american adult population

with celiac disease. Am J Gastroenterol 

2001;96(1):112-119. No prevalence or incidence 

reported 

Meyer L J, Zone J J. Familial incidence of dermatitis 

herpetiformis. J Am Acad Dermatol 1987;17(4):643-

647. No prevalence or incidence reported 

Michaelsen K F, Weile B, Larsen P et al. Does the low 

intake of wheat in Danish infants cause the low 

incidence rate of coeliac disease?. Acta Paediatr 

1993;82(6-7):605-606. No prevalence or incidence 

reported 

Michaelsson G, Gerden B, Hagforsen E et al. Psoriasis 

patients with antibodies to gliadin can be improved by

a gluten-free diet. Br J Dermatol 2000;142(1):44-51. 

No prevalence or incidence reported 

Michaelsson G, Gerden B, Ottosson M et al. Patients

with psoriasis often have increased serum levels of 

IgA antibodies to gliadin. Br J Dermatol 

1993;129(6):667-673. No prevalence or incidence 

reported 

Michaelsson G, Kraaz W, Gerden B et al. Increased 

lymphocyte infiltration in duodenal mucosa from 

patients with psoriasis and serum IgA antibodies to

gliadin. Br J Dermatol 1995;133(6):896-904. No

prevalence or incidence reported

Michalski J P, McCombs C C, Arai T et al. HLA-DR,

DQ genotypes of celiac disease patients and healthy 

subjects from the West of Ireland. Tissue Antigens 

1996;47(2):127-133. No prevalence or incidence 

reported 

Midhagen G, Jarnerot G, Kraaz W. Adult coeliac 

disease within a defined geographic area in Sweden. A

study of prevalence and associated diseases. Scand J

Gastroenterol 1988;23(8):1000-1004. Serology screen 

<1990 

Mignot E, Kimura A, Abbal M et al. DQCAR 

microsatellite polymorphisms in three selected HLA 

class II-associated diseases. Tissue Antigens

1995;46(4):299-304. No prevalence or incidence 

reported 

A-551
Miller Karen K. Mechanisms by which nutritional 

disorders cause reduced bone mass in adults. J 

Womens Health (Larchmt) 2003;12(2):145-150. No 

prevalence or incidence reported

Miller M L. Clinical aspects of juvenile rheumatoid

arthritis. Curr Opin Rheumatol 1997;9(5):423-427. No 

prevalence or incidence reported

Mitchell R M S, Robinson T J. Monitoring dietary 

compliance in coeliac disease using red cell

distribution width. Int J Clin Pract 2002;56(4):249-

250. No prevalence or incidence reported 

Mitt K, Uibo O. Low cereal intake in Estonian infants: 

the possible explanation for the low frequency of

coeliac disease in Estonia. Eur J Clin Nutr

1998;52(2):85-88. No prevalence or incidence 

reported 

Mittal K K. Immunobiology of the human major

histocompatibility complex: association of HLA 

antigens with disease. Acta Anthropogenet 1984;8(3-

4):245-268. No prevalence or incidence reported

Mittal S K. Chronic diarrhea in tropics. Indian J 

Pediatr 1999;66(1 Suppl):S4-15. No prevalence or

incidence reported 

Moayyedi P, O'Mahony S, Jackson P et al. Small 

intestine in lymphocytic and collagenous colitis: 

mucosal morphology, permeability, and secretory 

immunity to gliadin. J Clin Pathol 1997;50(6):527-

529. No prevalence or incidence reported 

Mody G M, Cassim B. Rheumatologic manifestations 

of gastrointestinal disorders. Curr Opin Rheumatol 

1998;10(1):67-72. No prevalence or incidence 

reported 

Mohindra S, Yachha S K, Srivastava A et al. Coeliac 

disease in Indian children: assessment of clinical,

nutritional and pathologic characteristics. J Health

Popul Nutr 2001;19(3):204-208. Not a relevant 

screening geography

Mohn A, Cerruto M, Lafusco D et al. Celiac disease in

children and adolescents with type I diabetes:

importance of hypoglycemia. J Pediatr Gastroenterol 

Nutr 2001;32(1):37-40. No prevalence or incidence 

reported 

Mokhallalaty M, Debek A, Naja Z et al. Celiac disease 

at Makassed General Hospital (8 years of experience).

Rev Med Liban 2002;14(2-3):49-53. No prevalence or

incidence reported 

Molteni N, Bardella M T, Bianchi P A. Obstetric and 

gynecological problems in women with untreated

celiac sprue. J Clin Gastroenterol 1990;12(1):37-39. 

No prevalence or incidence reported 

Molteni N, Bardella M T, Vezzoli G et al. Intestinal 

calcium absorption as shown by stable strontium test 

in celiac disease before and after gluten-free diet. Am

J Gastroenterol 1995;90(11):2025-2028. No 

prevalence or incidence reported

Molteni N, Caraceni M P, Bardella M T et al. Bone 

mineral density in adult celiac patients and the effect

of gluten-free diet from childhood. Am J Gastroenterol 

1990;85(1):51-53. No prevalence or incidence 

reported 

Moneo I, Alday E, Gonzalez-Munoz M et al. alphaamylase hypersensitivity in non-exposed millers. 

Occup Med 1994;44(2):91-94. No prevalence or 

incidence reported 

Moneret-Vautrin D A, Kanny G, Morisset M et al. The

food anaphylaxis Vigilance Network in France. 

Allergy Clin Immunol Int 2003;15(4):155-159. No 

prevalence or incidence reported

Monetini L, Cavallo M G, Manfrini S et al. Antibodies 

to bovine beta-casein in diabetes and other

autoimmune diseases. Hormone and Metabolic 

Research.Hormon- Und 

Stoffwechselforschung.Hormones Et Metabolisme 

2002;34(8):455-459. No prevalence or incidence 

reported 

Montalto G, Carroccio A, Soresi M et al. Chronic 

pancreatitis in Sicily. Preliminary reports. Ital J 

Gastroenterol 1990;22(1):33-35. No prevalence or

incidence reported 

Monteiro E, Menezes M L, Magalhaes Ramalho P.

Anti-reticulin antibodies: a diagnostic and monitoring 

test for childhood coeliac disease. Scand J 

Gastroenterol 1986;21(8):955-957. No prevalence or 

incidence reported 

Montgomery R D, Atiyeh M, Scales W R et al.

Intestinal absorption in Saudi Arabia: an evaluation of 

the one hour blood xylose test. Trans R Soc Trop Med 

Hyg 1982;76(1):25-28. No prevalence or incidence 

reported 

Montgomery R D, Shearer A C I. The cell population 

of the upper jejunal mucosa in tropical sprue and

postinfective malabsorption. Gut 1974;15(5):387-391. 

No prevalence or incidence reported 

Moodie S J, Norman P J, King A L et al. Analysis of 

candidate genes on chromosome 19 in coeliac disease:

an association study of the KIR and LILR gene

clusters. European Journal of Immunogenetics -

Official Journal of the British Society for

Histocompatibility and Immunogenetics 

2002;29(4):287-291. No prevalence or incidence 

reported 

A-552
Moodie S, Ciclitira P. Coeliac disease: Genetic factors 

and antigen presentation: MALADIE CoeLIAQUE: 

FACTEURS GENETIQUES ET PRESENTATION 

DES ANTIGENES. Acta Endoscopica 

2001;31(3):255-264. No prevalence or incidence 

reported 

Mooradian A D, Morley J E, Levine A S et al. 

Abnormal intestinal permeability to sugars in diabetes 

mellitus. Diabetologia 1986;29(4):221-224. No

prevalence or incidence reported

Moore R H, Hitman G A, Medcraft J et al. HLA-DP 

region gene polymorphism in primary IgA

nephropathy: No association. Nephrol Dial Transplant 

1992;7(3):200-204. No prevalence or incidence 

reported 

Mora Barbara, Bonamico Margherita, Indovina Paola 

et al. CTLA-4 +49 A/G dimorphism in Italian patients 

with celiac disease. Hum Immunol 2003;64(2):297-

301. No prevalence or incidence reported 

Mora S, Barera G, Beccio S et al. A prospective, 

longitudinal study of the long-term effect of treatment 

on bone density in children with celiac disease. Eur J 

Pediatr 2001;139(4):516-521. No prevalence or 

incidence reported 

Mora S, Barera G, Beccio S et al. Bone density and 

bone metabolism are normal after long-term glutenfree diet in young celiac patients. Am J Gastroenterol 

1999;94(2):398-403. No prevalence or incidence 

reported 

Mora S, Barera G, Ricotti A et al. Reversal of low

bone density with a gluten-free diet in children and 

adolescents with celiac disease. Am J Clin Nutr 

1998;67(3):477-481. No prevalence or incidence 

reported 

Mora S, Weber G, Barera G et al. Effect of gluten-free 

diet on bone mineral content in growing patients with 

celiac disease. Am J Clin Nutr 1993;57(2):224-228. 

No prevalence or incidence reported 

Moran C E, Sosa E G, Martinez S M et al. Bone

mineral density in patients with pancreatic

insufficiency and steatorrhea. Am J Gastroenterol 

1997;92(5):867-871. No prevalence or incidence 

reported 

Morelli M S, Zucker S D, Radford-smith G et al. A 

role for the appendix in inflammatory bowel disease?

Cut it out. Gastroenterology 2003;125(4):1270-1272. 

No prevalence or incidence reported 

Morellini M, Trabace S, Mazzilli M C et al. A study of 

HLA class II antigens in an Italian paediatric

population with coeliac disease. Dis Markers 

1988;6(1):23-28. No prevalence or incidence reported 

Morris M A, Yiannakou J Y, King A L et al. Coeliac 

disease and Down syndrome: associations not due to

genetic linkage on chromosome 21. Scand J 

Gastroenterol 2000;35(2):177-180. No prevalence or 

incidence reported 

Morrow-Brown H. A holistic view of allergic disease.

Human Nutrition.Applied Nutrition 1984;38(6):421-

434. No prevalence or incidence reported 

Mortimer P E, Stewart J S, Norman A P et al. Followup study of coeliac disease. Br Med J 1968;3(609):7-9. 

No prevalence or incidence reported 

Morton N E. An exact linkage test for multiple case

families. Hum Hered 1983;33(4):244-249. No 

prevalence or incidence reported

Moynahan E J. Skin disease and the gut. Br Med J

1970;4(734):559-560. No prevalence or incidence 

reported 

Muench R, Ammann R. Fecal immunoreactive lipase:

a new tubeless pancreatic function test. Scand J 

Gastroenterol 1992;27(4):289-294. No prevalence or 

incidence reported 

Muers M F, Faux J A, Ting A et al. HLA-A, B, C and 

HLA-DR antigens in extrinsic allergic alveolitis 

(budgerigar fancier's lung disease). Clin Allergy

1982;12(1):47-53. No prevalence or incidence 

reported 

Mugica F, Aranzadi M J, Recasens M et al. Adult

celiac disease and hypertransaminasemia. Revista

Espanola De Enfermedades Digestivas - Organo 

Oficial De La Sociedad Espanola De Patologia

Digestiva 2000;92(2):78-85. No prevalence or

incidence reported 

Mugica F, Castiella A, Otazua P et al. Prevalence of 

coeliac disease in unexplained chronic 

hypertransaminasemia. Revista Espanola De 

Enfermedades Digestivas - Organo Oficial De La

Sociedad Espanola De Patologia Digestiva 

2001;93(11):707-714. No prevalence or incidence 

reported 

Mulder C J J, Tytgat G N J, Groenland F et al. 

Combined coeliac disease and thyroid disease, a study 

of 17 cases. J Clin Nutr Gastroenterol 1988;3(3):89-

92. No prevalence or incidence reported 

Mulder C J. Do we have to screen the general

population for coeliac disease instead of only patients 

with so-called associated diseases?. Digestive and 

Liver Disease - Official Journal of the Italian Society

of Gastroenterology and the Italian Association for the

Study of the Liver 2000;32(9):780-781. No prevalence 

or incidence reported 

A-553
Mulder Chris J J, Hadithi Mohammed M, Rostami 

Kamran et al. Coeliac disease--has the time come for 

routine mass screening? In 2002--2010--2020?. Rom J 

Gastroenterol 2002;11(3):179-182. No prevalence or 

incidence reported 

Murray I A, Clenton S, McGeorge B A et al. 

Retrospective audit of the value of the pancreolauryl

test in a district general hospital. Postgrad Med J 

2003;79(934):471-473. No prevalence or incidence 

reported 

Murray I A, Coupland K, Smith J A et al. Intestinal 

trehalase activity in a UK population: establishing a 

normal range and the effect of disease. Br J Nutr

2000;83(3):241-245. No prevalence or incidence 

reported 

Murray Iain A, Daniels Ian, Coupland Kathryn et al. 

Increased activity and expression of iNOS in human 

duodenal enterocytes from patients with celiac 

disease. American Journal of 

Physiology.Gastrointestinal and Liver Physiology

2002;283(2):G319-G326. No prevalence or incidence 

reported 

Murray J A, Herlein J, Mitros F et al. Serologic testing 

for celiac disease in the United States: Results of a 

multilaboratory comparison study. Clin Diagn Lab 

Immunol 2000;7(4):584-587. No prevalence or

incidence reported 

Murray J A, Van Dyke C, Plevak M F et al. Trends in 

the identification and clinical features of celiac disease 

in a North American community, 1950-2001. Clin

Gastroenterol Hepatol 2003;1(1):19-27. No prevalence 

or incidence reported 

Murray J A. Serodiagnosis of celiac disease. Clin Lab 

Med 1997;17(3):445-464. No prevalence or incidence 

reported 

Murray J A. The widening spectrum of celiac disease. 

Am J Clin Nutr 1999;69(3):354-365. No prevalence or

incidence reported 

Mustalahti K, Holopainen P, Karell K et al. Genetic

dissection between silent and clinically diagnosed

symptomatic forms of coeliac disease in multiplex 

families. Digestive and Liver Disease - Official

Journal of the Italian Society of Gastroenterology and 

the Italian Association for the Study of the Liver 

2002;34(12):842-845. No prevalence or incidence 

reported 

Mustalahti Kirsi, Lohiniemi Susanna, Collin Pekka et

al. Gluten-free diet and quality of life in patients with 

screen-detected celiac disease. Effective Clinical

Practice - Ecp 2002;5(3):105-113. No prevalence or 

incidence reported 

Muzzo S, Burrows R, Burgueno M et al. Effect of

calcium and vitamin D supplementation on bone 

mineral density of celiac children. Nutr Res 

2000;20(9):1241-1247. No prevalence or incidence 

reported 

Myhre A G, Aarsetoy H, Undlien D E et al. High 

frequency of coeliac disease among patients with 

autoimmune adrenocortical failure. Scand J

Gastroenterol 2003;38(5):511-515. No prevalence or 

incidence reported 

Mylotte M, Egan-Mitchell B, Fottrell P F et al. Family

studies in coeliac disease. Q J Med 1974;43(171):359-

369. Serology screen <1990 

Mylotte M, Egan-Mitchell B, Fottrell P F et al. 

Fingerprints in patients with coeliac disease and their 

relatives. Br Med J 1972;4(833):144-146. No 

prevalence or incidence reported

Mylotte M, Egan-Mitchell B, McCarthy C F et al. 

Coeliac disease in the West of Ireland. Br Med J 

1973;3(5878):498-499. No prevalence or incidence 

reported 

Mylotte M, Egan-Mitchell B, McCarthy C F et al. 

Incidence of coeliac disease in the West of Ireland. Br

Med J 1973;1(5855):703-705. Serology screen <1990 

Myrelid A, Gustafsson J, Ollars B et al. Growth charts

for Down Syndrome from birth to 18 years of age. 

Arch Dis Child 2002;87(2):97-103. No prevalence or

incidence reported 

Nakamura T, Takeuchi T. Pancreatic steatorrhea, 

malabsorption, and nutrition biochemistry: a 

comparison of Japanese, European, and American 

patients with chronic pancreatitis. Pancreas 

1997;14(4):323-333. No prevalence or incidence 

reported 

Nakamura T, Tando Y, Terada A et al. Can pancreatic 

steatorrhea be diagnosed without chemical analysis?.

International Journal of Pancreatology - Official 

Journal of the International Association of

Pancreatology 1997;22(2):121-125. No prevalence or

incidence reported 

Nakamura T, Tando Y, Yamada N et al. Study on

pancreatic insufficiency (chronic pancreatitis) and

steatorrhea in Japanese patients with low fat intake. 

Digestion 1999;60(Suppl 1):93-96. No prevalence or

incidence reported 

Nakshabendi I M, Downie S, Russell R I et al. 

Increased rates of duodenal mucosal protein synthesis 

in vivo in patients with untreated coelia disease. Gut 

1996;39(2):176-179. No prevalence or incidence 

reported 

A-554
Naluai A T, Nilsson S, Gudjonsdottir A H et al.

Genome-wide linkage analysis of Scandinavian 

affected sib-pairs supports presence of susceptibility

loci for celiac disease on chromosomes 5 and 11.

European Journal of Human Genetics - Ejhg 

2001;9(12):938-944. No prevalence or incidence 

reported 

Naluai A T, Nilsson S, Samuelsson L et al. The

CTLA4/CD28 gene region on chromosome 2q33 

confers susceptibility to celiac disease in a way 

possibly distinct from that of type 1 diabetes and other 

chronic inflammatory disorders. Tissue Antigens

2000;56(4):350-355. No prevalence or incidence 

reported 

Nash Samantha. Does exclusive breast-feeding reduce 

the risk of coeliac disease in children?. Br J

Community Nurs 2003;8(3):127-132. No prevalence 

or incidence reported 

Naveh Y, Lightman A, Zinder O. A prospective study

of serum zinc concentration in children with celiac 

disease. Eur J Pediatr 1983;102(5):734-736. No

prevalence or incidence reported

Nazer H. Gastroenterological problems in childhood 

in Jordan. Ann Trop Paediatr 1982;2(2):69-72. No

prevalence or incidence reported

Neale G. Generalised disorders of bone associated 

with disease of the gastro-intestinal tract. Ir J Med Sci 

1974;0(Suppl):57-63. No prevalence or incidence 

reported 

Nelsen D A. Gluten-sensitive enteropathy (celiac

disease): More common than you think. Am Fam Phys

2002;66(12):2259-2266+2269. No prevalence or 

incidence reported 

Nelsen David A. Gluten-sensitive enteropathy (celiac

disease): more common than you think. Am Fam 

Physician 2002;66(12):2259-2266. No prevalence or 

incidence reported 

Nelson R, McNeish A S, Anderson C M. Coeliac 

disease in children of Asian immigrants. Lancet 

1973;1(7799):348-350. No prevalence or incidence 

reported 

Nepom G T, Erlich H. MHC class-II molecules and 

autoimmunity. Annu Rev Immunol 1991;9493-525. 

No prevalence or incidence reported 

Nepom G T. MHC genes in HLA-associated disease.

Curr Opin Immunol 1990;2(4):588-592. No 

prevalence or incidence reported

Neuberger J. PBC and the gut: the villi atrophy, the 

plot thickens. Gut 1999;44(5):594-595. No prevalence 

or incidence reported 

Neuhausen Susan L, Feolo Mike, Camp Nicola J et al. 

Genome-wide linkage analysis for celiac disease in 

North American families. Am J Med Genet

2002;111(1):1-9. No prevalence or incidence reported 

Neuhausen Susan L, Weizman Zvi, Camp Nicola J et

al. HLA DQA1-DQB1 genotypes in Bedouin families 

with celiac disease. Hum Immunol 2002;63(6):502-

507. No prevalence or incidence reported 

Nicolas M E O, Krause P K, Gibson L E et al. 

Dermatitis herpetiformis. Int J Dermatol 

2003;42(8):588-600. No prevalence or incidence 

reported 

Nielsen I M, Ornvold K, Jacobsen B B et al. Fatal 

familial cholestatic syndrome in Greenland Eskimo

children. Acta Paediatr Scand 1986;75(6):1010-1016. 

No prevalence or incidence reported 

Nielsen O H, Jacobsen O, Pedersen E R. Non-tropical 

sprue. Malignant diseases and mortality rate. Scand J

Gastroenterol 1985;20(1):13-18. No prevalence or

incidence reported 

Nieminen U, Kahri A, Savilahti E et al. Duodenal 

disaccharidase activities in the follow-up of villous

atrophy in coeliac disease. Scand J Gastroenterol 

2001;36(5):507-510. No prevalence or incidence 

reported 

Nieto A, Blanco Quiros A, Arranz E et al. Study of 

HLA-DQA1 alleles in celiac children. Journal of 

Investigational Allergology & Clinical Immunology - 

Official Organ of the International Association of

Asthmology (Interasma) and Sociedad

Latinoamericana De Alergia E Inmunologia 

1995;5(4):209-215. No prevalence or incidence 

reported 

Niggemann B, Reibel S, Roehr C C et al. Predictors of 

positive food challenge outcome in non-IgE-mediated 

reactions to food in children with atopic dermatitis. J 

Allergy Clin Immunol 2001;108(6):1053-1058. No 

prevalence or incidence reported

Niggemann B, Sielaff B, Beyer K et al. Outcome of 

double-blind, placebo-controlled food challenge tests 

in 107 children with atopic dermatitis. Clinical and 

Experimental Allergy - Journal of the British Society 

for Allergy and Clinical Immunology 1999;29(1):91-

96. No prevalence or incidence reported 

Nilssen D E, Brandtzaeg P, Froland S S et al. Subclass 

composition and J-chain expression of the 

'compensatory' gastrointestinal IgG cell population in 

selective IgA deficiency. Clin Exp Immunol 

1992;87(2):237-245. No prevalence or incidence 

reported 

Nilsson A. Lactose malabsorption and lactose 

intolerance in adults - A cause of irritable bowel

A-555
syndrome?. Scand J Nutr Naringsforsk 

2001;45(4):175-176. No prevalence or incidence 

reported 

Niveloni S, Dezi R, Pedreira S et al. Gluten sensitivity 

in patients with primary biliary cirrhosis. Am J 

Gastroenterol 1998;93(3):404-408. No prevalence or 

incidence reported 

Niveloni S, Fiorini A, Dezi R et al. Usefulness of 

videoduodenoscopy and vital dye staining as 

indicators of mucosal atrophy of celiac disease: 

assessment of interobserver agreement. Gastroenterol

Int 1998;47(3):223-229. No prevalence or incidence 

reported 

Niveloni S, Pedreira S, Sugai E et al. The natural 

history of gluten sensitivity: report of two new celiac

disease patients resulting from a long-term follow-up 

of nonatrophic, first-degree relatives. Am J 

Gastroenterol 2000;95(2):463-468. No prevalence or 

incidence reported 

Niven M J, Caffrey C, Moore R H et al. T-cell

receptor beta-subunit gene polymorphism and 

autoimmune disease. Hum Immunol 1990;27(4):360-

367. No prevalence or incidence reported 

Norgard B, Fonager K, Sorensen H T et al. Birth 

outcomes of women with celiac disease: a nationwide 

historical cohort study. Am J Gastroenterol 

1999;94(9):2435-2440. No prevalence or incidence 

reported 

Norris T S. Three familial cases of adult idiopathic 

steatorrhoea. Proc R Soc Med 1966;59(10):1005-

1006. No prevalence or incidence reported 

Nosari I, Casati A, Mora C et al. The use of IgAantiendomysial antibody test for screening coeliac 

disease in insulin-dependent diabetes mellitus.

Diabetes Nutr Metab Clin Exp 1996;9(5):267-272. No 

prevalence or incidence reported

Not T, Citta A, Lucchesi A et al. Anti-endomysium 

antibody on human umbilical cord vein tissue: an

inexpensive and sensitive diagnostic tool for the 

screening of coeliac disease. Eur J Pediatr

1997;156(8):616-618. No prevalence or incidence 

reported 

Not T, Ventura A, Peticarari S et al. A new, rapid, 

noninvasive screening test for celiac disease. Eur J 

Pediatr 1993;123(3):425-427. No prevalence or 

incidence reported 

Not Tarcisio, Faleschini Elena, Tommasini Alberto et 

al. Celiac disease in patients with sporadic and

inherited cardiomyopathies and in their relatives. Eur 

Heart J 2003;24(15):1455-1461. No prevalence or

incidence reported 

Nousia-Arvanitakis S, Karagiozoglou-Lamboudes T, 

Aggouridaki C et al. Influence of jejunal morphology

changes on exocrine pancreatic function in celiac 

disease. J Pediatr Gastroenterol Nutr 1999;29(1):81-

85. No prevalence or incidence reported 

Novacek G, Miehsler W, Wrba F et al. Prevalence and

clinical importance of hypertransaminasaemia in 

coeliac disease. Eur J Gastroenterol Hepatol

1999;11(3):283-288. No prevalence or incidence 

reported 

Novembre E, Cianferoni A, Bernardini R et al. 

Epidemiology of insect venom sensitivity in children 

and its correlation to clinical and atopic features. Clin 

Exp Allergy 1998;28(7):834-838. No prevalence or

incidence reported 

Nowak-Wegrzyn A, Conover-Walker M K, Wood R 

A. Food-allergic reactions in schools and preschools. 

Arch Pediatr Adolesc Med 2001;155(7):790-795. No 

prevalence or incidence reported

Nowowiejska B, Kaczmarski M, Dabrowska E J. A 

long-term study in children with a recognized gluten 

intolerance. Rocz Akad Med Bialymst 

1995;40(3):580-587. No prevalence or incidence 

reported 

O'Boyle C J, Kerin M J, Feeley K et al. Primary small 

intestinal tumours: increased incidence of lymphoma

and improved survival. Ann R Coll Surg Engl 

1998;80(5):332-334. No prevalence or incidence 

reported 

O'Connor T M, Cronin C C, Loane J F et al. Type 1 

diabetes mellitus, coeliac disease, and lymphoma: a 

report of four cases. Diabetic Medicine - a Journal of 

the British Diabetic Association 1999;16(7):614-617. 

No prevalence or incidence reported 

Oderda Giuseppina, Rapa Anna, Zavallone Annalisa et 

al. Thyroid autoimmunity in childhood celiac disease. 

J Pediatr Gastroenterol Nutr 2002;35(5):704-705. No 

prevalence or incidence reported

Odetti P, Valentini S, Aragno I et al. Oxidative stress 

in subjects affected by celiac disease. Free Radic Res

1998;29(1):17-24. No prevalence or incidence 

reported 

O'Farrelly C, Graeme-Cook F, Hourihane D O et al. 

Histological changes associated with wheat protein 

antibodies in the absence of villous atrophy. J Clin 

Pathol 1987;40(10):1228-1230. No prevalence or

incidence reported 

O'Farrelly C. Is villous atrophy always and only the 

result of gluten sensitive disease of the intestine?. Eur 

J Gastroenterol Hepatol 2000;12(6):605-608. No 

prevalence or incidence reported

A-556
Ogborn A D. Pregnancy in patients with coeliac 

disease. Br J Obstet Gynaecol 1975;82(4):293-296. No 

prevalence or incidence reported

O'Gorman P, Bennett D, Kavanagh E et al.

MALTectomy (appendectomy/tonsillectomy) does not 

influence the occurrence or mode of presentation of 

adult celiac disease. Am J Gastroenterol 

1996;91(4):723-725. No prevalence or incidence 

reported 

O'Grady J G, Stevens F M, Harding B et al. 

Hyposplenism and gluten-sensitive enteropathy.

Natural history, incidence, and relationship to diet and 

small bowel morphology. Gastroenterology

1984;87(6):1326-1331. No prevalence or incidence 

reported 

O'Grady J G, Stevens F M, McCarthy C F. Genetic

influences on splenic function in coeliac disease. Gut 

1985;26(10):1004-1007. No prevalence or incidence 

reported 

O'Keefe S J, O'Keefe E A, Burke E et al. Milkinduced malabsorption in malnourished African 

patients. Am J Clin Nutr 1991;54(1):130-135. No 

prevalence or incidence reported

Olden Kevin W. Diagnosis of irritable bowel 

syndrome. Gastroenterology 2002;122(6):1701-1714. 

No prevalence or incidence reported 

Olds G, McLoughlin R, O'Morian C et al. Celiac 

disease for the endoscopist. Gastrointest Endosc 

2002;56(3):407-415. No prevalence or incidence 

reported 

O'Leary C, Walsh C H, Wieneke P et al. Coeliac 

disease and autoimmune Addison's disease: a clinical 

pitfall. Qjm - Monthly Journal of the Association of 

Physicians 2002;95(2):79-82. No prevalence or

incidence reported 

O'Leary Clare, Quigley Eamonn M M. Small bowel 

bacterial overgrowth, celiac disease, and IBS: what are 

the real associations?. Am J Gastroenterol 

2003;98(4):720-722. No prevalence or incidence 

reported 

O'Leary Clare, Wieneke Peter, Buckley Sarah et al.

Celiac disease and irritable bowel-type symptoms. Am

J Gastroenterol 2002;97(6):1463-1467. No prevalence 

or incidence reported 

Olsson R, Kagevi I, Rydberg L. On the concurrence of

primary biliary cirrhosis and intestinal villous atrophy.

Scand J Gastroenterol 1982;17(5):625-628. No

prevalence or incidence reported

Olsson R, Lindberg J, Weiland O et al. Chronic active 

hepatitis in Sweden. The etiologic spectrum, clinical

presentation, and laboratory profile. Scand J 

Gastroenterol 1988;23(4):463-470. No prevalence or 

incidence reported 

O'Reilly D, Murphy J, McLaughlin J et al. The 

prevalence of coeliac disease and cystic fibrosis in

Ireland, Scotland, England and Wales. Int J Epidemiol 

1974;3(3):247-251. Serology screen <1990 

Orgad S, Avigad S, Jonas A et al. Immunogenetics of 

childhood celiac disease: the association with HDA 

DR3 and DR7 in unrelated patients with multiply

affected families. Isr J Med Sci 1981;17(11):1041-

1044. No prevalence or incidence reported 

Ortolani C, Ispano M, Scibilia J et al. Introducing

chemists to food allergy. Allergy 2001;56(Suppl 

67):5-8. No prevalence or incidence reported 

Ots M, Uibo O, Metskula K et al. IgA-antigliadin

antibodies in patients with IgA nephropathy: the 

secondary phenomenon?. Am J Nephrol 

1999;19(4):453-458. No prevalence or incidence 

reported 

Ott D J. Celiac disease: biopsy or enteroclysis better 

for evaluating response to a gluten-free diet?. Am J 

Gastroenterol 1997;92(4):715-716. No prevalence or 

incidence reported 

Oxentenko A S, Murray J A. Celiac disease and

dermatitis herpetiformis: The spectrum of glutensensitive enteropathy. Int J Dermatol 2003;42(8):585-

587. No prevalence or incidence reported 

Ozgenc F, Aksu G, Aydogdu S et al. Association

between anti-endomysial antibody and total intestinal

villous atrophy in children with coeliac disease. J

Postgrad Med 2003;49(1):21-24. No prevalence or

incidence reported 

Ozkan T, Ozeke T, Meral A. Gliadin-specific IgA 

antibodies in breast milk. J Int Med Res 

2000;28(5):234-240. No prevalence or incidence 

reported 

Padmanabhan Vijayalakshmi, Callas Peter W, Li

Shuan C et al. Histopathological features of the

terminal ileum in lymphocytic and collagenous colitis:

a study of 32 cases and review of literature. Modern 

Pathology - an Official Journal of the United States 

and Canadian Academy of Pathology, Inc 

2003;16(2):115-119. No prevalence or incidence 

reported 

Paerregaard A, Vilien M, Krasilnikoff P A et al. 

Supposed coeliac disease during childhood and its 

presentation 14-38 years later. Scand J Gastroenterol 

1988;23(1):65-70. No prevalence or incidence 

reported 

Paimela L, Kurki P, Leirisalo-Repo M et al. Gliadin 

immune reactivity in patients with rheumatoid

A-557
arthritis. Clin Exp Rheumatol 1995;13(5):603-607. No 

prevalence or incidence reported

Palavecino E A, Mota A H, Awad J et al. HLA and 

celiac disease in Argentina: involvement of the DQ

subregion. Dis Markers 1990;8(1):5-10. No

prevalence or incidence reported

Papadopoulos A J, Schwartz R A, Krysicka Janniger 

C. Alopecia areata: Emerging concepts. Acta

Dermatovenerol Alp Panonica Adriat 2000;9(3):83-

90. No prevalence or incidence reported 

Papadopoulos K I, Hornblad Y, Hallengren B. The 

occurrence of polyglandular autoimmune syndrome

type III associated with coeliac disease in patients with 

sarcoidosis. J Intern Med 1994;236(6):661-663. No 

prevalence or incidence reported

Papadopoulos K I, Sjoberg K, Lindgren S et al. 

Evidence of gastrointestinal immune reactivity in

patients with sarcoidosis. J Intern Med 

1999;245(5):525-531. No prevalence or incidence 

reported 

Papadopoulou A, Lloyd D R, Williams M D et al. 

Gastrointestinal and nutritional sequelae of bone 

marrow transplantation. Arch Dis Child 

1996;75(3):208-213. No prevalence or incidence 

reported 

Papo M, Quer J C, Pastor R M et al. Antineutrophil 

cytoplasmic antibodies in relatives of patients with 

inflammatory bowel disease. Am J Gastroenterol

1996;91(8):1512-1515. No prevalence or incidence 

reported 

Pare P, Douville P, Caron D et al. Adult celiac sprue: 

changes in the pattern of clinical recognition. J Clin 

Gastroenterol 1988;10(4):395-400. No prevalence or 

incidence reported 

Parke A L. Gastrointestinal disorders and rheumatic

diseases. Curr Opin Rheumatol 1993;5(1):79-84. No 

prevalence or incidence reported

Parnell N D, Ciclitira P J. Review article: coeliac 

disease and its management. Aliment Pharmacol Ther

1999;13(1):1-13. No prevalence or incidence reported 

Parnell N, Ciclitira P J. Celiac disease. Curr Opin

Gastroenterol 1999;15(2):120-124. No prevalence or 

incidence reported 

Parry Sally D, Welfare Mark R, Cobden Irving et al. 

Push enteroscopy in a UK district general hospital: 

experience of 51 cases over 2 years. Eur J 

Gastroenterol Hepatol 2002;14(3):305-309. No

prevalence or incidence reported

Partanen J, Milner C, Campbell R D et al. HLA-linked 

heat-shock protein 70 (HSP70-2) gene polymorphism 

and celiac disease. Tissue Antigens 1993;41(1):15-19. 

No prevalence or incidence reported 

Partanen J. The HLA-DRB4 gene does not explain 

genetic susceptibility in HLA-DQ2-negative celiac 

disease. Immunogenetics 2000;51(3):249-250. No 

prevalence or incidence reported

Passarge E, Valentine-Thon E. Everything the 

pediatrician ever wanted to know about HLA but was 

afraid to ask. Eur J Pediatr 1980;133(2):93-100. No 

prevalence or incidence reported

Pasternack A, Collin P, Mustonen J et al. Glomerular 

IgA deposits in patients with celiac disease. Clin

Nephrol 1990;34(2):56-60. No prevalence or

incidence reported 

Patel A H, Loftus E V, Murray J A et al. Cigarette 

smoking and celiac sprue: a case-control study. Am J 

Gastroenterol 2001;96(8):2388-2391. No prevalence 

or incidence reported 

Patel R S, Johlin F C, Murray J A. Celiac disease and 

recurrent pancreatitis. Gastroenterol Int 

1999;50(6):823-827. No prevalence or incidence 

reported 

Patey-Mariaud de, Serre Cellier C, Jabri B et al. 

Distinction between coeliac disease and refractory 

sprue: a simple immunohistochemical method. 

Histopathology 2000;37(1):70-77. No prevalence or 

incidence reported 

Patney N L, Srivastava V K, Wahal p k et al. A study 

of fat malabsorption and jejunal muscosal biopsy in 

diabetic neuropathy: a preliminary report. J Assoc 

Physicians India 1973;21(9):777-785. No prevalence 

or incidence reported 

Patterson R N, Johnston S D. Iron deficiency anaemia: 

are the British Society of Gastroenterology guidelines 

being adhered to?. Postgrad Med J 2003;79(930):226-

228. No prevalence or incidence reported 

Patwari A K, Anand V K, Kapur Gaurav et al. Clinical

and nutritional profile of children with celiac disease. 

Indian Pediatr 2003;40(4):337-342. No prevalence or

incidence reported 

Patwari A K. Diarrhoea and malnutrition interaction. 

Indian J Pediatr 1999;66(1 Suppl):S124-S134. No 

prevalence or incidence reported

Pearce C B, Sinclair D, Duncan H D et al. Use of the

anti-endomysial antibody test to diagnose coeliac 

disease in clinical practice. Clin Lab 2002;48(5-

6):319-325. No prevalence or incidence reported

Pellecchia M T, Scala R, Filla A et al. Idiopathic

cerebellar ataxia associated with celiac disease: lack of 

distinctive neurological features. J Neurol Neurosurg 

A-558
Psychiatry 1999;66(1):32-35. No prevalence or

incidence reported 

Pellegrini G, Scotta M S, Soardo S et al. Elevated IgA 

anti-gliadin antibodies in juvenile chronic arthritis. 

Clin Exp Rheumatol 1991;9(6):653-656. No 

prevalence or incidence reported

Pena A S, Garrote J A, Crusius J B. Advances in the 

immunogenetics of coeliac disease. Clues for

understanding the pathogenesis and disease 

heterogeneity. Scandinavian Journal of

Gastroenterology.Supplement 1998;22556-58. No

prevalence or incidence reported

Pena A S, Mann D L, Hague N E et al. Genetic basis

of gluten-sentitive enteropathy. Gastroenterology

1978;75(2):230-235. No prevalence or incidence 

reported 

Pena A S, Wijmenga C. Genetic factors underlying 

gluten-sensitive enteropathy. Curr Allergy Asthma

Rep 2001;1(6):526-533. No prevalence or incidence 

reported 

Pengiran Tengah D S N A, Wills A J, Holmes G K T.

Neurological complications of coeliac disease. 

Postgrad Med J 2002;78(921):393-398. No prevalence 

or incidence reported 

Peraaho M, Kaukinen K, Paasikivi K et al. Wheatstarch-based gluten-free products in the treatment of 

newly detected coeliac disease: prospective and 

randomized study. Aliment Pharmacol Ther 

2003;17(4):587-594. No prevalence or incidence 

reported 

Peracchi Maddalena, Trovato Cristina, Longhi

Massimo et al. Tissue transglutaminase antibodies in 

patients with end-stage heart failure. Am J

Gastroenterol 2002;97(11):2850-2854. No prevalence 

or incidence reported 

Perez-Bravo F, Araya M, Mondragon A et al. Genetic 

differences in HLA-DQA1* and DQB1* allelic 

distributions between celiac and control children in 

Santiago, Chile. Hum Immunol 1999;60(3):262-267. 

No prevalence or incidence reported 

Perez-Machado Miguel A, Ashwood Paul, Thomson 

Michael A et al. Reduced transforming growth factorbeta1-producing T cells in the duodenal mucosa of

children with food allergy. Eur J Immunol 

2003;33(8):2307-2315. No prevalence or incidence 

reported 

Persliden J, Pettersson H B L, Falth-Magnusson K. 

Intestinal biopsy in children with coeliac disease; A 

Swedish national study of radiation dose and risk. 

Radiat Prot Dosim 1995;57(1-4):459-462. No 

prevalence or incidence reported

Persliden J, Pettersson H B, Falth-Magnusson K. 

Small intestinal biopsy in children with coeliac 

disease: measurement of radiation dose and analysis of 

risk. Acta Paediatr 1993;82(3):296-299. No 

prevalence or incidence reported

Persson L A, Ivarsson A, Hernell O. Breast-feeding 

protects against celiac disease in childhood--

epidemiological evidence. Adv Exp Med Biol

2002;503115-123. No prevalence or incidence 

reported 

Perticarari S, Not T, Cauci S et al. ELISA method for 

quantitative measurement of IgA and IgG specific 

anti- gliadin antibodies. J Pediatr Gastroenterol Nutr 

1992;15(3):302-309. No prevalence or incidence 

reported 

Petaros P, Martelossi S, Tommasini A et al. 

Prevalence of autoimmune disorders in relatives of

patients with celiac disease. Dig Dis Sci 

2002;47(7):1427-1431. No prevalence or incidence 

reported 

Peters U, Schneeweiss S, Trautwein E A et al. A casecontrol study of the effect of infant feeding on celiac 

disease. Ann Nutr Metab 2001;45(4):135-142. No 

prevalence or incidence reported

Peters Ulrike, Askling Johan, Gridley Gloria et al. 

Causes of death in patients with celiac disease in a 

population-based Swedish cohort. Arch Intern Med 

2003;163(13):1566-1572. No prevalence or incidence 

reported 

Petronzelli F, Bonamico M, Ferrante P et al. Genetic 

contribution of the HLA region to the familial

clustering of coeliac disease. Ann Hum Genet 

1997;61(Pt 4):307-317. No prevalence or incidence 

reported 

Petronzelli F, Ferrante P, Triglione P et al.

Oligotyping of celiac multiplex families with the 11th 

International Histocompatibility Workshop reagents. 

Tissue Antigens 1991;38(5):238-239. No prevalence 

or incidence reported 

Petronzelli F, Multari G, Ferrante P et al. Different 

dose effect of HLA-DQ alpha beta heterodimers in

insulin-dependent diabetes mellitus and celiac disease 

susceptibility. Hum Immunol 1993;36(3):156-162. No 

prevalence or incidence reported

Phillips D L, Keeffe E B. Hematologic manifestations 

of gastrointestinal disease. Hematol Oncol Clin North 

Am 1987;1(2):207-228. No prevalence or incidence 

reported 

Phillips S, Donaldson L, Geisler K et al. Stool

composition in factitial diarrhea: a 6-year experience 

with stool analysis. Ann Intern Med 1995;123(2):97-

100. No prevalence or incidence reported 

A-559
Philotheou A. Epilogue: What have we learned to 

improve the treatment of children with diabetes 

mellitus and their families?. Journal of Pediatric 

Endocrinology & Metabolism - Jpem 2001;14(Suppl 

1):697-700. No prevalence or incidence reported

Piattella L, Zamponi N, Cardinali C et al. Endocranial 

calcifications, infantile celiac disease, and epilepsy.

Child's Nervous System - Chns - Official Journal of 

the International Society for Pediatric Neurosurgery

1993;9(3):172-175. No prevalence or incidence 

reported 

Picarelli A, Di Giovambattista F, Cedrone C et al.

Quantitative analysis of stool losses in adult celiac

disease: use of near-infrared analysis reconsidered. 

Scand J Gastroenterol 1998;33(10):1052-1056. No

prevalence or incidence reported

Picarelli A, Di Tola M, Sabbatella L et al.

Identification of a new coeliac disease subgroup: 

antiendomysial and anti-transglutaminase antibodies 

of IgG class in the absence of selective IgA

deficiency. J Intern Med 2001;249(2):181-188. No 

prevalence or incidence reported

Picarelli A, Di Tola M, Sabbatella L et al.

Immunologic evidence of no harmful effect of oats in 

celiac disease. Am J Clin Nutr 2001;74(1):137-140. 

No prevalence or incidence reported 

Picarelli A, Maiuri L, Frate A et al. Production of

antiendomysial antibodies after in-vitro gliadin 

challenge of small intestine biopsy samples from

patients with coeliac disease. Lancet

1996;348(9034):1065-1067. No prevalence or

incidence reported 

Picarelli A, Triglione P, Mariani P et al. Use of a

threshold serum level of anti-gliadin antibodies 

improves diagnostic efficiency of the test in adult 

coeliac disease but is unreliable as a screening test. Ital

J Gastroenterol 1996;28(2):70-75. No prevalence or 

incidence reported 

Pietroletti R, Bishop A E, Carlei F et al. Gut endocrine 

cell population in coeliac disease estimated by

immunocytochemistry using a monoclonal antibody to 

chromogranin. Gut 1986;27(7):838-843. No 

prevalence or incidence reported

Pietzak M M, Thomas D W. Childhood 

malabsorption. Pediatr Rev 2003;24(6):195-204. No 

prevalence or incidence reported

Pistorius L R, Sweidan W H, Purdie D W et al. 

Coeliac disease and bone mineral density in adult 

female patients. Gut 1995;37(5):639-642. No 

prevalence or incidence reported

Pittschieler K, Reissigl H, Mengarda G. Celiac disease 

in two different population groups of South Tirol. J 

Pediatr Gastroenterol Nutr 1988;7(3):400-402. Not a 

relevant screening geography

Ploski R, Ascher H, Sollid L M. HLA genotypes and 

the increased incidence of coeliac disease in Sweden. 

Scand J Gastroenterol 1996;31(11):1092-1097. No

prevalence or incidence reported

Pocecco M, Ventura A. Coeliac disease and insulindependent diabetes mellitus: a causal association?. 

Acta Paediatr 1995;84(12):1432-1433. No prevalence 

or incidence reported 

Poddar U. Celiac disease: clinical features and

diagnostic criteria. Indian J Pediatr 1999;66(1

Suppl):S21-S25. No prevalence or incidence reported 

Poddar Ujjal, Thapa Babu, Ram Nain et al. Celiac 

disease in India: are they true cases of celiac disease?. 

J Pediatr Gastroenterol Nutr 2002;35(4):508-512. Not 

a relevant screening geography

Podolsky D K, LaMont J T. So, where are all the 

celiacs?. Gastroenterology 1999;116(2):237No 

prevalence or incidence reported

Polanco I, Mearin M L, Larrauri J et al. Effect of

gluten supplementation in healthy siblings of children 

with celiac disease. Gastroenterology 1987;92(3):678-

681. No prevalence or incidence reported 

Poley J R, Bhatia M, Welsh J D. Disaccharidase

deficiency in infants with cow's milk protein 

intolerance. Response to treatment. Digestion

1978;17(2):97-107. No prevalence or incidence 

reported 

Polvi A, Arranz E, Fernandez-Arquero M et al. HLADQ2-Negative Celiac disease in Finland and Spain. 

Hum Immunol 1998;59(3):169-175. No prevalence or

incidence reported 

Polvi A, Garden O A, Elwood C M et al. Canine major 

histocompatibility complex genes DQA and DQB in 

Irish setter dogs. Tissue Antigens 1997;49(3 Pt 1):236-

243. No prevalence or incidence reported 

Polvi A, Maki M, Collin P et al. TNF microsatellite

alleles a2 and b3 are not primarily associated with

celiac disease in the Finnish population. Tissue 

Antigens 1998;51(5):553-555. No prevalence or 

incidence reported 

Polvi A, Maki M, Partanen J. Celiac patients

predominantly inherit HLA-DPB1*0101 positive 

haplotype from HLA-DQ2 homozygous parent. Hum 

Immunol 1997;53(2):156-158. No prevalence or 

incidence reported 

Poolman M, Hough S. Diabetic diarrhoea - A 

neglected complication. J Endocrinol Metab Diabetes 

A-560
S Afr 2003;8(2):52-59. No prevalence or incidence 

reported 

Poon E, Nixon R. Cutaneous spectrum of coeliac 

disease. Australas J Dermatol 2001;42(2):136-138. No 

prevalence or incidence reported

Popat S, Hearle N, Bevan S et al. Mutational analysis

of CD28 in coeliac disease. Scand J Gastroenterol 

2002;37(5):536-539. No prevalence or incidence 

reported 

Popat S, Hearle N, Hogberg L et al. Variation in the 

CTLA4/CD28 gene region confers an increased risk of 

coeliac disease. Ann Hum Genet 2002;66(Pt 2):125-

137. No prevalence or incidence reported 

Popat S, Hearle N, Wixey J et al. Analysis of the

CTLA4 gene in Swedish coeliac disease patients.

Scand J Gastroenterol 2002;37(1):28-31. No

prevalence or incidence reported

Popat S, Hogberg L, McGuire S et al. Germline 

mutations in TGM2 do not contribute to coeliac 

disease susceptibility in the Swedish population. Eur J 

Gastroenterol Hepatol 2001;13(12):1477-1479. No

prevalence or incidence reported

Porter K G, McMaster D, Elmes M E et al. Anemia

and low serum-copper during zinc therapy. Lancet 

1977;2(8041):774No prevalence or incidence reported 

Postel-Vinay M C, Saab C, Gourmelen M. Nutritional 

status and growth hormone-binding protein. Horm Res 

1995;44(4):177-181. No prevalence or incidence 

reported 

Prasad S, Thomas P, Nicholas D S et al. Adult

endomysial antibody-negative coeliac disease and 

cigarette smoking. Eur J Gastroenterol Hepatol 

2001;13(6):667-671. No prevalence or incidence 

reported 

Pratesi R, Gandolfi L, Friedman H et al. Serum IgA 

antibodies from patients with coeliac disease react 

strongly with human brain blood-vessel structures. 

Scand J Gastroenterol 1998;33(8):817-821. No

prevalence or incidence reported

Pratesi R, Gandolfi L, Garcia S G et al. Prevalence of 

coeliac disease: Unexplained age-related variation in 

the same population. Scand J Gastroenterol 

2003;38(7):747-750. Not a relevant screening 

geography

Pratesi R, Gandolfi L, Garcia S G et al. Prevalence of 

coeliac disease: Unexplained age-related variation in 

the same population. Scand J Gastroenterol 

2003;38(7):747-750. Not a relevant screening 

geography

Pratesi Riccardo, Gandolfi Lenora, Martins Rita C et 

al. Is the prevalence of celiac disease increased among 

epileptic patients?. Arq Neuropsiquiatr

2003;61(2b):330-334. No prevalence or incidence 

reported 

Prati D, Bardella M T, Peracchi M et al. High

frequency of anti-endomysial reactivity in candidates 

to heart transplant. Digestive and Liver Disease -

Official Journal of the Italian Society of

Gastroenterology and the Italian Association for the 

Study of the Liver 2002;34(1):39-43. No prevalence or

incidence reported 

Pratico G, Caltabiano L, Bottaro G et al. Serum levels 

of osteocalcin and type I procollagen in children with 

celiac disease. J Pediatr Gastroenterol Nutr 

1997;24(2):170-173. No prevalence or incidence 

reported 

Presotto F, Betterle C. Insulin-dependent diabetes 

mellitus: A constellation of autoimmune diseases. 

Journal of Pediatric Endocrinology & Metabolism - 

Jpem 1997;10(5):455-469. No prevalence or incidence 

reported 

Prichard M G, Ryan G, Musk A W. Wheat flour 

sensitisation and airways disease in urban bakers. Br J 

Ind Med 1984;41(4):450-454. No prevalence or 

incidence reported 

Pricolo V E, Mangi A A, Aswad B et al.

Gastrointestinal malignancies in patients with celiac

sprue. Am J Surg 1998;176(4):344-347. No 

prevalence or incidence reported

Primack S L, Miller R R, Muller N L. Diffuse 

pulmonary hemorrhage: Clinical, pathologic, and

imaging features. Am J Roentgenol 1995;164(2):295-

300. No prevalence or incidence reported 

Primignani M, Agape D, Ronchi G et al. Prevalence of

duodenal and jejunal lesions in dermatitis 

herpetiformis. Ric Clin Lab 1987;17(3):243-249. No 

prevalence or incidence reported

Prince M I, Jones D E J. Primary biliary cirrhosis: 

New perspectives in diagnosis and treatment. Postgrad 

Med J 2000;76(894):199-206. No prevalence or 

incidence reported 

Probert C S, Mayberry J F, Mann R. Inflammatory

bowel disease in the rural Indian subcontinent: a 

survey of patients attending mission hospitals. 

Digestion 1990;47(1):42-46. No prevalence or

incidence reported 

Procaccini E, Chianelli M, Pantano P et al. Imaging of 

autoimmune diseases. Q J Nucl Med 1999;43(1):100-

112. No prevalence or incidence reported 

A-561
Pruessner H T. Detecting celiac disease in your

patients. Am Fam Physician 1998;57(5):1023-34, 

1039. No prevalence or incidence reported 

Pryce D, Behrens R, Davidson R et al. Onchocerciasis

in members of an expedition to Cameroon: Role of 

advice before travel and long term follow up. Br Med 

J 1992;304(6837):1285-1286. No prevalence or 

incidence reported 

Pueschel S M, Romano C, Failla P et al. A prevalence

study of celiac disease in persons with Down 

syndrome residing in the United States of America. 

Acta Paediatr 1999;88(9):953-956. Not a relevant 

screening group

Pynnonen P, Isometsa E, Aalberg V et al. Is coeliac 

disease prevalent among adolescent psychiatric 

patients?. Acta Paediatr 2002;91(6):657-659. No

prevalence or incidence reported

Qari F A. Clinical presentation of adult celiac disease 

in Western Saudi Arabia. Saudi Med J 

2002;23(12):1514-1517. No prevalence or incidence 

reported 

Quisel Anna, Gill James M, Westerberg Dyanne. 

Guideline for diagnosis of celiac disease. Del Med J 

2002;74(5):229-241. No prevalence or incidence 

reported 

Rabassa E B, Sagaro E, Fragoso T et al. Coeliac 

disease in Cuban children. Arch Dis Child 

1981;56(2):128-131. Not a relevant screening 

geography

Rabinowitz L G, Esterly N B. Inflammatory bullous 

diseases in children. Dermatol Clin 1993;11(3):565-

581. No prevalence or incidence reported 

Raccuglia G, French A, Zarafonetis C J. Absorption 

and excretion of cyanocobalamine after oral 

administration of a large dose in various conditions. 

Acta Haematol 1969;42(1):1-7. No prevalence or 

incidence reported 

Radzikowski A, Kulus M, Krauze A et al. Growth, 

bone age and nutritional status in neglected coeliac 

disease. Materia Medica Polona.Polish Journal of

Medicine and Pharmacy 1991;23(2):146-150. No

prevalence or incidence reported

Raffensperger E C, D'Agostino F, Manfredo H et al. 

Fecal fat excretion. An analysis of four years'

experience. Arch Intern Med 1967;119(6):573-576. 

No prevalence or incidence reported 

Ralston S H, Willocks L, Pitkeathly D A et al. High 

prevalence of unrecognized osteomalacia in hospital 

patients with rheumatoid arthritis. Br J Rheumatol

1988;27(3):202-205. No prevalence or incidence 

reported 

Ramalingaswami V. Interface of protein nutrition and 

medicine in the tropics. Lancet 1969;2(7623):733-736. 

No prevalence or incidence reported 

Ramos-Arroyo M A, Feijoo E, Sanchez-Valverde F et 

al. Heat-shock protein 70-1 and HLA class II gene 

polymorphisms associated with celiac disease 

susceptibility in Navarra (Spain). Hum Immunol 

2001;62(8):821-825. No prevalence or incidence 

reported 

Ramos-Remus C, Bahlas S, Vaca-Morales O. 

Rheumatic features of gastrointestinal tract, hepatic, 

and pancreatic diseases. Curr Opin Rheumatol 

1997;9(1):56-61. No prevalence or incidence reported 

Ramot B, Many A. Primary intestinal lymphoma: 

clinical manifestations and possible effect of

environmental factors. Recent Results in Cancer 

Research.Fortschritte Der Krebsforschung.Progres 

Dans Les Recherches Sur Le Cancer 1972;39193-199. 

No prevalence or incidence reported 

Rampertab S D, Forde K A, Green P H R. Small 

bowel neoplasia in coeliac disease. Gut

2003;52(8):1211-1214. No prevalence or incidence 

reported 

Rannem T, Hylander E, Jarnum S et al. Calcium

absorption and bone mineral content in patients 

subjected to ileal bypass because of familial

hypercholesterolaemia. Scand J Gastroenterol 

1990;25(9):897-905. No prevalence or incidence 

reported 

Rapoport M J, Bistritzer T, Vardi O et al. Increased 

prevalence of diabetes-related autoantibodies in celiac 

disease. J Pediatr Gastroenterol Nutr 1996;23(5):524-

527. No prevalence or incidence reported 

Rasmusson C G, Eriksson M A. Celiac disease and 

mineralisation disturbances of permanent teeth. 

International Journal of Paediatric Dentistry / the 

British Paedodontic Society and the International

Association of Dentistry for Children 2001;11(3):179-

183. No prevalence or incidence reported 

Ratnam K V. IgA dermatosis in an adult Chinese

population. A 10-year study of linear IgA and

dermatitis herpetiformis in Singapore. Int J Dermatol 

1988;27(1):21-24. No prevalence or incidence 

reported 

Ratsch I M, Catassi C. Coeliac disease: a potentially 

treatable health problem of Saharawi refugee children. 

Bull World Health Organ 2001;79(6):541-545. No 

prevalence or incidence reported

Rautonen J, Rautonen N, Savilahti E. Antibodies to 

gliadin in children with coeliac disease. Acta Paediatr

A-562
Scand 1991;80(12):1200-1206. No prevalence or 

incidence reported 

Ravaglia Giovanni, Forti Paola, Maioli Fabiola et al.

Increased prevalence of coeliac disease in autoimmune 

thyroiditis is restricted to aged patients. Exp Gerontol 

2003;38(5):589-595. No prevalence or incidence 

reported 

Ravelli A M, Tobanelli P, Minelli L et al. Endoscopic 

features of celiac disease in children. Gastroenterol Int

2001;54(6):736-742. No prevalence or incidence 

reported 

Rawashdeh M O, Khalil B, Raweily E. Celiac disease 

in Arabs. J Pediatr Gastroenterol Nutr 1996;23(4):415-

418. No prevalence or incidence reported 

Rea F, Polito C, Marotta A et al. Restoration of body

composition in celiac children after one year of glutenfree diet. J Pediatr Gastroenterol Nutr 1996;23(4):408-

412. No prevalence or incidence reported 

Read M, O'Halloran E T, O'Sullivan C. Coeliac 

disease in adolescents/young adults: difficulties in 

monitoring. Br J Biomed Sci 2000;57(3):217-221. No 

prevalence or incidence reported

Reeder M M. RPC of the month from AFIP. 

Radiology 1969;93(2):427-433. No prevalence or

incidence reported 

Reen D J, O'Regan D. HLA antigen frequencies in an 

Irish population. Tissue Antigens 1980;15(4):369-372. 

No prevalence or incidence reported 

Rees T D, Binnie W H. Recurrent aphthous stomatitis. 

Dermatol Clin 1996;14(2):243-256. No prevalence or

incidence reported 

Reeves G E, Burns C, Hall S T et al. The measurement 

of IgA and IgG transglutaminase antibodies in celiac 

disease: a comparison with current diagnostic 

methods. Pathology 2000;32(3):181-185. No 

prevalence or incidence reported

Reibel S, Rohr C, Ziegert M et al. What safety

measures need to be taken in oral food challenges in 

children?. Allergy 2000;55(10):940-944. No 

prevalence or incidence reported

Reijonen H, Ilonen J, Knip M et al. Insulin-dependent 

diabetes mellitus associated with dermatitis 

herpetiformis: evidence for heterogeneity of HLAassociated genes. Tissue Antigens 1991;37(2):94-96. 

No prevalence or incidence reported 

Reiner E B, Patterson M. Intestinal disaccharidase

content. South Med J 1966;59(3):311-314. No

prevalence or incidence reported

Rejman F. Postgastrectomy syndrome. A clinical

study based upon 100 patients. Annales Chirurgiae Et 

Gynaecologiae Fenniae.Supplementum 1970;1701-63. 

No prevalence or incidence reported 

Rensch M J, Szyjkowski R, Shaffer R T et al. The

prevalence of celiac disease autoantibodies in patients 

with systemic lupus erythematosus. Am J 

Gastroenterol 2001;96(4):1113-1115. No prevalence 

or incidence reported 

Rettenbacher T, Hollerweger A, Macheiner P et al. 

Adult celiac disease: US signs. Radiology

1999;211(2):389-394. No prevalence or incidence 

reported 

Reunala T L, Koskimies S. Familial dermatitis

herpetiformis. Clin Dermatol 1991;9(3):335-339. No 

prevalence or incidence reported

Reunala T L. Dermatitis herpetiformis. Clin Dermatol 

2001;19(6):728-736. No prevalence or incidence 

reported 

Reunala T, Collin P. Diseases associated with 

dermatitis herpetiformis. Br J Dermatol 

1997;136(3):315-318. No prevalence or incidence 

reported 

Reunala T, Lokki J. Dermatitis herpetiformis in 

Finland. Acta Derm Venereol 1978;58(6):505-510. No 

prevalence or incidence reported

Reunala T, Salo O P, Tiilikainen A et al. Family

studies in dermatitis herpetiformis. Ann Clin Res 

1976;8(4):254-261. No prevalence or incidence 

reported 

Reunala T. Dermatitis herpetiformis: coeliac disease 

of the skin. Ann Med 1998;30(5):416-418. No 

prevalence or incidence reported

Reunala T. Incidence of familial dermatitis 

herpetiformis. Br J Dermatol 1996;134(3):394-398. 

No prevalence or incidence reported 

Reyes H, Radrigan M E, Gonzalez M C et al.

Steatorrhea in patients with intrahepatic cholestasis of 

pregnancy. Gastroenterology 1987;93(3):584-590. No 

prevalence or incidence reported

Rhim G S, McMorris M S. School readiness for 

children with food allergies. Annals of Allergy,

Asthma & Immunology - Official Publication of the 

American College of Allergy, Asthma, & Immunology

2001;86(2):172-176. No prevalence or incidence 

reported 

Ribeiro U, Posner M C, Safatle-Ribeiro A V et al. 

Risk factors for squamous cell carcinoma of the 

oesophagus. Br J Surg 1996;83(9):1174-1185. No

prevalence or incidence reported

A-563
Ribes C, Pena AS, Pereda A et al. IGA gliadin 

antibodies, a useful screening test for coeliac disease 

in family members of children with coeliac disease. J

Clin Nutr Gastroenterol 1991; 6(4):196-202. Unable to 

obtain full article

Ribes-Koninckx C, Alfonso P, Ortigosa L et al. A 

beta-turn rich oats peptide as an antigen in an ELISA

method for the screening of coeliac disease in a 

paediatric population. Eur J Clin Invest 

2000;30(8):702-708. No prevalence or incidence 

reported 

Riccabona M, Rossipal E. Sonographic findings in 

celiac disease. J Pediatr Gastroenterol Nutr 

1993;17(2):198-200. No prevalence or incidence 

reported 

Rich E J, Christie D L. Anti-gliadin antibody panel

and xylose absorption test in screening for celiac 

disease. J Pediatr Gastroenterol Nutr 1990;10(2):174-

178. No prevalence or incidence reported 

Rifkind E A, Logan R F A, Busuttil A. Coeliac disease 

in Edinburgh and the Lothians 1900-1980. Scott Med 

J 1982;27(4):342No prevalence or incidence reported 

Rifkind E A, Logan R F, Busuttil A et al. Coeliac 

disease in Edinburgh and the Lothians 1900-1980. 

Scott Med J 1982;27(3):256Serology screen <1990 

Riggs B L, Kelly P J, Kinney W R et al. Calcium

deficiency and osteoporosis. Observations in one 

hundred and sixty-six patients and critical review of 

the literature. Journal of Bone and Joint 

Surgery.American Volume 1967;49(5):915-924. No 

prevalence or incidence reported

Riley D. Changing paediatrics. 18 years admissions to 

a medical unit. Scott Med J 1968;13(5):159-161. No 

prevalence or incidence reported

Riordan S M, McIver C J, Duncombe V M et al. 

Factors influencing the 1-g 14C-D-xylose breath test 

for bacterial overgrowth. Am J Gastroenterol 

1995;90(9):1455-1460. No prevalence or incidence 

reported 

Risch N. Assessing the role of HLA-linked and

unlinked determinants of disease. Am J Hum Genet 

1987;40(1):1-14. No prevalence or incidence reported 

Rizzetto M, Bonino F, Pera A et al. Incidence and

significance of different types of connective tissue 

antibodies in adult and pediatric gastroenterological 

disorders. Digestion 1978;17(1):29-37. No prevalence 

or incidence reported 

Robbana-Barnat S, Fradin J. Cereal grains: IgE- and 

non-IgE-mediated reactions. J Nutr Environ Med

1997;7(1):35-46. No prevalence or incidence reported 

Robert M E, Ament M E, Weinstein W M. The

histologic spectrum and clinical outcome of refractory

and unclassified sprue. Am J Surg Pathol 

2000;24(5):676-687. No prevalence or incidence 

reported 

Robinson B N, Roberts D F, Mather B A et al. Coeliac 

disease and HLA: a family study. J Immunogenet 

1980;7(5):381-391. No prevalence or incidence 

reported 

Robinson F. FLAIR-FLOW 4: Synthesis report on

food allergy for health professionals. Nutr Bull 

2002;27(2):85-92. No prevalence or incidence 

reported 

Robinson F. Producing foods for consumers with food 

allergy. Nutr Bull 2003;28(1):65-67. No prevalence or

incidence reported 

Robles D T, Fain P R, Gottlieb P A et al. The genetics 

of autoimmune polyendocrine syndrome type II. 

Endocrinol Metab Clin North Am 2002;31(2):353-

368. No prevalence or incidence reported 

Rogers E L, Douglass W, Russell R M et al.

Deficiency of fat soluble vitamins after jejunoileal 

bypass surgery for morbid obesity. Am J Clin Nutr 

1980;33(6):1208-1214. No prevalence or incidence 

reported 

Roizen Nancy J, Patterson David. Down Syndrome. 

Lancet 2003;361(9365):1281-1289. No prevalence or 

incidence reported 

Roldan M B, Alonso M, Barrio R. Thyroid 

autoimmunity in children and adolescents with Type 1 

diabetes mellitus. Diabetes Nutr Metab 1999;12(1):27-

31. No prevalence or incidence reported 

Romiti A, Merli M, Martorano M et al. Malabsorption 

and nutritional abnormalities in patients with liver

cirrhosis. Ital J Gastroenterol 1990;22(3):118-123. No 

prevalence or incidence reported

Rona R J, Tanner J M. Aetiology of idiopathic growth 

hormone deficiency in England and Wales. Arch Dis 

Child 1977;52(3):197-208. No prevalence or incidence 

reported 

Rosa Utiyama S R, Silva Kotze L M, Nisihara R M et 

al. Spectrum of autoantibodies in celiac patients and 

relatives. Dig Dis Sci 2001;46(12):2624-2630. No

prevalence or incidence reported

Roschger P, Fratzl P, Eschberger J et al. Validation of 

quantitative backscattered electron imaging for the 

measurement of mineral density distribution in human 

bone biopsies. Bone 1998;23(4):319-326. No 

prevalence or incidence reported

A-564
Roschmann E, Wienker T F, Gerok W et al. Analysis

of marker genes contributing to coeliac disease 

susceptibility. Adv Exp Med Biol 1995;371b1339-

1343. No prevalence or incidence reported 

Roschmann E, Wienker T F, Gerok W et al. T-cell 

receptor variable genes and genetic susceptibility to 

celiac disease: an association and linkage study. 

Gastroenterology 1993;105(6):1790-1796. No 

prevalence or incidence reported

Roschmann E, Wienker T F, Volk B A. Role of T cell 

receptor delta gene in susceptibility to celiac disease. J 

Mol Med 1996;74(2):93-98. No prevalence or

incidence reported 

Rose G A. Clinical aspects of calcium metabolism.

Bone diseases. Trans Med Soc Lond 1970;8662-71. 

No prevalence or incidence reported 

Rosenberg W M, Wordsworth B P, Jewell D P et al. A 

locus telomeric to HLA-DPB encodes susceptibility to

coeliac disease. Immunogenetics 1989;30(4):307-310. 

No prevalence or incidence reported 

Ross J R. Postgastrectomy syndromes and their 

management. Surg Clin North Am 1971;51(3):615-

632. No prevalence or incidence reported 

Rossi E. Monosymptomatic forms of celiac disease. 

Eur J Pediatr 1982;138(1):4-5. No prevalence or 

incidence reported 

Rossiter M A, Barrowman J A, Dand A et al. Amylase 

content of mixed saliva in children. Acta Paediatr 

Scand 1974;63(3):389-392. No prevalence or

incidence reported 

Ross-Smith P, Jenner F A. Diet (gluten) and

schizophrenia. J Hum Nutr 1980;34(2):107-112. No 

prevalence or incidence reported

Rostami K, Mulder C J J. Coeliac disease. A 

challenging diagnosis. Rom J Gastroenterol 

1999;8(2):111-114. No prevalence or incidence 

reported 

Rostami K, Steegers E A, Wong W Y et al. Coeliac 

disease and reproductive disorders: a neglected 

association. Eur J Obstet Gynecol Reprod Biol 

2001;96(2):146-149. No prevalence or incidence 

reported 

Rostoker G, Delchier J C, Chaumette M T. Increased 

intestinal intra-epithelial T lymphocytes in primary 

glomerulonephritis: a role of oral tolerance breakdown 

in the pathophysiology of human primary

glomerulonephritides?. Nephrology, Dialysis, 

Transplantation - Official Publication of the European 

Dialysis and Transplant Association - European Renal 

Association 2001;16(3):513-517. No prevalence or

incidence reported 

Rotter J I, Landaw E M. Measuring the genetic 

contribution of a single locus to a multilocus disease. 

Clin Genet 1984;26(6):529-542. No prevalence or

incidence reported 

Rovner Alisha J, Schall Joan I, Jawad Abbas F et al. 

Rethinking growth failure in Alagille syndrome: the 

role of dietary intake and steatorrhea. J Pediatr

Gastroenterol Nutr 2002;35(4):495-502. No 

prevalence or incidence reported

Roy P K, Venzon D J, Feigenbaum K M et al. Gastric 

secretion in Zollinger-Ellison syndrome. Correlation 

with clinical expression, tumor extent and role in

diagnosis--a prospective NIH study of 235 patients 

and a review of 984 cases in the literature. Medicine 

2001;80(3):189-222. No prevalence or incidence 

reported 

Roy R N, Russell R I. Crohn's disease & aflatoxins. J 

R Soc Health 1992;112(6):277-279. No prevalence or

incidence reported 

Rude R K, Olerich M. Magnesium deficiency: 

possible role in osteoporosis associated with glutensensitive enteropathy. Osteoporosis International - a 

Journal Established as Result of Cooperation Between 

the European Foundation for Osteoporosis and the 

National Osteoporosis Foundation of the Usa 

1996;6(6):453-461. No prevalence or incidence 

reported 

Rueda B, Pascual M, Lopez-Nevot M A et al. A new 

allele within the transmembrane region of the human 

MICA gene with seven GCT repeats. Tissue Antigens 

2002;60(6):526-528. No prevalence or incidence 

reported 

Rueda B, Pascual M, Lopez-Nevot M A et al. 

Association of MICA-A5.1 allele with susceptibility 

to celiac disease in a family study. Am J Gastroenterol 

2003;98(2):359-362. No prevalence or incidence 

reported 

Rueda Blanca, Lopez-Nevot Miguel, Angel Pascual et

al. Polymorphism of the inducible nitric oxide 

synthase gene in celiac disease. Hum Immunol 

2002;63(11):1062-1065. No prevalence or incidence 

reported 

Ruiz del, Prado M Y, Olivares Lopez J L et al. HLA 

system. Phenotypic and gene frequencies in celiac and

healthy subjects from the same geographical area. 

Revista Espanola De Enfermedades Digestivas - 

Organo Oficial De La Sociedad Espanola De 

Patologia Digestiva 2001;93(2):106-113. No 

prevalence or incidence reported

Ruiz M Y, Olivares J L. Three-loci HLA haplotypes in 

Spanish celiac children and healthy subjects: 

estimation of linkage disequilibrium and haplotype 

A-565
frequencies. Am J Gastroenterol 2001;96(5):1455-

1459. No prevalence or incidence reported 

Rumbo M, Chirdo F G, Ben R et al. Evaluation of

coeliac disease serological markers in Down syndrome

patients. Digestive and Liver Disease - Official

Journal of the Italian Society of Gastroenterology and 

the Italian Association for the Study of the Liver 

2002;34(2):116-121. No prevalence or incidence 

reported 

Ruskone-Fourmestraux A, Rambaud J C.

Gastrointestinal lymphoma: prevention and treatment 

of early lesions. Best Practice & Research.Clinical

Gastroenterology 2001;15(2):337-354. No prevalence 

or incidence reported 

Russo M W, Fried M W. Side effects of therapy for 

chronic hepatitis C. Gastroenterology

2003;124(6):1711-1719. No prevalence or incidence 

reported 

Russo P A, Chartrand L J, Seidman E. Comparative 

analysis of serologic screening tests for the initial

diagnosis of celiac disease. Pediatrics 1999;104(1 Pt 

1):75-78. No prevalence or incidence reported 

Ryan J. Coeliac disease. Update 2000. Aust Fam 

Physician 2000;29(9):835-838. No prevalence or

incidence reported 

Ryder L P, Staub Nielsen L, Svejgaard A. 

Associations between HL A histocompatibility

antigens and non malignant diseases. Humangenetik 

1974;25(4):251-264. No prevalence or incidence 

reported 

Saalman R, Fallstrom S P. High incidence of urinary

tract infection in patients with coeliac disease. Arch 

Dis Child 1996;74(2):170-171. No prevalence or

incidence reported 

Sabra Aderbal, Bellanti Joseph A, Rais Jonathan et al.

IgE and non-IgE food allergy. Annals of Allergy,

Asthma & Immunology - Official Publication of the 

American College of Allergy, Asthma, & Immunology

2003;90(6 Suppl 3):71-76. No prevalence or incidence 

reported 

Sachdev A, Srinivasan V, Maheswary S et al. Adult 

onset celiac disease in north India. Tropical 

Gastroenterology - Official Journal of the Digestive 

Diseases Foundation 2002;23(3):117-119. No 

prevalence or incidence reported

Sagaro E, Jimenez N. Family studies of coeliac 

disease in Cuba. Arch Dis Child 1981;56(2):132-133. 

Not a relevant screening geography

Salmela M T, Pender S L, Reunala T et al. Parallel 

expression of macrophage metalloelastase (MMP-12) 

in duodenal and skin lesions of patients with

dermatitis herpetiformis. Gut 2001;48(4):496-502. No 

prevalence or incidence reported

Salur L, Uibo O, Talvik I et al. The high frequency of 

coeliac disease among children with neurological 

disorders. European Journal of Neurology - the 

Official Journal of the European Federation of

Neurological Societies 2000;7(6):707-711. No

prevalence or incidence reported

Salvati V M, Bajaj-Elliott M, Poulsom R et al. 

Keratinocyte growth factor and coeliac disease. Gut 

2001;49(2):176-181. No prevalence or incidence 

reported 

Salvetti M, Ristori G, Bomprezzi R et al. Twins:

Mirrors of the immune system. Immunol Today

2000;21(7):342-347. No prevalence or incidence 

reported 

Sampson H A, Scanlon S M. Natural history of food 

hypersensitivity in children with atopic dermatitis. Eur

J Pediatr 1989;115(1):23-27. No prevalence or

incidence reported 

Sampson H A. Food allergy. Curr Opin Immunol 

1990;2(4):542-547. No prevalence or incidence 

reported 

Sampson H A. Patient's perception of food allergy 

may not jibe with reality. Consultant 

1997;37(2):226+233No prevalence or incidence 

reported 

Sampson H A. Utility of food-specific IgE 

concentrations in predicting symptomatic food allergy.

J Allergy Clin Immunol 2001;107(5):891-896. No 

prevalence or incidence reported

Sanchez D, Tuckova L, Sebo P et al. Occurrence of 

IgA and IgG autoantibodies to calreticulin in coeliac 

disease and various autoimmune diseases. J 

Autoimmun 2000;15(4):441-449. No prevalence or

incidence reported 

Sanchez-Albisua Iciar, Storm Wolfgang, Wascher Iris 

et al. How frequent is coeliac disease in Down 

syndrome?. Eur J Pediatr 2002;161(12):683-684. Not 

a relevant screening group 

Sanchez-Borges M, Capriles-Hulett A, Suarez-Chacon 

R et al. Oral anaphylaxis from mite ingestion. Allergy 

Clin Immunol Int 2001;13(1):33-35. No prevalence or

incidence reported 

Sandberg-Bennich S, Dahlquist G, Kallen B. Coeliac 

disease is associated with intrauterine growth and

neonatal infections. Acta Paediatr 2002;91(1):30-33. 

No prevalence or incidence reported 

Sanders D S, Carter M J, Hurlstone D P et al. 

Association of adult coeliac disease with irritable

bowel syndrome: a case-control study in patients 

A-566
fulfilling ROME II criteria referred to secondary care.

Lancet 2001;358(9292):1504-1508. No prevalence or 

incidence reported 

Sanders D S, Hurlstone D P, Stokes R O et al. 

Changing face of adult coeliac disease: experience of a 

single university hospital in South Yorkshire. Postgrad 

Med J 2002;78(915):31-33. Not a relevant screening 

test 

Sanders D S. Coeliac disease. Br J Surg 

2002;89(6):676-677. Review article 

Saredi N, Bava J. Cryptosporidiosis in pediatric

patients. Rev Inst Med Trop Sao Paulo 

1998;40(3):197-200. No prevalence or incidence 

reported 

Sari Ramazan, Aydogdu Ismet, Sevinc Alper et al. 

Upper and lower gastrointestinal endoscopical 

investigation in elderly patients with iron deficiency

anaemia. Haematologia (Budap) 2002;31(4):327-332. 

Not a relevant screening geography

Sategna Guidetti C, Solerio E, Scaglione N et al. 

Duration of gluten exposure in adult coeliac disease 

does not correlate with the risk for autoimmune 

disorders. Gut 2001;49(4):502-505. No prevalence or

incidence reported 

Sategna Guidetti, Carla Scaglione, Nadia Martini et al.

Red cell distribution width as a marker of coeliac 

disease: a prospective study. Eur J Gastroenterol 

Hepatol 2002;14(2):177-181. No prevalence or

incidence reported 

Sategna-Guidetti C, Bianco L, Riffero P. Is watery

diarrhoea a feature of distal ileum resection in Crohn's

disease female patients?. Panminerva Med

1987;29(3):189-190. No prevalence or incidence 

reported 

Sategna-Guidetti C, Bruno M, Mazza E et al. 

Autoimmune thyroid diseases and coeliac disease. Eur

J Gastroenterol Hepatol 1998;10(11):927-931. No 

prevalence or incidence reported

Sategna-Guidetti C, Ferfoglia G, Bruno M et al. Do 

IgA antigliadin and IgA antiendomysium antibodies 

show there is latent coeliac disease in primary IgA 

nephropathy?. Gut 1992;33(4):476-478. No 

prevalence or incidence reported

Sategna-Guidetti C, Grosso S B, Grosso S et al. The

effects of 1-year gluten withdrawal on bone mass, 

bone metabolism and nutritional status in newlydiagnosed adult coeliac disease patients. Aliment 

Pharmacol Ther 2000;14(1):35-43. No prevalence or 

incidence reported 

Sategna-Guidetti C, Grosso S, Bruno M et al. 

Reliability of immunologic markers of celiac sprue in

the assessment of mucosal recovery after gluten 

withdrawal. J Clin Gastroenterol 1996;23(2):101-104. 

No prevalence or incidence reported 

Sategna-Guidetti C, Grosso S. Changing pattern in

adult coeliac disease: A 24-year survey. Eur J

Gastroenterol Hepatol 1994;6(1):15-19. Not a relevant 

screening test 

Sategna-Guidetti C, Volta U, Ciacci C et al. 

Prevalence of thyroid disorders in untreated adult

celiac disease patients and effect of gluten withdrawal:

an Italian multicenter study. Am J Gastroenterol 

2001;96(3):751-757. No prevalence or incidence 

reported 

Saukkonen T, Ilonen J, Akerblom H K et al. 

Prevalence of coeliac disease in siblings of patients

with Type I diabetes is related to the prevalence of

DQB1*02 allele. Diabetologia 2001;44(8):1051-1053. 

Not a relevant screening group 

Saukkonen T, Vaisanen S, Akerblom H K et al. 

Coeliac disease in children and adolescents with type

1 diabetes: a study of growth, glycaemic control, and 

experiences of families. Acta Paediatr 2002;91(3):297-

302. No prevalence or incidence reported 

Savage D A, Middleton D, Trainor F et al. HLA class

II frequencies in celiac disease patients in the west of 

Ireland. Hum Immunol 1992;34(1):47-52. No

prevalence or incidence reported

Saviana B, Quilliot D, Ziegler O et al. Diagnosis of 

lipid malabsorption in patients with chronic

pancreatitis: a new indirect test using postprandial 

plasma apolipoprotein B-48. Am J Gastroenterol 

1999;94(11):3229-3235. No prevalence or incidence 

reported 

Savidge T C, Shmakov A N, Walker-Smith J A et al. 

Epithelial cell proliferation in childhood enteropathies. 

Gut 1996;39(2):185-193. No prevalence or incidence 

reported 

Savilahti E, Ormala T, Saukkonen T et al. Jejuna of 

patients with insulin-dependent diabetes mellitus 

(IDDM) show signs of immune activation. Clin Exp 

Immunol 1999;116(1):70-77. No prevalence or

incidence reported 

Savilahti E, Simell O, Koskimies S et al. Celiac

disease in insulin-dependent diabetes mellitus. Eur J 

Pediatr 1986;108(5 Pt 1):690-693. Serology screen 

<1990 

Savilahti E, Verkasalo M. Intestinal cow's milk

allergy: pathogenesis and clinical presentation. Clin 

Rev Allergy 1984;2(1):7-23. No prevalence or

incidence reported 

Sawhney I M S, Chopra J S. Occipital seizures and 

epilepsies in children. Neurol India 1994;42(2):92No 

prevalence or incidence reported

A-567
Scalici C, Manzoni D, Licastro G et al. Celiac disease 

in the pediatric age, psychological difficulties

experienced on the gluten-free diet. A preliminary 

investigation at the Clinic for Celiac Disease of the 

"G. Di Cristina" Hospital ARNAS, Palermo, Italy.

Acta Med Mediterr 2003;19(1):63-66. No prevalence 

or incidence reported 

Schapira M, Maisin J M, Ghilain J M et al.

Epidemiology of coeliac disease. Acta Gastro-Enterol 

Belg 2003;66(3):234-236. Review article 

Schatz D A, Winter W E. Autoimmune polyglandular 

syndrome II: Clinical syndrome and treatment. 

Endocrinol Metab Clin North Am 2002;31(2):339-

352. No prevalence or incidence reported 

Schenker S. Adverse reactions to food. Nutr Bull 

2002;27(2):125-127. No prevalence or incidence 

reported 

Schlichting J, Leuschner U. Drug therapy of primary

biliary diseases: classical and modern strategies. J Cell

Mol Med 2001;5(1):98-115. No prevalence or

incidence reported 

Schmidt E, Schmidt F W. Clinical aspects of gut 

enzymology. Journal of Clinical Chemistry and 

Clinical Biochemistry.Zeitschrift Fur Klinische

Chemie Und Klinische Biochemie 1979;17(11):693-

704. No prevalence or incidence reported 

Schober Edith, Rami Birgit, Granditsch Gerhard et al. 

Coeliac disease in children and adolescents with type

1 diabetes mellitus: to screen or not, to treat or not?.

Horm Res 2002;57(Suppl 1):97-100. No prevalence or

incidence reported 

Scholz S, Albert E. HLA and diseases: involvement of

more than one HLA-linked determinant of disease 

susceptibility. Immunol Rev 1983;7077-88. No

prevalence or incidence reported

Schrumpf E, Abdelnoor M, Fausa O et al. Risk factors 

in primary sclerosing cholangitis. J Hepatol 

1994;21(6):1061-1066. No prevalence or incidence 

reported 

Schuppan D, Ciccocioppo R. Coeliac disease and 

secondary autoimmunity. Digestive and Liver Disease

- Official Journal of the Italian Society of 

Gastroenterology and the Italian Association for the 

Study of the Liver 2002;34(1):13-15. No prevalence or

incidence reported 

Schuppan D, Esslinger B, Dieterich W. Innate 

immunity and coeliac disease. Lancet

2003;362(9377):3-4. No prevalence or incidence 

reported 

Schuppan D, Hahn E G. Celiac disease and its link to 

type 1 diabetes mellitus. Journal of Pediatric 

Endocrinology & Metabolism - Jpem 2001;14(Suppl 

1):597-605. No prevalence or incidence reported

Schuppan D, Hahn E G. IgA anti-tissue 

transglutaminase: setting the stage for coeliac disease 

screening. Eur J Gastroenterol Hepatol 

2001;13(6):635-637. No prevalence or incidence 

reported 

Schuppan Detlef, Hahn Eckhart G. Biomedicine. 

Gluten and the gut-lessons for immune regulation.

Science 2002;297(5590):2218-2220. No prevalence or

incidence reported 

Schwartz M K, Sleisenger M H, Pert J H et al. The 

effect of a gluten-free diet on fat, nitrogen, and 

mineral metabolism in patients with sprue.

Gastroenterology 1968;54(4):Suppl 791-Suppl 792. 

No prevalence or incidence reported 

Schweizer J J, Oren A, Mearin M L. Cancer in 

children with celiac disease: a survey of the European 

Society of Paediatric Gastroenterology, Hepatology

and Nutrition. J Pediatr Gastroenterol Nutr 

2001;33(1):97-100. No prevalence or incidence 

reported 

Scolapio J S, Fleming C R, Kelly D G et al. Survival

of home parenteral nutrition-treated patients: 20 years 

of experience at the Mayo Clinic. Mayo Clin Proc

1999;74(3):217-222. No prevalence or incidence 

reported 

Scott B B, Young S, Rajah S M et al. Proceedings: 

The incidence of coeliac diseases and HL-A8 in

dermatitis herpetiformis. Gut 1975;16(10):845No 

prevalence or incidence reported

Scott E M, Gaywood I, Scott B B. Guidelines for 

osteoporosis in coeliac disease and inflammatory

bowel disease. British Society of Gastroenterology.

Gut 2000;46(Suppl 1):1-8. No prevalence or incidence 

reported 

Scott E M, Scott B B. A strategy for osteoporosis in 

gastroenterology. Eur J Gastroenterol Hepatol 

1998;10(8):689-696. No prevalence or incidence 

reported 

Scott F W, Rowsell P, Wang G-S et al. Oral exposure

to diabetes-promoting food or immunomodulators in 

neonates alters gut cytokines and diabetes. Diabetes

2002;51(1):73-78. No prevalence or incidence 

reported 

Scott H W, Law D H, Sandstead H H et al. Jejunoileal 

shunt in surgical treatment of morbid obesity. Ann 

Surg 1970;171(5):770-782. No prevalence or

incidence reported 

A-568
Scott H, Ek J, Havnen J et al. Serum antibodies to

dietary antigens: a prospective study of the diagnostic 

usefulness in celiac disease of children. J Pediatr

Gastroenterol Nutr 1990;11(2):215-220. No 

prevalence or incidence reported

Scott H, Fausa O, Ek J et al. Measurements of serum

IgA and IgG activities to dietary antigens. A 

prospective study of the diagnostic usefulness in adult 

coeliac disease. Scand J Gastroenterol

1990;25(3):287-292. No prevalence or incidence 

reported 

Seah P P, Fry L, Holborow E J et al. Antireticulin

antibody: incidence and diagnostic significance. Gut 

1973;14(4):311-315. No prevalence or incidence 

reported 

Sedghizadeh Parish P, Shuler Charles F, Allen Carl M 

et al. Celiac disease and recurrent aphthous stomatitis:

a report and review of the literature. Oral Surg Oral 

Med Oral Pathol Oral Radiol Endod 2002;94(4):474-

478. No prevalence or incidence reported 

Sela B-A. Homocysteine gets to the brain. Isr Med 

Assoc J 2002;4(3):204-206. No prevalence or

incidence reported 

Selby P L, Davies M, Adams J E et al. Bone loss in 

celiac disease is related to secondary 

hyperparathyroidism. Journal of Bone and Mineral 

Research - the Official Journal of the American

Society for Bone and Mineral Research 

1999;14(4):652-657. No prevalence or incidence 

reported 

Selby R, Barnard J M, Buehler S K et al. Tuberculosis 

associated with HLA--B8, BfS in a Newfoundland 

community study. Tissue Antigens 1978;11(5):403-

408. No prevalence or incidence reported 

Selby W S, Gallagher N D. Malignancy in a 19-year 

experience of adult celiac disease. Dig Dis Sci 

1979;24(9):684-688. No prevalence or incidence 

reported 

Selzer G, Sherman G, Callihan T R et al. Primary 

small intestinal lymphomas and alpha-heavy-chain 

disease. A study of 43 cases from a pathology

department in Israel. Isr J Med Sci 1979;15(2):111-

123. No prevalence or incidence reported 

Semrad C E. Bone mass and gastrointestinal disease.

Ann N Y Acad Sci 2000;904564-570. No prevalence 

or incidence reported 

Senarath Yapa R S. Coeliac disease in young and old 

patients. J Clin Exp Gerontol 1991;13(3):95-102. No 

prevalence or incidence reported

Sentongo T A, Rutstein R M, Stettler N et al. 

Association between steatorrhea, growth, and 

immunologic status in children with perinatally

acquired HIV infection. Arch Pediatr Adolesc Med 

2001;155(2):149-153. No prevalence or incidence 

reported 

Shah A, Mayberry J F, Williams G et al. 

Epidemiological survey of coeliac disease and 

inflammatory bowel disease in first-degree relatives of 

coeliac patients. Q J Med 1990;74(275):283-288. Not 

a relevant screening test 

Shah V H, Rotterdam H, Kotler D P et al. All that

scallops is not celiac disease. Gastroenterol Int 

2000;51(6):717-720. No prevalence or incidence 

reported 

Shahbazkhani Bijan, Malekzadeh Reza, Sotoudeh

Masoud et al. High prevalence of coeliac disease in 

apparently healthy Iranian blood donors. Eur J 

Gastroenterol Hepatol 2003;15(5):475-478. Not a 

relevant screening geography

Shaker J L, Brickner R C, Findling J W et al. 

Hypocalcemia and skeletal disease as presenting

features of celiac disease. Arch Intern Med

1997;157(9):1013-1016. No prevalence or incidence 

reported 

Shaker J L, Magill S B, Lalande B M et al. Endocrine 

manifestations of celiac disease. Endocr Pract 

2002;12(2):110-116. No prevalence or incidence 

reported 

Shaltout A A, Khuffash F A, Hilal A A et al. Pattern 

of protracted diarrhoea among children in Kuwait. 

Ann Trop Paediatr 1989;9(1):30-32. No prevalence or

incidence reported 

Shamir R, Eliakim R, Lahat N et al. ELISA of antiendomysial antibodies in the diagnosis of celiac 

disease: Comparison with immunofluorescence assay 

of anti-endomysial antibodies and tissue 

transglutaminase antibodies. Isr Med Assoc J 

2002;4(8):594-596. No prevalence or incidence 

reported 

Shamir R, Levine A, Yalon-Hacohen M et al. Faecal 

occult blood in children with coeliac disease. Eur J 

Pediatr 2000;159(11):832-834. No prevalence or

incidence reported 

Shamir R, Shoenfeld Y, Blank M et al. The prevalence

of coeliac disease antibodies in patients with the 

antiphospholipid syndrome. Lupus 2003;12(5):394-

399. No prevalence or incidence reported 

Shamir R. Advances in celiac disease. Gastroenterol 

Clin North Am 2003;32(3):931-947. No prevalence or

incidence reported 

Shamir Raanan, Lerner Aaron, Shinar Eilat et al. The 

use of a single serological marker underestimates the 

prevalence of celiac disease in Israel: a study of blood 

A-569
donors. Am J Gastroenterol 2002;97(10):2589-2594. 

Not a relevant screening geography

Shanahan F, McKenna R, McCarthy C F et al. Coeliac 

disease and diabetes mellitus: A study of 24 patients 

with HLA typing. Qjm - Monthly Journal of the

Association of Physicians 1982;51(203):329-335. No 

prevalence or incidence reported

Shand A G, Ciclitira P J. Celiac disease. Clin Perspect 

Gastroenterol 2002;5(5):277-283. No prevalence or

incidence reported 

Shaoul R, Marcon M A, Okada Y et al. Gastric

metaplasia: a frequently overlooked feature of

duodenal biopsy specimens in untreated celiac disease. 

J Pediatr Gastroenterol Nutr 2000;30(4):397-403. No 

prevalence or incidence reported

Sharma B C, Bhasin D K, Makharia G et al.

Diagnostic value of push-type enteroscopy: a report 

from India. Am J Gastroenterol 2000;95(1):137-140. 

No prevalence or incidence reported 

Sheldon W. Prognosis in early adult life of coeliac 

children treated with a gluten-free diet. Br Med J 

1969;2(654):401-404. No prevalence or incidence 

reported 

Shepherd N A, Blackshaw A J, Hall P A et al.

Malignant lymphoma with eosinophilia of the 

gastrointestinal tract. Histopathology 1987;11(2):115-

130. No prevalence or incidence reported 

Sher K S, Fraser R C, Wicks A C et al. High risk of 

coeliac disease in Punjabis. Epidemiological study in 

the south Asian and European populations of 

Leicestershire. Digestion 1993;54(3):178-182. Not a 

relevant screening geography

Sher K S, Mayberry J F. Female fertility, obstetric and 

gynaecological history in coeliac disease. A case

control study. Digestion 1994;55(4):243-246. No

prevalence or incidence reported

Sher K S, Mayberry J F. Female fertility, obstetric and 

gynaecological history in coeliac disease: a case 

control study. Acta Paediatr 1996;412(Suppl):76-77. 

No prevalence or incidence reported 

Sherman S L, Iselius L, Ellis A et al. Combined 

segregation and linkage analysis of coeliac disease. 

Genetic Epidemiology.Supplement 1986;1283-288. 

No prevalence or incidence reported 

Sherman S L. Genetic analysis workshop IV: 

summary for coeliac disease. Genetic 

Epidemiology.Supplement 1986;1(Suppl):271-276. 

No prevalence or incidence reported 

Shibahara M, Nanko H, Shimizu M et al. Dermatitis 

herpetiformis in Japan: An update. Arch Dermatol

2002;204(1):37-42. No prevalence or incidence 

reported 

Shidrawi R G, Ciclitira P J. Celiac disease. Curr Opin 

Gastroenterol 1996;12(2):159-163. No prevalence or 

incidence reported 

Shidrawi R G, Day P, Przemioslo R et al. In vitro

toxicity of gluten peptides in coeliac disease assessed 

by organ culture. Scand J Gastroenterol 

1995;30(8):758-763. No prevalence or incidence 

reported 

Shipman R T, Williams A L, Kay R et al. A family

study of coeliac disease. Aust N Z J Med

1975;5(3):250-255. Serology screen <1990 

Shmerling D H, Franckx J. Childhood celiac disease: a 

long-term analysis of relapses in 91 patients. J Pediatr

Gastroenterol Nutr 1986;5(4):565-569. No prevalence 

or incidence reported 

Sibert J R, Morgan R J H, O'Connell H I et al. Is

regional Paediatric Surveillance useful? Experience in

Wales. Arch Dis Child 2001;84(6):486-487. No

prevalence or incidence reported

Sicherer S H, Mun tilde, Murphy R et al. Symposium:

Pediatric food allergy. Pediatrics 2003;111(6 

III):1591-1594. No prevalence or incidence reported 

Sicherer S H, Sampson H A. Food hypersensitivity

and atopic dermatitis: pathophysiology, epidemiology, 

diagnosis, and management. J Allergy Clin Immunol 

1999;104(3 Pt 2):S114-S122. No prevalence or

incidence reported 

Signer E, Burgin-Wolff A, Berger R et al. Antibodies 

to gliadin as a screening test for coeliac disease. A

prospective study. Helv Paediatr Acta 1979;34(1):41-

52. No prevalence or incidence reported 

Signore A, Chianelli M, Annovazzi A et al. Imaging 

active lymphocytic infiltration in coeliac disease with 

iodine-123-interleukin-2 and the response to diet. Eur 

J Nucl Med 2000;27(1):18-24. No prevalence or 

incidence reported 

Signore A, Picarelli A, Annovazzi A et al. 123IInterleukin-2: biochemical characterization and in

vivo use for imaging autoimmune diseases. Nucl Med 

Commun 2003;24(3):305-316. No prevalence or 

incidence reported 

Signore A, Picarelli A, Chianelli M et al. sup 1sup

2sup 3I-Interleukin-2 scintigraphy: A new approach to

assess disease activity in autoimmunity. Journal of 

Pediatric Endocrinology & Metabolism - Jpem 

1996;9(Suppl 1):139-144. No prevalence or incidence 

reported 

Sigurgeirsson B, Agnarsson B A, Lindelof B. Risk of 

lymphoma in patients with dermatitis herpetiformis. 

A-570
BMJ 1994;308(6920):13-15. No prevalence or

incidence reported 

Sigurs N, Hattevig G, Kjellman B et al. Appearance of

atopic disease in relation to serum IgE antibodies in 

children followed up from birth for 4 to 15 years. J 

Allergy Clin Immunol 1994;94(4):757-763. No

prevalence or incidence reported

Silink M. How should we manage celiac disease in 

childhood diabetes?. Pediatr Diabetes 2001;2(3):95-

97. No prevalence or incidence reported 

Silton R P, Fernandez-Caldas E, Trudeau W L et al.

Prevalence of specific IgE to the storage mite,

Aleuroglyphus ovatus. J Allergy Clin Immunol 

1991;88(4):595-603. No prevalence or incidence 

reported 

Silva E M, Fernandes M I, Galvao L C et al. Human 

leukocyte antigen class II alleles in white Brazilian 

patients with celiac disease. J Pediatr Gastroenterol 

Nutr 2000;31(4):391-394. No prevalence or incidence 

reported 

Sipetic S, Vlajinac H, Kocev N et al. Family history

and risk of type 1 diabetes mellitus. Acta Diabetol

2002;39(3):111-115. No prevalence or incidence 

reported 

Sjoberg K, Lindgren S, Eriksson S. Frequent 

occurrence of non-specific gliadin antibodies in 

chronic liver disease. Endomysial but not gliadin 

antibodies predict coeliac disease in patients with 

chronic liver disease. Scand J Gastroenterol 

1997;32(11):1162-1167. No prevalence or incidence 

reported 

Sjogren A, Floren C H, Nilsson A. Measurements of 

magnesium in mononuclear cells. Sci Total Environ 

1985;42(1-2):77-82. No prevalence or incidence 

reported 

Skeen M B. Neurologic manifestations of

gastrointestinal disease. Neurol Clin 2002;20(1):195-

225. No prevalence or incidence reported 

Skovbjerg H, Sjostrom H, Noren O B. Coeliac disease 

- A diagnostic and scientific challenge. Ugeskr Laeg 

2002;164(25):3329-3333. No prevalence or incidence 

reported 

Skre H, Berg K. Cerebellar ataxia and total albinism: a 

kindred suggesting pleitotropism or linkage. Clin

Genet 1974;5(3):196-204. No prevalence or incidence 

reported 

Smecuol E, Bai J C, Vazquez H et al. Gastrointestinal

permeability in celiac disease. Gastroenterology

1997;112(4):1129-1136. No prevalence or incidence 

reported 

Smecuol E, Gonzalez D, Mautalen C et al.

Longitudinal study on the effect of treatment on body

composition and anthropometry of celiac disease 

patients. Am J Gastroenterol 1997;92(4):639-643. No 

prevalence or incidence reported

Smecuol E, Maurino E, Vazquez H et al. 

Gynaecological and obstetric disorders in coeliac

disease: frequent clinical onset during pregnancy or

the puerperium. Eur J Gastroenterol Hepatol 

1996;8(1):63-89. No prevalence or incidence reported 

Smecuol E, Vazquez H, Sugai E et al. Sugar tests 

detect celiac disease among first-degree relatives. Am 

J Gastroenterol 1999;94(12):3547-3552. No 

prevalence or incidence reported

Smith L J, Lacaille F, Lepage G et al. Taurine 

decreases fecal fatty acid and sterol excretion in cystic

fibrosis. A randomized double-blind trial. Am J Dis 

Child 1991;145(12):1401-1404. No prevalence or

incidence reported 

Smith R, Phillips A J. Osteoporosis during pregnancy

and its management. Scandinavian Journal of

Rheumatology.Supplement 1998;10766-67. No 

prevalence or incidence reported

Smith S E, Littlewood J M. The two-film barium meal 

in the exclusion of coeliac disease. Clin Radiol

1977;28(6):629-634. No prevalence or incidence 

reported 

Snook J A, Dwyer L, Lee-Elliott C et al. Adult coeliac 

disease and cigarette smoking. Gut 1996;39(1):60-62. 

No prevalence or incidence reported 

Sokol E M, Brown G M, Frucht H L. Nontropical 

sprue in siblings with dissimilar, unusual, and severe 

manifestations. Gastroenterology 1969;56(1):117-123. 

No prevalence or incidence reported 

Sollid L M, Lundin K E. Coeliac disease. An

inappropriate immune response. Lancet 

2001;358(Suppl):s13No prevalence or incidence 

reported 

Sollid L M, Markussen G, Ek J et al. Evidence for a 

primary association of celiac disease to a particular

HLA-DQ alpha/beta heterodimer. J Exp Med

1989;169(1):345-350. No prevalence or incidence 

reported 

Sollid L M, Thorsby E. HLA susceptibility genes in 

celiac disease: genetic mapping and role in 

pathogenesis. Gastroenterology 1993;105(3):910-922. 

No prevalence or incidence reported 

Sollid L M, Thorsby E. The primary association of

celiac disease to a given HLA-DQ alpha/beta 

heterodimer explains the divergent HLA-DR 

associations observed in various Caucasian 

A-571
populations. Tissue Antigens 1990;36(3):136-137. No 

prevalence or incidence reported

Sollid L, Bruserud O, Gaudernack G et al. The role of

the CD8-positive subset of T cells in proliferative 

responses to soluble antigens. I. Studies of healthy

subjects, type 1 diabetics, and coeliac disease patients. 

Scand J Immunol 1986;23(4):461-467. No prevalence 

or incidence reported 

Sollid Ludvig M. Coeliac disease: dissecting a 

complex inflammatory disorder. Nature

Reviews.Immunology 2002;2(9):647-655. No 

prevalence or incidence reported

Somech Raz, Spirer Zvi. Celiac disease: extraintestinal

manifestations, associated diseases, and

complications. Adv Pediatr 2002;49191-201. No

prevalence or incidence reported

Sonwalkar S A, Holbrook I B, Phillips I et al. A 

prospective, comparative study of the paraaminobenzoic acid test and faecal elastase 1 in the 

assessment of exocrine pancreatic function. Aliment 

Pharmacol Ther 2003;17(3):467-471. No prevalence 

or incidence reported 

Sood A, Midha V, Sood N et al. Adult celiac disease 

in northern India. Indian J Gastroenterol 

2003;22(4):124-126. No prevalence or incidence 

reported 

Sorensen H T, Fonager K. Risk estimation of disorders 

associated with coeliac disease. A 16-year Danish

nationwide follow-up study based on hospital 

discharge data. Implications for screening. Int J Risk 

Saf Med 1996;8(2):137-140. No prevalence or

incidence reported 

Sorensen H T, Thulstrup A M, Blomqvist P et al. Risk 

of primary biliary liver cirrhosis in patients with 

coeliac disease: Danish and Swedish cohort data. Gut 

1999;44(5):736-738. No prevalence or incidence 

reported 

Soresi M, Amplo M, Agliastro R et al. Screening for 

autoantibodies to tissue transglutaminase reveals a low 

prevalence of celiac disease in blood donors with

cryptogenic hypertransaminasemia. Digestion

2001;64(2):87-91. No prevalence or incidence 

reported 

Souroujon M, Ashkenazi A, Lupo M et al. Serum 

ferritin levels in celiac disease. Am J Clin Pathol

1982;77(1):82-86. No prevalence or incidence 

reported 

Specker B L. The significance of high bone density in

children. Eur J Pediatr 2001;139(4):473-475. No

prevalence or incidence reported

Spergel Jonathan M, Beausoleil Janet L, Mascarenhas 

Maria et al. The use of skin prick tests and patch tests 

to identify causative foods in eosinophilic esophagitis. 

J Allergy Clin Immunol 2002;109(2):363-368. No 

prevalence or incidence reported

Spiller Robin C. Postinfectious irritable bowel

syndrome. Gastroenterology 2003;124(6):1662-1671. 

No prevalence or incidence reported 

Spiro H M. About this issue. J Clin Gastroenterol 

1995;20(4):271No prevalence or incidence reported 

Spurkland A, Ingvarsson G, Falk E S et al. Dermatitis 

herpetiformis and celiac disease are both primarily 

associated with the HLA-DQ (alpha 1*0501, beta 

1*02) or the HLA-DQ (alpha 1*03, beta 1*0302)

heterodimers. Tissue Antigens 1997;49(1):29-34. No 

prevalence or incidence reported

Stahlberg M R, Hietanen E. Glutathione and

glutathione-metabolizing enzymes in the erythrocytes

of healthy children and in children with insulindependent diabetes mellitus, juvenile rheumatoid

arthritis, coeliac disease and acute lymphoblastic 

leukaemia. Scand J Clin Lab Invest 1991;51(2):125-

130. No prevalence or incidence reported 

Stahlberg M R, Savilahti E, Siimes M A. Iron

deficiency in coeliac disease is mild and it is detected 

and corrected by gluten-free diet. Acta Paediatr Scand 

1991;80(2):190-193. No prevalence or incidence 

reported 

Stanner S. Is breast best for the heart?. Nutr Bull 

2001;26(3):199-200. No prevalence or incidence 

reported 

Stazi A V, Mantovani A. A risk factor for female 

fertility and pregnancy: celiac disease. Gynecological 

Endocrinology - the Official Journal of the 

International Society of Gynecological Endocrinology

2000;14(6):454-463. No prevalence or incidence 

reported 

Stazi Maria, Antonietta Cotichini, Rodolfo Patriarca et 

al. The Italian Twin Project: from the personal 

identification number to a national twin registry. Twin 

Research - the Official Journal of the International 

Society for Twin Studies 2002;5(5):382-386. No

prevalence or incidence reported

Stein E, Shane E. Secondary osteoporosis. Endocrinol 

Metab Clin North Am 2003;32(1):115-134. No

prevalence or incidence reported

Steinfeld C M, Moertel C G, Woolner L B. Diarrhea 

and medullary carcinoma of the thyroid. Cancer 

1973;31(5):1237-1239. No prevalence or incidence 

reported 

A-572
Stenhammar L, Ansved P, Jansson G et al. The 

incidence of childhood celiac disease in Sweden. J 

Pediatr Gastroenterol Nutr 1987;6(5):707-709. 

Serology screen <1990 

Stenhammar L, Fallstrom S P, Jansson G et al. Coeliac 

disease in children of short stature without 

gastrointestinal symptoms. Eur J Pediatr

1986;145(3):185-186. No prevalence or incidence 

reported 

Stenhammar L, Johansson C G. The incidence of 

coeliac disease in children in south-east Sweden. Acta 

Paediatr Scand 1981;70(3):379-381. Serology screen 

<1990 

Stenhammar L. Transient gastro-intestinal disorders

during infancy and early childhood. A follow-up study

with special reference to coeliac disease. Acta Paediatr 

Scand 1981;70(3):383-387. No prevalence or

incidence reported 

Stern M, Bender S W, Gruttner R et al. Serum 

antibodies against gliadin and reticulin in a family

study of coeliac disease. Eur J Pediatr 1980;135(1):31-

36. No prevalence or incidence reported 

Stern M, Teuscher M, Wechmann T. Serological 

screening for coeliac disease: methodological 

standards and quality control. Acta Paediatr

1996;412(Suppl):49-51. No prevalence or incidence 

reported 

Stern M. Comparative evaluation of serologic tests for 

celiac disease: A European initiative toward 

standardization. J Pediatr Gastroenterol Nutr

2000;31(5):513-519. No prevalence or incidence 

reported 

Stevens F M, Egan-Mitchell B, Cryan E et al.

Decreasing incidence of coeliac disease. Arch Dis

Child 1987;62(5):465-468. Serology screen <1990 

Stevens F M, Hitchcock H T. Farmer's lung disease 

and coeliac disease: a prospective study. Ir J Med Sci 

1977;146(10):335-339. No prevalence or incidence 

reported 

Stevens F M, Lloyd R S, Geraghty S M et al.

Schizophrenia and coeliac disease--the nature of the 

relationship. Psychol Med 1977;7(2):259-263. No 

prevalence or incidence reported

Stevens F M, Lloyd R, Egan-Mitchell B et al. 

Proceedings: Antireticulin antibodies in coeliacs and 

their relatives. Gut 1973;14(10):829Not a relevant 

screening test 

Stevens F M, Lloyd R, Egan-Mitchell B et al. 

Reticulin antibodies in patients with coeliac disease 

and their relatives. Gut 1975;16(8):598-602. Serology

screen <1990 

Stevens R F, Meyer S. Fanconi and Glanzmann: The 

men and their works. Br J Haematol 2002;119(4):901-

904. No prevalence or incidence reported 

Stewart J. Child coeliacs in adult life. Ir Med J

1974;67(15):411-414. No prevalence or incidence 

reported 

Stocker F, Ammann P, Rossi E. Selective gamma-Aglobulin deficiency, with dominant autosomal 

inheritance in a Swiss family. Arch Dis Child 

1968;43(231):585-588. No prevalence or incidence 

reported 

Stockman J A. Clinical facts and curios. Curr Probl 

Pediatr 1992;22(9):413-419. No prevalence or

incidence reported 

Stokes P L, Asquith P, Cooke W T. Genetics of 

coeliac disease. Clin Gastroenterol 1973;2(3):547-556. 

No prevalence or incidence reported 

Stokes P L, Asquith P, Holmes G K et al. Inheritance

and influence of histocompatibility (HL-A) antigens in 

adult coeliac disease. Gut 1973;14(8):627-630. No 

prevalence or incidence reported

Stokes P L, Asquith P, Waterhouse J H et al. 

Malignancy in relatives of patients with adult coeliac 

disease. Gut 1972;13(10):836-837. No prevalence or 

incidence reported 

Stokes P L, Holmes G K, Smits B J. Immunoglobulin 

levels in families with coeliac disease. Lancet

1972;2(7777):608No prevalence or incidence reported 

Stokes P L, Prior P, Sorahan T M. Malignancy in 

relatives of patients with coeliac disease. Br J Prev

Soc Med 1976;30(1):17-21. No prevalence or

incidence reported 

Storm W. Prevalence and diagnostic significance of 

gliadin antibodies in children with Down syndrome. 

Eur J Pediatr 1990;149(12):833-834. No prevalence or

incidence reported 

Storsrud S, Olsson M, Arvidsson Lenner R et al. Adult 

coeliac patients do tolerate large amounts of oats. Eur 

J Clin Nutr 2003;57(1):163-169. No prevalence or

incidence reported 

Storsrud Stine, Hulthen Lena R, Lenner Ragnhild A. 

Beneficial effects of oats in the gluten-free diet of

adults with special reference to nutrient status, 

symptoms and subjective experiences. Br J Nutr 

2003;90(1):101-107. No prevalence or incidence 

reported 

Stringer Veysi V T, Puntis J W, Batcup G et al. 

Gastroduodenal ulcers in the Helicobacter pylori era. 

Acta Paediatr 2000;89(10):1181-1185. No prevalence 

or incidence reported 

A-573
Strobel S, Brydon W G, Ferguson A. 

Cellobiose/mannitol sugar permeability test 

complements biopsy histopathology in clinical 

investigation of the jejunum. Gut 1984;25(11):1241-

1246. No prevalence or incidence reported 

Strobel S, Busuttil A, Ferguson A. Human intestinal 

mucosal mast cells: expanded population in untreated

coeliac disease. Gut 1983;24(3):222-227. No 

prevalence or incidence reported

Strober W. Genetic and anthropologic factors in

gluten-sensitive enteropathy. Am J Phys Anthropol 

1983;62(1):119-126. No prevalence or incidence 

reported 

Stromberg L. Diagnostic accuracy of the atopy patch 

test and the skin-prick test for the diagnosis of food

allergy in young children with atopic 

eczema/dermatitis syndrome. Acta Paediatr Int J

Paediatr 2002;91(10):1044-1049. No prevalence or

incidence reported 

Suarez R M, Suarez R M. Diseases of the digestive 

system in Puerto Ricans aged 80 and older. J Am 

Geriatr Soc 1967;15(4):383-385. Not a relevant 

screening geography

Sugai E, Srur G, Vazquez H et al. Steatocrit: a reliable

semiquantitative method for detection of steatorrhea. J 

Clin Gastroenterol 1994;19(3):206-209. No 

prevalence or incidence reported

Sugai Emilia, Chernavsky Alejandra, Pedreira Silvia

et al. Bone-specific antibodies in sera from patients

with celiac disease: characterization and implications 

in osteoporosis. J Clin Immunol 2002;22(6):353-362. 

No prevalence or incidence reported 

Suharjono. Intestinal biopsy and coeliac disease. 

Paediatr Indones 1971;11(3):116-134. No prevalence 

or incidence reported 

Suliman G I. Coeliac disease in Sudanese children. 

Gut 1978;19(2):121-125. No prevalence or incidence 

reported 

Sullivan A. Coeliac disease. Nursing Standard (Royal

College of Nursing (Great Britain) - 1987)

1999;14(11):48-52. No prevalence or incidence 

reported 

Suman Shivani, Williams Elizabeth J, Thomas Peter

W et al. Is the risk of adult coeliac disease causally

related to cigarette exposure?. Eur J Gastroenterol 

Hepatol 2003;15(9):995-1000. No prevalence or 

incidence reported 

Sumnik Z, Kolouskova S, Cinek O et al. HLADQA1*05-DQB1*0201 positivity predisposes to

coeliac disease in Czech diabetic children. Acta

Paediatr 2000;89(12):1426-1430. Not a relevant 

screening geography

Susi M, Holopainen P, Mustalahti K et al. Candidate

gene region 15q26 and genetic susceptibility to coeliac 

disease in Finnish families. Scand J Gastroenterol 

2001;36(4):372-374. No prevalence or incidence 

reported 

Sutton D R, Baird I M, Stewart J S et al. 

Gastrointestinal iron losses in atrophic gastritis, 

postgastrectomy states and adult coeliac disease. Gut 

1971;12(10):869-870. No prevalence or incidence 

reported 

Sutton D R, Stewart J S, Baird I M et al. "Free" iron 

loss in atrophic gastritis, post-gastrectomy states, and 

adult coeliac disease. Lancet 1970;2(7669):387-389. 

No prevalence or incidence reported 

Sutton G. Coeliac disease: Testing the New Zealand 

iceberg. New Zealand J Med Lab Sci 2000;54(2):46-

48. No prevalence or incidence reported 

Svedberg P, Johansson S, Wallander M-A et al. Extraintestinal manifestations associated with irritable

bowel syndrome: a twin study. Aliment Pharmacol 

Ther 2002;16(5):975-983. No prevalence or incidence 

reported 

Svejgaard A, Lobitz W C. HL A histocompability 

antigens and skin diseases. Br J Dermatol 

1974;91(2):237-241. No prevalence or incidence 

reported 

Svejgaard A. HLA and disease. Rev Fr Transfus

Immuno-Hematol 1977;20(1):27-30. No prevalence or

incidence reported 

Swerdlow A J, Whittaker S, Carpenter L M et al.

Mortality and cancer incidence in patients with 

dermatitis herpetiformis: a cohort study. Br J Dermatol 

1993;129(2):140-144. No prevalence or incidence 

reported 

Swincow G, Chrobot A M, Bala G et al. Comparative 

analysis of etiologic factors, frequency and diagnostic 

approach to malabsorption syndrome in two time 

periods: 1980-1986 and 1994- 1997. Med Sci Monit 

1999;5(5):891-895. No prevalence or incidence 

reported 

Swinson C M, Levi A J. Is coeliac disease 

underdiagnosed?. Br Med J 1980;281(6250):1258-

1260. No prevalence or incidence reported 

Swinson C M, Slavin G, Coles E C et al. Coeliac 

disease and malignancy. Lancet 1983;1(8316):111-

115. No prevalence or incidence reported 

Sylvester F A. Bone abnormalities in gastrointestinal 

and hepatic disease. Curr Opin Pediatr 

A-574
1999;11(5):402-407. No prevalence or incidence 

reported 

Szaflarska-Szczepanik A, Adamska I, Swincow G et 

al. Occurrence of allergy symptoms in celiac disease 

children - Preliminary report. Med Sci Monit 

1998;4(6):942-944. No prevalence or incidence 

reported 

Szaflarska-Szczepanik A, Czerwionka-Szaflarska M. 

The frequency of occurrence and clinical picture of 

celiac disease in the parents of children with the

disease. Medical Science Monitor - International 

Medical Journal of Experimental and Clinical 

Research 2001;7(5):971-976. Not a relevant screening 

geography

Szaflarska-Szczepanik Anna. Assessment of 

correlation between the presence of antiendomysial 

antibodies and small intestine mucosal villous atrophy

in the diagnostics of celiac disease. Medical Science 

Monitor - International Medical Journal of 

Experimental and Clinical Research 2002;8(3):Cr185-

Cr188. No prevalence or incidence reported 

Szathmari M, Tulassay T, Arato A et al. Bone mineral

content and density in asymptomatic children with 

coeliac disease on a gluten-free diet. Eur J 

Gastroenterol Hepatol 2001;13(4):419-424. No

prevalence or incidence reported

Tabrez S, Roberts I M. Malabsorption and 

malnutrition. Prim Care 2001;28(3):505-22, V. No

prevalence or incidence reported

Taggart D P, Imrie C W. A new pattern of histologic 

predominance and distribution of malignant diseases 

of the small intestine. Surg Gynecol Obstet

1987;165(6):515-518. No prevalence or incidence 

reported 

Tai V, Crowe M, O'Keefe S. Celiac disease in older 

people. J Am Geriatr Soc 2000;48(12):1690-1696. No 

prevalence or incidence reported

Talstad I, Fretheim B, Myren J et al. Graded 

gastrectomy for duodenal ulcer -- a five-year

prospective study. Scand J Gastroenterol 

1975;33(Suppl):1-27. No prevalence or incidence 

reported 

Taminiau J A. Celiac disease. Curr Opin Pediatr

1996;8(5):483-486. No prevalence or incidence 

reported 

Tandon N, Shtauvere-Brameus A, Hagopian W A et 

al. Prevalence of ICA-12 and other autoantibodies in 

north Indian patients with early-onset diabetes. Ann N 

Y Acad Sci 2002;958214-217. No prevalence or

incidence reported 

Teahon K, Somasundaram S, Smith T et al. Assessing 

the site of increased intestinal permeability in coeliac

and inflammatory bowel disease. Gut 1996;38(6):864-

869. No prevalence or incidence reported 

Tedeschi A, Tuccari G, Magazzu G et al. 

Immunohistochemical localization of lactoferrin in 

duodenojejunal mucosa from celiac children. J Pediatr 

Gastroenterol Nutr 1987;6(3):328-334. No prevalence 

or incidence reported 

Tessier J L, Davies G A L. Giardiasis. Prim Care 

Update Ob Gyns 1999;6(1):8-11. No prevalence or

incidence reported 

Thain M E, Hamilton J R, Ehrlich R M. Coexistence 

of diabetes mellitus and celiac disease. Eur J Pediatr 

1974;85(4):527-529. No prevalence or incidence 

reported 

Thapa B R. Celiac disease in India. Indian J Pediatr 

1999;66(1 Suppl):S16-S20. No prevalence or

incidence reported 

Thimister P W, Hopman W P, Rosenbusch G et al. 

Plasma cholecystokinin and gallbladder responses to 

increasing doses of bombesin in celiac disease. Dig 

Dis Sci 1998;43(3):668-672. No prevalence or

incidence reported 

Thirup P. Steatorrhea cannot be excluded where there

is a fecal weight below 0.200 kg per day and a high 

fecal consistency. Scand J Clin Lab Invest 

1998;58(7):577-583. No prevalence or incidence 

reported 

Thomas G E, Clain D J. Proceedings: Tropical sprue 

in Rhodesia. Gut 1974;15(10):823No prevalence or 

incidence reported 

Thomas P D, Forbes A, Green J et al. Guidelines for 

the investigation of chronic diarrhoea, 2nd edition. 

Gut 2003;52(Suppl 5):v1-v15. No prevalence or 

incidence reported 

Thomason K, West J, Logan R F A et al. Fracture

experience of patients with coeliac disease: a

population based survey. Gut 2003;52(4):518-522. No 

prevalence or incidence reported

Thompson N P, Montgomery S M, Pounder R E et al. 

Is measles vaccination a risk factor for inflammatory

bowel disease?. Lancet 1995;345(8957):1071-1074. 

No prevalence or incidence reported 

Thompson N P, Montgomery S M, Pounder R E et al. 

Is measles vaccination a risk factor for inflammatory

bowel disease?. Lancet 1995;345(8957):1062-

1063+1071. No prevalence or incidence reported

Thomson G. HLA disease associations: models for the 

study of complex human genetic disorders. Crit Rev 

Clin Lab Sci 1995;32(2):183-219. No prevalence or

incidence reported 

A-575
Thomson G. Investigation of the mode of inheritance 

of the HLA associated diseases by the method of

antigen genotype frequencies among diseased

individuals. Tissue Antigens 1983;21(2):81-104. No 

prevalence or incidence reported

Thornquist H, Jacobsen G S, Dahl L B et al. Coeliac 

disease and gluten-free diet: a following-up study of 

fifteen young adults. Ann Nutr Metab 1993;37(6):295-

301. No prevalence or incidence reported 

Thorsby E, Lundin K E A, Ronningen K S et al. 

Molecular and functional aspects of some diseaseassociated HLA polymorphisms. Genes and Gene 

Products in the Development of Diabetes Mellitus: 

Proceedings of the 3rd Nordisk Insulin Symposium

'genes Ane Gene Products in the Development of

Diabetes Mellitus' Ics866 1989;55-67. No prevalence 

or incidence reported 

Thorsby E, Lundin K E, Ronningen K S et al. 

Molecular basis and functional importance of some 

disease-associated HLA polymorphisms. Tissue 

Antigens 1989;34(1):39-49. No prevalence or

incidence reported 

Thorsby E. Invited anniversary review: HLA 

associated diseases. Hum Immunol 1997;53(1):1-11. 

No prevalence or incidence reported 

Thurley C A, Kwan W C, Freeman H J et al. T cell 

receptor gene expression and genotypes in celiac

disease. Pathobiology - Journal of Immunopathology,

Molecular and Cellular Biology 1994;62(5-6):311-

318. No prevalence or incidence reported 

Tighe M R, Ciclitira P J. The gluten-host interaction. 

Bailliere's Clin Gastroenterol 1995;9(2):211-230. No 

prevalence or incidence reported

Tighe M R, Hall M A, Ashkenazi A et al. Celiac 

disease among Ashkenazi Jews from Israel. A study of 

the HLA class II alleles and their associations with

disease susceptibility. Hum Immunol 1993;38(4):270-

276. No prevalence or incidence reported 

Tighe M R, Hall M A, Barbado M et al. HLA class II 

alleles associated with celiac disease susceptibility in a 

southern European population. Tissue Antigens 

1992;40(2):90-97. No prevalence or incidence 

reported 

Tighe M R, Hall M A, Cardi E et al. Associations

between alleles of the major histocompatibility 

complex- encoded ABC transporter gene TAP2, HLA 

class II alleles, and celiac disease susceptibility. Hum

Immunol 1994;39(1):9-16. No prevalence or incidence 

reported 

Tighe R, Ciclitira P J. Celiac disease. Curr Opin

Gastroenterol 1995;11(2):112-115. No prevalence or 

incidence reported 

Tighe R, Ciclitira P J. Molecular biology of coeliac 

disease. Arch Dis Child 1995;73(3):189-191. No

prevalence or incidence reported

Tiwari J L, Betuel H, Gebuhrer L et al. Genetic 

epidemiology of coeliac disease. Genet Epidemiol

1984;1(1):37-42. No prevalence or incidence reported 

Toffolon E P, Goldfinger S E. Malabsorption 

following gastrectomy and ileal resection. Surg Clin 

North Am 1974;54(3):647-653. No prevalence or

incidence reported 

Tomei E, Marini M, Messineo D et al. Computed

tomography of the small bowel in adult celiac disease:

the jejunoileal fold pattern reversal. Eur Radiol

2000;10(1):119-122. No prevalence or incidence 

reported 

Tomkin G H, Mawhinney M, Nevin N C. Isolated 

absence of IgA with autosomal dominant inheritance.

Lancet 1971;2(7716):124-125. No prevalence or 

incidence reported 

Torinsson Naluai A, Nilsson S, Samuelsson L et al. 

The CTLA4/CD28 gene region on chromosome 2q33 

confers susceptibility to celiac disease in a way 

possibly distinct from that of type 1 diabetes and other 

chronic inflammatory disorders. Tissue Antigens

2000;56(4):350-355. No prevalence or incidence 

reported 

Toskes P P, Dawson W, Curington C et al. Nondiabetic retinal abnormalities in chronic pancreatitis. 

N Engl J Med 1979;300(17):942-946. No prevalence 

or incidence reported 

Tovey F I, Godfrey J E, Lewin M R. A gastrectomy

population: 25-30 years on. Postgrad Med J 

1990;66(776):450-456. No prevalence or incidence 

reported 

Trabace S, Giunta A, Rosso M et al. HLA-ABC and 

DR antigens in celiac disease. A study in a pediatric 

Italian population. Vox Sang 1984;46(2):102-106. No 

prevalence or incidence reported

Tran T M, Van den, Neucker A et al. Effects of a 

proton-pump inhibitor in cystic fibrosis. Acta Paediatr

1998;87(5):553-558. No prevalence or incidence 

reported 

Trejdosiewicz L K, Calabrese A, Smart C J et al.

Gamma delta T cell receptor-positive cells of the 

human gastrointestinal mucosa: occurrence and V 

region gene expression in Heliobacter pyloriassociated gastritis, coeliac disease and inflammatory

A-576
bowel disease. Clin Exp Immunol 1991;84(3):440-

444. No prevalence or incidence reported 

Trevisiol C, Ventura A, Baldas V et al. A reliable

screening procedure for coeliac disease in clinical

practice. Scand J Gastroenterol 2002;37(6):679-684. 

Not a relevant screening group 

Triolo G, Accardo-Palumbo A, Dieli F et al. Humoral 

and cell mediated immune response to cow's milk 

proteins in Behcet's disease. Ann Rheum Dis 

2002;61(5):459-462. No prevalence or incidence 

reported 

Tripp E J, MacKay E H. Silver staining of bone prior 

to decalcification for quantitative determination of 

osteoid in sections. Stain Technol 1972;47(3):129-

136. No prevalence or incidence reported 

Troncone R, Greco L, Auricchio S. Gluten-sensitive 

enteropathy. Pediatr Clin North Am 1996;43(2):355-

373. No prevalence or incidence reported 

Troncone R, Greco L, Auricchio S. The controversial 

epidemiology of coeliac disease. Acta Paediatr 

2000;89(2):140-141. No prevalence or incidence 

reported 

Troncone R, Greco L, Mayer M et al. In siblings of

celiac children, rectal gluten challenge reveals gluten 

sensitization not restricted to celiac HLA.

Gastroenterology 1996;111(2):318-324. No 

prevalence or incidence reported

Troncone R, Mayer M, Spagnuolo F et al. Endomysial 

antibodies as unreliable markers for slight dietary

transgressions in adolescents with celiac disease. J

Pediatr Gastroenterol Nutr 1995;21(1):69-72. No 

prevalence or incidence reported

Troncone R, Mazzarella G, Leone N et al. Gliadin 

activates mucosal cell mediated immunity in cultured 

rectal mucosa from coeliac patients and a subset of 

their siblings. Gut 1998;43(4):484-489. No prevalence 

or incidence reported 

Troncone Riccardo, Franzese Adriana, Mazzarella

Giuseppe et al. Gluten sensitivity in a subset of 

children with insulin dependent diabetes mellitus. Am

J Gastroenterol 2003;98(3):590-595. No prevalence or

incidence reported 

Tumer L, Hasanoglu A, Aybay C. Endomysium 

antibodies in the diagnosis of celiac disease in shortstatured children with no gastrointestinal symptoms. 

Pediatrics International - Official Journal of the Japan 

Pediatric Society 2001;43(1):71-73. No prevalence or 

incidence reported 

Turner J M, Lawrence S, Fellows I W et al. [14C]-

triolein absorption: a useful test in the diagnosis of 

malabsorption. Gut 1987;28(6):694-700. No 

prevalence or incidence reported

Turowski G, Ke cedil. Soluble HLA class I antigens as

a familial genetic background in coeliac disease. CentEur J Immunol 2001;26(1):28-30. No prevalence or

incidence reported 

Tursi A, Brandimarte G, Giorgetti G et al. Low 

prevalence of antigliadin and anti-endomysium 

antibodies in subclinical/silent celiac disease. Am J 

Gastroenterol 2001;96(5):1507-1510. No prevalence 

or incidence reported 

Tursi A, Brandimarte G, Giorgetti G M. Sorbitol H2-

breath test versus anti-endomysium antibodies for the 

diagnosis of subclinical/silent coeliac disease. Scand J 

Gastroenterol 2001;36(11):1170-1172. No prevalence 

or incidence reported 

Tursi A, Giorgetti G, Brandimarte G et al. Prevalence

and clinical presentation of subclinical/silent celiac

disease in adults: an analysis on a 12-year observation.

Hepatogastroenterology 2001;48(38):462-464. No 

prevalence or incidence reported

Tursi Antonio, Brandimarte Giovanni, Giorgetti Gian 

et al. Prevalence of antitissue transglutaminase

antibodies in different degrees of intestinal damage in

celiac disease. J Clin Gastroenterol 2003;36(3):219-

221. No prevalence or incidence reported 

Tursi Antonio, Brandimarte Giovanni, Giorgetti 

GianMarco. High prevalence of small intestinal

bacterial overgrowth in celiac patients with persistence

of gastrointestinal symptoms after gluten withdrawal.

Am J Gastroenterol 2003;98(4):839-843. No 

prevalence or incidence reported

Tursi Antonio, Brandimarte Giovanni. The 

symptomatic and histologic response to a gluten-free 

diet in patients with borderline enteropathy. J Clin 

Gastroenterol 2003;36(1):13-17. No prevalence or

incidence reported 

Tuysuz B, Dursun A, Kutlu T et al. HLA-DQ alleles 

in patients with celiac disease in Turkey. Tissue 

Antigens 2001;57(6):540-542. No prevalence or 

incidence reported 

Uibo O, Maaroos H I. Hospital screening of coeliac 

disease in Estonian children by anti-gliadin antibodies

of IgA class. Acta Paediatr 1993;82(3):233-234. No 

prevalence or incidence reported

Uibo O, Metskula K, Kukk T et al. Results of coeliac 

disease screening in Estonia in 1990-1994. Acta 

Paediatr 1996;412(Suppl):39-41. Not a relevant 

screening geography

Uibo O, Uibo R, Kleimola V et al. Serum IgA antigliadin antibodies in an adult population sample. High 

A-577
prevalence without celiac disease. Dig Dis Sci

1993;38(11):2034-2037. Not a relevant screening

geography

Uibo O. Childhood celiac disease in Estonia: efficacy

of the IgA-class antigliadin antibody test in the search 

for new cases. J Pediatr Gastroenterol Nutr 

1994;18(1):53-55. Not a relevant screening geography

Uibo R, Sullivan E P, Uibo O et al. Comparison of the 

prevalence of glutamic acid decarboxylase (GAD65) 

and gliadin antibodies (AGA) in a randomly selected 

adult estonian population. Hormone and Metabolic 

Research.Hormon- Und 

Stoffwechselforschung.Hormones Et Metabolisme 

2001;33(9):564-567. No prevalence or incidence 

reported 

Uil J J, van Elburg R M, Janssens P M et al.

Sensitivity of a hyperosmolar or "low"-osmolar test 

solution for sugar absorption in recognizing small 

intestinal mucosal damage in coeliac disease.

Digestive and Liver Disease - Official Journal of the 

Italian Society of Gastroenterology and the Italian 

Association for the Study of the Liver 2000;32(3):195-

200. No prevalence or incidence reported 

Uil J J, van Elburg R M, Mulder C J et al. The value

of the D-xylose test compared with the differential

sugar absorption test in recognizing coeliac disease. 

Neth J Med 1996;49(2):68-72. No prevalence or 

incidence reported 

Uil J J, van Elburg R M, van Overbeek F M et al. 

Follow-up of treated coeliac patients: sugar absorption 

test and intestinal biopsies compared. Eur J

Gastroenterol Hepatol 1996;8(3):219-223. No

prevalence or incidence reported

umnik Z, Kolous caron, Cinek O et al. HLA -

DQA1*05-DQB1*0201 positivity predisposes to

coeliac disease in Czech diabetic children. Acta

Paediatr Int J Paediatr 2000;89(12):1426-1430. No

prevalence or incidence reported

Ung K A, Kilander A F, Lindgren A et al. Impact of 

bile acid malabsorption on steatorrhoea and symptoms 

in patients with chronic diarrhoea. Eur J Gastroenterol 

Hepatol 2000;12(5):541-547. No prevalence or

incidence reported 

Unsworth D J, Brown D L. Serological screening

suggests that adult coeliac disease is underdiagnosed 

in the UK and increases the incidence by up to 12%. 

Gut 1994;35(1):61-64. Not a relevant screening test 

Usai P, Bassotti G, Satta P et al. Oesophageal motility

in adult coeliac disease. Neurogastroenterol Motil 

1995;7(4):239-244. No prevalence or incidence 

reported 

Usai P, Boi M F, Piga M et al. Adult celiac disease is

frequently associated with sacroiliitis. Dig Dis Sci

1995;40(9):1906-1908. No prevalence or incidence 

reported 

Usai P, Minerba L, Marini B et al. Case control study 

on health-related quality of life in adult coeliac 

disease. Digestive and Liver Disease - Official Journal 

of the Italian Society of Gastroenterology and the 

Italian Association for the Study of the Liver 

2002;34(8):547-552. No prevalence or incidence 

reported 

Ussher R, Yeong M L, Stace N. Coeliac disease:

incidence and prevalence in Wellington 1985-92. N Z 

Med J 1994;107(978):195-197. Not a relevant 

screening geography

Vader Willemijn, Kooy Yvonne, Van Veelen et al. 

The gluten response in children with celiac disease is 

directed toward multiple gliadin and glutenin peptides.

Gastroenterology 2002;122(7):1729-1737. No 

prevalence or incidence reported

Vahedi Kouroche, Mascart Francoise, Mary Jean et al. 

Reliability of antitransglutaminase antibodies as 

predictors of gluten-free diet compliance in adult 

celiac disease. Am J Gastroenterol 2003;98(5):1079-

1087. No prevalence or incidence reported 

Vaknin-Dembinsky A, Eliakim R, Steiner I.

Neurological deficits in patients with celiac disease. 

Arch Neurol 2002;59(4):647-648. No prevalence or

incidence reported 

Valdimarsson T, Lofman O, Toss G et al. Reversal of 

osteopenia with diet in adult coeliac disease. Gut 

1996;38(3):322-327. No prevalence or incidence 

reported 

Valdimarsson T, Toss G, Lofman O et al. Three years'

follow-up of bone density in adult coeliac disease: 

significance of secondary hyperparathyroidism. Scand 

J Gastroenterol 2000;35(3):274-280. No prevalence or

incidence reported 

Valdimarsson T, Toss G, Ross I et al. Bone mineral 

density in coeliac disease. Scand J Gastroenterol 

1994;29(5):457-461. No prevalence or incidence 

reported 

Valentine R J, Martin J D, Myers S I et al. 

Asymptomatic celiac and superior mesenteric artery

stenoses are more prevalent among patients with 

unsuspected renal artery stenoses. Journal of Vascular

Surgery - Official Publication, the Society for 

Vascular Surgery and International Society for 

Cardiovascular Surgery, North American Chapter 

1991;14(2):195-199. No prevalence or incidence 

reported 

A-578
Valentini R A, Andreani M L, Corazza G R et al. IgA 

endomysium antibody: a valuable tool in the screening 

of coeliac disease but not its follow-up. Ital J

Gastroenterol 1994;26(6):279-282. No prevalence or 

incidence reported 

Valentino R, Savastano S, Tommaselli A P et al. 

Prevalence of coeliac disease in patients with thyroid 

autoimmunity. Horm Res 1999;51(3):124-127. No 

prevalence or incidence reported

Valentino Rossella, Savastano Silvia, Maglio Maria et

al. Markers of potential coeliac disease in patients

with Hashimoto's thyroiditis. Eur J Endocrinol 

2002;146(4):479-483. No prevalence or incidence 

reported 

Valleta E A, Mastella G. Incidence of celiac disease in

a cystic fibrosis population. Acta Paediatr Scand

1989;78(5):784-785. No prevalence or incidence 

reported 

Valletta E A, Trevisiol D, Mastella G. IgA anti-gliadin

antibodies in the monitoring of gluten challenge in 

celiac disease. J Pediatr Gastroenterol Nutr 

1990;10(2):169-173. No prevalence or incidence 

reported 

Valman H B. Proceedings: Diet and growth after

resection of ileum in childhood. Gut 

1974;15(10):822No prevalence or incidence reported 

van Belzen M J, Mulder C J, Pearson P L et al. The 

tissue transglutaminase gene is not a primary factor 

predisposing to celiac disease. Am J Gastroenterol 

2001;96(12):3337-3340. No prevalence or incidence 

reported 

Van Cutsem E, Vantrappen G. Epidemiology and

clinical aspects of esophageal cancer. J Belge Radiol 

1991;74(5):365-368. No prevalence or incidence 

reported 

van den, Boom S A, Kimber A C et al. Weaning

practices in children up to 19 months of age in 

Madrid. Acta Paediatr 1995;84(8):853-858. No

prevalence or incidence reported

van den, Bosch H C, Tham R T et al. Celiac disease: 

small-bowel enteroclysis findings in adult patients

treated with a gluten-free diet. Radiology

1996;201(3):803-808. No prevalence or incidence 

reported 

Van den, Neucker A, Pestel N et al. Clinical use of 

acid steatocrit. Acta Paediatr 1997;86(5):466-469. No 

prevalence or incidence reported

Van der, Vliet H J J, Von Blomberg B M E et al. 

Circulating Valpha24SUP+ Vbeta11SUP+ NKT cell 

numbers are decreased in a wide variety of diseases

that are characterized by autoreactive tissue damage.

Clin Immunol 2001;100(2):144-148. No prevalence or

incidence reported 

van Elburg R M, Uil J J, Mulder C J et al. Intestinal

permeability in patients with coeliac disease and 

relatives of patients with coeliac disease. Gut 

1993;34(3):354-357. No prevalence or incidence 

reported 

van Overbeek F M, Uil-Dieterman I G, Mol I W et al. 

The daily gluten intake in relatives of patients with

coeliac disease compared with that of the general 

Dutch population. Eur J Gastroenterol Hepatol 

1997;9(11):1097-1099. No prevalence or incidence 

reported 

van Stirum J, Baerlocher K, Fanconi A et al. The 

incidence of coeliac disease in children in Switzerland.

Helv Paediatr Acta 1982;37(5):421-430. Serology

screen <1990 

Van Wouwe J P. Clinical and laboratory diagnosis of 

acrodermatitis enteropathica. Eur J Pediatr 

1989;149(1):2-8. No prevalence or incidence reported 

Vancikova Z, Chlumecky V, Sokol D et al. The 

serologic screening for celiac disease in the general 

population (blood donors) and in some high-risk 

groups of adults (patients with autoimmune diseases, 

osteoporosis and infertility) in the Czech republic. 

Folia Microbiol (Praha) 2002;47(6):753-758. Not a 

relevant screening geography

Vanelli M, de Fanti A, Adinolfi B et al. Clinical data

regarding the growth of diabetic children. Horm Res 

1992;37(Suppl 3):65-69. No prevalence or incidence 

reported 

Varkonyi A, Boda M, Endreffy E et al. Coeliac 

disease: always something to discover. Scandinavian 

Journal of Gastroenterology.Supplement 

1998;228122-129. No prevalence or incidence 

reported 

Varma S, Malhotra P, Kochhar R et al. Celiac disease 

presenting as iron-deficiency anemia in northern India. 

Indian Journal of Gastroenterology - Official Journal 

of the Indian Society of Gastroenterology

2001;20(6):234-236. Not a relevant screening 

geography

Vartdal F, Johansen B H, Friede T et al. The peptide 

binding motif of the disease associated HLA-DQ 

(alpha 1* 0501, beta 1* 0201) molecule. Eur J 

Immunol 1996;26(11):2764-2772. No prevalence or 

incidence reported 

Vasquez H, Mazure R, Gonzalez D et al. Risk of 

fractures in celiac disease patients: a cross-sectional,

case-control study. Am J Gastroenterol

2000;95(1):183-189. No prevalence or incidence 

reported 

A-579
Vazquez H, Cabanne A, Sugai E et al. Serological

markers identify histologically latent coeliac disease 

among first-degree relatives. Eur J Gastroenterol 

Hepatol 1996;8(1):15-21. Not a relevant screening 

geography

Vazquez H, Smecuol E, Flores D et al. Relation 

between cigarette smoking and celiac disease:

evidence from a case-control study. Am J

Gastroenterol 2001;96(3):798-802. No prevalence or 

incidence reported 

Vazquez H, Sugai E, Pedreira S et al. Screening for 

asymptomatic celiac sprue in families. J Clin 

Gastroenterol 1995;21(2):130-133. No prevalence or 

incidence reported 

Vecchi M, Bianchi M B, Sinico R A et al. Antibodies

to neutrophil cytoplasm in Italian patients with 

ulcerative colitis: sensitivity, specificity and

recognition of putative antigens. Digestion 

1994;55(1):34-39. No prevalence or incidence 

reported 

Vecchi M, Folli C, Donato M F et al. High rate of

positive anti-tissue transglutaminase antibodies in

chronic liver disease. Role of liver decompensation 

and of the antigen source. Scand J Gastroenterol 

2003;38(1):50-54. No prevalence or incidence 

reported 

Veitch A M, Kelly P, Zulu I S et al. Tropical

enteropathy: a T-cell-mediated crypt hyperplastic

enteropathy. Eur J Gastroenterol Hepatol 

2001;13(10):1175-1181. No prevalence or incidence 

reported 

Velluzzi F, Caradonna A, Boy M F et al. Thyroid and 

celiac disease: clinical, serological, and echographic 

study. Am J Gastroenterol 1998;93(6):976-979. No 

prevalence or incidence reported

Ventura A, Magazzu G, Greco L. Duration of

exposure to gluten and risk for autoimmune disorders 

in patients with celiac disease. SIGEP Study Group for 

Autoimmune Disorders in Celiac Disease.

Gastroenterology 1999;117(2):297-303. No 

prevalence or incidence reported

Ventura A, Neri E, Ughi C et al. Gluten-dependent 

diabetes-related and thyroid-related autoantibodies in 

patients with celiac disease. Eur J Pediatr

2000;137(2):263-265. No prevalence or incidence 

reported 

Venturini I, Cosenza R, Miglioli L et al. Adult celiac

disease and primary sclerosing cholangitis: two case 

reports. Hepatogastroenterology 1998;45(24):2344-

2347. No prevalence or incidence reported 

Verge C F, Howard N J, Rowley M J et al. Antiglutamate decarboxylase and other antibodies at the 

onset of childhood IDDM: a population-based study. 

Diabetologia 1994;37(11):1113-1120. No prevalence 

or incidence reported 

Verkarre V, Asnafi V, Lecomte T et al. Refractory

coeliac sprue is a diffuse gastrointestinal disease. Gut 

2003;52(2):205-211. No prevalence or incidence 

reported 

Verkasalo M, Kuitunen P, Leisti S et al. Growth 

failure from symptomless celiac disease. A study of 14 

patients. Helv Paediatr Acta 1978;33(6):489-495. No 

prevalence or incidence reported

Verkasalo M, Kuitunen P, Savilahti E et al. Changing 

pattern of cow's milk intolerance. An analysis of the 

occurrence and clinical course in the 60s and mid-70s. 

Acta Paediatr Scand 1981;70(3):289-295. No 

prevalence or incidence reported

Vermeer B J, Lindeman J, Harst-Oostveen C J et al.

The immunoglobulin-bearing cells in the lamina 

propria and the clinical response to a gluten-free diet 

in dermatitis herpetiformis. Archives for 

Dermatological Research.Archiv Fur Dermatologische 

Forschung 1977;258(3):223-230. No prevalence or

incidence reported 

Vestergaard Peter, Mosekilde Leif. Fracture risk in 

patients with celiac Disease, Crohn's disease, and

ulcerative colitis: a nationwide follow-up study of

16,416 patients in Denmark. Am J Epidemiol 

2002;156(1):1-10. No prevalence or incidence 

reported 

Vestergaard Peter. Bone loss associated with 

gastrointestinal disease: prevalence and pathogenesis. 

Eur J Gastroenterol Hepatol 2003;15(8):851-856. No 

prevalence or incidence reported

Veyrieres M, Baillet P, Hay J M et al. Factors 

influencing long-term survival in 100 cases of small 

intestine primary adenocarcinoma. Am J Surg 

1997;173(3):237-239. No prevalence or incidence 

reported 

Visakorpi J K, Kuitunen P, Savilahti E. Frequency and 

nature of relapses in children suffering from the 

malabsorption syndrome with gluten intolerance. Acta

Paediatr Scand 1970;59(5):481-486. No prevalence or

incidence reported 

Vissers M, Doekes G, Heederik D. Exposure to wheat 

allergen and fungal alpha-amylase in the homes of

bakers. Clinical and Experimental Allergy - Journal of

the British Society for Allergy and Clinical

Immunology 2001;31(10):1577-1582. No prevalence 

or incidence reported 

Viteri F E, Schneider R E. Gastrointestinal alterations 

in protein-calorie malnutrition. Med Clin North Am

A-580
1974;58(6):1487-1505. No prevalence or incidence 

reported 

Vivas Santiago, Ruiz de, Morales Jose M et al. Human 

recombinant anti-transglutaminase antibody testing is

useful in the diagnosis of silent coeliac disease in a 

selected group of at-risk patients. Eur J Gastroenterol 

Hepatol 2003;15(5):479-483. No prevalence or

incidence reported 

Vjero K, Martucci S, Alvisi C et al. Defining a proper 

setting for endoscopy in coeliac disease. Eur J 

Gastroenterol Hepatol 2003;15(6):675-678. No

prevalence or incidence reported

Vlissides D N, Venulet A, Jenner F A. A double-blind 

gluten-free/gluten-load controlled trial in a secure

ward population. Br J Psychiatry 1986;148447-452. 

No prevalence or incidence reported 

Vogelsang H, Oberhuber G, Wyatt J. Lymphocytic 

gastritis and gastric permeability in patients with

celiac disease. Gastroenterology 1996;111(1):73-77. 

No prevalence or incidence reported 

Vogelsang H, Schwarzenhofer M, Granditsch G et al. 

In vitro production of endomysial antibodies in

cultured duodenal mucosa from patients with celiac 

disease. Am J Gastroenterol 1999;94(4):1057-1061. 

No prevalence or incidence reported 

Vogelsang H, Schwarzenhofer M, Oberhuber G. 

Changes in gastrointestinal permeability in celiac

disease. Dig Dis 1998;16(6):333-336. No prevalence 

or incidence reported 

Vogelsang H, Schwarzenhofer M, Steiner B et al. In 

vivo and in vitro permeability in coeliac disease.

Aliment Pharmacol Ther 2001;15(9):1417-1425. No 

prevalence or incidence reported

Vogelsang H, Suk E K, Janisiw M et al. Calcaneal 

ultrasound attenuation and vitamin-D-receptor 

genotypes in celiac disease. Scand J Gastroenterol 

2000;35(2):172-176. No prevalence or incidence 

reported 

Vogelsang H, Wyatt J, Penner E et al. Screening for 

celiac disease in first-degree relatives of patients with 

celiac disease by lactulose/mannitol test. Am J

Gastroenterol 1995;90(10):1838-1842. Not a relevant 

screening test 

Vogelsang H. The changing features of celiac disease.

Preface. Dig Dis 1998;16(6):328-329. No prevalence 

or incidence reported 

Vogelsang Harald, Panzer Simon, Mayr Wolfgang R 

et al. Distribution of HLA class I alleles differs in

celiac disease patients according to age of onset. Dig 

Dis Sci 2003;48(3):611-614. No prevalence or

incidence reported 

Volta U, Bonazzi C, Baldoni A M et al. Clinical

presentation of adult coeliac disease. Ann Med Interne

(Paris) 1988;139(2):123-124. No prevalence or

incidence reported 

Volta U, Bonazzi C, Pisi E et al. Antigliadin and 

antireticulin antibodies in coeliac disease and at onset 

of diabetes in children. Lancet 1987;2(8566):1034-

1035. No prevalence or incidence reported 

Volta U, De Franceschi L, Lari F et al. Coeliac disease 

hidden by cryptogenic hypertransaminasaemia. Lancet

1998;352(9121):26-29. No prevalence or incidence 

reported 

Volta U, De Franceschi L, Molinaro N et al. 

Frequency and significance of anti-gliadin and antiendomysial antibodies in autoimmune hepatitis. Dig 

Dis Sci 1998;43(10):2190-2195. No prevalence or

incidence reported 

Volta U, De Franceschi L, Molinaro N et al. Organspecific autoantibodies in coeliac disease: do they 

represent an epiphenomenon or the expression of 

associated autoimmune disorders?. Ital J Gastroenterol

Hepatol 1997;29(1):18-21. No prevalence or incidence 

reported 

Volta U, De Giorgio R, Petrolini N et al. Clinical

findings and anti-neuronal antibodies in coeliac

disease with neurological disorders. Scand J

Gastroenterol 2002;37(11):1276-1281. No prevalence 

or incidence reported 

Volta U, Granito A, De Franceschi L et al. Anti tissue

transglutaminase antibodies as predictors of silent 

coeliac disease in patients with 

hypertransaminasaemia of unknown origin. Digestive 

and Liver Disease - Official Journal of the Italian

Society of Gastroenterology and the Italian

Association for the Study of the Liver 2001;33(5):420-

425. No prevalence or incidence reported 

Volta U, Lenzi M, Lazzari R et al. Antibodies to

gliadin detected by immunofluorescence and a microELISA method: markers of active childhood and adult 

coeliac disease. Gut 1985;26(7):667-671. No 

prevalence or incidence reported

Volta U, Molinaro N, De Franceschi L et al. Human 

umbilical cord as substrate for IgA antiendomysial 

antibodies allows large scale screening for celiac 

sprue. J Clin Gastroenterol 1996;23(1):18-20. Not a 

relevant screening group 

Volta U, Molinaro N, De Franceschi L et al. IgA antiendomysial antibodies on human umbilical cord tissue 

for celiac disease screening. Save both money and 

monkeys. Dig Dis Sci 1995;40(9):1902-1905. No

prevalence or incidence reported

A-581
Volta U, Ravaglia G, Granito A et al. Coeliac disease

in patients with autoimmune thyroiditis. Digestion 

2001;64(1):61-65. No prevalence or incidence 

reported 

Volta Umberto, Rodrigo Luis, Granito Alessandro et 

al. Celiac disease in autoimmune cholestatic liver

disorders. Am J Gastroenterol 2002;97(10):2609-

2613. No prevalence or incidence reported 

Von Muhlendahl K E, Herkenhoff H. Long-term 

course of neonatal diabetes. N Engl J Med

1995;333(11):704-708. No prevalence or incidence 

reported 

von Tirpitz, Christian Reinshagen, Max. Management 

of osteoporosis in patients with gastrointestinal 

diseases. Eur J Gastroenterol Hepatol 2003;15(8):869-

876. No prevalence or incidence reported 

Wahab P J, Hopman W P, Jansen J B. Basal and fatstimulated plasma peptide YY levels in celiac disease. 

Dig Dis Sci 2001;46(11):2504-2509. No prevalence or

incidence reported 

Wahab P J, Meijer J W R, Goerres M S et al. Coeliac

disease: changing views on gluten-sensitive

enteropathy. Scandinavian Journal of

Gastroenterology.Supplement 2002;(236):60-65. No 

prevalence or incidence reported

Wahab Peter J, Meijer Jos W R, Dumitra Daniela et al. 

Coeliac disease: more than villous atrophy. Rom J

Gastroenterol 2002;11(2):121-127. No prevalence or 

incidence reported 

Wahab Peter J, Meijer Jos W R, Mulder Chris J J.

Histologic follow-up of people with celiac disease on 

a gluten-free diet: slow and incomplete recovery. Am

J Clin Pathol 2002;118(3):459-463. No prevalence or

incidence reported 

Walker W A. Immunology: Editorial overview. Curr 

Opin Gastroenterol 1991;7(3):418-420. No prevalence 

or incidence reported 

Walker-Smith J A, Grigor W. Coeliac disease in a

diabetic child. Lancet 1969;1(7603):1021No 

prevalence or incidence reported

Walker-Smith J A, Reye R D. Small intestinal

morphology in aboriginal children. Aust N Z J Med 

1971;1(4):377-384. No prevalence or incidence 

reported 

Walker-Smith J A, Talley N A. Coeliac disease and 

dermatitis herpetiformis. Med J Aust 1973;1(1):10-12. 

No prevalence or incidence reported 

Walker-Smith J A, Vines R, Grigor W. Coeliac 

disease and diabetes. Lancet 1969;2(7621):650No 

prevalence or incidence reported

Walker-Smith J A. Celiac disease and Down 

syndrome. Eur J Pediatr 2000;137(6):743-744. No 

prevalence or incidence reported

Walker-Smith J A. Coeliac disease in children of

Asian immigrants. Lancet 1973;1(7800):428No 

prevalence or incidence reported

Walker-Smith J A. Diabetes and coeliac disease.

Lancet 1969;2(7634):1366No prevalence or incidence 

reported 

Walmsley R S, Ibbotson J P, Chahal H et al. 

Antibodies against Mycobacterium paratuberculosis in 

Crohn's disease. Qjm - Monthly Journal of the 

Association of Physicians 1996;89(3):217-221. No 

prevalence or incidence reported

Walsh C H, Cooper B T, Wright A D et al. Diabetes

mellitus and coeliac disease: a clinical study. Q J Med 

1978;47(185):89-100. No prevalence or incidence 

reported 

Walsh D. Coeliac disease and schizophrenia. Br Med J 

1973;2(5860):242No prevalence or incidence reported 

Walsh S V, Egan L J, Connolly C E et al. 

Enteropathy-associated T-cell lymphoma in the West 

of Ireland: low-frequency of Epstein-Barr virus in

these tumors. Modern Pathology - an Official Journal 

of the United States and Canadian Academy of

Pathology, Inc 1995;8(7):753-757. No prevalence or 

incidence reported 

Walters J R F, Banks L M, Butcher G P et al. 

Detection of low bone mineral density by dual energy

x ray absorptiometry in unsuspected suboptimally

treated coeliac disease. Gut 1995;37(2):220-224. No 

prevalence or incidence reported

Walters J R. Bone mineral density in coeliac disease. 

Gut 1994;35(2):150-151. No prevalence or incidence 

reported 

Warngard O, Stenhammar L, Ascher H et al. Small 

bowel biopsy in Swedish paediatric clinics. Acta 

Paediatr 1996;85(2):240-241. No prevalence or

incidence reported 

Wasmuth H E, Matern S. Nutrition in childhood and 

immune-mediated diseases. Ann Nestle 

2002;60(1):22-31. No prevalence or incidence 

reported 

Weile B, Cavell B, Nivenius K et al. Striking 

differences in the incidence of childhood celiac 

disease between Denmark and Sweden: a plausible 

explanation. J Pediatr Gastroenterol Nutr 

1995;21(1):64-68. Serology screen <1990 

Weile B, Krasilnikoff P A. Low incidence rates by

birth of symptomatic coeliac disease in a Danish

A-582
population of children. Acta Paediatr 1992;81(5):394-

398. Serology screen <1990 

Weile B. Aspects of classic symptomatic childhood 

coeliac disease in Denmark: Retrospectively 

illustrated by local, regional, and national studies.

APMIS Suppl 2003;111(113):5-46. Review article 

Weile Birgitte, Heegaard Niels H H, Hoier-Madsen 

Mimi et al. Tissue transglutaminase and endomysial 

autoantibodies measured in an historical cohort of

children and young adults in whom coeliac disease 

was suspected. Eur J Gastroenterol Hepatol 

2002;14(1):71-76. No prevalence or incidence 

reported 

Weinstein W M, Brow J R, Parker F et al. The small 

intestinal mucosa in dermatitis herpetiformis. II. 

Relationship of the small intestinal lesion to gluten. 

Gastroenterology 1971;60(3):362-369. No prevalence 

or incidence reported 

Weir D G, Hourihane D O. Coeliac disease during the

teenage period: the value of serial serum folate 

estimations. Gut 1974;15(6):450-457. No prevalence 

or incidence reported 

Weir D G. The pathogenesis of folic acid deficiency in

man. Ir J Med Sci 1974;143(1):3-20. No prevalence or

incidence reported 

Weizman Z, Ben Zion Y Z, Binsztok M et al. 

Correlation of clinical characteristics and small bowel 

histopathology in celiac disease. J Pediatr

Gastroenterol Nutr 1997;24(5):555-558. No 

prevalence or incidence reported

Weizman Z, Stringer D A, Durie P R. Radiologic 

manifestations of malabsorption: a nonspecific 

finding. Pediatrics 1984;74(4):530-533. No prevalence 

or incidence reported 

Weizman Z, Vardi O, Binsztok M. Dermatoglyphic 

(fingerprint) patterns in celiac disease. J Pediatr

Gastroenterol Nutr 1990;10(4):451-453. No 

prevalence or incidence reported

West Joe, Logan Richard F A, Card Tim R et al.

Fracture risk in people with celiac disease: a

population-based cohort study. Gastroenterology

2003;125(2):429-436. No prevalence or incidence 

reported 

West R J, Fosbrooke A S, Lloyd J K. Treatment of 

children with familial hypercholesterolaemia. Postgrad 

Med J 1975;51(8):Suppl 82-Suppl 87. No prevalence 

or incidence reported 

Westerholm-Ormio Mia, Vaarala Outi, Pihkala Paivi

et al. Immunologic activity in the small intestinal 

mucosa of pediatric patients with type 1 diabetes. 

Diabetes 2003;52(9):2287-2295. No prevalence or

incidence reported 

Westman E, Ambler G R, Royle M et al. Children 

with coeliac disease and insulin dependent diabetes

mellitus--growth, diabetes control and dietary intake. 

Journal of Pediatric Endocrinology & Metabolism - 

Jpem 1999;12(3):433-442. No prevalence or incidence 

reported 

Wharton B A. Coeliac disease in childhood. Br J Hosp 

Med 1974;12(4):452-466. No prevalence or incidence 

reported 

Wharton B, Wharton P. Nutrition in adolescence. Nutr 

Health 1987;4(4):195-203. No prevalence or incidence 

reported 

White A G, Barnetson R S C, Da Costa J A G et al. 

The incidence of HL A antigens in dermatitis

herpetiformis. Br J Dermatol 1973;89(2):133-136. No 

prevalence or incidence reported

White T T, Slavotinek A H. Results of surgical

treatment of chronic pancreatitis. Report of 142 cases. 

Ann Surg 1979;189(2):217-224. No prevalence or

incidence reported 

Whitfield C R. Obstetric sprue. J Obstet Gynaecol Br 

Commonw 1970;77(7):577-586. No prevalence or

incidence reported 

Whorwell P J, Alderson M R, Foster K J et al. Death 

from ischaemic heart-disease and malignancy in adult

patients with coeliac disease. Lancet

1976;2(7977):113-114. No prevalence or incidence 

reported 

Wicks A C, Clain D J. Chronic pancreatitis in African

diabetics. Am J Dig Dis 1975;20(1):1-8. No

prevalence or incidence reported

Wicks A C, Jones J J. Ethnic differences in coronary

heart disease. South African Medical Journal.SuidAfrikaanse Tydskrif Vir Geneeskunde 

1973;47(9):362No prevalence or incidence reported 

Wiggins H S, Pearson J R, Walker J G et al. Incidence

and significance of faecal hydroxystearic acid in

alimentary disease. Gut 1974;15(8):614-621. No

prevalence or incidence reported

Williams A J, Annis P, Lock R J et al. Evaluation of a

high-throughput second antibody radiobinding assay

for measuring IgA antibodies to human tissue 

transglutaminase. J Immunol Methods 1999;228(1-

2):81-85. No prevalence or incidence reported 

Williams A J, Asquith P, Stableforth D E.

Susceptibility to tuberculosis in patients with coeliac

disease. Tubercle 1988;69(4):267-274. No prevalence 

or incidence reported 

A-583
Williams A J, Norcross A J, Lock R J et al. The high 

prevalence of autoantibodies to tissue 

transglutaminase in first-degree relatives of patients 

with type 1 diabetes is not associated with islet 

autoimmunity. Diabetes Care 2001;24(3):504-509. 

Not a relevant screening group 

Williams C N, Dickson R C. Cholestyramine and

medium-chain triglyceride in prolonged management 

of patients subjected to ileal resection or bypass. Can 

Med Assoc J 1972;107(7):626-631. No prevalence or

incidence reported 

Williamson Debbie, Marsh Michael N. Celiac disease.

Mol Biotechnol 2002;22(3):293-299. No prevalence or

incidence reported 

Williamson N, Asquith P, Stokes L et al. 

Anticonnective tissue and other antitissue 'antibodies' 

in the sera of patients with coeliac disease compared 

with the findings in a mixed hospital population. J

Clin Pathol 1976;29(6):484-494. No prevalence or

incidence reported 

Willoughby J M T, Laitner S M. Audit of the 

investigation of iron deficiency anaemia in a distinct 

general hospital, with sample guidelines for future

practice. Postgrad Med J 2000;76(894):218-222. No 

prevalence or incidence reported

Wills A J, Unsworth D J. The neurology of gluten

sensitivity: Separating the wheat from the chaff. Curr 

Opin Neurol 2002;15(5):519-523. No prevalence or

incidence reported 

Wills A J. The neurology and neuropathology of 

coeliac disease. Neuropathol Appl Neurobiol

2000;26(6):493-496. No prevalence or incidence 

reported 

Wilson M-M. Undernutrition in medical outpatients. 

Clin Geriatr Med 2002;18(4):759-771. No prevalence 

or incidence reported 

Winklhofer-Roob B M, Rossipal E, Lanzer G. Human 

leucocyte class I and II antigens in coeliac disease: a

study in an Austrian paediatric population. Eur J 

Pediatr 1991;150(10):704-707. No prevalence or

incidence reported 

Witas H W, Mlynarski W, Rozalski M et al. Study of 

Polish coeliac patients: HLA-DQ amino acid variants 

involved in antigen presentation. Cent-Eur J Immunol 

1997;22(4):266-271. No prevalence or incidence 

reported 

Witas H W, Mlynarski W, Sychowski R.

Polymorphism of genes located on chromosome 2q is 

associated with coeliac disease. Cent-Eur J Immunol 

2001;26(1):31-36. No prevalence or incidence 

reported 

Wolters Victorien, Vooijs-Moulaert Anne, Burger

Huib et al. Human tissue transglutaminase enzyme

linked immunosorbent assay outperforms both the 

guinea pig based tissue transglutaminase assay and 

anti-endomysium antibodies when screening for 

coeliac disease. Eur J Pediatr 2002;161(5):284-287. 

No prevalence or incidence reported 

Wonke B. Clinical management of beta-thalassemia 

major. Semin Hematol 2001;38(4):350-359. No

prevalence or incidence reported

Woodruff C W. Milk intolerances. Nutr Rev 

1976;34(2):33-37. No prevalence or incidence 

reported 

Woods R K, Stoney R M, Raven J et al. Reported

adverse food reactions overestimate true food allergy

in the community. Eur J Clin Nutr 2002;56(1):31-36. 

No prevalence or incidence reported 

Woods Rosalie K, Thien Frank, Raven Joan et al. 

Prevalence of food allergies in young adults and their

relationship to asthma, nasal allergies, and eczema. 

Annals of Allergy, Asthma & Immunology - Official 

Publication of the American College of Allergy,

Asthma, & Immunology 2002;88(2):183-189. No 

prevalence or incidence reported

Woolley N, Holopainen P, Bourgain C et al. CD80 

(B7-1) and CD86 (B7-2) genes and genetic 

susceptibility to coeliac disease. European Journal of 

Immunogenetics - Official Journal of the British 

Society for Histocompatibility and Immunogenetics 

2002;29(4):331-333. No prevalence or incidence 

reported 

Woolley Niina, Holopainen Paivi, Ollikainen Vesa et

al. A new locus for coeliac disease mapped to 

chromosome 15 in a population isolate. Hum Genet 

2002;111(1):40-45. No prevalence or incidence 

reported 

Wordsworth B P, Salmon M. The HLA class II 

component of susceptibility to rheumatoid arthritis. 

Bailliere's Clin Rheumatol 1992;6(2):325-336. No

prevalence or incidence reported

Wordsworth P. PCR-SSO typing in HLA-disease 

association studies. European Journal of

Immunogenetics - Official Journal of the British 

Society for Histocompatibility and Immunogenetics 

1991;18(1-2):139-146. No prevalence or incidence 

reported 

Wright D H. Enteropathy associated T cell lymphoma. 

Cancer Surv 1997;30(-):249-261. No prevalence or

incidence reported 

Wright D H. The major complications of coeliac

disease. Bailliere's Clin Gastroenterol 1995;9(2):351-

369. No prevalence or incidence reported 

A-584
Wu T T, Hamilton S R. Lymphocytic gastritis:

association with etiology and topology. Am J Surg

Pathol 1999;23(2):153-158. No prevalence or

incidence reported 

Wucherpfennig K W. Insights into autoimmunity

gained from structural analysis of MHC-peptide

complexes. Curr Opin Immunol 2001;13(6):650-656. 

No prevalence or incidence reported 

Wurm P, Wicks A C. Iron deficiency anaemia - A

clinical challenge. Postgrad Med J 2000;76(894):193-

194. No prevalence or incidence reported 

Wyburn G M. The scanning micrograph as a clinical 

dimension. N Z Med J 1974;80(520):51-56. No

prevalence or incidence reported

Yamashiro Y. Pediatric gastroenterology in Japan: A 

personal perspective. J Pediatr Gastroenterol Nutr

2002;34(5):493-495. No prevalence or incidence 

reported 

Yeboah F A, White D. AlphaB-crystallin expression 

in celiac disease - a preliminary study. Croat Med J

2001;42(5):523-526. No prevalence or incidence 

reported 

Yiannakou J Y, Brett P M, Morris M A et al. Family

linkage study of the T-cell receptor genes in coeliac 

disease. Ital J Gastroenterol Hepatol 1999;31(3):198-

201. No prevalence or incidence reported 

Yong J M. Cause of raised serum-alkalinephosphatase after partial gastrectomy and in other

malabsorption states. Lancet 1966;1(7447):1132-1134. 

No prevalence or incidence reported 

Young W F, Pringle E M. 110 children with coeliac 

disease, 1950-1969. Arch Dis Child 

1971;46(248):421-436. No prevalence or incidence 

reported 

Zachor D A, Mroczek-Musulman E, Brown P.

Prevalence of celiac disease in Down syndrome in the

United States. J Pediatr Gastroenterol Nutr 

2000;31(3):275-279. Not a relevant screening group 

Zadik Z, Kowarski A. Incidence of neurosecretory

dysfunction among children aged 6-14 years in

Rehovot, Israel. Acta Paediatrica 

Scandinavica.Supplement 1989;34977-83. No 

prevalence or incidence reported

Zalev A H, Gardiner G W, Warren R E. NSAID injury

to the small intestine. Abdom Imaging 1998;23(1):40-

44. No prevalence or incidence reported 

Zauli D, Grassi A, Granito A et al. Prevalence of silent

coeliac disease in atopics. Digestive and Liver Disease 

- Official Journal of the Italian Society of 

Gastroenterology and the Italian Association for the 

Study of the Liver 2000;32(9):775-779. No prevalence 

or incidence reported 

Zelissen P M, Bast E J, Croughs R J. Associated 

autoimmunity in Addison's disease. J Autoimmun

1995;8(1):121-130. No prevalence or incidence 

reported 

Zhong F, McCombs C C, Olson J M et al. An 

autosomal screen for genes that predispose to celiac

disease in the western counties of Ireland. Nat Genet 

1996;14(3):329-333. No prevalence or incidence 

reported 

Ziegler Anette, Schmid Sandra, Huber Doris et al. 

Early infant feeding and risk of developing type 1 

diabetes-associated autoantibodies. Jama - the Journal 

of the American Medical Association 

2003;290(13):1721-1728. No prevalence or incidence 

reported 

Ziem G E. Profile of patients with chemical injury and 

sensitivity, part II. Int J Toxicol 1999;18(6):401-409. 

No prevalence or incidence reported 

Zins B J, Tremaine W J, Carpenter H A. Collagenous 

colitis: mucosal biopsies and association with fecal 

leukocytes. Mayo Clin Proc 1995;70(5):430-433. No 

prevalence or incidence reported

Zipser Robert D, Patel Sunil, Yahya Kareem Z et al.

Presentations of adult celiac disease in a nationwide 

patient support group. Dig Dis Sci 2003;48(4):761-

764. No prevalence or incidence reported 

Zollinger R M. Islet cell tumors of the pancreas and 

the alimentary tract. Am J Surg 1975;129(2):102-110. 

No prevalence or incidence reported 

Zubillaga P, Vitoria J C, Arrieta A et al. Down 

Syndrome and celiac disease. J Pediatr Gastroenterol 

Nutr 1993;16(2):168-171. No prevalence or incidence 

reported 

Zucca E, Roggero E, Bertoni F et al. Primary

extranodal non-Hodgkin's lymphomas. Part 1:

Gastrointestinal, cutaneous and genitourinary

lymphomas. Ann Oncol 1997;8(8):727-737. No

prevalence or incidence reported

A-585
Objective 3 – Celiac Associated Lymphoma 

Abdulkarim A S, Burgart L J, See J et al. Etiology of 

nonresponsive celiac disease: results of a systematic 

approach. Am J Gastroenterol 2002;97(8):2016-2021. 

Does not address the question 

Acalovschi M. Coeliac disease and lymphoma. Rom J 

Gastroenterol 2001;10(4):317-320. Review article 

Al Mondhiry H. Primary lymphomas of the small 

intestine: east-west contrast. Am J Hematol 

1986;22(1):89-105. Review article 

Aljurf M D, Owaidah T W, Ezzat A et al. Antigenand/or immune-driven lymphoproliferative disorders. 

Ann Oncol 2003;14(11):1595-1606. Not about celiac 

and GI lymphoma 

Andersson H, Dotevall G, Mobacken H. Malignant 

mesenteric lymphoma in a patient with dermatitis 

herpetiformis, hypochlorhydria, and small-bowel 

abnormalities. Scand J Gastroenterol 1971;6(5):397-

399. Does not address the question 

Anonymous. Coeliac disease in the elderly. Lancet 

1984;1(8380):775-776. Not about celiac and GI

lymphoma 

Anonymous. A new type intestinal lymphoma. J Clin

Pathol Mol Pathol 2002;55(5):314Not about celiac and

GI lymphoma 

Anonymous. Primary gut lymphomas. Lancet

1991;337(8754):1384-1385. Not about celiac and GI 

lymphoma 

Anonymous. A guide for patients. Pract Gastroenterol 

2002;26(11):58-61. Not about celiac and GI 

lymphoma 

Aozasa K. Villous atrophy with crypt hyperplasia in

malignant histiocytosis of the nose. J Clin Pathol 

1982;35(6):606-610. Not about celiac and GI

lymphoma 

Ashton-Key M, Diss T C, Pan L et al. Molecular 

analysis of T-cell clonality in ulcerative jejunitis and 

enteropathy-associated T-cell lymphoma. Am J Pathol 

1997;151(2):493-498. Does not address the question 

Asquith P. Adult coeliac disease and malignancy. Ir 

Med J 1974;67(15):417-420. Review article 

Austad W I, Cornes J S, Gough K R et al. Steatorrhea 

and malignant lymphoma. The relationship of 

malignant tumors of lymphoid tissue and celiac 

disease. Am J Dig Dis 1967;12(5):475-490. Does not 

address the question 

Baer A N, Bayless T M, Yardley J H. Intestinal 

ulceration and malabsorption syndromes. 

Gastroenterology 1980;79(4):754-765. Not about 

celiac and GI lymphoma 

Bagdi E, Diss T C, Munson P et al. Mucosal intraepithelial lymphocytes in enteropathy-associated Tcell lymphoma, ulcerative jejunitis, and refractory

celiac disease constitute a neoplastic population. 

Blood 1999;94(1):260-264. Does not address the 

question 

Bank S, Marks I N, Novis B. Progress in small-bowel 

physiology and disease. South African Medical

Journal.Suid-Afrikaanse Tydskrif Vir Geneeskunde 

1971;45(41):1141-1144. Not about celiac and GI 

lymphoma 

Barry R E. Coeliac disease and malignancy. Tijdschr 

Gastroenterol 1973;16(1):23-34. Does not address the 

question 

Barry R E, Read A E. Coeliac disease and malignancy.

Qjm - Monthly Journal of the Association of

Physicians 1973;42(168):665-675. Not about celiac 

and GI lymphoma 

Barry R E, Read A E. Two types of 'coeliac' disease?. 

Gut 1972;13(10):846-847. Not about celiac and GI 

lymphoma 

Barry R E, Baker P, Read A E. Coeliac disease. The 

clinical presentation. Clin Gastroenterol 1974;3(1):55-

69. Not about celiac and GI lymphoma 

Barry R E, Morris J S, Kenwright S et al. Coeliac 

disease and malignancy. The possible importance of 

familial involvement. Scand J Gastroenterol 

1971;6(3):205-207. Not about celiac and GI 

lymphoma 

Bell S, Green P H R, Kagnoff M F. American 

gastroenterological association medical position

statement: Celiac sprue. Gastroenterology

2001;120(6):1522-1525. Not about celiac and GI 

lymphoma 

Berndt H. Malabsorption in cancer of and outside the 

bowel. Digestion 1968;1(5):305-310. Not about celiac 

and GI lymphoma 

Biagi F, Corazza G R. Defining gluten refractory 

enteropathy. Eur J Gastroenterol Hepatol 

2001;13(5):561-565. Not about celiac and GI

lymphoma 

Biagi F, Lorenzini P, Corazza G R. Literature review

on the clinical relationship between ulcerative 

A-586
jejunoileitis, coeliac disease, and enteropathyassociated T-cell. Scand J Gastroenterol 

2000;35(8):785-790. Review article 

Bontems P, Deprettere A, Cadranel S et al. The

coeliac iceberg: A consensus in paediatrics. Acta

Gastro-Enterol Belg 2000;63(2):157-162. Not about 

celiac and GI lymphoma 

Booth S N, King J P G, Leonard J C et al. Serum 

carcinoembryonic antigen in clinical disorders. Gut 

1973;14(10):794-799. Not about celiac and GI 

lymphoma 

Boucher B J, Wright J T. Steatorrhoea and jejunal 

reticulum cell sarcoma occurring in a patient on longterm colchicine therapy for gout. Postgrad Med J 

1973;49(568):106-107. Not about celiac and GI

lymphoma 

Bourke M A, McLoughlin D M, Stevens F M et al. 

Serum lysozyme: is it a useful marker of malignant 

lymphoma in coeliac disease?. Ir J Med Sci 

1983;152(3):125-128. Not about celiac and GI 

lymphoma 

Brandborg L L. Histologic diagnosis of diseases of 

malabsorption. Am J Med 1979;67(6):999-1006. Not 

about celiac and GI lymphoma 

Brandt L, Hagander B, Norden A et al. Lymphoma of 

the small intestine in adult coeliac disease. Acta Med 

Scand 1978;204(6):467-470. Does not address the 

question 

Brunt P W, Sircus W, Maclean N. Neoplasia and the

coeliac syndrome in adults. Lancet 1969;1(7587):180-

184. Not about celiac and GI lymphoma 

Brunton F J, Guyer P B. Malignant histiocytosis and 

ulcerative jejunitis of the small intestine. Clin Radiol 

1983;34(3):291-295. Not about celiac and GI

lymphoma 

Brzechwa-Ajdukiewicz A, McCarthy C F, Austad W

et al. Carcinoma, villous atrophy, and steatorrhoea. 

Gut 1966;7(6):572-577. Not about celiac and GI 

lymphoma 

Buckley D B, English J, Molloy W et al. Dermatitis 

herpetiformis: a review of 119 cases. Clin Exp

Dermatol 1983;8(5):477-487. Not about celiac and GI 

lymphoma 

Burrows F G, Toye D K. Coeliac disease. Barium

studies. Clin Gastroenterol 1974;3(1):91-107. Not 

about celiac and GI lymphoma 

Cammarota G, Tursi A, Papa A et al. Helicobacter 

pylori, gastric mucosa-associated lymphoid tissue and 

autoimmune thyroid diseases. Gastroenterol Int

1997;10(SUPPL. 1):43-45. Not about celiac and GI 

lymphoma 

Carbonnel F, D'Almagne H, Lavergne A et al. The 

clinicopathological features of extensive small 

intestinal CD4 T cell infiltration. Gut 1999;45(5):662-

667. Not about celiac and GI lymphoma 

Carbonnel F, Grollet-Bioul L, Brouet J C et al. Are 

complicated forms of celiac disease cryptic T-cell

lymphomas?. Blood 1998;92(10):3879-3886. Does not 

address the question 

Carroccio A, Iannitto E, Di Prima L et al. Screening 

for celiac disease in non-Hodgkin's lymphoma 

patients: a serum anti-transglutaminase-based

approach. Dig Dis Sci 2003;48(8):1530-1536. Not 

about celiac and GI lymphoma 

Casellas F, Chicharro L, Malagelada J R. Potential 

usefulness of hydrogen breath test with D-xylose in 

clinical management of intestinal malabsorption. Dig 

Dis Sci 1993;38(2):321-327. Not about celiac and GI 

lymphoma 

Catassi C, Fabiani E, Corrao G et al. Risk of nonHodgkin lymphoma in celiac disease. Jama - the 

Journal of the American Medical Association

2002;287(11):1413-1419. Risk of CD in lymphoma 

Ceccarelli M, Cortigiani L, Ughi C et al. Placental 

isoferritin as a marker of immune system involvement 

in coeliac disease. Riv Ital Pediatr 1990;16(3):300-

302. Not about celiac and GI lymphoma 

Cellier C, Cuillerier E, Patey-Mariaud de et al. Push 

enteroscopy in celiac sprue and refractory sprue.

Gastrointest Endosc 1999;50(5):613-617. Not about 

celiac and GI lymphoma 

Cellier C, Delabesse E, Helmer C et al. Refractory 

sprue, coeliac disease, and enteropathy-associated Tcell lymphoma. French Coeliac Disease Study Group. 

Lancet 2000;356(9225):203-208. Pathogenesis only

Cellier C, Patey N, Mauvieux L et al. Abnormal 

intestinal intraepithelial lymphocytes in refractory

sprue. Gastroenterology 1998;114(3):471-481. Not 

about celiac and GI lymphoma 

Cello J P. Inflammatory and malignant diseases of the

small bowel causing malabsorption. Clin 

Gastroenterol 1983;12(2):511-532. Not about celiac 

and GI lymphoma 

Cerf-Bensussan N, Brousse N, Cellier C. From 

hyperplasia to T cell lymphoma. Gut 2002;51(3):304-

305. Review article 

Chantar C, Escartin P, Plaza A G. Diffuse plasma cell 

infiltration of the small intestine with malabsorption 

associated to IgA monoclonal gammapathy. Cancer 

A-587
1974;34(5):1620-1630. Not about celiac and GI

lymphoma 

Cheng H, Wang J, Zhang C et al. Clinicopathologic 

study of mucosa-associated lymphoid tissue 

lymphoma in gastroscopic biopsy. World Journal of 

Gastroenterology - Wjg 2003;9(6):1270-1272. Not 

about celiac and GI lymphoma 

Chott A, Dragosics B, Radaszkiewicz T. Peripheral Tcell lymphomas of the intestine. Am J Pathol 

1992;141(6):1361-1371. Does not address the question 

Chott A, Haedicke W, Mosberger I et al. Most

CD56sup + intestinal lymphomas are CD8sup 

+CD5sup - T-cell lymphomas of monomorphic small 

to medium size histology. Am J Pathol 

1998;153(5):1483-1490. Not about celiac and GI 

lymphoma 

Ciacci C, Squillante A, Rendina D et al. Helicobacter

pylori infection and peptic disease in coeliac disease. 

Eur J Gastroenterol Hepatol 2000;12(12):1283-1287. 

Not about celiac and GI lymphoma 

Ciclitira Paul J, Moodie Simon J. Transition of care 

between paediatric and adult gastroenterology. Coeliac 

disease. Best Practice & Research.Clinical

Gastroenterology 2003;17(2):181-195. Not about 

celiac and GI lymphoma 

Cluysenaer O J J, Van Tongeren J H M. The natural 

history of coeliac sprue, and factors which may

influence it. Neth J Med 1978;21(1):35-43. Not about 

celiac and GI lymphoma 

Collin P, Reunala T, Pukkala E et al. Coeliac disease--

associated disorders and survival. Gut

1994;35(9):1215-1218. Double publication of 

included data 

Connon J J, McFarland J, Kelly A. Acute abdominal 

complications of coeliac disease. Scand J

Gastroenterol 1975;10(8):843-846. Not about celiac 

and GI lymphoma 

Cooke W T, Thompson H, Williams J A. Malignancy

and adult coeliac disease. Gut 1969;10(2):108-111. 

Not a controlled study

Cooper B T, Read A E. Small intestinal lymphoma. 

World J Surg 1985;9(6):930-937. Review article 

Cooper B T, Read A E. Coeliac disease and 

lymphoma. Qjm - Monthly Journal of the Association 

of Physicians 1987;63(240):269-274. Review article 

Cooper B T, Holmes G K T, Ferguson R. Celiac 

disease and malignancy. Medicine 1980;59(4):249-

261. Not a controlled study

Cooper B T, Holmes G K, Cooke W T. Lymphoma 

risk in coeliac disease of later life. Digestion 

1982;23(2):89-92. Double publication of included data 

Cooper B T, Ukabam S O, Barry R E et al. Serum 

lysozyme activity in coeliac disease: A possible aid to

the diagnosis of malignant change. J Clin Pathol 

1981;34(12):1358-1360. Not about celiac and GI 

lymphoma 

Cooper D L, Doria R, Salloum E. Primary

gastrointestinal lymphomas. Gastroenterologist 

1996;4(1):54-64. Not about celiac and GI lymphoma 

Corazza G R, Di Stefano M, Ciccocioppo R et al. 

Immune-mediated complications of coeliac disease. 

Int J Immunopathol Pharmacol 1997;10(2 Suppl):83-

85. Not about celiac and GI lymphoma 

Corazza G R, Zoli G, Di Sabatino A et al. A 

reassessment of splenic hypofunction in celiac disease.

Am J Gastroenterol 1999;94(2):391-397. Not about 

celiac and GI lymphoma 

Cornes J S. Hodgkin's disease of the gastrointestinal 

tract. Proc R Soc Med 1967;60(8):732-733. Not about 

celiac and GI lymphoma 

Crabbe P A, Heremans J F. Normal and defective 

production of immunoglobulins in the intestinal tract. 

Bibl Paediatr 1968;87161-181. Not about celiac and 

GI lymphoma 

Cronin C C, Shanahan F. Exploring the iceberg - The 

spectrum of celiac disease. Am J Gastroenterol

2003;98(3):518-520. Not about celiac and GI

lymphoma 

Crump M, Gospodarowicz M, Shepherd F A.

Lymphoma of the gastrointestinal tract. Semin Oncol 

1999;26(3):324-337. Review article 

Cuillerier E, Landi B, Cellier C. Is push enteroscopy

useful in patients with malabsorption of unclear

origin?. Am J Gastroenterol 2001;96(7):2103-2106. 

Not about celiac and GI lymphoma 

Cuoco L, Cammarota G, Tursi A et al. Disappearance 

of gastric mucosa-associated lymphoid tissue in

coeliac patients after gluten withdrawal. Scand J

Gastroenterol 1998;33(4):401-405. Not about celiac 

and GI lymphoma 

Czaja A J. Autoimmune liver disease. Curr Opin

Gastroenterol 1999;15(3):240-248. Not about celiac 

and GI lymphoma 

D'Agostino L, Ciacci C, Daniele B et al. Postheparin 

plasma diamine oxidase in subjects with small bowel 

mucosal atrophy. Dig Dis Sci 1987;32(3):313-317. 

Not about celiac and GI lymphoma 

A-588
D'Agostino L, Contegiacomo A, Pignata S et al. 

Plasma postheparin diamine oxidase in patients with 

small intestinal lymphoma. Cancer 1991;67(2):511-

515. Not about celiac and GI lymphoma 

D'Agostino L, Daniele B, Pignata S et al. Postheparin 

plasma diamine oxidase in subjects with small bowel 

disease. Diagnostic efficiency of a simplified test. 

Digestion 1988;41(1):46-54. Not about celiac and GI 

lymphoma 

Daum S, Weiss D, Hummel M et al. Frequency of

clonal intraepithelial T lymphocyte proliferations in 

enteropathy-type intestinal T cell lymphoma, coeliac 

disease, and refractory sprue. Gut 2001;49(6):804-812. 

Does not address the question 

David T J, Ajdukiewicz A B, Read A E. Dermal and 

epidermal ridge atrophy in celiac sprue.

Gastroenterology 1973;64(4):539-544. Not about 

celiac and GI lymphoma 

de Bruin P C, Jiwa N M, Oudejans J J et al. EpsteinBarr virus in primary gastrointestinal T cell

lymphomas. Association with gluten-sensitive 

enteropathy, pathological features, and

immunophenotype. Am J Pathol 1995;146(4):861-867. 

Not about celiac and GI lymphoma 

de Bruin P C, Kummer J A, van der V et al. Granzyme 

B-expressing peripheral T-cell lymphomas: neoplastic 

equivalents of activated cytotoxic T cells with

preference for mucosa-associated lymphoid tissue 

localization. Blood 1994;84(11):3785-3791. Not about 

celiac and GI lymphoma 

De Giacomo C, Gianatti A, Negrini R et al.

Lymphocytic gastritis: a positive relationship with

celiac disease. Eur J Pediatr 1994;124(1):57-62. Not 

about celiac and GI lymphoma 

Deprez Pierre H, Sempoux Christine, De Saeger et al. 

Expression of cholecystokinin in the duodenum of

patients with coeliac disease: respective role of 

atrophy and lymphocytic infiltration. Clinical Science 

(London, England - 1979) 2002;103(2):171-177. Not 

about celiac and GI lymphoma 

Devi Rampertab S, Fleischauer A, Neugut A I et al. 

Risk of duodenal adenoma in celiac disease. Scand J 

Gastroenterol 2003;38(8):831-833. Not about celiac 

and GI lymphoma 

Dewar D, Pereira S P, Ciclitira P J. The pathogenesis 

of coeliac disease. Int J Biochem Cell Biol

2004;36(1):17-24. Not about celiac and GI lymphoma 

Dickey W. Colon neoplasia co-existing with coeliac

disease in older patients: coincidental, probably;

important, certainly. Scand J Gastroenterol 

2002;37(9):1054-1056. Not about celiac and GI

lymphoma 

Dieterich W, Ehnis T, Bauer M et al. Identification of 

tissue transglutaminase as the autoantigen of celiac 

disease. Nat Med 1997;3(7):797-801. Review article 

Dinari G, Zahavi I, Marcus H et al. Placental ferritin 

in coeliac disease: relation to clinical stage, origin, and

possible role in the pathogenesis of malignancy. Gut 

1991;32(9):999-1003. Does not address the question 

Doe W F. An overview of intestinal immunity and 

malabsorption. Am J Med 1979;67(6):1077-1084. Not 

about celiac and GI lymphoma 

Douglas A P. The immunological basis of coeliac 

disease. Front Gastrointest Res 1975;149-73. Not 

about celiac and GI lymphoma 

Driessen A, Ectors N. Lymphomas of the gastrointestinal tract: Uncommon types: LYMPHOMES DU 

TRACTUS GASTRO-INTESTINAL: TYPES

RARES. Acta Endoscopica 2003;33(3):327-345. Not 

about celiac and GI lymphoma 

Duffy L F. Gastrointestinal manifestations in AIDS. 

Pediatr AIDS HIV Infect 1993;4(3):151-156. Not 

about celiac and GI lymphoma 

Dutz W, Asvadi S, Sadri S et al. Intestinal lymphoma

and sprue: a systematic approach. Gut

1971;12(10):804-810. Does not address the question 

Egan C A, O'Loughlin S, Gormally S et al. Dermatitis

Herpetiformis: a review of fifty-four patients. Ir J Med 

Sci 1997;166(4):241-244. Not about celiac and GI 

lymphoma 

Egan L J, Walsh S V, Stevens F M et al. Celiacassociated lymphoma. A single institution experience

of 30 cases in the combination chemotherapy era. J 

Clin Gastroenterol 1995;21(2):123-129. Does not 

address the question 

Elsborg L, Mosbech J. Sprue: a follow-up study of an 

old series. Dan Med Bull 1978;25(5):205-206. Not 

about celiac and GI lymphoma 

Ermacora E, Prampolini L, Tribbia G. Long-term 

follow-up of dermatitis herpetiformis in children. J 

Am Acad Dermatol 1986;15(1):24-30. Not about 

celiac and GI lymphoma 

Farrell R J, Kelly C P. Diagnosis of celiac sprue. Am J 

Gastroenterol 2001;96(12):3237-3246. Not about 

celiac and GI lymphoma 

Farstad I N, Lundin K E A. Gastrointestinal

intraepithelial lymphocytes and T cell lymphomas. 

Gut 2003;52(2):163-164. Not about celiac and GI 

lymphoma 

Farstad I N, Johansen F-E, Vlatkovic L et al. 

Heterogeneity of intraepithelial lymphocytes in

A-589
refractory sprue: Potential implications of CD30 

expression. Gut 2002;51(3):372-378. Not about celiac 

and GI lymphoma 

Farthing M J, Rees L H, Edwards C R et al. Male 

gonadal function in coeliac disease: 2. Sex hormones. 

Gut 1983;24(2):127-135. Not about celiac and GI 

lymphoma 

Feeley K M, Heneghan M A, Stevens F M et al. 

Lymphocytic gastritis and coeliac disease: evidence of

a positive association. J Clin Pathol 1998;51(3):207-

210. Not about celiac and GI lymphoma 

Fehmers M C, Wilderink F, Oushoorn H H et al. 

Gluten-sensitive enteropathy and intestinal

lymphoreticulosis. A case report. Neth J Med

1975;18(2):83-88. Not about celiac and GI lymphoma 

Ferguson A, Kingstone K. Coeliac disease and 

malignancies. Acta Paediatr 1996;41278-81. Does not 

address the question 

Ferguson R, Asquith P, Cooke W T. The cellular

infiltrate of the jejunum in coeliac patients with

complicating lymphoma. Gut 1974;15(4):338-339. 

Not about celiac and GI lymphoma 

Ferguson R, Asquith P, Cooke W T. The jejunal 

cellular infiltrate in coeliac disease complicated by

lymphoma. Gut 1974;15(6):458-461. Not about celiac 

and GI lymphoma 

Festen H P. Intrinsic factor secretion and cobalamin 

absorption. Physiology and pathophysiology in the 

gastrointestinal tract. Scandinavian Journal of 

Gastroenterology.Supplement 1991;1881-7. Not about 

celiac and GI lymphoma 

Finan P J, Thompson M R. Surgical presentation of 

small bowel lymphoma in adult coeliac disease. 

Postgrad Med J 1980;56(662):859-861. Does not 

address the question 

Fine K D, Stone M J. Alpha-heavy chain disease,

Mediterranean lymphoma, and immunoproliferative

small intestinal disease: a review of 

clinicopathological features, pathogenesis, and 

differential diagnosis. Am J Gastroenterol 

1999;94(5):1139-1152. Not about celiac and GI

lymphoma 

Fine K D, Lee E L, Meyer R L. Colonic 

histopathology in untreated celiac sprue or refractory

sprue: is it lymphocytic colitis or colonic

lymphocytosis?. Hum Pathol 1998;29(12):1433-1440. 

Not about celiac and GI lymphoma 

Fisher C M. Neoplasia and the coeliac syndrome.

Lancet 1969;1(7597):730Not about celiac and GI 

lymphoma 

Foss H D, Stein H. Pathology of intestinal 

lymphomas. Recent Results in Cancer 

Research.Fortschritte Der Krebsforschung.Progres 

Dans Les Recherches Sur Le Cancer 2000;15633-41. 

Not about celiac and GI lymphoma 

Foster P N, Heatley R V, Losowsky M S. Natural 

killer cells in coeliac disease. J Clin Lab Immunol 

1985;17(4):173-176. Not about celiac and GI

lymphoma 

Freeman H J. Survey of gastroenterologists on the 

diagnosis and treatment of adult patients with celiac 

disease in British Columbia. Can J Gastroenterol

1998;12(2):149-152. Does not address the question 

Freeman H J. Hepatobiliary tract and pancreatic

disorders in celiac disease. Can J Gastroenterol

1997;11(1):77-81. Not about celiac and GI lymphoma 

Freeman H J. Celiac-associated autoimmune thyroid 

disease: A study of 16 patients with overt

hypothyroidism: Maladie thyroidienne auto-immune 

de nature coeliaque: etude portant sur 16 patients 

atteints d'hypothyroidie averee. Can J Gastroenterol 

1995;9(5):242-246. Not about celiac and GI 

lymphoma 

Freeman H J. Clinical spectrum of biopsy defined 

celiac disease in the elderly. Can J Gastroenterol 

1995;9(1):42-46. Not about celiac and GI lymphoma 

Freeman H J. Neoplastic disorders in 100 patients with 

adult celiac disease. Can J Gastroenterol 

1996;10(3):163-166. Not about celiac and GI

lymphoma 

Freeman H J. Free perforation due to intestinal 

lymphoma in biopsy-defined or suspected celiac 

disease. J Clin Gastroenterol 2003;37(4):299-302. Not 

about celiac and GI lymphoma 

Freeman H J, Weinstein W M, Shnitka T K. Primary 

abdominal lymphoma. Presenting manifestation of 

celiac sprue or complicating dermatitis herpetiformis. 

Am J Med 1977;63(4):585-594. Not about celiac and 

GI lymphoma 

Freeman Hugh, Lemoyne Michel, Pare Pierre. Coeliac 

disease. Best Practice & Research.Clinical

Gastroenterology 2002;16(1):37-49. Review article 

Fry L. Dermatitis herpetiformis. Bailliere's Clinical 

Gastroenterology 1995;9(2):371-393. Not about celiac 

and GI lymphoma 

Fry L, McMinn R M. Morphology and functional 

cytology of the small intestinal mucosa in

malabsorptive disorders and other diseases. J Clin

Pathol 1966;19(3):260-265. Not about celiac and GI 

lymphoma 

A-590
Fu K, Stewart J R. Radiotherapeutic management of 

small intestinal lymphoma with malabsorption. Cancer

1973;31(2):286-290. Not about celiac and GI

lymphoma 

Fundia A F, Gonzalez Cid M B, Bai J et al. 

Chromosome instability in lymphocytes from patients 

with celiac disease. Clin Genet 1994;45(2):57-61. 

Does not address the question 

Fundia A, Gomez J C, Maurino E et al. Chromosome 

instability in untreated adult celiac disease patients. 

Acta Paediatr 1996;41282-84. Does not address the 

question 

Gale J, Simmonds P D, Mead G M et al. Enteropathytype intestinal T-cell lymphoma: clinical features and 

treatment of 31 patients in a single center. Journal of 

Clinical Oncology - Official Journal of the American

Society of Clinical Oncology 2000;18(4):795-803. 

Does not address the question 

Garioch J J. Dermatitis herpetiformis and its

management. Prescr J 1996;36(3):141-145. Not about 

celiac and GI lymphoma 

Gasbarrini G, Ciccocioppo R, De Vitis I et al. Coeliac 

disease in the elderly. A multicentre Italian study. 

Gerontology 2001;47(6):306-310. Not a controlled

study

Gasbarrini G, Miglio F, Serra M A et al. 

Immunological studies of the jejunal mucosa in 

normal subjects and adult celiac patients. Digestion 

1974;10(2):122-128. Not about celiac and GI

lymphoma 

Gawkrodger D J, Blackwell J N, Gilmour H M et al. 

Dermatitis herpetiformis: diagnosis, diet and 

demography. Gut 1984;25(2):151-157. Not about 

celiac and GI lymphoma 

Gay G J, Delmotte J S. Enteroscopy in small intestinal

inflammatory diseases. Gastrointest Endosc Clin N 

Am 1999;9(1):115-123. Not about celiac and GI 

lymphoma 

Gerson D E, Lewicki A M. Intramural small bowel 

hemorrhage: complication of sprue. Radiology 

1973;108(3):521-522. Not about celiac and GI 

lymphoma 

Gheorghe L, Gheorghe C, Aposteanu G et al. Clinical 

spectrum of adult celiac disease in a referral center for 

Southern Romania. Associated disorders and shortterm survival. Rom J Gastroenterol 1996;5(4):223-

228. Not about celiac and GI lymphoma 

Gill S S, Heuman D M, Mihas A A. Small intestinal 

neoplasms. J Clin Gastroenterol 2001;33(4):267-282. 

Not about celiac and GI lymphoma 

Gillet H, Ferguson A, Frier B. Coeliac disease often 

co-exists with Type 1 diabetes mellitus. Pract Diabetes

Int 1998;15(4):117-120. Not about celiac and GI 

lymphoma 

Goerres M S, Meijer J W R, Wahab P J et al. 

Azathioprine and prednisone combination therapy in 

refractory coeliac disease. Aliment Pharmacol Ther 

2003;18(5):487-494. Not a controlled study

Goldberg H I, Sheft D J. Abnormalities in small

intestine contour and caliber: a working classification. 

Radiol Clin North Am 1976;14(3):461-475. Not about 

celiac and GI lymphoma 

Goodwin P, Fry L. Reticulum cell sarcoma 

complicating dermatitis herpetiformis. Proc R Soc

Med 1973;66(7):625-626. Not about celiac and GI 

lymphoma 

Gould D J, Howell R. Dermatitis herpetiformis and 

reticulum cell sarcoma, a rare complication. Br J 

Dermatol 1977;96(5):561-562. Not about celiac and 

GI lymphoma 

Gourtsoyiannis N C, Nolan D J. Lymphoma of the 

small intestine: radiological appearances. Clin Radiol 

1988;39(6):639-645. Not about celiac and GI

lymphoma 

Green Peter H R, Jabri Bana. Celiac disease and other 

precursors to small-bowel malignancy. Gastroenterol 

Clin North Am 2002;31(2):625-639. Review article 

Green P H R, Jabri B. Coeliac disease. Lancet

2003;362(9381):383-391. Does not address the 

question 

Green P H R, Stavropoulos S N, Panagi S G et al. 

Characteristics of adult celiac disease in the USA:

results of a national survey. Am J Gastroenterol

2001;96(1):126-131. Not about celiac and GI

lymphoma 

Gritzmann N, Hollerweger A, Macheiner P et al.

Transabdominal sonography of the gastrointestinal 

tract. Eur Radiol 2002;12(7):1748-1761. Not about 

celiac and GI lymphoma 

Habeshaw J A, Hayward M J, McVie J G. 

Extramedullary plasmacytoma of stomach. Scand J

Haematol 1975;14(1):57-64. Not about celiac and GI 

lymphoma 

Hadziselimovic F, Emmons L R, Schaub U et al. 

Occurrence of large granular lymphocytes and natural 

killer cells in the epithelium of the gut distinguishes 

two different coeliac diseases. Gut 1992;33(6):767-

772. Not about celiac and GI lymphoma 

Halkin H, Meytes D, Militeanu J et al. Multiple

lymphomatous polyposis of the gastrointestinal tract. 

A-591
Isr J Med Sci 1973;9(5):648-654. Not about celiac and 

GI lymphoma 

Hall R P. Dietary management of dermatitis 

herpetiformis. Arch Dermatol 1987;123(10):1378a1380a. Not about celiac and GI lymphoma 

Halme L, Mecklin J P, Juhola M et al. Primary

gastrointestinal non-Hodgkin's lymphoma. A 

population based study in central Finland in 1975-

1993. Acta Oncol 1997;36(1):69-74. Does not address 

the question 

Hardman C M, Anstey A. The management of

dermatitis herpetiformis. J Dermatol Treat 

1998;9(2):125-130. Not about celiac and GI 

lymphoma 

Harris O D, Cooke W T, Thompson H et al. 

Malignancy in adult coeliac disease and idiopathic

steatorrhoea. Am J Med 1967;42(6):899-912. Double 

publication of included data 

Harvey Richard F, Shaw Ian S. Current thinking in 

coeliac disease. Br J Gen Pract 2002;246(1638):596-

602. Not about celiac and GI lymphoma 

Hayat M, Cairns A, Dixon M F et al. Quantitation of 

intraepithelial lymphocytes in human duodenum: what 

is normal?. J Clin Pathol 2002;55(5):393-394. Not 

about celiac and GI lymphoma 

Hekimgil M, Soydan S, Nart D et al. Histopathologic 

and immunophenotypic features of childhood and

adult anaplastic large-cell lymphomas. Turk J 

Haematol 2001;18(4):265-274. Not about celiac and 

GI lymphoma 

Heneghan M A, Stevens F M, Cryan E M et al. Celiac 

sprue and immunodeficiency states: a 25-year review. 

J Clin Gastroenterol 1997;25(2):421-425. Not about 

celiac and GI lymphoma 

Herron M D, Zone J J. Treatment of dermatitis 

herpetiformis and linear IgA bullous dermatosis. 

Dermatol Ther 2002;15(4):374-381. Not about celiac 

and GI lymphoma 

Hobbs J R. Immunoflobulins and malabsorption. Proc 

R Soc Med 1969;62(10):982-985. Not about celiac 

and GI lymphoma 

Hodges J R, Isaacson P, Eade O E et al. Serum 

lysozyme levels in malignant histiocytosis of the

intestine. Gut 1979;20(10):854-857. Does not address 

the question 

Hodges J R, Isaacson P, Smith C L et al. Malignant 

histiocytosis of the intestine. Dig Dis Sci 

1979;24(8):631-638. Does not address the question 

Hodgson J R, Hoffman H N, Huizenga K A. 

Roentgenologic features of lymphoid hyperplasia of 

the small intestine associated with 

dysgammaglobulinemia. Radiology 1967;88(5):883-

888. Not about celiac and GI lymphoma 

Hoffmann M, Vogelsang H, Kletter K et al. 18Ffluoro-deoxy-glucose positron emission tomography

(18F-FDG-PET) for assessment of enteropathy-type T 

cell lymphoma. Gut 2003;52(3):347-351. Not about 

celiac and GI lymphoma 

Hoggan R. Considering wheat, rye, and barley

proteins as aids to carcinogens. Med Hypotheses

1997;49(3):285-288. Not about celiac and GI

lymphoma 

Holmes G K. Celiac disease and malignancy. J Pediatr

Gastroenterol Nutr 1997;24(5):S20-S23. Review 

article 

Holmes G K T. Coeliac disease and malignancy.

Digestive and Liver Disease - Official Journal of the 

Italian Society of Gastroenterology and the Italian 

Association for the Study of the Liver 2002;34(3):229-

237. Review article 

Holmes G K T. Coeliac disease and malignancy. Ann 

Nestle 1993;51(2):66-74. Review article 

Holmes G K T. Coeliac disease and Type 1 diabetes

mellitus - The case for screening. Diabetic Medicine - 

a Journal of the British Diabetic Association 

2001;18(3):169-177. Not about celiac and GI

lymphoma 

Holmes G K, Stokes P L, Sorahan T M et al. Coeliac 

disease, gluten-free diet, and malignancy. Gut

1976;17(8):612-619. Double publication of included 

data 

Hourihane D O, Weir D G. Malignant celiac 

syndrome. Report of two cases with malabsorption 

and microscopic foci of intestinal lymphoma. 

Gastroenterology 1970;59(1):130-139. Does not 

address the question 

Howdle P D, Jalal P K, Holmes G K T et al. Primary

small-bowel malignancy in the UK and its association 

with coeliac disease. Qjm - Monthly Journal of the 

Association of Physicians 2003;96(5):345-353. Does 

not address the question 

Howell W M, Jones D B. The role of human leucocyte 

antigen genes in the development of malignant 

disease. J Clin Pathol Clin Mol Pathol

1995;48(6):M302-M306. Not about celiac and GI 

lymphoma 

Howell W M, Leung S T, Jones D B et al. HLA-DRB, 

-DQA, and -DQB polymorphism in celiac disease and 

enteropathy-associated T-cell lymphoma. Common 

A-592
features and additional risk factors for malignancy.

Hum Immunol 1995;43(1):29-37. Does not address 

the question 

Howell W, Martin Calder, Philip C et al. Gene

polymorphisms, inflammatory diseases and cancer. 

Proc Nutr Soc 2002;61(4):447-456. Not about celiac 

and GI lymphoma 

Ilyas M, Niedobitek G, Agathanggelou A et al. NonHodgkin's lymphoma, coeliac disease, and EpsteinBarr virus: a study of 13 cases of enteropathyassociated T- and B-cell lymphoma. Am J Pathol

1995;177(2):115-122. Does not address the question 

Isaacson P. Malignant histiocytosis of the intestine: 

the early histological lesion. Gut 1980;21(5):381-386. 

Not about celiac and GI lymphoma 

Isaacson P. Primary gastrointestinal lymphoma. 

Virchows Archiv.A, Pathological Anatomy and 

Histology 1981;391(1):1-8. Not about celiac and GI 

lymphoma 

Isaacson P, Wright D H. Intestinal lymphoma

associated with malabsorption. Lancet 

1978;1(8055):67-70. Does not address the question 

Isaacson P, Wright D H. Malignant histiocytosis of the

intestine. Its relationship to malabsorption and

ulcerative jejunitis. Hum Pathol 1978;9(6):661-677. 

Does not address the question 

Isaacson P G. Gastrointestinal lymphoma. Hum Pathol

1994;25(10):1020-1029. Review article 

Isaacson P G. Gastrointestinal lymphomas of T- and 

B-cell types. Modern Pathology - an Official Journal 

of the United States and Canadian Academy of

Pathology, Inc 1999;12(2):151-158. Review article 

Isaacson P G. Intestinal lymphoma and enteropathy. 

Am J Pathol 1995;177(2):111-113. Review article 

Isaacson P G. Relation between cryptic intestinal

lymphoma and refractory sprue. Lancet 

2000;356(9225):178-179. Does not address the 

question 

Isaacson P G. B-cell lymphomas of the gastrointestinal

tract. Am J Surg Pathol 1985;9(3 Suppl):117-128. Not 

about celiac and GI lymphoma 

Isaacson P G. T-cell lymphoma: The real thing. Gut 

1999;45(5):638-639. Not about celiac and GI

lymphoma 

Isaacson P, Wright D H, Judd M A et al. Primary

gastrointestinal lymphomas: a classification of 66 

cases. Cancer 1979;43(5):1805-1809. Not about celiac 

and GI lymphoma 

Jacobsen M B, Fausa O, Elgjo K et al. Hepatic lesions

in adult coeliac disease. Scand J Gastroenterol 

1990;25(7):656-662. Does not address the question 

James D G, Sharma O P. Overlap syndromes with

sarcoidosis. Postgrad Med J 1985;61(719):769-771. 

Not about celiac and GI lymphoma 

James S P. 19. Immunologic, gastroenterologic, and 

hepatobiliary disorders. J Allergy Clin Immunol 

2003;111(2 Suppl 2):S645-S658. Not about celiac and

GI lymphoma 

Jennings J S R, Howdle P D. Celiac disease. Curr

Opin Gastroenterol 2001;17(2):118-126. Not about 

celiac and GI lymphoma 

Johnston S D, Watson R G P. Small bowel lymphoma 

in unrecognized coeliac disease: A cause for concern?. 

Eur J Gastroenterol Hepatol 2000;12(6):645-648. 

Does not address the question 

Johnston S D, Watson R G, McMillan S A et al. 

Coeliac disease detected by screening is not silent--

simply unrecognized. Qjm - Monthly Journal of the 

Association of Physicians 1998;91(12):853-860. Not 

about celiac and GI lymphoma 

Jones B, Bayless T M, Fishman E K et al. 

Lymphadenopathy in celiac disease: computed 

tomographic observations. Ajr.American Journal of 

Roentgenology 1984;142(6):1127-1132. Not about 

celiac and GI lymphoma 

Jones D B, Foreman R. Cell origin of lymphoma 

complicating coeliac disease. Lancet

1985;2(8463):1067-1068. Not about celiac and GI 

lymphoma 

Jones P E, Gleeson M H. Mucosal ulceration and 

mesenteric lymphadenopathy in coeliac disease. Br 

Med J 1973;3(5873):212-213. Not about celiac and GI 

lymphoma 

Joshi V V. Pathology of acquired immunodeficiency

syndrome (AIDS) in children. Keio J Med

1996;45(4):306-312. Not about celiac and GI

lymphoma 

Kaerlev L, Teglbjaerg P S, Sabroe S et al. Medical 

risk factors for small-bowel adenocarcinoma with

focus on Crohn disease: a European population-based 

case-control study. Scand J Gastroenterol 

2001;36(6):641-646. Not about celiac and GI

lymphoma 

Katoh A, Ohshima K, Kanda M et al. Gastrointestinal

T cell lymphoma: predominant cytotoxic phenotypes, 

including alpha/beta, gamma/delta T cell and natural 

killer cells. Leuk Lymphoma 2000;39(1-2):97-111. 

Not about celiac and GI lymphoma 

A-593
Katz K D. Celiac Disease - Current Clinical

Considerations in Treatment and Avoidance of 

Nutritional Deficiencies. Today's Ther Trends

2003;21(4):379-389. Not about celiac and GI

lymphoma 

Keating J P. Is celiac disease a premalignant state?. J

Pediatr Gastroenterol Nutr 1984;3(1):4-5. Not about 

celiac and GI lymphoma 

Kelly C P, Feighery C F, Gallagher R B et al. 

Diagnosis and treatment of gluten-sensitive 

enteropathy. Adv Intern Med 1990;35341-363. Does 

not address the question 

Kepczyk T, Kadakia S C. Prospective evaluation of 

gastrointestinal tract in patients with iron-deficiency

anemia. Dig Dis Sci 1995;40(6):1283-1289. Not about 

celiac and GI lymphoma 

Khilnani M T, Keller R J, Cuttner J.

Macroglobulinemia and steatorrhea: roentgen and 

pathologic findings in the intestinal tract. Radiol Clin 

North Am 1969;7(1):43-55. Not about celiac and GI 

lymphoma 

Koning F. Celiac disease and malignancy: an 

immunological basis?. J Pediatr Gastroenterol Nutr 

1997;24(5):S18-S19. Does not address the question 

Kowlessar O D. Dietary gluten sensitivity updated. J 

Am Diet Assoc 1972;60(6):475-477. Not about celiac 

and GI lymphoma 

Krawitt E L, Beeken W L. Limitations of the 

usefulness of the d-xylose absorption test. Am J Clin 

Pathol 1975;63(2):261-263. Not about celiac and GI 

lymphoma 

Krikler D M. Steatorrhoea and plasma-alkalinephosphatase. Lancet 1968;2(7558):51Not about celiac 

and GI lymphoma 

Kruschwitz M, Fritzsche G, Schwarting R et al. BerACT8: new monoclonal antibody to the mucosa 

lymphocyte antigen. J Clin Pathol 1991;44(8):636-

645. Not about celiac and GI lymphoma 

Lahdeaho M-L, Lehtinen T, Aine R et al. Antibody

response to adenovirus E1b-derived synthetic peptides 

and serum levels of p53 in patients with 

gastrointestinal and other malignant lymphomas. J

Med Virol 1994;43(4):393-396. Not about celiac and 

GI lymphoma 

Lang-Muritano M, Molinari L, Dommann-Scherrer C

et al. Incidence of enteropathy-associated T-cell 

lymphoma in celiac disease: Implications for children 

and adolescents with type 1 diabetes. Pediatr Diabetes

2002;3(1):42-45. Does not address the question 

Lasch E E, Ramot B, Neumann G. Childhood celiac 

disease in Israel. Epidemiological aspects. Isr J Med 

Sci 1968;4(6):1260-1264. Not about celiac and GI 

lymphoma 

Leonard J N, Tucker W F, Fry J S et al. Increased

incidence of malignancy in dermatitis herpetiformis. 

Br Med J (Clin Res Ed) 1983;286(6358):16-18. Not 

about celiac and GI lymphoma 

Levinson J D, Kirsner J B. Infiltrative diseases of the 

small bowel and malabsorption. Am J Dig Dis 

1970;15(8):741-766. Not about celiac and GI

lymphoma 

Lewin K J, Kahn L B, Novis B H. Primary intestinal

lymphoma of "Western" and "Mediterranean" type, 

alpha chain disease and massive plasma cell

infiltration: a comparative study of 37 cases. Cancer 

1976;38(6):2511-2528. Not about celiac and GI

lymphoma 

Little A-M, Stern P L. Does HLA type predispose 

some individuals to cancer?. Mol Med Today

1999;5(8):337-342. Not about celiac and GI 

lymphoma 

Lojda Z. Proteinases in pathology. Usefulness of 

histochemical methods. Journal of Histochemistry and 

Cytochemistry - Official Journal of the Histochemistry

Society 1981;29(3a Suppl):481-493. Not about celiac 

and GI lymphoma 

Luzi G, Zullo A, Iebba F et al. Duodenal pathology

and clinical-immunological implications in common 

variable immunodeficiency patients. Am J 

Gastroenterol 2003;98(1):118-121. Not about celiac 

and GI lymphoma 

Machulla H K G, Muller L P, Schaaf A et al.

Association of chronic lymphocytic leukemia with 

specific alleles of the HLA-DR4:DR53:DQ8 

haplotype in German patients. Int J Cancer 

2001;92(2):203-207. Not about celiac and GI

lymphoma 

Maclaurin B P, Cooke W T, Ling N R. Impaired

lymphocyte reactivity against tumour cells in patients 

with coeliac disease. Gut 1971;12(10):794-800. Not 

about celiac and GI lymphoma 

Marsh M N. Studies of intestinal lymphoid tissue. IV--

The predictive value of raised mitotic indices among 

jejunal epithelial lymphocytes in the diagnosis of

gluten-sensitive enteropathy. J Clin Pathol 

1982;35(5):517-525. Not about celiac and GI

lymphoma 

Marsh M N, Haeney M R. Studies of intestinal 

lymphoid tissue. VI. Proliferative response of small 

intestinal epithelial lymphocytes distinguishes glutenfrom non-gluten-induced enteropathy. J Clin Pathol 

A-594
1983;36(2):149-160. Not about celiac and GI

lymphoma 

Marsh M N, Mathan M, Mathan V I. Studies of 

intestinal lymphoid tissue. VII. The secondary nature 

of lymphoid cell "activation" in the jejunal lesion of 

tropical sprue. Am J Pathol 1983;112(3):302-312. Not 

about celiac and GI lymphoma 

Marshak R H, Hazzi C, Lindner A E et al. The 

radiology corner: the small bowel in immunoglobulin 

deficiency syndromes. Am J Gastroenterol 

1975;64(1):59-73. Not about celiac and GI lymphoma 

Marshak R H, Hazzi C, Lindner A E et al. Small 

bowel in immunoglobulin deficiency syndromes. Am 

J Roentgenol Radium Ther Nucl Med 

1974;122(2):227-240. Not about celiac and GI 

lymphoma 

Marshak R H, Linder A E, Maklansky D. 

Immunoglobulin disorders of the small bowel. Radiol 

Clin North Am 1976;14(3):477-491. Not about celiac 

and GI lymphoma 

Marshak R H, Lindner A E, Maklansky D. 

Lymphoreticular disorders of the gastrointestinal tract: 

roentgenographic features. Gastrointest Radiol

1979;4(2):103-120. Not about celiac and GI 

lymphoma 

Mathus-Vliegen E M. Coeliac disease and lymphoma: 

current status. Neth J Med 1996;49(5):212-220. 

Review article 

Mathus-Vliegen E M H. Lymphoma in coeliac 

disease. J R Soc Med 1995;88(12):672-677. Review 

article 

Mathus-Vliegen E M, Van Halteren H, Tytgat G N.

Malignant lymphoma in coeliac disease: various

manifestations with distinct symptomatology and 

prognosis?. J Inter Med 1994;236(1):43-49. Does not 

address the question 

Maurino Eduardo, Niveloni Sonia, Chernavsky

Alejandra et al. Azathioprine in refractory sprue:

results from a prospective, open-label study. Am J 

Gastroenterol 2002;97(10):2595-2602. Not about 

celiac and GI lymphoma 

Mazzacca G. Diet, coeliac disease and gastrointestinal

neoplasm. Adv Exp Med Biol 1993;348133-136. Not 

about celiac and GI lymphoma 

McCrae W M, Eastwood M A, Martin M R et al. 

Neglected coeliac disease. Lancet 1975;1(7900):187-

190. Does not address the question 

McElvaney N G, Duignan R, Fielding J F. Coeliac 

disease: clinical presentations, correlations of dietary 

compliance, symptomatic response and repeat biopsy

findings. Ulster Med J 1992;61(2):134-138. Does not 

address the question 

McPherson J R. Jejunal biopsy. Med Clin North Am 

1970;54(4):851-862. Not about celiac and GI

lymphoma 

McPherson J R. Jejunal biopsy in the diagnosis of

malabsorption syndromes. Dis Colon Rectum 

1965;8(6):425-430. Not about celiac and GI 

lymphoma 

McPhillips J. Understanding coeliac disease: 

symptoms and long-term risks. Br J Nurs 

2000;9(8):479-483. Not about celiac and GI 

lymphoma 

Mead G M, Whitehouse J M, Thompson J et al. 

Clinical features and management of malignant

histiocytosis of the intestine. Cancer 

1987;60(11):2791-2796. Does not address the question 

Mention Jean, Ben Ahmed, Melika Begue et al. 

Interleukin 15: a key to disrupted intraepithelial 

lymphocyte homeostasis and lymphomagenesis in

celiac disease. Gastroenterology 2003;125(3):730-745. 

Not about celiac and GI lymphoma 

Michalski J P, McCombs C C. Celiac disease: clinical

features and pathogenesis. Am J Med Sci 

1994;307(3):204-211. Not about celiac and GI 

lymphoma 

Milovic V, Stein J, Caspary W F. Intestinal

malabsorption: Patophysiology, clinical signs and

symptoms, diagnosis and treatment (First part). Arch 

Gastroenterohepatol 1999;18(3-4):65-74. Not about 

celiac and GI lymphoma 

Montgomery R D, Atiyeh M, Scales W R et al.

Intestinal absorption in Saudi Arabia: an evaluation of 

the one hour blood xylose test. Trans R Soc Trop Med 

Hyg 1982;76(1):25-28. Not about celiac and GI

lymphoma 

Morgan D R, Holgate C S, Dixon M F et al. Primary 

small intestinal lymphoma: a study of 39 cases. Am J 

Pathol 1985;147(3):211-221. Not about celiac and GI 

lymphoma 

Mulder Chris J J, Hadithi Mohammed M, Rostami 

Kamran et al. Coeliac disease--has the time come for 

routine mass screening? In 2002--2010--2020?. Rom J 

Gastroenterol 2002;11(3):179-182. Not about celiac 

and GI lymphoma 

Mulder C J, Wahab P J, Moshaver B et al. Refractory 

coeliac disease: a window between coeliac disease and

enteropathy associated T cell lymphoma. 

Scandinavian Journal of Gastroenterology.Supplement 

2000;(232):32-37. Review article 

A-595
Murray A, Cuevas E C, Jones D B et al. Study of the 

immunohistochemistry and T cell clonality of

enteropathy-associated T cell lymphoma. Am J Pathol 

1995;146(2):509-519. Not about celiac and GI 

lymphoma 

Mussche M, Thienpont L. Adult celiac disease 

complicated by intestinal reticulum cell sarcoma with 

high serum IgA level. Acta Clin Belg 1974;29(6):388-

393. Does not address the question 

Neild G H. Coeliac disease: a graft-versus-host-like 

reaction localised to the small bowel wall?. Lancet

1981;1(8224):811-812. Does not address the question 

Nelsen D A. Gluten-sensitive enteropathy (celiac

disease): More common than you think. Am Fam Phys

2002;66(12):2259-2266+2269. Not about celiac and 

GI lymphoma 

Nicolas M E O, Krause P K, Gibson L E et al. 

Dermatitis herpetiformis. Int J Dermatol 

2003;42(8):588-600. Not about celiac and GI

lymphoma 

Novis B H, Bank S, Marks I N. Gastric acid secretion

and intestinal malabsorption. South African Medical 

Journal.Suid-Afrikaanse Tydskrif Vir Geneeskunde 

1973;47(26):1139-1142. Not about celiac and GI 

lymphoma 

Novis B H, Bank S, Marks I N et al. Abdominal 

lymphoma presenting with malabsorption. Qjm -

Monthly Journal of the Association of Physicians 

1971;40(160):521-540. Does not address the question 

O'Boyle C J, Kerin M J, Feeley K et al. Primary small 

intestinal tumours: increased incidence of lymphoma

and improved survival. Ann R Coll Surg Engl 

1998;80(5):332-334. Does not address the question 

O'Connor T M, Cronin C C, Loane J F et al. Type 1 

diabetes mellitus, coeliac disease, and lymphoma: a 

report of four cases. Diabetic Medicine - a Journal of 

the British Diabetic Association 1999;16(7):614-617. 

Does not address the question 

O'Driscoll B R, Stevens F M, O'Gorman T A et al.

HLA type of patients with coeliac disease and 

malignancy in the west of Ireland. Gut

1982;23(8):662-665. Pathogenesis only

O'Farrelly C. Is villous atrophy always and only the 

result of gluten sensitive disease of the intestine?. Eur 

J Gastroenterol Hepatol 2000;12(6):605-608. Not 

about celiac and GI lymphoma 

O'Farrelly C, Feighery C, O'Briain D S et al. Humoral 

response to wheat protein in patients with coeliac 

disease and enteropathy associated T cell lymphoma. 

Br Med J (Clin Res Ed) 1986;293(6552):908-910. Not 

about celiac and GI lymphoma 

O'Grady J G, Stevens F M, McCarthy C F. Celiac

disease: does hyposplenism predispose to the 

development of malignant disease?. Am J 

Gastroenterol 1985;80(1):27-29. Does not address the 

question 

O'Grady J G, Stevens F M, Harding B et al. 

Hyposplenism and gluten-sensitive enteropathy.

Natural history, incidence, and relationship to diet and 

small bowel morphology. Gastroenterology

1984;87(6):1326-1331. Not about celiac and GI

lymphoma 

O'Mahony S, Howdle P D, Losowsky M S. Review 

article: management of patients with non-responsive 

coeliac disease. Aliment Pharmacol Ther

1996;10(5):671-680. Review article 

O'Malley Martin E, Wilson Stephanie R. US of 

gastrointestinal tract abnormalities with CT 

correlation. Radiographics - a Review Publication of 

the Radiological Society of North America, Inc 

2003;23(1):59-72. Not about celiac and GI lymphoma 

Oberhuber G. Histopathology of celiac disease. 

Biomed Pharmacother 2000;54(7):368-372. Not about 

celiac and GI lymphoma 

Otto H F, Bettmann I, Weltzien J V et al. Primary 

intestinal lymphomas. Virchows Archiv.A,

Pathological Anatomy and Histology 1981;391(1):9-

31. Review article 

Parnell N D, Ciclitira P J. Review article: coeliac 

disease and its management. Aliment Pharmacol Ther

1999;13(1):1-13. Not about celiac and GI lymphoma 

Parry Sally D, Welfare Mark R, Cobden Irving et al. 

Push enteroscopy in a UK district general hospital: 

experience of 51 cases over 2 years. Eur J 

Gastroenterol Hepatol 2002;14(3):305-309. Not about 

celiac and GI lymphoma 

Patey-Mariaud de, Serre Cellier C, Jabri B et al. 

Distinction between coeliac disease and refractory 

sprue: a simple immunohistochemical method. 

Histopathology 2000;37(1):70-77. Not about celiac 

and GI lymphoma 

Pearce Allum B, Sinclair David, Duncan Hamish D et 

al. Use of the anti-endomysial antibody test to

diagnose coeliac disease in clinical practice. Clin Lab 

2002;48(5-6):319-325. Not about celiac and GI

lymphoma 

Perera D R, Weinstein W M, Rubin C E. Symposium 

on pathology of the gastrointestinal tract-Part II. Small 

intestinal biopsy. Hum Pathol 1975;6(2):157-217. Not 

about celiac and GI lymphoma 

Peters U, Askling J, Gridley G et al. Causes of death 

in patients with celiac disease in a population-based 

A-596
Swedish cohort. Arch Intern Med 2003;163(13):1566-

1572. Double publication of included data 

Pricolo V E, Mangi A A, Aswad B et al.

Gastrointestinal malignancies in patients with celiac

sprue. Am J Surg 1998;176(4):344-347. Does not 

address the question 

Pruessner H T. Detecting celiac disease in your

patients. Am Fam Physician 1998;57(5):1023-34, 

1039. Not about celiac and GI lymphoma 

Purtilo D T, Greally J. Coeliac disease and

malignancy. Lancet 1983;1(8327):771Not about celiac 

and GI lymphoma 

Ramot B, Many A. Primary intestinal lymphoma: 

clinical manifestations and possible effect of

environmental factors. Recent Results in Cancer 

Research.Fortschritte Der Krebsforschung.Progres 

Dans Les Recherches Sur Le Cancer 1972;39193-199. 

Review article 

Rampertab S D, Forde K A, Green P H R. Small 

bowel neoplasia in coeliac disease. Gut

2003;52(8):1211-1214. Not about celiac and GI

lymphoma 

Read A E. Malignancy and steatorrhea. Bibl Paediatr 

1968;87182-190. Not about celiac and GI lymphoma 

Reunala T L, Leonard J N. Malignant disease in 

dermatitis herpetiformis. Clin Dermatol 

1991;9(3):369-373. Not about celiac and GI 

lymphoma 

Reunala T, Helin H, Kuokkanen K et al. Lymphoma in 

dermatitis herpetiformis: Report of four cases. Acta 

Derm-Venereol 1982;62(4):343-346. Not about celiac 

and GI lymphoma 

Ricart E, Bouma G, Salvador Pen et al. The 

therapeutic spectrum of infliximab and tumor necrosis 

factor immunomodulation in chronic inflammatory

diseases. Drugs Today 2002;38(11):725-744. Not 

about celiac and GI lymphoma 

Risch N. Assessing the role of HLA-linked and

unlinked determinants of disease. Am J Hum Genet 

1987;40(1):1-14. Not about celiac and GI lymphoma 

Robert M E, Ament M E, Weinstein W M. The

histologic spectrum and clinical outcome of refractory

and unclassified sprue. Am J Surg Pathol 

2000;24(5):676-687. Not about celiac and GI

lymphoma 

Robertson D A F, Dixon M F, Scott B B. Small 

intestinal ulceration: Diagnostic difficulties in relation

to coeliac disease. Gut 1983;24(6):565-574. Not about 

celiac and GI lymphoma 

Robertson D A F, Swinson C M, Hall R et al. Coeliac 

disease, splenic function, and malignancy. Gut 

1982;23(8):666-669. Not about celiac and GI

lymphoma 

Rossini F P. Quo vadis capsule endoscopy?. Dig Liver

Dis 2002;34(8):537-539. Not about celiac and GI 

lymphoma 

Rowland M, Imrie C, Bourke B et al. How should 

Helicobacter pylori infected children be managed?. 

Gut 1999;45(Suppl 1):36-39. Not about celiac and GI 

lymphoma 

Ruan E A, Komorowski R A, Hogan W J et al.

Nongranulomatous chronic idiopathic enterocolitis: 

Clinicopathologic profile and response to 

corticosteroids. Gastroenterology 1996;111(3):629-

637. Not about celiac and GI lymphoma 

Rubesin S E. Simplified approach to differential 

diagnosis of small bowel abnormalities. Radiol Clin 

North Am 2003;41(2):343-364. Not about celiac and 

GI lymphoma 

Rubesin S E, Gilchrist A M, Bronner M et al. NonHodgkin lymphoma of the small intestine. 

Radiographics - a Review Publication of the 

Radiological Society of North America, Inc 

1990;10(6):985-998. Review article 

Rubesin S E, Herlinger H, Saul S H et al. Adult celiac 

disease and its complications. Radiographics - a 

Review Publication of the Radiological Society of

North America, Inc 1989;9(6):1045-1066. Review 

article 

Ruskone-Fourmestraux A, Rambaud J C.

Gastrointestinal lymphoma: prevention and treatment 

of early lesions. Best Practice & Research.Clinical

Gastroenterology 2001;15(2):337-354. Review article 

Ryan B M, Kelleher D. Refractory celiac disease.

Gastroenterology 2000;119(1):243-251. Review 

article 

Ryan J C. Premalignant conditions of the small 

intestine. Semin Gastrointest Dis 1996;7(2):88-93. 

Review article 

Sampson H A. Food allergy. Curr Opin Immunol 

1989;2(4):542-547. Not about celiac and GI 

lymphoma 

Sategna-Guidetti C, Grosso S, Bruno M et al. 

Comparison of serum anti-gliadin, anti-endomysium, 

and anti-jejunum antibodies in adult celiac sprue. J 

Clin Gastroenterol 1995;20(1):17-21. Not about celiac 

and GI lymphoma 

Savilahti E, Ormala T, Saukkonen T et al. Jejuna of 

patients with insulin-dependent diabetes mellitus 

A-597
(IDDM) show signs of immune activation. Clin Exp 

Immunol 1999;116(1):70-77. Not about celiac and GI 

lymphoma 

Schattner A, Kozak N, Lassry Y et al. Primary 

intestinal T-cell lymphoma and sclerosing cholangitis: 

A cytokine-mediated association?. J Intern Med 

1998;244(6):537-541. Not about celiac and GI 

lymphoma 

Schmitt-Graff A, Hummel M, Zemlin M et al.

Intestinal T-cell lymphoma: a reassessment of 

cytomorphological and phenotypic features in relation

to patterns of small bowel remodelling. Virchows 

Archiv - an International Journal of Pathology 

1996;429(1):27-36. Not about celiac and GI 

lymphoma 

Schweizer J J, Oren A, Mearin M L. Cancer in 

children with celiac disease: a survey of the European 

Society of Paediatric Gastroenterology, Hepatology

and Nutrition. J Pediatr Gastroenterol Nutr 

2001;33(1):97-100. Not about celiac and GI 

lymphoma 

Scott B B, Losowsky M S. Depressed cell mediated 

immunity in coeliac disease. Gut 1976;17(11):900-

905. Not about celiac and GI lymphoma 

Seaman W B, Galdabini J J. Intestinal obstruction

complicating adult Celiac disease. New Engl J Med 

1976;295(22):1242-1248. Not about celiac and GI 

lymphoma 

Sedghizadeh Parish P, Shuler Charles F, Allen Carl M 

et al. Celiac disease and recurrent aphthous stomatitis:

a report and review of the literature. Oral Surg Oral 

Med Oral Pathol Oral Radiol Endod 2002;94(4):474-

478. Not about celiac and GI lymphoma 

Selby W, Gallagher N D. Development of malignancy

in 9 of 96 patients with adult coeliac disease. Aust

New Zealand J Med 1978;8(6):669Does not address 

the question 

Seligmann M. Alpha heavy chain disease. Blut 

1975;31(1):1-4. Not about celiac and GI lymphoma 

Selzer G, Sherman G, Callihan T R et al. Primary 

small intestinal lymphomas and alpha-heavy-chain 

disease. A study of 43 cases from a pathology

department in Israel. Isr J Med Sci 1979;15(2):111-

123. Not about celiac and GI lymphoma 

Seraphin Peter, Mobarhan Sohrab. Mortality in

patients with celiac disease. Nutr Rev 2002;60(4):116-

118. Review article 

Shaoul R, Marcon M A, Okada Y et al. Gastric

metaplasia: a frequently overlooked feature of

duodenal biopsy specimens in untreated celiac disease. 

J Pediatr Gastroenterol Nutr 2000;30(4):397-403. Not 

about celiac and GI lymphoma 

Sharma B C, Bhasin D K, Makharia G et al.

Diagnostic value of push-type enteroscopy: A report 

from India. Am J Gastroenterol 2000;95(1):137-140. 

Not about celiac and GI lymphoma 

Sheldon W. Prognosis in early adult life of coeliac 

children treated with a gluten-free diet. Br Med J 

1969;2(654):401-404. Not about celiac and GI 

lymphoma 

Shepherd N A, Blackshaw A J, Hall P A et al.

Malignant lymphoma with eosinophilia of the 

gastrointestinal tract. Histopathology 1987;11(2):115-

130. Does not address the question 

Shils M E. Nutritional problems associated with

gastrointestinal and genitourinary cancer. Cancer Res 

1977;37(7 Pt 2):2366-2372. Not about celiac and GI 

lymphoma 

Shiner M. Present trends in coeliac disease. Postgrad 

Med J 1984;60(709):773-778. Not about celiac and GI 

lymphoma 

Shiner M, Pearson J R. Abnormalities in the jejunal 

mucosa in Arab children. Gastroenterol Clin Biol

1981;5(6-7):663-673. Not about celiac and GI 

lymphoma 

Shreeve D R, Horrocks P, Mainwaring A R.

Steatorrhoea and intra-abdominal lymphoma. Scand J 

Gastroenterol 1968;3(6):577-585. Does not address 

the question 

Signore A, Chianelli M, Annovazzi A et al. Imaging 

active lymphocytic infiltration in coeliac disease with 

iodine-123-interleukin-2 and the response to diet. Eur 

J Nucl Med 2000;27(1):18-24. Not about celiac and 

GI lymphoma 

Sigurgeirsson B, Agnarsson B A, Lindelof B. Risk of 

lymphoma in patients with dermatitis herpetiformis. 

BMJ 1994;308(6920):13-15. Not about celiac and GI 

lymphoma 

Simu G, Jung J, Vojth V et al. Microscopic 

observations concerning the autoimmune response 

escalation into malignant lymphoma. Morphol 

Embryol (Bucur) 1986;32(2):99-104. Not about celiac 

and GI lymphoma 

Sjaastad O. Urinary excretion of free and conjugated 

histamine in various gastrointestinal disorders. Acta

Med Scand 1969;185(6):495-499. Not about celiac 

and GI lymphoma 

Skinner J M. Gastrointestinal lymphoma. Pathology

1985;17(2):193-203. Review article 

A-598
Skinner J M, Whitehead R. Immunological aspects of 

gastro-intestinal pathology. Curr Top Pathol

1976;63259-288. Not about celiac and GI lymphoma 

Slavutsky I, Gomez J C, Pedreira S et al. Increased 

rDNA transcriptional activity in celiac disease. J Clin 

Gastroenterol 1992;14(1):11-14. Not about celiac and 

GI lymphoma 

Sleisenger M H, Brandborg L L. Malabsorption.

Major Probl Intern Med 1977;131-261. Not about 

celiac and GI lymphoma 

Smith E P, Zone J J. Dermatitis herpetiformis and

linear IgA bullous dermatosis. Dermatol Clin

1993;11(3):511-526. Not about celiac and GI

lymphoma 

Sollid L, Bruserud O, Gaudernack G et al. The role of

the CD8-positive subset of T cells in proliferative 

responses to soluble antigens. I. Studies of healthy

subjects, type 1 diabetics, and coeliac disease patients. 

Scand J Immunol 1986;23(4):461-467. Not about 

celiac and GI lymphoma 

Sorensen H T, Fonager K. Risk estimation of disorders 

associated with coeliac disease. A 16-year Danish

nationwide follow-up study based on hospital 

discharge data. Implications for screening. Int J Risk 

Saf Med 1996;8(2):137-140. Unable to extract data 

Spence W J, Ritchie S. Lymphomas of small bowel 

and their relationship to idiopathic steatorrhea. 

Canadian Journal of Surgery.Journal Canadien De 

Chirurgie 1969;12(2):207-209. Not about celiac and 

GI lymphoma 

Spencer J, Cerf-Bensussan N, Jarry A et al.

Enteropathy-associated T cell lymphoma (malignant 

histiocytosis of the intestine) is recognized by a 

monoclonal antibody (HML-1) that defines a 

membrane molecule on human mucosal lymphocytes. 

Am J Pathol 1988;132(1):1-5. Not about celiac and GI 

lymphoma 

Spencer J, MacDonald T T, Diss T C et al. Changes in 

intraepithelial lymphocyte subpopulations in coeliac 

disease and enteropathy associated T cell lymphoma

(malignant histiocytosis of the intestine). Gut

1989;30(3):339-346. Not about celiac and GI

lymphoma 

Spiro H M. About this issue. J Clin Gastroenterol 

1995;21(2):81Not about celiac and GI lymphoma 

Stazi Maria, Antonietta Cotichini, Rodolfo Patriarca et 

al. The Italian Twin Project: from the personal 

identification number to a national twin registry. Twin 

Research - the Official Journal of the International 

Society for Twin Studies 2002;5(5):382-386. Not 

about celiac and GI lymphoma 

Stein E, Shane E. Secondary osteoporosis. Endocrinol 

Metab Clin North Am 2003;32(1):115-134. Not about 

celiac and GI lymphoma 

Stein H, Dienemann D, Sperling M et al. Identification

of a T cell lymphoma category derived from intestinalmucosa-associated T cells. Lancet 1988;2(8619):1053-

1054. Not about celiac and GI lymphoma 

Stenhammar L, Brandt A, Wagermark J. A family

study of coeliac disease. Acta Paediatr Scand

1982;71(4):625-628. Not about celiac and GI

lymphoma 

Stenstam M, Brandt L, Hallberg T. Subnormal 

response of blood lymphocytes to 

phytohaemagglutinin in adult coeliac disease 

complicated by intestinal lymphoma. Scand J 

Gastroenterol 1983;18(6):777-781. Not about celiac 

and GI lymphoma 

Stewart J. Child coeliacs in adult life. Ir Med J

1974;67(15):411-414. Not about celiac and GI 

lymphoma 

Stokes P L, Holmes G K T. Malignancy. Clin

Gastroenterol 1974;3(1):159-170. Not about celiac and 

GI lymphoma 

Stokes P L, Asquith P, Waterhouse J H et al. 

Malignancy in relatives of patients with adult coeliac 

disease. Gut 1972;13(10):836-837. Not about celiac 

and GI lymphoma 

Stokes P L, Prior P, Sorahan T M. Malignancy in 

relatives of patients with coeliac disease. Br J Prev

Soc Med 1976;30(1):17-21. Not about celiac and GI 

lymphoma 

Swerdlow A J, Whittaker S, Carpenter L M et al.

Mortality and cancer incidence in patients with 

dermatitis herpetiformis: a cohort study. Br J Dermatol 

1993;129(2):140-144. Not about celiac and GI 

lymphoma 

Swinson C M, Hall P J, Bedford P A et al. HLA

antigens in coeliac disease associated with

malignancy. Gut 1983;24(10):925-928. Not about 

celiac and GI lymphoma 

Swinson C M, Slavin G, Coles E C et al. Coeliac 

disease and malignancy. Lancet 1983;1(8316):111-

115. Not about celiac and GI lymphoma 

Taggart D P, Imrie C W. A new pattern of histologic 

predominance and distribution of malignant diseases 

of the small intestine. Surg Gynecol Obstet

1987;165(6):515-518. Not about celiac and GI 

lymphoma 

A-599
Thompson H. Necropsy studies on adult coeliac 

disease. J Clin Pathol 1974;27(9):710-721. Not about 

celiac and GI lymphoma 

Thompson H. Pathology of coeliac disease. Curr Top 

Pathol 1976;6349-75. Not about celiac and GI 

lymphoma 

Thompson H. The small intestine at autopsy. Clin 

Gastroenterol 1974;3(1):171-181. Not about celiac and 

GI lymphoma 

Thornquist H, Jacobsen G S, Dahl L B et al. Coeliac 

disease and gluten-free diet: a following-up study of 

fifteen young adults. Ann Nutr Metab 1993;37(6):295-

301. Not about celiac and GI lymphoma 

Trejdosiewicz L K, Malizia G, Oakes J et al. 

Expression of the common acute lymphoblastic 

leukaemia antigen (CALLA gp100) in the brush 

border of normal jejunum and jejunum of patients with 

coeliac disease. J Clin Pathol 1985;38(9):1002-1006. 

Not about celiac and GI lymphoma 

Trier J S. Diagnostic value of peroral biopsy of the 

proximal small intestine. N Engl J Med 

1971;285(26):1470-1473. Not about celiac and GI 

lymphoma 

Troncone R, Greco L, Auricchio S. Gluten-sensitive 

enteropathy. Pediatr Clin North Am 1996;43(2):355-

373. Not about celiac and GI lymphoma 

Tursi A, Gasbarrini G. Acquired gastric mucosaassociated lymphoid tissue (MALT): a review with 

special emphasis on association with extragastric

diseases and management problems of gastric MALT. 

J Clin Gastroenterol 1999;29(2):133-137. Review 

article 

Vahedi Kouroche, Mascart Francoise, Mary Jean et al. 

Reliability of antitransglutaminase antibodies as 

predictors of gluten-free diet compliance in adult 

celiac disease. Am J Gastroenterol 2003;98(5):1079-

1087. Not about celiac and GI lymphoma 

Verkarre V, Asnafi V, Lecomte T et al. Refractory

coeliac sprue is a diffuse gastrointestinal disease. Gut 

2003;52(2):205-211. Does not address the question 

Verkarre V, Romana S, Cellier C et al. Recurrent 

partial trisomy 1q22-q44 in clonal intraepithelial 

lymphocytes in refractory celiac sprue. 

Gastroenterology 2003;125(1):40-46. Does not 

address the question 

Veyrieres M, Baillet P, Hay J M et al. Factors 

influencing long-term survival in 100 cases of small 

intestine primary adenocarcinoma. Am J Surg 

1997;173(3):237-239. Not about celiac and GI 

lymphoma 

Wahab P J, Crusius J B A, Meijer J W R et al.

Cyclosporin in the treatment of adults with refractory

coeliac disease - An open pilot study. Aliment 

Pharmacol Ther 2000;14(6):767-774. Not about celiac 

and GI lymphoma 

Wahab P J, Meijer Jos W R, Mulder C J J. Histologic

follow-up of people with celiac disease on a glutenfree diet: slow and incomplete recovery. Am J Clin 

Pathol 2002;118(3):459-463. Not a controlled study

Walker W A, Hong R. Immunology of the 

gastrointestinal tract. II. Eur J Pediatr 1973;83(5):711-

720. Not about celiac and GI lymphoma 

Walsh S V, Egan L J, Connolly C E et al. 

Enteropathy-associated T-cell lymphoma in the West 

of Ireland: low-frequency of Epstein-Barr virus in

these tumors. Modern Pathology - an Official Journal 

of the United States and Canadian Academy of

Pathology, Inc 1995;8(7):753-757. Does not address 

the question 

Wartiovaara J, Tarpila S. Cell contacts and polysomes

in irradiated human jejunal mucosa at onset of 

epithelial repair. Laboratory Investigation: A Journal 

of Technical Methods and Pathology 1977;36(6):660-

665. Not about celiac and GI lymphoma 

Washington K, Stenzel T T, Buckley R H et al. 

Gastrointestinal pathology in patients with common 

variable immunodeficiency and X-linked 

agammaglobulinemia. Am J Surg Pathol 

1996;20(10):1240-1252. Not about celiac and GI 

lymphoma 

Westergaard H. The sprue syndromes. Am J Med Sci 

1985;290(6):249-262. Not about celiac and GI 

lymphoma 

Whitehead R. Primary lymphadenopathy complicating

idiopathic steatorrhoea. Gut 1968;9(5):569-575. Not 

about celiac and GI lymphoma 

Whitehead R, Skinner J M. Morphology of the gut 

associated lymphoid system in health and disease: a

review. Pathology 1978;10(1):3-16. Review article 

Whorwell P J, Alderson M R, Foster K J et al. Death 

from ischaemic heart-disease and malignancy in adult

patients with coeliac disease. Lancet

1976;2(7977):113-114. Does not address the question 

Williamson R C, Welch C E, Malt R A.

Adenocarcinoma and lymphoma of the small intestine. 

Distribution and etiologic associations. Ann Surg

1983;197(2):172-178. Does not address the question 

Wilson F A, Dietschy J M. Differential diagnostic 

approach to clinical problems of malabsorption. 

Gastroenterology 1971;61(6):911-931. Not about 

celiac and GI lymphoma 

A-600
Wright D H. Enteropathy associated T cell lymphoma. 

Cancer Surv 1997;30249-261. Review article 

Wright D H. The major complications of coeliac

disease. Bailliere's Clinical Gastroenterology

1995;9(2):351-369. Review article 

Wright D H. The identification and classification of 

non-Hodgkin's lymphoma: A review. Diagn 

Histopathol 1982;5(2):73-111. Not about celiac and 

GI lymphoma 

Wu T T, Hamilton S R. Lymphocytic gastritis:

association with etiology and topology. Am J Surg

Pathol 1999;23(2):153-158. Not about celiac and GI 

lymphoma 

Young W F, Pringle E M. 110 children with coeliac 

disease, 1950-1969. Arch Dis Child 

1971;46(248):421-436. Not about celiac and GI

lymphoma 

Zarrabi M H, Rosner F. Middle Eastern intestinal

lymphoma: report of a case and review of the 

literature. Am J Med Sci 1976;272(1):101-119. Not 

about celiac and GI lymphoma 

Zoli G, Corazza G R, Parente R et al. Defective

phagocyte activity in adult coeliac disease. Eur J

Gastroenterol Hepatol 1992;4(8):675-678. Not about 

celiac and GI lymphoma 

Zucca E, Roggero E, Bertoni F et al. Primary

extranodal non-Hodgkin's lymphomas. Part 1:

Gastrointestinal, cutaneous and genitourinary

lymphomas. Ann Oncol 1997;8(8):727-737. Not about 

celiac and GI lymphoma

Objective 4 – Expected Consequences of Testing for CD 

Aarbakke J, Schjonsby H. Value of urinary simple 

phenol and indican determinations in the diagnosis of 

the stagnant loop syndrome. Scand J Gastroenterol 

1976;11(4):409-414. Not about consequences of

testing 

Abdulkarim Ahmad S, Burgart Lawrence J, See 

Jacalyn et al. Etiology of nonresponsive celiac disease:

results of a systematic approach. Am J Gastroenterol 

2002;97(8):2016-2021. Not about consequences of

testing 

Acalovschi M, Jayanthi V, Probert C S et al. 

Management of coeliac disease: a changing diagnostic 

approach but what value in follow up?. Qual Health 

Care 1992;1(1):26-28. Not about consequences of

testing 

Acerini C L, Ahmed M L, Ross K M et al. Coeliac 

disease in children and adolescents with IDDM: 

clinical characteristics and response to gluten-free 

diet. Diabet Med 1998;15(1):38-44. Not about 

consequences of testing 

Ackerman Z, Eliakim R, Stalnikowicz R et al. Role of 

small bowel biopsy in the endoscopic evaluation of 

adults with iron deficiency anemia. Am J 

Gastroenterol 1996;91(10):2099-2102. Not about 

consequences of testing 

Adrian T E, Besterman H S, Mallinson C N et al. 

Plasma trypsin in chronic pancreatitis and pancreatic

adenocarcinoma. Clin Chim Acta 1979;97(2-3):205-

212. Not about consequences of testing 

Agardh D, Nilsson A, Carlsson A et al. Tissue 

transglutaminase autoantibodies and human leucocyte 

antigen in Down Syndrome patients with coeliac 

disease. Acta Paediatr 2002;91(1):34-38. Not about 

consequences of testing 

Agardh Daniel, Borulf Stefan, Lernmark Ake et al.

Tissue transglutaminase immunoglobulin isotypes in 

children with untreated and treated celiac disease. J 

Pediatr Gastroenterol Nutr 2003;36(1):77-82. Not 

about consequences of testing 

Agreus L, Svardsudd K, Tibblin G et al. Endomysium 

antibodies are superior to gliadin antibodies in

screening for coeliac disease in patients presenting 

supposed functional gastrointestinal symptoms. Scand 

J Prim Health Care 2000;18(2):105-110. Not about 

consequences of testing 

Aine L. Coeliac-type permanent-tooth enamel defects.

Ann Med 1996;28(1):9-12. Not about consequences of

testing 

Akesson B, Floren C H. Use of the triolein breath test

for the demonstration of fat malabsorption in coeliac

disease. Scand J Gastroenterol 1984;19(3):307-314. 

Not about consequences of testing 

Aktay A N, Lee P C, Kumar V et al. The prevalence 

and clinical characteristics of celiac disease in juvenile

diabetes in Wisconsin. J Pediatr Gastroenterol Nutr 

2001;33(4):462-465. Not about consequences of

testing 

Al Attas R A. How common is celiac disease in

Eastern Saudi Arabia?. Ann Saudi Med 2002;22(5-

6):315-319. Not about consequences of testing 

A-601
Altuntas B, Filik B, Ensari A et al. Can zinc 

deficiency be used as a marker for the diagnosis of 

celiac disease in Turkish children with short stature?.

Pediatr Int 2000;42(6):682-684. Not about 

consequences of testing 

Altuntas B, Kansu A, Ensari A et al. Celiac disease in

Turkish short-statured children and the value of

antigliadin antibody in diagnosis. Acta Paediatr Jpn 

1998;40(5):457-460. Not about consequences of

testing 

Amann S T, Josephson S A, Toskes P P. Acid 

steatocrit: a simple, rapid gravimetric method to 

determine steatorrhea. Am J Gastroenterol 

1997;92(12):2280-2284. Not about consequences of 

testing 

Amara W, Husebekk A. Improved method for

serological testing in celiac disease--IgA antiendomysium antibody test: a comparison between 

monkey oesophagus and human umbilical cord as

substrate in indirect immunofluorescence test. Scand J 

Clin Lab Invest 1998;58(7):547-554. Not about 

consequences of testing 

Ament M E, Perera D R, Esther L J. Sucraseisomaltase deficiency-a frequently misdiagnosed 

disease. Eur J Pediatr 1973;83(5):721-727. Not about 

consequences of testing 

Amenta J S. Lipiodol absorption and urinary lodide 

excretion as a screening test for steatorrhea. Clin

Chem 1969;15(4):295-306. Not about consequences of 

testing 

Amin M, Eckhardt T, Kapitza S et al. Correlation

between tissue transglutaminase antibodies and

endomysium antibodies as diagnostic markers of 

coeliac disease. Clin Chim Acta 1999;282(1-2):219-

225. Not about consequences of testing 

Ammann R W, Akovbiantz A, Hacki W et al. 

Diagnostic value of the fecal chymotrypsin test in

pancreatic insufficiency, particularly chronic 

pancreatitis: correlation with the pancreozyminsecretin test, fecal fat excretion and final clinical

diagnosis. Digestion 1981;21(6):281-289. Not about 

consequences of testing 

Ammann R, Kashiwagi H. Pancreatic exocrine 

insufficiency and proteolytic enzymes in stool. A 

critical evaluation of a new diagnostic test in various 

forms of steatorrhea. Helv Med Acta 1966;33(3):220-

228. Not about consequences of testing 

Anand A C, Elias E, Neuberger J M. End-stage 

primary biliary cirrhosis in a first generation migrant 

south Asian population. Eur J Gastroenterol Hepatol 

1996;8(7):663-666. Not about consequences of testing 

Anand B S, Piris J, Jerrome D W et al. The timing of 

histological damage following a single challenge with 

gluten in treated coeliac disease. Q J Med 

1981;50(197):83-94. Not about consequences of

testing 

Anand B S, Piris J, Truelove S C. The role of various 

cereals in coeliac disease. Q J Med 1978;47(185):101-

110. Not about consequences of testing 

Anand B S, Truelove S C, Offord R E. Skin test for 

coeliac disease using a subfraction of gluten. Lancet

1977;1(8003):118-120. Not about consequences of

testing 

Andersson H, Dotevall G, Mobacken H. Malignant 

mesenteric lymphoma in a patient with dermatitis 

herpetiformis, hypochlorhydria, and small-bowel 

abnormalities. Scand J Gastroenterol 1971;6(5):397-

399. Not about consequences of testing 

Anonymous. A long-term survey of coeliac disease. 

Med J Aust 1971;2(20):992Not about consequences of

testing 

Anonymous. American Gastroenterological 

Association medical position statement: Celiac Sprue. 

Gastroenterology 2001;120(6):1522-1525. Not about 

consequences of testing 

Anonymous. American Thoracic Society/European 

Respiratory Society statement: Standards for the

diagnosis and management of individuals with alpha-1 

antitrypsin deficiency. Am J Respir Crit Care Med

2003;168(7):818-900. Not about consequences of

testing 

Anonymous. Beyond the iceberg: the present and

future of coeliac disease screening. Proceedings of a 

symposium. Ancona, Italy, 20-21 October 1995. Acta 

Paediatr 1996; 412(Suppl):1-84. Unable to obtain

article 

Anonymous. Catch-up growth in celiac disease. Nutr 

Rev 1973;31(1):13-14. Not about consequences of

testing 

Anonymous. Celiac disease and how to live with it. 

Harvard Women's Health Watch 2001;8(9):3-4. Not 

about consequences of testing 

Anonymous. Celiac disease: more than an irritable 

bowel. Harvard Women's Health Watch

2000;7(11):7Not about consequences of testing 

Anonymous. Coeliac disease. Br Med J

1970;4(726):1-2. Not about consequences of testing 

Anonymous. HIV-associated enteropathy. Lancet 

1989;2(8666):777-778. Not about consequences of

testing 

A-602
Anonymous. Screening for coeliac disease has

benefits in Williams syndrome. Arch Dis Child

2002;86(4):275Not about consequences of testing 

Anonymous. Small-intestinal morphology in

infectious hepatitis. JAMA 1969;209(11):1713-1714. 

Not about consequences of testing 

Anson O, Weizman Z, Zeevi N. Celiac disease:

parental knowledge and attitudes of dietary

compliance. Pediatrics 1990;85(1):98-103. Not about 

consequences of testing 

Aoun J P, Moukarbel N, Aftimos G. Value of 

duodenal endoscopic markers of villous atrophy. J 

Med Liban 2001;49(6):319-324. Not about 

consequences of testing 

Araya M, Mondragon A, Perez-Bravo F et al. Celiac 

disease in a Chilean population carrying Amerindian 

traits. J Pediatr Gastroenterol Nutr 2000; 31(4):381-

386. Not about consequences of testing 

Artan R. Antigliadin antibody measurement as a 

screening test for childhood coeliac disease. Int Med J 

1998;5(3):209-212. Not about consequences of testing 

Ascher H, Hahn-Zoric M, Hanson L A et al. Value of 

serologic markers for clinical diagnosis and population

studies of coeliac disease. Scand J Gastroenterol 

1996;31(1):61-67. Not about consequences of testing 

Ascher H, Lanner A, Kristiansson B. A new 

laboratory kit for anti-gliadin IgA at diagnosis and 

follow-up of childhood celiac disease. J Pediatr

Gastroenterol Nutr 1990;10(4):443-450. Not about 

consequences of testing 

Ascher H. Paediatric aspects of coeliac disease: old 

challenges and new ones... Digestive and Liver 

Disease - Official Journal of the Italian Society of 

Gastroenterology and the Italian Association for the 

Study of the Liver 2002;34(3):216-224. Not about 

consequences of testing 

Ashabani A, Abushofa U, Abusrewill S et al. The 

prevalence of coeliac disease in Libyan children with 

type 1 diabetes mellitus. Diabetes Metab Res Rev 

2003;19(1):69-75. Not about consequences of testing 

Ashabani A, Errabtea H, Shapan A et al. Serologic 

markers of untreated celiac disease in Libyan children: 

antigliadin, antitransglutaminase, antiendomysial, and 

anticalreticulin antibodies. J Pediatr Gastroenterol 

Nutr 2001;33(3):276-282. Not about consequences of 

testing 

Auricchio S, Cardelli M, De Ritis G. An in vitro 

animal model for the study of cereal components toxic 

in celiac disease. Pediatr Res 1984;18(12):1372-1378. 

Not about consequences of testing 

Auricchio S, Greco L, Troncone R. What is the true 

prevalence of coeliac disease?. Gastroenterol Int 

1990;3(3):140-142. Not about consequences of testing 

Auricchio S, Mazzacca G, Tosi R et al. Coeliac

disease as a familial condition: Identification of

asymptomatic coeliac patients within family groups.

Gastroenterol Int 1988;1(1):25-31. Not about 

consequences of testing 

Babron M-C, Nilsson S, Adamovic S et al. Meta and 

pooled analysis of European coeliac disease data. Eur 

J Hum Genet 2003;11(11):828-834. Not about 

consequences of testing 

Bagnasco M, Montagna P, De Alessandri A et al. IgA 

antiendomysium antibodies in human umbilical cord 

sections as a screening test in relatives of patients with 

celiac disease. Allergy 1997;52(10):1017-1021. Not 

about consequences of testing 

Bahia M, Rabello A, Brasileiro Filho G et al. Serum 

antigliadin antibody levels as a screening criterion 

before jejunal biopsy indication for celiac disease in a

developing country. Brazilian Journal of Medical and 

Biological Research = Revista Brasileira De Pesquisas 

Medicas E Biologicas / Sociedade Brasileira De

Biofisica ...Et Al 2001;34(11):1415-1420. Not about 

consequences of testing 

Bahna S L, Gandhi M D. Milk hypersensitivity. II. 

Practical aspects of diagnosis, treatment and 

prevention. Ann Allergy 1983;50(5):295-301. Not 

about consequences of testing 

Bai J C, Andrush A, Matelo G et al. Fecal fat 

concentration in the differential diagnosis of 

steatorrhea. Am J Gastroenterol 1989;84(1):27-30. 

Not about consequences of testing 

Bai J, Moran C, Martinez C et al. Celiac sprue after 

surgery of the upper gastrointestinal tract. Report of 

10 patients with special attention to diagnosis, clinical 

behavior, and follow-up. J Clin Gastroenterol 

1991;13(5):521-524. Not about consequences of

testing 

Bailey D S, Freedman A R, Price S C et al. Early

biochemical responses of the small intestine of coeliac 

patients to wheat gluten. Gut 1989;30(1):78-85. Not 

about consequences of testing 

Baker P G, Barry R E, Read A E. Detection of

continuing gluten ingestion in treated coeliac patients. 

Br Med J 1975;1(5956):486-488. Not about 

consequences of testing 

Balasekaran R, Porter J L, Santa Ana C A et al. 

Positive results on tests for steatorrhea in persons 

consuming olestra potato chips. Ann Intern Med 

2000;132(4):279-282. Not about consequences of

testing 

A-603
Baldas V, Tommasini A, Trevisiol C et al.

Development of a novel rapid non-invasive screening 

test for coeliac disease. Gut 2000;47(5):628-631. Not 

about consequences of testing 

Bamforth J, Murray P J, Roberts A H. Spurious 

steatorrhoea. Br Med J 1967;2(553):682Not about 

consequences of testing 

Banks Sara M, Salovey Peter, Greener Susan et al. 

The effects of message framing on mammography

utilization. Health Psychol 1995;14(2):178-184. Not 

about consequences of testing 

Barakat M H, Ali S M, Badawi A R et al. Peroral

endoscopic duodenal biopsy in infants and children. 

Acta Paediatr Scand 1983;72(4):563-569. Not about 

consequences of testing 

Barbato M, Miglietta M R, Viola F et al. Impact of

modification of diagnostic techniques and criteria on 

the presentation of celiac disease in the last 16 years.

Observation in Rome. Minerva Pediatr

1996;48(9):359-363. Not about consequences of

testing 

Bardella M T, Minoli G, Radaelli F et al. Reevaluation

of duodenal endoscopic markers in the diagnosis of 

celiac disease. Gastrointest Endosc 2000;51(6):714-

716. Not about consequences of testing 

Bardella M T, Minoli G, Ravizza D et al. Increased 

prevalence of celiac disease in patients with dyspepsia. 

Arch Intern Med 2000;160(10):1489-1491. Not about 

consequences of testing 

Bardella M T, Molteni N, Cesana B et al. IgA 

antigliadin antibodies, cellobiose/mannitol sugar test, 

and carotenemia in the diagnosis of and screening for 

celiac disease. Am J Gastroenterol 1991;86(3):309-

311. Not about consequences of testing 

Bardella M T, Trovato C, Cesana B M et al.

Serological markers for coeliac disease: is it time to

change?. Digestive and Liver Disease - Official

Journal of the Italian Society of Gastroenterology and 

the Italian Association for the Study of the Liver 

2001;33(5):426-431. Not about consequences of

testing 

Bardella M T, Vecchi M, Conte D et al. Chronic 

unexplained hypertransaminasemia may be caused by

occult celiac disease. Hepatology 1999;29(3):654-657. 

Not about consequences of testing 

Barera G, Bianchi C, Calisti L et al. Screening of

diabetic children for coeliac disease with antigliadin 

antibodies and HLA typing. Arch Dis Child

1991;66(4):491-494. Not about consequences of

testing 

Barera G, Bonfanti R, Viscardi M et al. Occurrence of

celiac disease after onset of type 1 diabetes: a 6-year 

prospective longitudinal study. Pediatrics 

2002;109(5):833-838. Not about consequences of

testing 

Barry R E, Barry R, Ene M D et al. Fluorescein 

dilaurate--tubeless test for pancreatic exocrine failure. 

Lancet 1982;2(8301):742-744. Not about 

consequences of testing 

Barry R E, Morris J S, Read A E. A case of smallintestinal mucosal atrophy. Gut 1970;11(9):743-747. 

Not about consequences of testing 

Barton D M, Baskar V, Kamalakannan D et al. An 

assessment of care of paediatric and adolescent

patients with diabetes in a large district general 

hospital. Diabet Med 2003;20(5):394-398. Not about 

consequences of testing 

Basso D, Gallo N, Guariso G et al. Role of antitransglutaminase (anti-tTG), anti-gliadin, and antiendomysium serum antibodies in diagnosing celiac 

disease: a comparison of four different commercial 

kits for anti-tTG determination. J Clin Lab Anal 

2001;15(3):112-115. Not about consequences of

testing 

Baur X, Sander I, Posch A et al. Baker's asthma due to

the enzyme xylanase - A new occupational allergen. 

Clin Exp Allergy 1998;28(12):1591-1593. Not about 

consequences of testing 

Beckett C G, Ciclitira P J. Celiac disase. Curr Opin 

Gastroenterol 1997;13(2):107-111. Not about 

consequences of testing 

Beckett C. A gut issue. Nurs Times 1999;95(8):65-6, 

69. Not about consequences of testing 

Beers M H, Fink A, Beck J C. Screening

recommendations for the elderly. Am J Public Health 

1991;81(9):1131-1140. Not about consequences of

testing 

Bejes C, Marvel M K. Attempting the improbable: 

Offering colorectal cancer screening to all appropriate 

patients. Fam Pract Res J 1992;12(1):83-90. Not about 

consequences of testing 

Bell D R. Differential diagnosis of diarrhoea in adults. 

Br J Gen Pract 1974;213(1273):47-53. Not about 

consequences of testing 

Belloni C, Avanzini M A, De Silvestri A et al. No

evidence of autoimmunity in 6-year-old children

immunized at birth with recombinant hepatitis B 

vaccine. Pediatrics 2002;110(1 Pt 1):E4Not about 

consequences of testing 

A-604
Bengtsson U, Nilsson-Balknas U, Hanson L A et al. 

Double blind, placebo controlled food reactions do not 

correlate to IgE allergy in the diagnosis of staple food 

related gastrointestinal symptoms. Gut 

1996;39(1):130-135. Not about consequences of

testing 

Benini L, Caliari S, Bonfante F et al. Fecal fat 

concentration in the screening of steatorrhea. 

Digestion 1992;53(1-2):94-100. Not about 

consequences of testing 

Berg N O, Borulf S, Jakobsson I et al. How to 

approach the child suspected of malabsorption. 

Experience from a prospective investigation of

suspected malabsorption in children 1968-1976 in 

Malmo. Acta Paediatr Scand 1978;67(4):403-411. Not 

about consequences of testing 

Berger R, Schmidt G. Evaluation of six anti-gliadin 

antibody assays. J Immunol Methods 1996;191(1):77-

86. Not about consequences of testing 

Berrill W T, Eade O E, Fitzpatrick P F. Bird Fancier's 

lung and jejunal villous atrophy. Lancet 

1975;2(7943):1006-1008. Not about consequences of 

testing 

Bertele R M, Burgin-Wolff A, Berger R et al. The 

fluorescent immunosorbent test for IgG gliadin

antibodies and the leucocyte migration inhibition test

in coeliac disease; comparison of diagnostic value. Eur

J Pediatr 1985;144(1):58-62. Not about consequences 

of testing 

Berti I, Trevisiol C, Tommasini A et al. Usefulness of 

screening program for celiac disease in autoimmune 

thyroiditis. Dig Dis Sci 2000;45(2):403-406. Not 

about consequences of testing 

Beutner E H, Kumar V, Chorzelski Craig T P R M et 

al. Screening for celiac disease. New Engl J Med

1989;320(16):1087-1089. Not about consequences of 

testing 

Bhatnagar S, Bhan M K. Serological diagnosis of 

celiac disease. Indian J Pediatr 1999;66(1 Suppl):S26-

S31. Not about consequences of testing 

Biagi F, Corazza G R. Defining gluten refractory 

enteropathy. Eur J Gastroenterol Hepatol 

2001;13(5):561-565. Not about consequences of

testing 

Biagi F, Corazza G R. Tissue transglutaminase

antibodies: is sensitivity more important than 

specificity?. Digestive and Liver Disease - Official

Journal of the Italian Society of Gastroenterology and 

the Italian Association for the Study of the Liver 

2001;33(5):401-402. Not about consequences of

testing 

Biagi F, Ellis H J, Parnell N D et al. A non-toxic 

analogue of a coeliac-activating gliadin peptide: a 

basis for immunomodulation?. Aliment Pharmacol 

Ther 1999;13(7):945-950. Not about consequences of 

testing 

Biagi F, Ellis H J, Yiannakou J Y et al. Tissue 

transglutaminase antibodies in celiac disease. Am J 

Gastroenterol 1999;94(8):2187-2192. Not about 

consequences of testing 

Biagi F, Parnell N D, Ellis H J et al. Endomysial 

antibody production is not related to histological 

damage after in vitro gluten challenge. Eur J 

Gastroenterol Hepatol 2000;12(1):57-60. Not about 

consequences of testing 

Biagi F, Pezzimenti D, Campanella J et al.

Endomysial and tissue transglutaminase antibodies in 

coeliac sera: a comparison not influenced by previous 

serological testing. Scand J Gastroenterol 

2001;36(9):955-958. Not about consequences of

testing 

Bilbao J R, Vitoria Juan C, Ortiz Lourdes et al.

Immunoglobulin G autoantibodies against tissuetransglutaminase. A sensitive, cost-effective assay for 

the screening of celiac disease. Autoimmunity

2002;35(4):255-259. Not about consequences of

testing 

Binder H J. Cediac sprue--"unmasking" after 

vagotomy and hiatal-hernia repair. N Engl J Med 

1970;283(10):520-521. Not about consequences of

testing 

Bischoff S C, Mayer J, Wedemeyer J et al. 

Colonoscopic allergen provocation (COLAP): a new 

diagnostic approach for gastrointestinal food allergy.

Gut 1997;40(6):745-753. Not about consequences of 

testing 

Bittinger M, Barnert J, Schmidbaur W et al. D-xylose 

hydrogen-breath test as a noninvasive screening test 

for Coeliac disease. What is the optimum xylose

dose?. Rom J Gastroenterol 1997;6(4):235-238. Not 

about consequences of testing 

Bjarnason I, MacPherson A, Hollander D. Intestinal

permeability: an overview. Gastroenterology

1995;108(5):1566-1581. Not about consequences of 

testing 

Bjarnason I, Peters T J, Veall N. A persistent defect in 

intestinal permeability in coeliac disease demonstrated

by a 51Cr-labelled EDTA absorption test. Lancet 

1983;1(8320):323-325. Not about consequences of

testing 

Blackwell P J, Hill P G, Holmes G K T.

Autoantibodies to human tissue transglutaminase: 

superior predictors of coeliac disease. Scand J

A-605
Gastroenterol 2002;37(11):1282-1285. Not about 

consequences of testing 

Bodanszky H, Horvath K, Bata A et al. Hydrogen 

breath test in small intestinal malabsorption. Acta

Paediatr Hung 1987;28(1):45-49. Not about 

consequences of testing 

Bodanszky H, Horvath K, Horn G. The D-xylose test 

in coeliac disease. Acta Paediatr Hung 1983;24(1):17-

22. Not about consequences of testing 

Bode S, Gudmand-Hoyer E. Evaluation of the gliadin 

antibody test for diagnosing coeliac disease. Scand J 

Gastroenterol 1994;29(2):148-152. Not about 

consequences of testing 

Bode S, Gudmand-Hoyer E. Symptoms and 

haematologic features in consecutive adult coeliac 

patients. Scand J Gastroenterol 1996;31(1):54-60. Not 

about consequences of testing 

Bode S, Weile B, Krasilnikoff P A et al. The 

diagnostic value of the gliadin antibody test in celiac 

disease in children: a prospective study. J Pediatr 

Gastroenterol Nutr 1993;17(3):260-264. Not about 

consequences of testing 

Boldrini R, Biselli R, Bosman C. Chylomicron

retention disease--the role of ultrastructural 

examination in differential diagnosis. Pathol Res Pract 

2001;197(11):753-757. Not about consequences of

testing 

Bonamico M, Ballati G, Mariani P et al. Screening for 

coeliac disease: the meaning of low titers of antigliadin antibodies (AGA) in non-coeliac children. Eur 

J Epidemiol 1997;13(1):55-59. Not about 

consequences of testing 

Bonamico M, Bottaro G, Pasquino A M et al. Celiac 

disease and turner syndrome. J Pediatr Gastroenterol 

Nutr 1998;26(5):496-499. Not about consequences of 

testing 

Bonamico M, Mariani P, Danesi H M et al. Prevalence

and clinical picture of celiac disease in italian down 

syndrome patients: a multicenter study. J Pediatr

Gastroenterol Nutr 2001;33(2):139-143. Not about 

consequences of testing 

Bonamico M, Mariani P, Mazzilli M C et al.

Frequency and clinical pattern of celiac disease among 

siblings of celiac children. J Pediatr Gastroenterol

Nutr 1996;23(2):159-163. Not about consequences of 

testing 

Bonamico M, Morellini M, Mariani P et al. HLA

antigens and antigliadin antibodies in coeliac disease. 

Dis Markers 1991;9(6):313-317. Not about 

consequences of testing 

Bonamico M, Rasore-Quartino A, Mariani P et al.

Down syndrome and coeliac disease: Usefulness of 

antigliadin and antiendomysium antibodies. Acta 

Paediatr 1996;85(12):1503-1505. Not about 

consequences of testing 

Bonamico M, Scire G, Mariani P et al. Short stature as

the primary manifestation of monosymptomatic celiac 

disease. J Pediatr Gastroenterol Nutr 1992;14(1):12-

16. Not about consequences of testing 

Bonamico M, Tiberti C, Picarelli A et al.

Radioimmunoassay to detect antitransglutaminase 

autoantibodies is the most sensitive and specific 

screening method for celiac disease. Am J

Gastroenterol 2001;96(5):1536-1540. Not about 

consequences of testing 

Bonamico Margherita, Pasquino Anna M, Mariani 

Paolo et al. Prevalence and clinical picture of celiac 

disease in Turner syndrome. J Clin Endocrinol Metab

2002;87(12):5495-5498. Not about consequences of 

testing 

Bontems P, Deprettere A, Cadranel S et al. The

coeliac iceberg: a consensus in paediatrics. Acta

Gastroenterol Belg 2000;63(2):157-162. Review 

article 

Book L, Hart A, Black J et al. Prevalence and clinical 

characteristics of celiac disease in Downs syndrome in 

a US study. Am J Med Genet 2001;98(1):70-74. Not 

about consequences of testing 

Book Linda, Zone John J, Neuhausen Susan L. 

Prevalence of celiac disease among relatives of sib 

pairs with celiac disease in U.S. families. Am J 

Gastroenterol 2003;98(2):377-381. Not about 

consequences of testing 

Book LS. Diagnosing celiac disease in 2002: who, 

why, and how? Pediatrics 2002; 109(5):952-954. Not 

about consequences of testing 

Booth S N, King J P G, Leonard J C et al. The 

significance of elevation of serum carcinoembryonic 

antigen (CEA) levels in inflammatory diseases of the

intestine. Scand J Gastroenterol 1974;9(7):651-656. 

Not about consequences of testing 

Bostick Roberd M, Sprafka J, Michael Virnig et al. 

Predictors of cancer prevention attitudes and 

participation in cancer screening examinations. Am J

Prev Med 1994;23(6):816-826. Not about 

consequences of testing 

Bottaro G, Cataldo F, Rotolo N et al. The clinical

pattern of subclinical/silent celiac disease: an analysis

on 1026 consecutive cases. Am J Gastroenterol 

1999;94(3):691-696. Not about consequences of

testing 

A-606
Bottaro G, Failla P, Rotolo N et al. Changes in coeliac 

disease behaviour over the years. Acta Paediatr 

1993;82(6-7):566-568. Not about consequences of

testing 

Boudraa G, Hachelaf W, Benbouabdellah M et al. 

Prevalence of coeliac disease in diabetic children and 

their first- degree relatives in west Algeria: screening 

with serological markers. Acta Paediatr 

1996;412(Suppl):58-60. Not about consequences of

testing 

Bradlow B A, Haggan J M. A comparison of the 

plasma viscosity and the erythrocyte sedimentation 

rate as screening tests. S Afr Med J 1979;55(11):415-

420. Not about consequences of testing 

Bramble M G, Zucoloto S, Wright N A et al. Acute 

gluten challenge in treated adult coeliac disease: a 

morphometric and enzymatic study. Gut 

1985;26(2):169-174. Not about consequences of

testing 

Brett P M, Yiannakou J Y, Morris M A et al. A 

pedigree-based linkage study of coeliac disease:

failure to replicate previous positive findings. Ann 

Hum Genet 1998;62(Pt 1):25-32. Not about 

consequences of testing 

Brett P M, Yiannakou J Y, Morris M A et al. Common 

HLA alleles, rather than rare mutants, confer 

susceptibility to coeliac disease. Ann Hum Genet

1999;63(Pt 3):217-225. Not about consequences of

testing 

Brocchi E, Tomassetti P, Misitano B et al. Endoscopic 

markers in adult coeliac disease. Digestive and Liver 

Disease - Official Journal of the Italian Society of 

Gastroenterology and the Italian Association for the 

Study of the Liver 2002;34(3):177-182. Not about 

consequences of testing 

Brooklyn Trevor N, Di Mambro, Alexandra J et al. 

Patients over 45 years with iron deficiency require 

investigation. Eur J Gastroenterol Hepatol 

2003;15(5):535-538. Not about consequences of

testing 

Brusco G, Di Stefano M, Corazza G R. Increased red 

cell distribution width and coeliac disease. Digestive 

and Liver Disease - Official Journal of the Italian

Society of Gastroenterology and the Italian

Association for the Study of the Liver 2000;32(2):128-

130. Not about consequences of testing 

Brusco G, Izzi L, Corazza G R. Tissue 

transglutaminase antibodies for coeliac disease 

screening. Ital J Gastroenterol Hepatol 

1998;30(5):496-497. Not about consequences of

testing 

Bulpitt C J, Benos A S, Nicholl C G et al. Should 

medical screening of the elderly population be 

promoted?. Gerontology 1990;36(4):230-245. Not 

about consequences of testing 

Bundek Nancy I, Marks Gary, Richardson Jean L. 

Role of health locus of control beliefs in cancer 

screening of elderly Hispanic women. Health Psychol 

1993;12(3):193-199. Not about consequences of

testing 

Burgin-Wolff A, Berger R, Gaze H et al. IgG, IgA and 

IgE gliadin antibody determinations as screening test 

for untreated coeliac disease in children, a multicentre 

study. Eur J Pediatr 1989;148(6):496-502. Not about 

consequences of testing 

Burgin-Wolff A, Bertele R M, Berger R et al. A

reliable screening test for childhood celiac disease:

fluorescent immunosorbent test for gliadin antibodies. 

A prospective multicenter study. Eur J Pediatr

1983;102(5):655-660. Not about consequences of

testing 

Burgin-Wolff A, Dahlbom I, Hadziselimovic F et al.

Antibodies against human tissue transglutaminase and 

endomysium in diagnosing and monitoring coeliac 

disease. Scand J Gastroenterol 2002;37(6):685-691. 

Not about consequences of testing 

Burgin-Wolff A, Hernandez R, Just M et al. 

Immunofluorescent antibodies against gliadin: a 

screening test for coeliac disease. Helv Paediatr Acta

1976;31(4-5):375-380. Not about consequences of

testing 

Burks A W, James J M, Hiegel A et al. Atopic 

dermatitis and food hypersensitivity reactions. Eur J 

Pediatr 1998;132(1):132-136. Not about consequences 

of testing 

Bushara K O, Goebel S U, Shill H et al. Gluten 

sensitivity in sporadic and hereditary cerebellar ataxia. 

Ann Neurol 2001;49(4):540-543. Not about 

consequences of testing 

Buts J P, Morin C L, Roy C C et al. One-hour blood 

xylose test: a reliable index of small bowel function. 

Eur J Pediatr 1978;92(5):729-733. Not about 

consequences of testing 

Caffarelli C, Romanini E, Caruana P et al. Clinical 

food hypersensitivity: the relevance of duodenal 

immunoglobulin E-positive cells. Pediatr Res 

1998;44(4):485-490. Not about consequences of

testing 

Calabuig M, Torregosa R, Polo P et al. Serological 

markers and celiac disease: a new diagnostic 

approach?. J Pediatr Gastroenterol Nutr 

1990;10(4):435-442. Not about consequences of

testing 

A-607
Calero P, Ribes-Koninckx C, Albiach V et al. IgA 

antigliadin antibodies as a screening method for 

nonovert celiac disease in children with insulindependent diabetes mellitus. J Pediatr Gastroenterol 

Nutr 1996;23(1):29-33. Not about consequences of

testing 

Calkhoven P G, Aalbers M, Koshte V L et al. 

Relationship between IgGinf 1 and IgGinf 4

antibodies to foods and the development of IgE 

antibodies to inhalant allergens. I. Establishment of a 

scoring system for the overall food responsiveness and 

its application to 213 unselected children. Clin Exp 

Allergy 1991;21(1):91-98. Not about consequences of 

testing 

Camarero C, Eiras P, Asensio A et al. Intraepithelial

lymphocytes and coeliac disease: permanent changes 

in CD3-/CD7+ and T cell receptor gammadelta 

subsets studied by flow cytometry. Acta Paediatr

2000;89(3):285-290. Not about consequences of

testing 

Campbell C B, Roberts R K, Cowen A E. The 

changing clinical presentation of coeliac disease in

adults. Med J Aust 1977;1(4):89-93. Not about 

consequences of testing 

Carlsson A K, Axelsson I E, Borulf S K et al. 

Prevalence of IgA-antiendomysium and IgAantigliadin autoantibodies at diagnosis of insulindependent diabetes mellitus in Swedish children and 

adolescents. Pediatrics 1999;103(6 Pt 1):1248-1252. 

Not about consequences of testing 

Carlsson A K, Axelsson I E, Borulf S K et al. 

Serological screening for celiac disease in healthy 2.5-

year-old children in Sweden. Pediatrics

2001;107(1):42-45. Not about consequences of testing 

Carlsson A, Axelsson I, Borulf S et al. Prevalence of 

IgA-antigliadin antibodies and IgA-antiendomysium 

antibodies related to celiac disease in children with 

Down syndrome. Pediatrics 1998;101(2):272-275. Not 

about consequences of testing 

Carnicer J, Farre C, Varea V et al. Prevalence of 

coeliac disease in Down Syndrome. Eur J

Gastroenterol Hepatol 2001;13(3):263-267. Not about 

consequences of testing 

Carroccio A, Cavataio F, Iacono G et al. IgA 

antiendomysial antibodies on the umbilical cord in

diagnosing celiac disease. Sensitivity, specificity, and 

comparative evaluation with the traditional kit. Scand 

J Gastroenterol 1996;31(8):759-763. Not about 

consequences of testing 

Carroccio A, Custro N, Montalto G et al. Evidence of 

transient IgA anti-endomysial antibody positivity in a 

patient with Graves' disease. Digestion 1999;60(1):86-

88. Not about consequences of testing 

Carroccio A, Fabiani E, Iannitto E et al. Tissue 

transglutaminase autoantibodies in patients with nonHodgkin's lymphoma: Case reports. Digestion 

2000;62(4):271-275. Not about consequences of

testing 

Carroccio A, Giannitrapani L, Soresi M et al. Guinea

pig transglutaminase immunolinked assay does not 

predict coeliac disease in patients with chronic liver 

disease. Gut 2001;49(4):506-511. Not about 

consequences of testing 

Carroccio A, Iacono G, D'Amico D et al. Production 

of anti-endomysial antibodies in cultured duodenal 

mucosa: usefulness in coeliac disease diagnosis. Scand 

J Gastroenterol 2002;37(1):32-38. Not about 

consequences of testing 

Carroccio A, Iacono G, Ippolito S et al. Usefulness of 

faecal elastase-1 assay in monitoring pancreatic

function in childhood coeliac disease. Ital J 

Gastroenterol Hepatol 1998;30(5):500-504. Not about 

consequences of testing 

Carroccio A, Iacono G, Montalto G et al. 

Immunologic and absorptive tests in celiac disease: 

can they replace intestinal biopsies?. Scand J

Gastroenterol 1993;28(8):673-676. Not about 

consequences of testing 

Carroccio A, Iannitto E, Cavataio F et al. Sideropenic 

anemia and celiac disease: one study, two points of 

view. Dig Dis Sci 1998;43(3):673-678. Not about 

consequences of testing 

Carroccio Antonio, Iannitto Emilio, Di Prima et al. 

Screening for celiac disease in non-Hodgkin's 

lymphoma patients: a serum anti-transglutaminasebased approach. Dig Dis Sci 2003;48(8):1530-1536. 

Not about consequences of testing 

Carroccio Antonio, Vitale Giustina, Di Prima et al. 

Comparison of anti-transglutaminase ELISAs and an 

anti-endomysial antibody assay in the diagnosis of

celiac disease: a prospective study. Clin Chem

2002;48(9):1546-1550. Not about consequences of

testing 

Carroll Jerome F X, McGinley John J. Managing 

MICA clients in a modified therapeutic community

with enhanced staffing. J Subst Abuse Treat 

1998;15(6):565-577. Not about consequences of

testing 

Carswell F, Ferguson A. Food antibodies in serum--a 

screening test for coeliac disease. Arch Dis Child 

1972;47(254):594-596. Not about consequences of

testing 

A-608
Casellas F, de Torres I, Malagelada J R. Improved 

screening for intestinal villous atrophy by D-xylose 

breath test. Dig Dis Sci 2000;45(1):18-22. Not about 

consequences of testing 

Casellas F, Sardi J, de Torres I et al. Hydrogen breath 

test with D-xylose for celiac disease screening is as

useful in the elderly as in other age groups. Dig Dis 

Sci 2001;46(10):2201-2205. Not about consequences 

of testing 

Castellano Penny Z, Wenger Nanette K, Graves 

William L. Adherence to screening guidelines for 

breast and cervical cancer in postmenopausal women 

with coronary heart disease: An ancillary study of 

volunteers for HERS. Journal of Women's Health & 

Gender-Based Medicine 2001;10(5):451-461. Not 

about consequences of testing 

Castellino F, Scaglione N, Grosso S B et al. A novel 

method for detecting IgA endomysial antibodies by

using human umbilical vein endothelial cells. Eur J 

Gastroenterol Hepatol 2000;12(1):45-49. Not about 

consequences of testing 

Cataldo F, Lio D, Marino V et al. IgG(1) 

antiendomysium and IgG antitissue transglutaminase 

(anti-tTG) antibodies in coeliac patients with selective 

IgA deficiency. Working Groups on Celiac Disease of 

SIGEP and Club del Tenue. Gut 2000;47(3):366-369. 

Not about consequences of testing 

Cataldo F, Marino V, Bottaro G et al. Celiac disease 

and selective immunoglobulin A deficiency. Eur J 

Pediatr 1997;131(2):306-308. Not about consequences 

of testing 

Cataldo F, Marino V, Ventura A et al. Prevalence and

clinical features of selective immunoglobulin A 

deficiency in coeliac disease: an Italian multicentre 

study. Italian Society of Paediatric Gastroenterology

and Hepatology (SIGEP) and "Club del Tenue" 

Working Groups on Coeliac Disease. Gut 

1998;42(3):362-365. Not about consequences of

testing 

Cataldo F, Ventura A, Lazzari R et al.

Antiendomysium antibodies and coeliac disease: 

solved and unsolved questions. An Italian multicentre 

study. Acta Paediatr 1995;84(10):1125-1131. Not 

about consequences of testing 

Cataldo Francesco, Marino Vincenzo. Increased

prevalence of autoimmune diseases in first-degree

relatives of patients with celiac disease. J Pediatr 

Gastroenterol Nutr 2003;36(4):470-473. Not about 

consequences of testing 

Catapani W R, da Silva A N, de Morais M B et al. 

Clinical usefulness of acid steatocrit in pediatric

practice. Arq Gastroenterol 1999;36(2):105-108. Not 

about consequences of testing 

Catassi C, Fabiani E, Gasparin M et al. Quantitative

antigliadin antibody measurement in clinical practice: 

an Italian multicentre study. SIGEP Working Group 

on Quantitative AGA Standardization. Ital J 

Gastroenterol Hepatol 1999;31(5):366-370. Not about 

consequences of testing 

Catassi C, Fabiani E, Ratsch I M et al. Celiac disease 

in the general population: should we treat 

asymptomatic cases?. J Pediatr Gastroenterol Nutr

1997;24(5):S10-S12. Not about consequences of

testing 

Catassi C, Fabiani E, Ratsch I M et al. Is the sugar 

intestinal permeability test a reliable investigation for 

coeliac disease screening?. Gut 1997;40(2):215-217. 

Not about consequences of testing 

Catassi C, Fabiani E, Ratsch I M et al. The coeliac 

iceberg in Italy. A multicentre antigliadin antibodies 

screening for coeliac disease in school-age subjects. 

Acta Paediatr 1996;412(Suppl):29-35. Not about 

consequences of testing 

Catassi C, Fabiani E. The spectrum of coeliac disease 

in children. Bailliere's Clinical Gastroenterology

1997;11(3):485-507. Not about consequences of

testing 

Catassi C, Fanciulli G, D'Appello A R et al. 

Antiendomysium versus antigliadin antibodies in 

screening the general population for coeliac disease. 

Scand J Gastroenterol 2000;35(7):732-736. Not about 

consequences of testing 

Catassi C, Fornaroli F, Fasano A. Celiac disease:

From basic immunology to bedside practice. Clin

Appl Immunol Rev 2002;3(1-2):61-71. Not about 

consequences of testing 

Catassi C, Ratsch I M, Fabiani E et al. Coeliac disease 

in the year 2000: exploring the iceberg. Lancet 

1994;343(8891):200-203. Not about consequences of 

testing 

Catassi C, Ratsch I M, Fabiani E et al. High 

prevalence of undiagnosed coeliac disease in 5280 

Italian students screened by antigliadin antibodies. 

Acta Paediatr 1995;84(6):672-676. Not about 

consequences of testing 

Catassi C, Rossini M, Ratsch I M et al. Dose

dependent effects of protracted ingestion of small 

amounts of gliadin in coeliac disease children: a 

clinical and jejunal morphometric study. Gut 

1993;34(11):1515-1519. Not about consequences of 

testing 

A-609
Catassi Carlo, Fabiani Elisabetta, Corrao Giovanni et

al. Risk of non-Hodgkin lymphoma in celiac disease. 

JAMA 2002;287(11):1413-1419. Not about 

consequences of testing 

Catino M, Tumini S, Mezzetti A et al. Coeliac disease 

and diabetes mellitus in children: A non casual 

association. Diabetes Nutr Metab Clin Exp

1998;11(5):296-302. Not about consequences of

testing 

Cellier C, Cuillerier E, Patey-Mariaud de et al. Push 

enteroscopy in celiac sprue and refractory sprue.

Gastrointest Endosc 1999;50(5):613-617. Not about 

consequences of testing 

Cellier C, Delabesse E, Helmer C et al. Refractory 

sprue, coeliac disease, and enteropathy-associated Tcell lymphoma. French Coeliac Disease Study Group. 

Lancet 2000;356(9225):203-208. Not about 

consequences of testing 

Chadwick V S, Phillips S F, Hofmann A F. 

Measurements of intestinal permeability using low 

molecular weight polyethylene glycols (PEG 400). II. 

Application to normal and abnormal permeability 

states in man and animals. Gastroenterology

1977;73(2):247-251. Not about consequences of

testing 

Challacombe D N. Screening tests for coeliac disease.

Arch Dis Child 1995;73(1):3-4. Not about 

consequences of testing 

Challacombe D. When is a coeliac?. Lancet 

1994;343(8891):188Not about consequences of testing 

Chambers Ruth. The effectiveness of lifestyle-related 

health screening: A 2 year follow-up study of doctors 

and teachers. Fam Pract 1992;9(4):500-505. Not about 

consequences of testing 

Chan A W, Butzner J D, McKenna R et al. Tissue 

transglutaminase enzyme-linked immunosorbent assay

as a screening test for celiac disease in pediatric

patients. Pediatrics 2001;107(1):E8Not about 

consequences of testing 

Chan K N, Phillips A D, Mirakian R et al. Endomysial 

antibody screening in children. J Pediatr Gastroenterol 

Nutr 1994;18(3):316-320. Not about consequences of 

testing 

Chapman B A, Pattinson N R, Cook H B et al. Skin

testing for coeliac disease. N Z Med J

1979;90(649):463-464. Not about consequences of

testing 

Chartrand L J, Agulnik J, Vanounou T et al. 

Effectiveness of antigliadin antibodies as a screening 

test for celiac disease in children. Cmaj - Canadian

Medical Association Journal = Journal De 

L'association Medicale Canadienne 1997;157(5):527-

533. Not about consequences of testing 

Chartrand L J, Russo P A, Duhaime A G et al. Wheat

starch intolerance in patients with celiac disease. J Am

Diet Assoc 1997;97(6):612-618. Not about 

consequences of testing 

Chatzicostas Costantinos, Roussomoustakaki Maria, 

Drygiannakis Dimitrios et al. Primary biliary cirrhosis 

and autoimmune cholangitis are not associated with 

coeliac disease in Crete. Bmc Gastroenterology

Electronic Resource 2002;2(1):5Not about 

consequences of testing 

Cheung Bruno M H, Jeng Kee-Ching G, Lau Yen. 

Screening for diseases in elderly persons: The

correlation between physical checkup findings and 

chief complaints. Gerontology 1999;45(5):283-288. 

Not about consequences of testing 

Chimenti C, Pieroni M, Frustaci A. Celiac disease in

idiopathic dilated cardiomyopathy. Ital Heart J 

2001;2(9):658-659. Not about consequences of testing 

Chirdo F G, Rumbo M, Carabajal P et al. Analysis of 

anti-gliadin antibodies by immunoblot analysis and 

enzyme-linked immunosorbent assay using gliadin 

fractions as antigens. J Pediatr Gastroenterol Nutr

1999;29(2):171-177. Not about consequences of

testing 

Chirdo F G, Rumbo M, Carabajal P et al. 

Determination of anti-omega-gliadin antibodies in 

serologic tests for coeliac disease. Scand J

Gastroenterol 2000;35(5):508-516. Not about 

consequences of testing 

Ciacci C, Cavallaro R, Romano R et al. Increased risk

of surgery in undiagnosed celiac disease. Dig Dis Sci 

2001;46(10):2206-2208. Not about consequences of 

testing 

Ciacci C, Cirillo M, Cavallaro R et al. Long-term 

follow-up of celiac adults on gluten-free diet: 

prevalence and correlates of intestinal damage.

Digestion 2002; 66(3):178-185. Not about 

consequences of testing 

Ciacci C, Cirillo M, Giorgetti G et al. Low plasma

cholesterol: a correlate of nondiagnosed celiac disease 

in adults with hypochromic anemia. Am J 

Gastroenterol 1999;94(7):1888-1891. Not about 

consequences of testing 

Ciacci C, De Rosa A, De Michele G et al. Sexual

behaviour in untreated and treated coeliac patients. 

Eur J Gastroenterol Hepatol 1998; 10(8):649-651. Not 

about consequences of testing 

Ciacci C, Iavarone A, Siniscalchi M et al.

Psychological dimensions of celiac disease: toward an 

A-610
integrated approach. Dig Dis Sci 2002;47(9):2082-

2087. Not about consequences of testing 

Ciclitira P J, Ellis H J. In vivo gluten ingestion in

coeliac disease. Dig Dis 1998;16(6):337-340. Not 

about consequences of testing 

Ciclitira Paul J. Recent advances in coeliac disease. 

Clin Med 2003;3(2):166-169. Not about consequences 

of testing 

Clasen Carla M, Vernon Sally W, Mullen Patricia D et 

al. A survey of physician beliefs and self-reported

practices concerning screening for early detection of 

cancer. Soc Sci Med 1994;39(6):841-849. Not about 

consequences of testing 

Cleghorn G, Benjamin L, Corey M et al. Serum 

immunoreactive pancreatic lipase and cationic 

trypsinogen for the assessment of exocrine pancreatic 

function in older patients with cystic fibrosis. 

Pediatrics 1986;77(3):301-306. Not about 

consequences of testing 

Clemente Maria, Grazia Musu, Maria Paola et al. 

Antitissue transglutaminase antibodies outside celiac

disease. J Pediatr Gastroenterol Nutr 2002;34(1):31-

34. Not about consequences of testing 

Cobden I, Hamilton I, Rothwell J et al. 

Cellobiose/mannitol test: physiological properties of 

probe molecules and influence of extraneous factors. 

Clin Chim Acta 1985;148(1):53-62. Not about 

consequences of testing 

Cobden I, Rothwell J, Axon A T. Intestinal 

permeability and screening tests for coeliac disease. 

Gut 1980;21(6):512-518. Not about consequences of 

testing 

Cockburn Jill, Murphy Barbara, Schofield Penelope et 

al. Development of a strategy to encourage attendance

for screening mammography. Health Educ Res 

1991;6(3):279-290. Not about consequences of testing 

Cogulu O, Ozkinay F, Gunduz C et al. Celiac disease 

in children with down syndrome: Importance of

follow-up and serologic screening. Pediatr Int 

2003;45(4):395-399. Not about consequences of

testing 

Colaco J, Egan-Mitchell B, Stevens F M et al.

Compliance with gluten free diet in coeliac disease. 

Arch Dis Child 1987;62(7):706-708. Not about 

consequences of testing 

Collin P, Hallstrom O, Maki M et al. Atypical coeliac 

disease found with serologic screening. Scand J 

Gastroenterol 1990;25(3):245-250. Not about 

consequences of testing 

Collin P, Helin H, Maki M et al. Follow-up of patients

positive in reticulin and gliadin antibody tests with

normal small-bowel biopsy findings. Scand J 

Gastroenterol 1993;28(7):595-598. Not about 

consequences of testing 

Collin P, Kaukinen K, Maki M. Clinical features of 

celiac disease today. Dig Dis 1999;17(2):100-106. Not 

about consequences of testing 

Collin P, Korpela M, Hallstrom O et al. Rheumatic 

complaints as a presenting symptom in patients with 

coeliac disease. Scand J Rheumatol 1992;21(1):20-23. 

Not about consequences of testing 

Collin P, Maki M. Associated disorders in coeliac 

disease: clinical aspects. Scand J Gastroenterol 

1994;29(9):769-775. Not about consequences of

testing 

Collin P, Rasmussen M, Kyronpalo S et al. The hunt 

for coeliac disease in primary care. QJM

2002;95(2):75-77. Not about consequences of testing 

Collin P, Reunala T, Rasmussen M et al. High

incidence and prevalence of adult coeliac disease.

Augmented diagnostic approach. Scand J 

Gastroenterol 1997;32(11):1129-1133. Not about 

consequences of testing 

Collin P, Salmi J, Hallstrom O et al. Autoimmune 

thyroid disorders and coeliac disease. Eur J Endocrinol 

1994;130(2):137-140. Not about consequences of

testing 

Collin P, Salmi J, Hallstrom O et al. High frequency 

of coeliac disease in adult patients with type-I 

diabetes. Scand J Gastroenterol 1989;24(1):81-84. Not 

about consequences of testing 

Collin P, Vilska S, Heinonen P K et al. Infertility and 

coeliac disease. Gut 1996;39(3):382-384. Not about 

consequences of testing 

Collin P. New diagnostic findings in coeliac disease. 

Ann Med 1999;31(6):399-405. Not about 

consequences of testing 

Collin P. Serologic screening for coeliac disease--time 

for tissue transglutaminase test?. Ital J Gastroenterol 

Hepatol 1998;30(5):498-499. Not about consequences 

of testing 

Collin Pekka, Kaukinen Katri, Valimaki Matti et al.

Endocrinological disorders and celiac disease. Endocr 

Rev 2002;23(4):464-483. Not about consequences of 

testing 

Collin Pekka, Reunala Timo. Recognition and 

management of the cutaneous manifestations of celiac 

disease: a guide for dermatologists. Am J Clin

A-611
Dermatol 2003;4(1):13-20. Not about consequences of 

testing 

Collin Pekka, Syrjanen Jaana, Partanen Jukka et al. 

Celiac disease and HLA DQ in patients with IgA 

nephropathy. Am J Gastroenterol 2002;97(10):2572-

2576. Not about consequences of testing 

Cook H B, Burt M J, Collett J A et al. Adult coeliac 

disease: prevalence and clinical significance. Eur J

Gastroenterol Hepatol 2000;15(9):1032-1036. Not 

about consequences of testing 

Cooke W T, Asquith P. Coeliac disease. Introduction 

and definition. Clin Gastroenterol 1974;3(1):3-10. Not 

about consequences of testing 

Coombs R R, McLaughlan P. Allergenicity of food

proteins and its possible modification. Ann Allergy

1984;53(6 Pt 2):592-596. Not about consequences of 

testing 

Coplan James. "The infant or young child with

developmental delay": Erratum. N Engl J Med 

1994;331(1):56Not about consequences of testing 

Corazza G R, Andreani M L, Biagi F et al. The

smaller size of the 'coeliac iceberg' in adults. Scand J 

Gastroenterol 1997;32(9):917-919. Not about 

consequences of testing 

Corazza G R, Andreani M L, Venturo N et al. Celiac 

disease and alopecia areata: Report of a new 

association. Gastroenterology 1995;109(4):1333-1337. 

Not about consequences of testing 

Corazza G R, Brusco G, Andreani M L et al. Previous

misdiagnosis and diagnostic delay in adult celiac 

sprue. J Clin Gastroenterol 1996;22(4):324-325. Not 

about consequences of testing 

Corazza G R, Caletti G C, Lazzari R et al. Scalloped 

duodenal folds in childhood celiac disease. 

Gastrointest Endosc 1993;39(4):543-545. Not about 

consequences of testing 

Corazza G R, Di Sario A, Sacco G et al. Subclinical

coeliac disease: an anthropometric assessment. J 

Intern Med 1994;236(2):183-187. Not about 

consequences of testing 

Corazza G R, Falasca A, Strocchi A et al. Decreased 

plasma postheparin diamine oxidase levels in celiac 

disease. Dig Dis Sci 1988;33(8):956-961. Not about 

consequences of testing 

Corazza G R, Gasbarrini G. Coeliac disease in adults. 

Bailliere's Clinical Gastroenterology 1995;9(2):329-

350. Not about consequences of testing 

Corazza G R, Ginaldi L, Falasca A et al. Diamine

oxidase plasma activities after treatment with heparin 

and jejunal morphometry in untreated coeliac disease. 

Am J Clin Pathol 1989;42(11):1136-1139. Not about 

consequences of testing 

Corazza G R, Valentini R A, Andreani M L et al.

Subclinical coeliac disease is a frequent cause of irondeficiency anaemia. Scand J Gastroenterol 

1995;30(2):153-156. Not about consequences of

testing 

Corazza G, Valentini R A, Frisoni M et al. Gliadin 

immune reactivity is associated with overt and latent 

enteropathy in relatives of celiac patients. 

Gastroenterology 1992;103(5):1517-1522. Not about 

consequences of testing 

Corlin R F, Nichaman M Z, Grier O T. The use of 

plasma and erythrocyte phospholipid linoleate levels 

as a screening test for malabsorption. Am J Dig Dis 

1970;15(10):953-957. Not about consequences of

testing 

Cornell H J, Maxwell R J. Amino acid composition of 

gliadin fractions which may be toxic to individuals 

with coeliac disease. Clin Chim Acta 

1982;123(3):311-319. Not about consequences of

testing 

Corrao G, Corazza G R, Andreani M L et al.

Serological screening of coeliac disease: choosing the 

optimal procedure according to various prevalence

values. Gut 1994;35(6):771-775. Not about 

consequences of testing 

Cox M A, Lewis K O, Cooper B T. Sucrosemia in

untreated celiac disease: a potential screening test. Dig

Dis Sci 1998;43(5):1096-1101. Not about 

consequences of testing 

Crawford L V, Herrod H G. Allergy diets for infants 

and children. Curr Probl Pediatr 1981;11(12):1-44. 

Not about consequences of testing 

Crenn Pascal, Vahedi Kouroche, Lavergne-Slove

Anne et al. Plasma citrulline: A marker of enterocyte

mass in villous atrophy-associated small bowel 

disease. Gastroenterology 2003;124(5):1210-1219. 

Not about consequences of testing 

Crone J, Rami B, Huber W D et al. Prevalence of

Celiac Disease and Follow-up of Ema in Children and 

Adolescents With Type 1 Diabetes Mellitus. J Pediatr

Gastroenterol Nutr 2003;37(1):67-71. Not about 

consequences of testing 

Cronin C C, Feighery A, Ferriss J B et al. High 

prevalence of celiac disease among patients with 

insulin-dependent (type I) diabetes mellitus. Am J 

Gastroenterol 1997;92(12):2210-2212. Not about 

consequences of testing 

A-612
Cronin C C, Jackson L M, Feighery C et al. Coeliac 

disease and epilepsy. QJM 1998;91(4):303-308. Not 

about consequences of testing 

Cronin C C, Shanahan F. Exploring the iceberg - The 

spectrum of celiac disease. Am J Gastroenterol

2003;98(3):518-520. Not about consequences of

testing 

Cronin C C, Shanahan F. Why is celiac disease so

common in Ireland?. Perspect Biol Med 

2001;44(3):342-352. Not about consequences of

testing 

Croyle Robert T, Sun Yi, Louie Douglas H. 

Psychological minimization of cholesterol test results: 

Moderators of appraisal in college students and

community residents. Health Psychol 1993;12(6):503-

507. Not about consequences of testing 

Csizmadia C G, Mearin M L, Oren A et al. Accuracy

and cost-effectiveness of a new strategy to screen for 

celiac disease in children with Down syndrome. Eur J

Pediatr 2000;137(6):756-761. Not about consequences 

of testing 

Cummins A G, Thompson F M, Butler R N et al. 

Improvement in intestinal permeability precedes

morphometric recovery of the small intestine in

coeliac disease. Clin Sci (Lond) 2001;100(4):379-386. 

Not about consequences of testing 

Cuoco L, Cammarota G, Tursi A et al. Disappearance 

of gastric mucosa-associated lymphoid tissue in

coeliac patients after gluten withdrawal. Scand J

Gastroenterol 1998; 33(4):401-405. Not about 

consequences of testing 

Cuoco L, Certo M, Jorizzo R A et al. Prevalence and 

early diagnosis of coeliac disease in autoimmune 

thyroid disorders. Ital J Gastroenterol Hepatol 

1999;31(4):283-287. Not about consequences of

testing 

Cuomo A, Romano M, Rocco A et al. Reflux 

oesophagitis in adult coeliac disease: beneficial effect

of a gluten free diet. Gut 2003;52(4):514-517. Not 

about consequences of testing 

Dahele A, Ghosh S. Vitamin B12 deficiency in 

untreated celiac disease. Am J Gastroenterol 

2001;96(3):745-750. Not about consequences of

testing 

Dahlqvist A, Lindberg T, Meeuwisse G et al. 

Intestinal dipeptidases and disaccharidases in children 

with malabsorption. Acta Paediatr Scand 

1970;59(6):621-630. Not about consequences of

testing 

Dahlqvist G. Celiac disease and insulin-dependent

diabetes mellitus no proof for a causal association.

Acta Paediatr 1995;84(12):1337-1338. Not about 

consequences of testing 

Damoiseaux J G M C, Tervaert J W C. Celiac disease:

the role of (auto)antibody detection in diagnosis and 

follow-up. Neth J Med 2002;60(7):303-304. Not about 

consequences of testing 

Danielsson L, Stenhammar L, Astrom E. Is gluten

challenge necessary for the diagnosis of coeliac

disease in young children?. Scand J Gastroenterol 

1990;25(9):957-960. Not about consequences of

testing 

David T J, Ajdukiewicz A B, Read A E. Fingerprint 

changes in coeliac disease. Br Med J 1970;4(735):594-

596. Not about consequences of testing 

Davidson A G, Hassall E G. Screening for celiac 

disease. Cmaj - Canadian Medical Association Journal 

= Journal De L'association Medicale Canadienne

1997;157(5):547-548. Not about consequences of

testing 

Davison S. Coeliac disease and liver dysfunction. 

Arch Dis Child 2002;87(4):293-296. Not about 

consequences of testing 

Day A S, Abbott G D. Simultaneous presentation of 

coeliac disease and ulcerative colitis in a child. J 

Paediatr Child Health 1999;35(2):204-206. Not about 

consequences of testing 

Day A S, Cook H B, Whitehead M et al. Antiendomysial and anti-gliadin antibodies in screening 

for coeliac disease in children at greater risk of 

developing coeliac disease. N Z Med J

2000;113(1119):412-413. Not about consequences of 

testing 

de la, Concha E G, Fernandez-Arquero M et al. Celiac 

disease and TNF promoter polymorphisms. Hum 

Immunol 2000;61(5):513-517. Not about 

consequences of testing 

de Lecea A, Ribes-Koninckx C, Polanco I et al. 

Serological screening (antigliadin and 

antiendomysium antibodies) for non-overt coeliac 

disease in children of short stature. Acta Paediatr

1996;412(Suppl):54-55. Not about consequences of

testing 

De Vitis I, Ghirlanda G, Gasbarrini G. Prevalence of 

coeliac disease in type I diabetes: a multicentre study. 

Acta Paediatr 1996;412(Suppl):56-57. Not about 

consequences of testing 

de Vizia B, Poggi V, Conenna R et al. Iron absorption 

and iron deficiency in infants and children with 

gastrointestinal diseases. J Pediatr Gastroenterol Nutr 

1992;14(1):21-26. Not about consequences of testing 

A-613
Dean G, Hanniffy L, Stevens F. Schizophrenia and 

coeliac disease. Ir Med J 1975;68(21):545-546. Not 

about consequences of testing 

Del Rosario M A, Fitzgerald J F, Chong S K et al. 

Further studies of anti-endomysium and anti-gliadin 

antibodies in patients with suspected celiac disease. J 

Pediatr Gastroenterol Nutr 1998;27(2):191-195. Not 

about consequences of testing 

Demir H, Yuce A, Kocak N et al. Celiac disease in

Turkish children: presentation of 104 cases. Pediatr Int 

2000;42(5):483-487. Not about consequences of

testing 

Deutsch J C, Santhosh-Kumar C R, Kolli V R. A 

noninvasive stable-isotope method to simultaneously

assess pancreatic exocrine function and small bowel 

absorption. Am J Gastroenterol 1995;90(12):2182-

2185. Not about consequences of testing 

Devi Rampertab S, Fleischauer A, Neugut A I et al. 

Risk of duodenal adenoma in celiac disease. Scand J 

Gastroenterol 2003;38(8):831-833. Not about 

consequences of testing 

Devine P L, Birrell G W, Golder J P et al. Screening 

and monitoring coeliac disease: multicentre trial of a 

new serum antibody test kit. Dis Markers 

1994;12(1):71-80. Not about consequences of testing 

Dezi R, Niveloni S, Sugai E et al. Gluten sensitivity in

the rectal mucosa of first-degree relatives of celiac

disease patients. Am J Gastroenterol 1997;92(8):1326-

1330. Not about consequences of testing 

Dhar A, Goenka M K. Endomysial antibody and celiac 

disease. Indian Journal of Gastroenterology - Official 

Journal of the Indian Society of Gastroenterology

1993;12(4):157-158. Not about consequences of

testing 

Di Cagno, Raffaella De, Angelis Maria et al. 

Proteolysis by sourdough lactic acid bacteria: effects 

on wheat flour protein fractions and gliadin peptides 

involved in human cereal intolerance. Appl Environ 

Microbiol 2002;68(2):623-633. Not about 

consequences of testing 

Di Leo M, Weisz G, Ansaldi Balocco N. Serum and 

salivary antiendomysium antibodies in the screening 

of coeliac disease. Panminerva Med 1999;41(1):68-71. 

Not about consequences of testing 

Dias J, Unsworth D J, Walker-Smith J A. Antigliadin 

and antireticulin antibodies in screening for coeliac 

disease. Lancet 1987;2(8551):157-158. Not about 

consequences of testing 

Dickey W, Hughes D F, McMillan S A. Reliance on 

serum endomysial antibody testing underestimates the 

true prevalence of coeliac disease by one fifth. Scand J

Gastroenterol 2000;35(2):181-183. Not about 

consequences of testing 

Dickey W, Hughes D. Disappointing sensitivity of

endoscopic markers for villous atrophy in a high-risk 

population: implications for celiac disease diagnosis 

during routine endoscopy. Am J Gastroenterol 

2001;96(7):2126-2128. Not about consequences of

testing 

Dickey W, Hughes D. Prevalence of celiac disease and 

its endoscopic markers among patients having routine 

upper gastrointestinal endoscopy. Am J Gastroenterol 

1999;94(8):2182-2186. Not about consequences of

testing 

Dickey W, McConnell J B. How many hospital visits 

does it take before celiac sprue is diagnosed?. J Clin 

Gastroenterol 1996;23(1):21-23. Not about 

consequences of testing 

Dickey W, McMillan S A, Bharucha C et al.

Antigliadin antibodies in blood donors in Northern

Ireland. Eur J Gastroenterol Hepatol 1992;4(9):739-

741. Not about consequences of testing 

Dickey W, McMillan S A, Callender M E. High 

prevalence of celiac sprue among patients with 

primary biliary cirrhosis. J Clin Gastroenterol 

1997;25(1):328-329. Not about consequences of

testing 

Dickey W, McMillan S A, Hughes D F. Identification 

of coeliac disease in primary care. Scand J

Gastroenterol 1998;33(5):491-493. Not about 

consequences of testing 

Dickey W, McMillan S A, Hughes D F. Sensitivity of 

serum tissue transglutaminase antibodies for

endomysial antibody positive and negative coeliac 

disease. Scand J Gastroenterol 2001;36(5):511-514. 

Not about consequences of testing 

Dickey W, McMillan S A, McCrum E E et al.

Association between serum levels of total IgA and IgA 

class endomysial and antigliadin antibodies: 

implications for coeliac disease screening. Eur J

Gastroenterol Hepatol 1997;9(6):559-562. Not about 

consequences of testing 

Dickey W, Stewart F, Nelson J et al. Screening for 

coeliac disease as a possible maternal risk factor for 

neural tube defect. Clin Genet 1996;49(2):107-108. 

Not about consequences of testing 

Dieterich W, Ehnis T, Bauer M et al. Identification of 

tissue transglutaminase as the autoantigen of celiac 

disease. Nat Med 1997;3(7):797-801. Not about 

consequences of testing 

Dieterich W, Laag E, Bruckner-Tuderman L et al. 

Antibodies to tissue transglutaminase as serologic 

A-614
markers in patients with dermatitis herpetiformis. J 

Invest Dermatol 1999;113(1):133-136. Not about 

consequences of testing 

Dieterich W, Laag E, Schopper H et al. 

Autoantibodies to tissue transglutaminase as

predictors of celiac disease. Gastroenterology

1998;115(6):1317-1321. Not about consequences of 

testing 

Digilio M C, Giannotti A, Castro M et al. Screening 

for Celiac Disease in Patients With Deletion 22q11.2 

(Digeorge/Velo-Cardio-Facial Syndrome). Am J Med 

Genet 2003;121A(3):286-288. Not about 

consequences of testing 

Dinari G, Rosenbach Y, Zahavi I et al. Random fecal 

alpha 1-antitrypsin excretion in children with intestinal

disorders. Am J Dis Child 1984;138(10):971-973. Not 

about consequences of testing 

Dinari G, Zahavi I, Marcus H et al. Placental ferritin 

in coeliac disease: relation to clinical stage, origin, and

possible role in the pathogenesis of malignancy. Gut 

1991;32(9):999-1003. Not about consequences of

testing 

Dissanayake A S, Truelove S C, Whitehead R. Jejunal 

mucosal recovery in coeliac disease in relation to the

degree of adherence to a gluten-free diet. Q J Med 

1974;43(170):161-185. Not about consequences of

testing 

Drossman D A. Irritable bowel syndrome: how far do 

you go in the workup?. Gastroenterology

2001;121(6):1512-1515. Not about consequences of 

testing 

Duncan A, Park R P, Lee F D et al. A retrospective 

assessment of the clinical value of jejunal

disaccharidase analysis. Scand J Gastroenterol 

1994;29(12):1111-1116. Not about consequences of 

testing 

Eade O E, Lloyd R S, Lang C et al. IgA and IgG 

reticulin antibodies in coeliac and non-coeliac 

patients. Gut 1977;18(12):991-993. Not about 

consequences of testing 

Eigenmann P A, Calza A-M. Diagnosis of IgEmediated food allergy among Swiss children with

atopic dermatitis. Pediatr Allergy Immunol 

2000;11(2):95-100. Not about consequences of testing 

Eigenmann P A, Sicherer S H, Borkowski T A et al.

Prevalence of IgE-mediated food allergy among 

children with atopic dermatitis. Pediatrics 

1998;101(3):E8Not about consequences of testing 

Einarsson K, Bjorkhem I, Eklof R et al. 14C-triolein 

breath test as a rapid and convenient screening test for 

fat malabsorption. Scand J Gastroenterol 

1983;18(1):9-12. Not about consequences of testing 

Elewaut A, Dacremont G, Robberecht E et al. IgA 

isotyping of antigliadin antibodies. A possible clue for

a less invasive diagnosis of coeliac disease. Clin Chim 

Acta 1989;183(3):285-294. Not about consequences of 

testing 

Ensari A, Marsh M N, Morgan S et al. Diagnosing 

coeliac disease by rectal gluten challenge: a

prospective study based on immunopathology,

computerized image analysis and logistic regression 

analysis. Clin Sci (Lond) 2001;101(2):199-207. Not 

about consequences of testing 

Enzenauer R J, Root S. Arthropathy and celiac 

disease. J Clin Rheumatol 1998;4(4):205-208. Not 

about consequences of testing 

Erfurt John C, Foote Andrea, Heirich Max A. 

Worksite wellness programs: Incremental comparison 

of screening and referral alone, health education, 

follow-up counseling, and plant organization. Am J 

Health Promot 1991;5(6):438-448. Not about 

consequences of testing 

Exner G U, Sacher M, Shmerling D H et al. Growth 

retardation and bone mineral status in children with 

coeliac disease recognized after the age of 3 years.

Helv Paediatr Acta 1978;33(6):497-507. Not about 

consequences of testing 

Fabiani E, Catassi C. The serum IgA class anti-tissue 

transglutaminase antibodies in the diagnosis and

follow up of coeliac disease. Results of an 

international multi-centre study. International 

Working Group on Eu-tTG. Eur J Gastroenterol 

Hepatol 2001;13(6):659-665. Not about consequences 

of testing 

Farre C, Esteve M, Curcoy A et al. 

Hypertransaminasemia in pediatric celiac disease

patients and its prevalence as a diagnostic clue. Am J 

Gastroenterol 2002;97(12):3176-3181. Not about 

consequences of testing 

Farre C, Humbert P, Vilar P et al. Serological markers 

and HLA-DQ2 haplotype among first-degree relatives 

of celiac patients. Catalonian Coeliac Disease Study

Group. Dig Dis Sci 1999;44(11):2344-2349. Not about 

consequences of testing 

Farrell R J, Kelly C P. Diagnosis of celiac sprue. Am J 

Gastroenterol 2001;96(12):3237-3246. Not about 

consequences of testing 

Farrell Richard J, Kelly Ciaran P. Celiac sprue. N Engl 

J Med 2002;346(3):180-188. Not about consequences 

of testing 

A-615
Fasano A, Catassi C. Current approaches to diagnosis

and treatment of celiac disease: an evolving spectrum. 

Gastroenterology 2001;120(3):636-651. Not about 

consequences of testing 

Fasano A. European and North American populations 

should be screened for coeliac disease. Gut 

2003;52(2):168-169. Not about consequences of

testing 

Fasano A. Where have all the American celiacs gone?.

Acta Paediatr 1996;412(Suppl):20-24. Not about 

consequences of testing 

Fasano Alessio, Berti Irene, Gerarduzzi Tania et al.

Prevalence of celiac disease in at-risk and not-at-risk 

groups in the United States: a large multicenter study.

Arch Intern Med 2003;163(3):286-292. Not about 

consequences of testing 

Fasano Alessio. Celiac disease--how to handle a 

clinical chameleon. N Engl J Med 2003;348(25):2568-

2570. Not about consequences of testing 

Feighery C, Weir D G, Whelan A et al. Diagnosis of 

gluten-sensitive enteropathy: is exclusive reliance on 

histology appropriate?. Eur J Gastroenterol Hepatol 

1998;10(11):919-925. Not about consequences of

testing 

Feighery C. Coeliac disease. Br Med J 

1999;319(7204):236-239. Not about consequences of 

testing 

Ferfoglia G, Pulitano R, Sategna-Guidetti C. Do 

dietary antibodies still play a role in the diagnosis and 

follow-up of coeliac disease? A comparison among 

different serological tests. Panminerva Med 

1995;37(2):55-59. Not about consequences of testing 

Ferguson A, Denton-Miller P, Lai C L. Coeliac 

disease--objectives of life-long follow-up. Health Bull 

(Edinb) 1977;35(2):78-80. Not about consequences of 

testing 

Fernandez-Calle P, Codoceo R, Polanco I et al. Is an 

intestinal permeability test a valid marker for slight 

dietary transgressions in adolescents with coeliac 

disease?. Gut 1993;34(6):774-777. Not about 

consequences of testing 

Fernhall Bo, Tymeson Garth, Millar Lynn et al. 

Cardiovascular fitness testing and fitness levels of

adolescents and adults with mental retardation 

including Down syndrome. Education & Training in 

Mental Retardation 1989;24(2):133-138. Not about 

consequences of testing 

Ferreira M, Davies S L, Butler M et al. Endomysial 

antibody: is it the best screening test for coeliac

disease?. Gut 1992;33(12):1633-1637. Not about 

consequences of testing 

Fiasse R. Screening for gastrointestinal diseases -

Therapeutic impact. Acta Gastro-Enterol Belg 1995; 

58(5-6):343-347. Unable to obtain article 

Fielding Jonathan E. Frequency of health risk 

assessment activities at U.S. worksites. Am J Prev

Med 1989;5(2):73-81. Not about consequences of

testing 

Fine K D, Lee E L, Meyer R L. Colonic 

histopathology in untreated celiac sprue or refractory

sprue: is it lymphocytic colitis or colonic

lymphocytosis?. Hum Pathol 1998;29(12):1433-1440. 

Not about consequences of testing 

Fine K D, Ogunji F, George J et al. Utility of a rapid 

fecal latex agglutination test detecting the neutrophil 

protein, lactoferrin, for diagnosing inflammatory

causes of chronic diarrhea. Am J Gastroenterol

1998;93(8):1300-1305. Not about consequences of

testing 

Fine K D, Ogunji F, Saloum Y et al. Celiac sprue: 

another autoimmune syndrome associated with

hepatitis C. Am J Gastroenterol 2001;96(1):138-145. 

Not about consequences of testing 

Fink Raymond, Shapiro Sam. Significance of 

increased efforts to gain participation in screening for 

breast cancer. Am J Prev Med 1990;6(1):34-41. Not 

about consequences of testing 

First Lewis R, Palfrey Judith S. The infant or young 

child with developmental delay. N Engl J Med 

1994;330(7):478-483. Not about consequences of

testing 

Fisher S E, Markowitz J, Lifshitz F. Food intolerance 

in childhood. Compr Ther 1984;10(5):5-11. Not about 

consequences of testing 

Fitzpatrick K P, Sherman P M, Ipp M et al. Screening 

for celiac disease in children with recurrent abdominal 

pain. J Pediatr Gastroenterol Nutr 2001;33(3):250-

252. Not about consequences of testing 

Flanders G, Graves P, Rewers M. Prevention of type 1 

diabetes from laboratory to public health. 

Autoimmunity 1999;29(3):235-246. Not about 

consequences of testing 

Floreani A, Betterle C, Baragiotta A et al. Prevalence

of coeliac disease in primary biliary cirrhosis and of 

antimitochondrial antibodies in adult coeliac disease 

patients in Italy. Digestive and Liver Disease - Official 

Journal of the Italian Society of Gastroenterology and 

the Italian Association for the Study of the Liver 

2002;34(4):258-261. Not about consequences of

testing 

A-616
Foldes-Papp Zeno, Demel Ulrike, Berry Desiree et al. 

Tissue transglutaminase antibody determination in

celiac disease. Analysis of diagnostic specificity of 

anti-human IgA-type assays. J Immunoassay

Immunochem 2002;23(2):211-227. Not about 

consequences of testing 

Foster P N, Will E J, Kelleher J et al. Oxalate-loading 

tests to screen for steatorrhoea: an appraisal. Clin

Chim Acta 1984;144(2-3):155-161. Not about 

consequences of testing 

Fotherby K J, Wraight E P, Neale G. 51CrEDTA/14C-mannitol intestinal permeability test. 

Clinical use in screening for coeliac disease. Scand J

Gastroenterol 1988;23(2):171-177. Not about 

consequences of testing 

Fotoulaki M, Nousia-Arvanitakis S, AugoustidouSavvopoulou P et al. Clinical application of 

immunological markers as monitoring tests in celiac 

disease. Dig Dis Sci 1999;44(10):2133-2138. Not 

about consequences of testing 

Fox Sarah A, Klos Dennis S, Tsou Carole V et al.

Breast cancer screening recommendations: Current 

status of women's knowledge. Fam Community Health 

1987;10(3):39-50. Not about consequences of testing 

Fox Sarah A, Stein Judith A. The effect of

physician^patient communication on mammography

utilization by different ethnic groups. Med Care

1991;29(11):1065-1082. Not about consequences of 

testing 

Francis James, Carty John E, Scott Brian B. The 

prevalence of coeliac disease in rheumatoid arthritis. 

Eur J Gastroenterol Hepatol 2002;14(12):1355-1356. 

Not about consequences of testing 

Francis Rupert A, Ernst Frederick A, Nevels Harold et 

al. The relationship of blood pressure to a brief

measure of anger during routine health screening. J

Natl Med Assoc 1991;83(7):601-604. Not about 

consequences of testing 

Franklin R H. Post-vagotomy diarrhoea?. Br Med J 

1970;1(693):412Not about consequences of testing 

Franks Peter, Clancy Carolyn M. Physician gender 

bias in clinical decisionmaking: Screening for cancer 

in primary care. Med Care 1993;31(3):213-218. Not 

about consequences of testing 

Fraser-Reynolds K A, Butzner J D, Stephure D K et 

al. Use of immunoglobulin A-antiendomysial antibody

to screen for celiac disease in North American 

children with type 1 diabetes. Diabetes Care

1998;21(11):1985-1989. Not about consequences of 

testing 

Fredriksson Hans. Screening of mental disturbances in

occupational health services in Finland. Psychiatria 

Fennica 1987;18133-143. Not about consequences of 

testing 

Freeman H J. Failure of added dietary gluten to induce 

small intestinal histopathological changes in patients 

with watery diarrhea and lymphocytic colitis. Can J

Gastroenterol 1996;10(7):436-439. Not about 

consequences of testing 

Freeman H J. Small intestinal mucosal biopsy for 

investigation of diarrhea and malabsorption in adults. 

Gastrointest Endosc Clin N Am 2000;10(4):739-53, 

Vii. Not about consequences of testing 

Freeman H J. Solid-phase ELISA for tissue

transglutaminase, an endomysial target for possible 

serological diagnosis of celiac disease. Can J

Gastroenterol 1998;12(5):323-324. Not about 

consequences of testing 

Freeman H J. Survey of gastroenterologists on the 

diagnosis and treatment of adult patients with celiac 

disease in British Columbia. Can J Gastroenterol

1998;12(2):149-152. Not about consequences of

testing 

Freeman Hugh, Lemoyne Michel, Pare Pierre. Coeliac 

disease. Baillieres Best Pract Res Clin Gastroenterol 

2002;16(1):37-49. Not about consequences of testing 

Freemark M, Levitsky LL. Screening for celiac 

disease in children with type 1 diabetes: Two views of 

the controversy. Diabetes Care 2003; 26(6):1932-

1939. Not about consequences of testing 

Freier S. Paediatric gastrointestinal allergy. Clin

Allergy 1973;3(Suppl):597-618. Not about 

consequences of testing 

Fried Terri R, Rosenberg Roberta R, Lipsitz Lewis A. 

Older community-dwelling adults' attitudes toward

and practices of health promotion and advance 

planning activities. J Am Geriatr Soc 1995;43(6):645-

649. Not about consequences of testing 

Friedman Lawrence S, Johnson Brenda, Brett Allan S. 

Evaluation of substance-abusing adolescents by

primary care physicians. J Adolesc Health Care

1990;11(3):227-230. Not about consequences of

testing 

Friedman Lois C, Woodruff Amy, Lane Montague et 

al. Breast cancer screening behaviors and intentions 

among asymptomatic women 50 years of age and

older. Am J Prev Med 1995;11(4):218-223. Not about 

consequences of testing 

Friis S U, Gudmand-Hoyer E. Screening for coeliac 

disease in adults by simultaneous determination of

IgA and IgG gliadin antibodies. Scand J Gastroenterol 

A-617
1986;21(9):1058-1062. Not about consequences of

testing 

Frisoni G B, Carabellese N, Longhi M et al. Is celiac 

disease associated with Alzheimer's disease?. Acta

Neurol Scand 1997;95(3):147-151. Not about 

consequences of testing 

Fromm H, Hofmann A F. Breath test for altered bileacid metabolism. Lancet 1971;2(7725):621-625. Not 

about consequences of testing 

Frustaci Andrea, Cuoco Lucio, Chimenti Cristina et al. 

Celiac disease associated with autoimmune 

myocarditis. Circulation 2002;105(22):2611-2618. 

Not about consequences of testing 

Fry L. Dermatitis herpetiformis. Bailliere's Clinical 

Gastroenterology 1995;9(2):371-393. Not about 

consequences of testing 

Fry L. The gut and dermatitis herpetiformis. Br Med J 

1971;4(780):172Not about consequences of testing 

Fung V S, Duggins A, Morris J G et al. Progressive 

myoclonic ataxia associated with celiac disease

presenting as unilateral cortical tremor and dystonia.

Mov Disord 2000;15(4):732-734. Not about 

consequences of testing 

Gale J, Simmonds P D, Mead G M et al. Enteropathytype intestinal T-cell lymphoma: clinical features and 

treatment of 31 patients in a single center. Journal of 

Clinical Oncology - Official Journal of the American

Society of Clinical Oncology 2000;18(4):795-803. Not 

about consequences of testing 

Gandolfi L, Catassi C, Garcia S et al. Antiendomysial 

antibody test reliability in children with frequent

diarrhea and malnutrition: is it celiac disease?. J 

Pediatr Gastroenterol Nutr 2001;33(4):483-487. Not 

about consequences of testing 

Gandolfi L, Pratesi R, Cordoba J C et al. Prevalence of

celiac disease among blood donors in Brazil. Am J 

Gastroenterol 2000;95(3):689-692. Not about 

consequences of testing 

Gardiner A, Porteous N, Walker-Smith JA. The effect

of coeliac disease on the mother-child relationship. 

Aust Paediatr J 1972; 8(1):39-43. Unable to obtain

article 

Garioch J J, Lewis H M, Sargent S A et al. 25 years'

experience of a gluten-free diet in the treatment of

dermatitis herpetiformis. Br J Dermatol 

1994;131(4):541-545. Not about consequences of

testing 

Garn S M, Poznanski A K, Nagy J M. Bone 

measurement in the differential diagnosis of 

osteopenia and osteoporosis. Radiology

1971;100(3):509-518. Not about consequences of

testing 

Garrote J A, Sorell L, Alfonso P et al. A novel visual 

immunoassay for coeliac disease screening. Eur J Clin 

Invest 1999;29(8):697-699. Not about consequences 

of testing 

Gasbarrini Antonio, Ojetti Veronica, Cuoco Lucio et

al. Lack of endoscopic visualization of intestinal villi

with the "immersion technique" in overt atrophic 

celiac disease. Gastrointest Endosc 2003;57(3):348-

351. Not about consequences of testing 

Gaston Marilyn, Hughes Moody, Lanardo E. 

Improving utilization of breast and cervical cancer 

screening in your office practice. J Natl Med Assoc 

1995;87(9):700-704. Not about consequences of

testing 

Gath D H, Hallam N, Mynors-Wallis L et al. 

Emotional reactions in women attending a UK 

colposcopy clinic. J Epidemiol Community Health

1995;49(1):79-83. Not about consequences of testing 

Gawkrodger D J, Vestey J P, O'Mahony S et al. 

Dermatitis herpetiformis and established coeliac 

disease. Br J Dermatol 1993;129(6):694-695. Not 

about consequences of testing 

George E K, Hertzberger-ten Cate R, Suijlekom-Smit 

L W et al. Juvenile chronic arthritis and coeliac

disease in The Netherlands. Clin Exp Rheumatol 

1996;14(5):571-575. Not about consequences of

testing 

George E K, Mearin M L, Bouquet J et al. High

frequency of celiac disease in Down syndrome. Eur J 

Pediatr 1996;128(4):555-557. Not about consequences 

of testing 

George E K, Mearin M L, Bouquet J et al. Screening 

for coeliac disease in Dutch children with associated 

diseases. Acta Paediatr 1996;412(Suppl):52-53. Not 

about consequences of testing 

George Sharon A. Barriers to breast cancer screening: 

An integrative review. Health Care Women Int 

2000;21(1):53-65. Not about consequences of testing 

Gerrard J W, Lubos M C. The malabsorption 

syndromes. Pediatr Clin North Am 1967;14(1):73-91. 

Not about consequences of testing 

Gersch Irvine, Kelly Catherine, Cohen Sara et al. The 

Chingford Hall School Screening Project: Can we

have some more educational psychologist time 

please?. Educational Psychology in Practice 

2001;17(2):135-156. Not about consequences of

testing 

A-618
Ghosh S K, Littlewood J M, Goddard D et al. Stool 

microscopy in screening for steatorrhoea. Am J Clin 

Pathol 1977;30(8):749-753. Not about consequences 

of testing 

Giannotti A, Tiberio G, Castro M et al. Coeliac 

disease in Williams syndrome. J Med Genet 

2001;38(11):767-768. Not about consequences of

testing 

Gilchrist C N, Espinar E A, Cook H B. Familial short 

stature and coeliac disease: A family case report. N Z

Med J 1983;96(736):563-565. Not about consequences 

of testing 

Gilett P M, Gilett H R, Israel D M et al. Increased 

prevalence of celiac disease in girls with Turner

syndrome detected using antibodies to endomysium 

and tissue transglutaminase. Can J Gastroenterol 

2000;14(11):915-918. Not about consequences of

testing 

Gillberg R, Ahren C. Coeliac disease diagnosed by

means of duodenoscopy and endoscopic duodenal 

biopsy. Scand J Gastroenterol 1977;12(8):911-916. 

Not about consequences of testing 

Gillett H R, Cauch-Dudek K, Jenny E et al. Prevalence

of IgA antibodies to endomysium and tissue 

transglutaminase in primary biliary cirrhosis. Can J 

Gastroenterol 2000;14(8):672-675. Not about 

consequences of testing 

Gillett H R, Freeman H J. Comparison of IgA 

endomysium antibody and IgA tissue transglutaminase 

antibody in celiac disease. Can J Gastroenterol 

2000;14(8):668-671. Not about consequences of

testing 

Gillett H R, Freeman H J. Serological testing in 

screening for adult celiac disease. Can J Gastroenterol

1999;13(3):265-269. Not about consequences of

testing 

Gillett P M, Gillett H R, Israel D M et al. High 

prevalence of celiac disease in patients with type 1 

diabetes detected by antibodies to endomysium and 

tissue transglutaminase. Can J Gastroenterol 

2001;15(5):297-301. Not about consequences of

testing 

Gillett P M, Gillett H R, Israel D M et al. Increased 

prevalence of celiac disease in girls with Turner

syndrome detected using antibodies to endomysium 

and tissue transglutaminase. Can J Gastroenterol 

2000;14(11):915-918. Not about consequences of

testing 

Gillett P M, Israel D M. Tissue transglutaminase: does 

the key fit the celiac lock?. J Pediatr Gastroenterol

Nutr 2000;30(2):222-223. Not about consequences of 

testing 

Gomez J C, Selvaggio G S, Viola M et al. Prevalence 

of celiac disease in Argentina: screening of an adult 

population in the La Plata area. Am J Gastroenterol 

2001;96(9):2700-2704. Not about consequences of

testing 

Gomez Juan C, Selvaggio Gisella, Pizarro Bibiana et

al. Value of a screening algorithm for celiac disease 

using tissue transglutaminase antibodies as first level 

in a population-based study. Am J Gastroenterol 

2002;97(11):2785-2790. Not about consequences of 

testing 

Gonczi J, Skerritt J H, Mitchell J D. A reliable

screening test for coeliac disease: enzyme-linked 

immunosorbent assay to detect anti-gliadin antibodies 

in serum. Aust N Z J Med 1991;21(5):723-731. Not 

about consequences of testing 

Gonczi J, Skerritt J H, Mitchell J D. Differentiation of 

coeliac disease and other malabsorption diseases using 

specific serum antigliadin IgG subclass profiles and 

IgA1 levels. Int Arch Allergy Immunol 

1992;98(4):377-385. Not about consequences of

testing 

Gonzalez D, Sugai E, Gomez J C et al. Is it necessary

to screen for celiac disease in postmenopausal 

osteoporotic women?. Calcif Tissue Int 

2002;71(2):141-144. Not about consequences of

testing 

Gordon N. Cerebellar ataxia and gluten sensitivity: a 

rare but possible cause of ataxia, even in childhood. 

Dev Med Child Neurol 2000;42(4):283-286. Not 

about consequences of testing 

Gould S R, Chinn G L, Nobbs B T et al. Evaluation of 

a tubeless pancreatic function test in patients with

steatorrhoea in a district general hospital. J R Soc Med 

1988;81(5):270-273. Not about consequences of

testing 

Gracey M. Another screening test for coeliac disease?.

Aust Paediatr J 1974;10(6):367-370. Not about 

consequences of testing 

Granot E, Korman S M, Sallon S et al. "Early" vs.

"late" diagnosis of celiac disease in two ethnic groups 

living in the same geographic area. Isr J Med Sci 

1994;30(4):271-275. Not about consequences of

testing 

Greco L, Babron M C, Corazza G R et al. Existence of 

a genetic risk factor on chromosome 5q in Italian

coeliac disease families. Ann Hum Genet 2001;65(Pt 

1):35-41. Not about consequences of testing 

Greco L, Corazza G, Babron M C et al. Genome 

search in celiac disease. Am J Hum Genet 

A-619
1998;62(3):669-675. Not about consequences of

testing 

Greco L, D'Adamo G, Truscelli A et al. Intestinal

permeability after single dose gluten challenge in

coeliac disease. Arch Dis Child 1991;66(7):870-872. 

Not about consequences of testing 

Greco L, Percopo S, Clot F et al. Lack of correlation 

between genotype and phenotype in celiac disease. J

Pediatr Gastroenterol Nutr 1998;26(3):286-290. Not 

about consequences of testing 

Greco L, Percopo S. The coeliac disease task force " 

Free from Gluten," " Improved knowledge to cure

coeliac disease". Acta Paediatr 1996;412(Suppl):25-

28. Not about consequences of testing 

Greco L, Romino R, Coto I et al. The first large 

population based twin study of coeliac disease. Gut 

2002;50(5):624-628. Not about consequences of

testing 

Greco L, Troncone R, de Vizia B et al. Discriminant

analysis for the diagnosis of childhood celiac disease. 

J Pediatr Gastroenterol Nutr 1987;6(4):538-542. Not 

about consequences of testing 

Greco L, Troncone R. Coeliac families. Acta Paediatr

2002;91(1):16-17. Not about consequences of testing 

Green P H, Shane E, Rotterdam H et al. Significance 

of unsuspected celiac disease detected at endoscopy. 

Gastrointest Endosc 2000;51(1):60-65. Not about 

consequences of testing 

Green PHR, Stavropoulos SN, Panagi SG et al. 

Characteristics of adult celiac disease in the USA:

results of a national survey. Am J Gastroenterol 2001; 

96(1):126-131. Not about consequences of testing 

Greenberger N J, Saegh S, Ruppert R D. Urine indican

excretion in malabsorptive disorders. 

Gastroenterology 1968;55(2):204-211. Not about 

consequences of testing 

Grodzinsky E, Hed J, Lieden G et al. Presence of IgA 

and IgG antigliadin antibodies in healthy adults as 

measured by micro-ELISA. Effect of various cutoff 

levels on specificity and sensitivity when diagnosing 

coeliac disease. Int Arch Allergy Appl Immunol 

1990;92(2):119-123. Not about consequences of

testing 

Grodzinsky E, Hed J, Skogh T. IgA antiendomysium 

antibodies have a high positive predictive value for 

celiac disease in asymptomatic patients. Allergy 

1994;49(8):593-597. Not about consequences of

testing 

Grodzinsky E, Ivarsson A, Juto P et al. New 

automated immunoassay measuring immunoglobulin 

A antigliadin antibodies for prediction of celiac 

disease in childhood. Clin Diagn Lab Immunol 

2001;8(3):564-570. Not about consequences of testing 

Grodzinsky E, Jansson G, Skogh T et al. Antiendomysium and anti-gliadin antibodies as serological 

markers for coeliac disease in childhood: a clinical 

study to develop a practical routine. Acta Paediatr

1995;84(3):294-298. Not about consequences of

testing 

Grodzinsky E. Screening for coeliac disease in

apparently healthy blood donors. Acta Paediatr

1996;412(Suppl):36-38. Not about consequences of

testing 

Grunbaum Jo A, Rodriguez Beatriz L, Labarthe

Darwin R. Parental response to identification of

elevated blood pressure or cholesterol following

school-based screening. J Adolesc Health

1993;14(2):99-103. Not about consequences of testing 

Guandalini Stefano. Celiac disease. School Nurse

News 2003;20(2):24-27. Not about consequences of 

testing 

Guinnepain M T, Eloit C, Raffard M et al. Exerciseinduced anaphylaxis: useful screening of food 

sensitization. Annals of Allergy, Asthma & 

Immunology - Official Publication of the American 

College of Allergy, Asthma, & Immunology

1996;77(6):491-496. Not about consequences of

testing 

Gupta S K, Bhu N, Singh P P et al. Oxalate loading 

test for screening steatorrhoea in diabetics. Jpn J Exp 

Med 1987;57(3):141-143. Not about consequences of 

testing 

Guvenc cedil, Kaymakog caron, Gurel N et al. The 

prevalence of manifest and latent celiac disease in type

1 diabetes mellitus. Turk J Gastroenterol 

2002;13(2):103-107. Not about consequences of

testing 

Habior Andrzej, Lewartowska Aleksandra, Orlowska 

Janina et al. Association of coeliac disease with

primary biliary cirrhosis in Poland. Eur J 

Gastroenterol Hepatol 2003;15(2):159-164. Not about 

consequences of testing 

Hadjivassiliou M, Davies-Jones G A B, Sanders D S 

et al. Dietary treatment of gluten ataxia. J Neurol

Neurosurg Psychiatry 2003;74(9):1221-1224. Not 

about consequences of testing 

Hadjivassiliou M, Gibson A, Davies-Jones G A et al. 

Does cryptic gluten sensitivity play a part in

neurological illness?. Lancet 1996;347(8998):369-

371. Not about consequences of testing 

A-620
Hadjivassiliou M, Grunewald R A, Chattopadhyay A 

K et al. Clinical, radiological, neurophysiological, and 

neuropathological characteristics of gluten ataxia.

Lancet 1998;352(9140):1582-1585. Not about 

consequences of testing 

Hadjivassiliou Marios, Grunewald Richard, Sharrack 

Basil et al. Gluten ataxia in perspective: epidemiology, 

genetic susceptibility and clinical characteristics.

Brain Dev 2003;126(Pt 3):685-691. Not about 

consequences of testing 

Hadziselimovic F, Emmons L R, Schaub U et al. 

Occurrence of large granular lymphocytes and natural 

killer cells in the epithelium of the gut distinguishes 

two different coeliac diseases. Gut 1992;33(6):767-

772. Not about consequences of testing 

Hakeem V, Fifield R, al Bayaty H F et al. Salivary 

IgA antigliadin antibody as a marker for coeliac 

disease. Arch Dis Child 1992;67(6):724-727. Not 

about consequences of testing 

Hall W H. Proximal muscle atrophy in adult celiac 

disease. Am J Dig Dis 1968;13(8):697-704. Not about 

consequences of testing 

Hallert C, Astrom J. Intellectual ability of adults after

lifelong intestinal malabsorption due to coeliac 

disease. J Neurol Neurosurg Psychiatry

1983;46(1):87-89. Not about consequences of testing 

Hallert C, Granno C, Grant C et al. Quality of life of 

adult coeliac patients treated for 10 years. Scand J

Gastroenterol 1998;33(9):933-938. Not about 

consequences of testing 

Hallert C, Granno C, Hulten S et al. Living with 

coeliac disease: controlled study of the burden of 

illness. Scand J Gastroenterol 2002;37(1):39-42. Not 

about consequences of testing 

Hallert C, Lohiniemi S. Quality of life of celiac

patients living on a gluten-free diet. Nutrition

1999;15(10):795-797. Not about consequences of

testing 

Hallert C, Tobiasson P, Walan A. Serum folate

determinations in tracing adult coeliacs. Scand J 

Gastroenterol 1981;16(2):263-267. Not about 

consequences of testing 

Hallstrom O. Comparison of IgA-class reticulin and 

endomysium antibodies in coeliac disease and 

dermatitis herpetiformis. Gut 1989;30(9):1225-1232. 

Not about consequences of testing 

Hamilton J R, McNeill L K. Childhood celiac disease: 

response of treated patients to a small uniform daily

dose of wheat gluten. Eur J Pediatr 1972;81(5):885-

893. Not about consequences of testing 

Hanasz-Jarzynska T, Ignys I. Infantile colic and food 

allergy. Int Rev Allergol Clin Immunol 

1998;4(3):111-114. Not about consequences of testing 

Hankey G L, Holmes G K. Coeliac disease in the

elderly. Gut 1994;35(1):65-67. Not about 

consequences of testing 

Hansen D, Bennedbaek F N, Hansen L K et al. High 

prevalence of coeliac disease in Danish children with 

type I diabetes mellitus. Acta Paediatr 

2001;90(11):1238-1243. Not about consequences of 

testing 

Hanson L A. Human milk and host defence: 

immediate and long-term effects. Acta Paediatr Suppl 

1999;88(430):42-46. Not about consequences of

testing 

Hansson T, Anneren G, Sjoberg O et al. Celiac disease 

in relation to immunologic serum markers, trace 

elements, and HLA-DR and DQ antigens in Swedish 

children with Down syndrome. J Pediatr Gastroenterol 

Nutr 1999;29(3):286-292. Not about consequences of 

testing 

Hansson T, Dahlbom I, Hall J et al. Antibody 

reactivity against human and guinea pig tissue 

transglutaminase in children with celiac disease. J

Pediatr Gastroenterol Nutr 2000;30(4):379-384. Not 

about consequences of testing 

Hansson T, Dannaeus A, Kraaz W et al. Production of 

antibodies to gliadin by peripheral blood lymphocytes 

in children with celiac disease: the use of an enzymelinked immunospot technique for screening and 

follow-up. Pediatr Res 1997;41(4 Pt 1):554-559. Not 

about consequences of testing 

Hansson Tony, Dahlbom Ingrid, Rogberg Siv et al. 

Recombinant human tissue transglutaminase for 

diagnosis and follow-up of childhood coeliac disease. 

Pediatr Res 2002;51(6):700-705. Not about 

consequences of testing 

Hanukoglu A, Mizrachi A, Dalal I et al. 

Extrapancreatic autoimmune manifestations in type 1 

diabetes patients and their first-degree relatives: A 

multicenter study. Diabetes Care 2003;26(4):1235-

1240. Not about consequences of testing 

Harper G D, Wheeler D C, Wicks A C B. Butterfat 

absorption - a valuable screening test in 

malabsorption. Postgrad Med J 1994;70(819):23-26. 

Not about consequences of testing 

Harvey Richard F, Shaw Ian S. Current thinking in 

coeliac disease. Br J Gen Pract 2002;246(1638):596-

602. Not about consequences of testing 

A-621
Haycock G B. Screening test for coeliac disease. Arch 

Dis Child 1976;51(5):401Not about consequences of 

testing 

Healy D A, Neumyer M M, Atnip R G et al.

Evaluation of celiac and mesenteric vascular disease 

with duplex ultrasonography. Journal of Ultrasound in 

Medicine - Official Journal of the American Institute 

of Ultrasound in Medicine 1992;11(9):481-485. Not 

about consequences of testing 

Heikkinen M, Janatuinen E, Mayo K et al. Usefulness 

of anti-Helicobacter pylori and anti-CagA antibodies

in the selection of patients for gastroscopy. Am J 

Gastroenterol 1997;92(12):2225-2229. Not about 

consequences of testing 

Heikkinen M, Pikkarainen P, Takala J et al. Etiology

of dyspepsia: four hundred unselected consecutive

patients in general practice. Scand J Gastroenterol 

1995;30(6):519-523. Not about consequences of

testing 

Heneghan M A, Mchugh P, Stevens F M et al. 

Addison's disease and selective IgA deficiency in two 

coeliac patients. Scand J Gastroenterol

1997;32(5):509-511. Not about consequences of

testing 

Henker J, Zugehor M, Morrenz J. Reticulin antibodies 

in coeliac disease. Acta Paediatr Hung 

1983;24(4):349-353. Not about consequences of

testing 

Hennessy W B, Ralston M. Ileocaecal carcinoma and 

the coeliac syndrome. Gut 1969;10(11):951-952. Not 

about consequences of testing 

Hernandez M A, Colina G, Ortigosa L. Epilepsy,

cerebral calcifications and clinical or subclinical

coeliac disease. Course and follow up with gluten-free 

diet. Seizure 1998;7(1):49-54. Not about 

consequences of testing 

Hertervig E, Wieslander J, Johansson C et al. Antineutrophil cytoplasmic antibodies in chronic 

inflammatory bowel disease. Prevalence and 

diagnostic role. Scand J Gastroenterol 1995;30(7):693-

698. Not about consequences of testing 

Hill I, Fasano A, Schwartz R et al. The prevalence of 

celiac disease in at-risk groups of children in the 

United States. Eur J Pediatr 2000;136(1):86-90. Not 

about consequences of testing 

Hill Ivor D, Bhatnagar Shinjini, Cameron Donald J S 

et al. Celiac disease: Working Group Report of the 

First World Congress of Pediatric Gastroenterology, 

Hepatology, and Nutrition. J Pediatr Gastroenterol 

Nutr 2002;35(Suppl 2):78-88. Not about consequences 

of testing 

Hill P G, Thompson S P, Holmes G K. IgA antigliadin antibodies in adult celiac disease. Clin Chem 

1991;37(5):647-650. Not about consequences of

testing 

Hill R E, Durie P R, Gaskin K J et al. Steatorrhea and 

pancreatic insufficiency in Shwachman syndrome. 

Gastroenterology 1982;83(1 Pt 1):22-27. Not about 

consequences of testing 

Hin H, Bird G, Fisher P et al. Coeliac disease in 

primary care: case finding study. BMJ 

1999;318(7177):164-167. Not about consequences of 

testing 

Hjelt K, Krasilnikoff P A. The impact of gluten on

haematological status, dietary intakes of haemopoietic 

nutrients and vitamin B12 and folic acid absorption in 

children with coeliac disease. Acta Paediatr Scand 

1990;79(10):911-919. Not about consequences of

testing 

Hoey John. Irritable bowel syndrome: could it be 

celiac disease?. Cmaj - Canadian Medical Association

Journal = Journal De L'association Medicale 

Canadienne 2002;166(4):479-480. Not about 

consequences of testing 

Hoffbrand A V. Anaemia in adult coeliac disease. Clin

Gastroenterol 1974;3(1):71-89. Not about 

consequences of testing 

Hoffenberg E J, Bao F, Eisenbarth G S et al. 

Transglutaminase antibodies in children with a genetic 

risk for celiac disease. Eur J Pediatr 2000;137(3):356-

360. Not about consequences of testing 

Hoffenberg E J, Haas J, Drescher A et al. A trial of

oats in children with newly diagnosed celiac disease. 

Eur J Pediatr 2000;137(3):361-366. Not about 

consequences of testing 

Hogberg L, Falth-Magnusson K, Grodzinsky E et al. 

Familial prevalence of coeliac disease: A twenty-year 

follow-up study. Scand J Gastroenterol 2003;38(1):61-

65. Not about consequences of testing 

Holdstock G, Eade O E, Isaacson P et al. Endoscopic 

duodenal biopsies in coeliac disease and duodenitis. 

Scand J Gastroenterol 1979;14(6):717-720. Not about 

consequences of testing 

Holdstock G. Jejunal biopsy without the need for 

screening. Lancet 1978;1(8076):1236-1237. Not about 

consequences of testing 

Holmes G K T. Coeliac disease and malignancy.

Digestive and Liver Disease - Official Journal of the 

Italian Society of Gastroenterology and the Italian 

Association for the Study of the Liver 2002;34(3):229-

237. Not about consequences of testing 

A-622
Holmes G K T. Screening for coeliac disease in type 1 

diabetes. Arch Dis Child 2002;87(6):495-498. Not 

about consequences of testing 

Holmes G K. Coeliac disease and Type 1 diabetes

mellitus - the case for screening. Diabet Med 

2001;18(3):169-177. Not about consequences of

testing 

Holmes G K. Non-malignant complications of coeliac 

disease. Acta Paediatr 1996;412(Suppl):68-75. Not 

about consequences of testing 

Holt Peter R. Gastrointestinal diseases in the elderly. 

Curr Opin Clin Nutr Metab Care 2003;6(1):41-48. Not 

about consequences of testing 

Holt Worthe S. Factors affecting compliance with

screening sigmoidoscopy. J Fam Pract 

1991;32(6):585-589. Not about consequences of

testing 

Horvath K, Mehta D I. Celiac disease--a worldwide 

problem. Indian J Pediatr 2000;67(10):757-763. Not 

about consequences of testing 

Horvath Karoly, Hill Ivor D. Anti-tissue 

transglutaminase antibody as the first line screening 

for celiac disease: good-bye antigliadin tests?. Am J 

Gastroenterol 2002;97(11):2702-2704. Not about 

consequences of testing 

Hourihane D O, Weir D G. Malignant celiac 

syndrome. Report of two cases with malabsorption 

and microscopic foci of intestinal lymphoma. 

Gastroenterology 1970;59(1):130-139. Not about 

consequences of testing 

Hovell C J, Collett J A, Vautier G et al. High 

prevalence of coeliac disease in a population-based 

study from Western Australia: a case for screening?. 

Med J Aust 2001;175(5):247-250. Not about 

consequences of testing 

Howard MR, Turnbull AJ, Morley P et al. A 

prospective study of the prevalence of undiagnosed 

coeliac disease in laboratory defined iron and folate 

deficiency. J Clinl Path 2002; 55(10):754-757. Not 

about consequences of testing 

Hulse J A. Referral criteria for growth screening. J

Med Screen 1995;2(3):168-170. Not about 

consequences of testing 

Hummel M, Bonifacio E, Stern M et al. Development 

of celiac disease-associated antibodies in offspring of 

parents with type I diabetes. Diabetologia 

2000;43(8):1005-1011. Not about consequences of

testing 

Hurley T H, Sullivan J R, Hurley J V. Reaction to 

Kveim test material in sarcoidosis and other diseases. 

Lancet 1975;1(7905):494-496. Not about 

consequences of testing 

Hyams J S, Treem W R, Justinich C J et al.

Characterization of symptoms in children with

recurrent abdominal pain: resemblance to irritable 

bowel syndrome. J Pediatr Gastroenterol Nutr

1995;20(2):209-214. Not about consequences of

testing 

Hyer W, Cotterill A M, Savage M O. Common causes 

of short stature detectable by a height surveillance 

programme. J Med Screen 1995;2(3):150-153. Not 

about consequences of testing 

Iacono G, Carroccio A, Montalto G et al. Steatocrit 

test after a standard fatty meal: a new simple and 

sensitive test to detect malabsorption. J Pediatr 

Gastroenterol Nutr 1991;13(2):161-167. Not about 

consequences of testing 

Iacono G, Carroccio A, Montalto G et al. Steatocrit 

test: normal range and physiological variations in

preterm and low-birth-weight full-term newborns. 

Acta Paediatr 1992;81(11):933-934. Not about 

consequences of testing 

Iancu T, Elian E. The intestinal microvillus. 

Ultrastructural variability in coeliac disease and cow's

milk intolerance. Acta Paediatr Scand 1976;65(1):65-

73. Not about consequences of testing 

Iglesias S, Chapon F, Baron J C. Familial occipital 

calcifications, hemorrhagic strokes,

leukoencephalopathy, dementia, and external carotid 

dysplasia. Neurology 2000;55(11):1661-1667. Not 

about consequences of testing 

Iovino P, Ciacci C, Sabbatini F et al. Esophageal 

impairment in adult celiac disease with steatorrhea.

Am J Gastroenterol 1998;93(8):1243-1249. Not about 

consequences of testing 

Ivarsson A, Persson L A, Juto P et al. High prevalence 

of undiagnosed coeliac disease in adults: a Swedish 

population-based study. J Intern Med 1999;245(1):63-

68. Not about consequences of testing 

Ivarsson S A, Carlsson A, Bredberg A et al. 

Prevalence of coeliac disease in Turner syndrome. 

Acta Paediatr 1999;88(9):933-936. Not about 

consequences of testing 

Jaeger C, Hatziagelaki E, Petzoldt R et al. 

Comparative analysis of organ-specific autoantibodies

and celiac disease--associated antibodies in type 1

diabetic patients, their first-degree relatives, and

healthy control subjects. Diabetes Care 2001;24(1):27-

32. Not about consequences of testing 

James MW, Scott BB. Evidence-based clinical

medicine: Application of a diagnostic test using the 

A-623
example of coeliac disease. Cme J Gastroenterol 

Hepatol Nutr 2001; 4(1):28-31. Unable to obtain

article 

Janatkova I, Malic caron, Fu caron et al. Diagnostic 

asset of assessment of autoantibodies in glutensensitive enteropathy. Epidemiol Mikrobiol Imunol 

2002;51(3):125-130. Not about consequences of

testing 

Janatuinen E K, Kemppainen T A, Julkunen R J K et 

al. No harm from five year ingestion of oats in coeliac 

disease. Gut 2002;50(3):332-335. Not about 

consequences of testing 

Jansson U H, Gudjonsdottir A H, Ryd W et al. Two 

different doses of gluten show a dose-dependent

response of enteropathy but not of serological markers 

during gluten challenge in children with coeliac 

disease. Acta Paediatr 2001;90(3):255-259. Not about 

consequences of testing 

Jansson Ulf H G, Kristiansson Bengt, AlbertssonWikland Kerstin et al. Short-term gluten challenge in

children with coeliac disease does not impair

spontaneous growth hormone secretion. J Pediatr

Endocrinol Metab 2003;16(5):771-778. Not about 

consequences of testing 

Jaskowski T D, Schroder C, Martins T B et al. IgA 

antibodies against endomysium and transglutaminase: 

a comparison of methods. J Clin Lab Anal 

2001;15(3):108-111. Not about consequences of

testing 

Jennings J S R, Howdle P D. Celiac disease. Curr

Opin Gastroenterol 2001;17(2):118-126. Not about 

consequences of testing 

Johansen B H, Gjertsen H A, Vartdal F et al. Binding 

of peptides from the N-terminal region of alphagliadin to the celiac disease-associated HLA-DQ2 

molecule assessed in biochemical and T cell assays. 

Clin Immunol Immunopathol 1996;79(3):288-293. 

Not about consequences of testing 

Johnson R E, Green T A, Schachter J et al. Evaluation

of nucleic acid amplification tests as reference tests for 

Chlamydia trachomatis infections in asymptomatic 

men. J Clin Microbiol 2000;38(12):4382-4386. Not 

about consequences of testing 

Johnston S D, Peter Watson R G, McMillan S A. Soda 

bread provocation test for subjects with transient

serology for coeliac disease 3 years after a population 

screening survey. Eur J Gastroenterol Hepatol 

2000;12(9):1013-1015. Not about consequences of

testing 

Johnston S D, Ritchie C, Robinson J. Application of 

red cell distribution width to screening for coeliac

disease in insulin-dependent diabetes mellitus. Ir J 

Med Sci 1999;168(3):167-170. Not about 

consequences of testing 

Johnston S D, Smye M, Watson R G P et al. 

Lactulose-mannitol intestinal permeability test: A 

useful screening test for adult coeliac disease. Ann

Clin Biochem 2000;37(4):512-519. Not about 

consequences of testing 

Johnston S D, Smye M, Watson R P. Intestinal 

permeability tests in coeliac disease. Clin Lab 

2001;47(3-4):143-150. Not about consequences of

testing 

Johnston S D, Watson R G P. Small bowel lymphoma 

in unrecognized coeliac disease: A cause for concern?. 

Eur J Gastroenterol Hepatol 2000;12(6):645-648. Not 

about consequences of testing 

Johnston S D, Watson R G, McMillan S A et al. 

Preliminary results from follow-up of a large-scale 

population survey of antibodies to gliadin, reticulin 

and endomysium. Acta Paediatr 1996;412(Suppl):61-

64. Not about consequences of testing 

Johnston S D, Watson R G, McMillan S A et al. 

Serological markers for coeliac disease: changes with 

time and relationship to enteropathy. Eur J 

Gastroenterol Hepatol 1998;10(3):259-264. Not about 

consequences of testing 

Johnston S D, Watson R G, Middleton D et al. 

Genetic, morphometric and immunohistochemical 

markers of latent coeliac disease. Eur J Gastroenterol 

Hepatol 1999;11(11):1283-1288. Not about 

consequences of testing 

Johnston Simon D, McMillan Stanley A, Collins John 

S et al. A comparison of antibodies to tissue 

transglutaminase with conventional serological tests in 

the diagnosis of coeliac disease. Eur J Gastroenterol 

Hepatol 2003;15(9):1001-1004. Not about 

consequences of testing 

Johnstone D E. Food allergy in children under two 

years of age. Pediatr Clin North Am 1969;16(1):211-

216. Not about consequences of testing 

Jokinen J, Peters U, Maki M et al. Celiac sprue in 

patients with chronic oral mucosal symptoms. J Clin 

Gastroenterol 1998;26(1):23-26. Not about 

consequences of testing 

Juby L D, Rothwell J, Axon A T. Lactulose/mannitol 

test: an ideal screen for celiac disease.

Gastroenterology 1989;96(1):79-85. Not about 

consequences of testing 

Juto P, Fredrikzon B, Hernell O. Gliadin-specific

serum immunoglobulins A, E, G, and M in childhood: 

relation to small intestine mucosal morphology. J 

A-624
Pediatr Gastroenterol Nutr 1985;4(5):723-729. Not 

about consequences of testing 

Kalapesi Z, Rees J P R. Coeliac disease in 

schoolchildren. Ir Med J 1978;71(6):188-191. Not 

about consequences of testing 

Kallikorm R, Uibo O, Uibo R. Coeliac disease in

spondyloarthropathy: usefulness of serological 

screening. Clin Rheumatol 2000;19(2):118-122. Not 

about consequences of testing 

Kapadia C. The reliability of noninvasive tests for

celiac disease. Gastroenterology 1995;108(2):608-610. 

Not about consequences of testing 

Kapuscinska A, Zalewski T, Chorzelski TP et al. 

Disease specificity and dynamics of changes in IgA 

class anti-endomysial antibodies in celiac disease. J

Pediatr Gastroenterol Nutr 1987; 6(4):529-534. Not 

about consequences of testing 

Karczewska K, Lukasik M, Kasner J et al. Familial

occurrence of celiac disease and isolated

immunoglobulin a deficiency. Med Sci Monit 

1998;4(5):836-839. Not about consequences of testing 

Katz A J, Falchuk Z M. Current concepts in gluten

sensitive enteropathy (celiac sprue). Pediatr Clin 

North Am 1975;22(4):767-785. Not about 

consequences of testing 

Kaukinen K, Collin P, Holm K et al. Small-bowel

mucosal inflammation in reticulin or gliadin antibodypositive patients without villous atrophy. Scand J 

Gastroenterol 1998;33(9):944-949. Not about 

consequences of testing 

Kaukinen K, Collin P, Holm K et al. Wheat starchcontaining gluten-free flour products in the treatment 

of coeliac disease and dermatitis herpetiformis. A

long-term follow-up study. Scand J Gastroenterol 

1999;34(2):163-169. Not about consequences of

testing 

Kaukinen K, Halme L, Collin P et al. Celiac disease in

patients with severe liver disease: Gluten-free diet

may reverse hepatic failure. Gastroenterology 2002; 

122(4):881-888. Not about consequences of testing 

Kaukinen Katri, Partanen Jukka, Maki Markku et al. 

HLA-DQ typing in the diagnosis of celiac disease. Am 

J Gastroenterol 2002;97(3):695-699. Not about 

consequences of testing 

Kaukinen Katri, Sulkanen Satu, Maki Markku et al. 

IgA-class transglutaminase antibodies in evaluating 

the efficacy of gluten-free diet in coeliac disease. Eur J 

Gastroenterol Hepatol 2002;14(3):311-315. Not about 

consequences of testing 

Kawasaki E, Eisenbarth G S. High-throughput 

radioassays for autoantibodies to recombinant

autoantigens. Front Biosci 2000;5181-190. Not about 

consequences of testing 

Kelly C P, Feighery C F, Gallagher R B et al. Mucosal 

and systemic IgA anti-gliadin antibody in celiac

disease. Contrasting patterns of response in serum, 

saliva, and intestinal secretions. Dig Dis Sci 

1991;36(6):743-751. Not about consequences of

testing 

Kelly J, O'Farrelly C, Rees J P et al. Humoral response 

to alpha gliadin as serological screening test for

coeliac disease. Arch Dis Child 1987;62(5):469-473. 

Not about consequences of testing 

Kelly J, Whelan C A, Weir D G et al. Removal of 

endogenous peroxidase activity from cryostat sections 

for immunoperoxidase visualisation of monoclonal 

antibodies. J Immunol Methods 1987;96(1):127-132. 

Not about consequences of testing 

Kennedy N P, Feighery C. Clinical features of coeliac 

disease today. Biomed Pharmacother 2000;54(7):373-

380. Not about consequences of testing 

Kerlin P, Wong L. Breath hydrogen testing in bacterial 

overgrowth of the small intestine. Gastroenterology

1988;95(4):982-988. Not about consequences of

testing 

Khoshoo V, Bhan M K, Unsworth D J et al. Antireticulin antibodies: useful adjunct to histopathology

in diagnosing celiac disease, especially in a 

developing country. J Pediatr Gastroenterol Nutr

1988;7(6):864-866. Not about consequences of testing 

Khuffash F A, Barakat M H, Shaltout A A et al. 

Coeliac disease among children in Kuwait: difficulties

in diagnosis and management. Gut 1987;28(12):1595-

1599. Not about consequences of testing 

Kieffer M. Serum antibodies to gliadin and other

cereal proteins in patients with coeliac disease and 

dermatitis herpetiformis. Dan Med Bull 

1985;32(5):251-262. Not about consequences of

testing 

Kieslich M, Errazuriz G, Posselt H G et al. Brain

white-matter lesions in celiac disease: a prospective 

study of 75 diet-treated patients. Pediatrics 

2001;108(2):E21Not about consequences of testing 

Kilander A F, Dotevall G, Fallstrom S P et al. 

Evaluation of gliadin antibodies for detection of

coeliac disease. Scand J Gastroenterol

1983;18(3):377-383. Not about consequences of

testing 

A-625
King A L, Fraser J S, Moodie S J et al. Coeliac 

disease: follow-up linkage study provides further

support for existence of a susceptibility locus on

chromosome 11p11. Ann Hum Genet 2001;65(Pt 

4):377-386. Not about consequences of testing 

Kingham J G, Parker D R. The association between 

primary biliary cirrhosis and coeliac disease: a study

of relative prevalences. Gut 1998;42(1):120-122. Not 

about consequences of testing 

Klasen E C, Polanco I, Biemond I et al. alpha 1-

Antitrypsin and coeliac disease in spain. Gut 

1980;21(11):948-950. Not about consequences of

testing 

Knivsberg A M. Urine patterns, peptide levels and

IgA/IgG antibodies to food proteins in children with 

dyslexia. Pediatr Rehabil 1997;1(1):25-33. Not about 

consequences of testing 

Kocna Petr, Vanickova Zdislava, Perusicova Jindriska 

et al. Tissue transglutaminase-serology markers for 

coeliac disease. Clin Chem Lab Med 2002;40(5):485-

492. Not about consequences of testing 

Kokkonen J, Viitanen A, Simila S. Coping with a 

coeliac diet after adolescence. Helv Paediatr Acta

1989; 43(4):261-265. Unable to obtain article 

Kolek A, Fischerova E, Kos V et al. Application of 

ELISA method to determine antigliadin antibodies in 

children with coeliac disease. Acta Univ Palacki

Olomuc Fac Med 1989;122183-192. Not about 

consequences of testing 

Kolek A, Vospelova J, Hermanova Z et al. Occurrence 

of Coeliac Disease in Children With Down Syndrome 

in North Moravia, Czech Republic. Eur J Pediatr 

2003;162(3):207-208. Not about consequences of

testing 

Koletzko S, Burgin-Wolff A, Koletzko B et al. 

Prevalence of coeliac disease in diabetic children and 

adolescents. A multicentre study. Eur J Pediatr

1988;148(2):113-117. Not about consequences of

testing 

Kolho K L, Farkkila M A, Savilahti E. Undiagnosed 

coeliac disease is common in Finnish adults. Scand J

Gastroenterol 1998;33(12):1280-1283. Not about 

consequences of testing 

Kolho K L, Jusufovic J, Miettinen A et al. Parietal cell

antibodies and Helicobacter pylori in children. J 

Pediatr Gastroenterol Nutr 2000;30(3):265-268. Not 

about consequences of testing 

Kolho K L, Savilahti E. IgA endomysium antibodies 

on human umbilical cord: an excellent diagnostic tool 

for celiac disease in childhood. J Pediatr Gastroenterol 

Nutr 1997;24(5):563-567. Not about consequences of 

testing 

Kolho K L, Tiitinen A, Tulppala M et al. Screening 

for coeliac disease in women with a history of

recurrent miscarriage or infertility. Br J Obstet 

Gynaecol 1999;106(2):171-173. Not about 

consequences of testing 

Kolsteren M M, Koopman H M, Schalekamp G et al. 

Health-related quality of life in children with celiac 

disease. Eur J Pediatr 2001;138(4):593-595. Not about 

consequences of testing 

Koop I, Ilchmann R, Izzi L et al. Detection of

autoantibodies against tissue transglutaminase in 

patients with celiac disease and dermatitis

herpetiformis. Am J Gastroenterol 2000;95(8):2009-

2014. Not about consequences of testing 

Korponay-Szabo I R, Kovacs J B, Czinner A et al. 

High prevalence of silent celiac disease in preschool 

children screened with IgA/IgG antiendomysium 

antibodies. J Pediatr Gastroenterol Nutr 

1999;28(1):26-30. Not about consequences of testing 

Korponay-Szabo I R, Kovacs J B, Lorincz M et al. 

Prospective significance of antiendomysium antibody

positivity in subsequently verified celiac disease. J 

Pediatr Gastroenterol Nutr 1997;25(1):56-63. Not 

about consequences of testing 

Korponay-Szabo I, Kovacs J, Lorincz M et al. 

Families with multiple cases of gluten-sensitive

enteropathy. Z Gastroenterol 1998;36(7):553-558. Not 

about consequences of testing 

Kotze L M, Utiyama S R, Nisihara R M et al.

Antiendomysium antibodies in Brazilian patients with 

celiac disease and their first-degree relatives. Arq

Gastroenterol 2001;38(2):94-103. Not about 

consequences of testing 

Kowalska E, Wasowska-Krolikowska K, ToporowskaKowalska E. Estimation of antithyroid antibodies 

occurrence in children with coeliac disease. Medical

Science Monitor - International Medical Journal of 

Experimental and Clinical Research 2000;6(4):719-

721. Not about consequences of testing 

Kowlessar O D, Phillips L D. Celiac disease. Med

Clin North Am 1970;54(3):647-656. Not about 

consequences of testing 

Krasilnikoff P A, Gudman-Hoyer E, Moltke H H.

Diagnostic value of disaccharide tolerance tests in

children. Acta Paediatr Scand 1975;64(5):693-698. 

Not about consequences of testing 

Krawitt E L, Chastenay B F. 25-hydroxy vitamin D 

absorption test in patients with gastrointestinal

A-626
disorders. Calcif Tissue Int 1980;32(3):183-187. Not 

about consequences of testing 

Kristiansson B, Karlberg J, Fallstrom S P. Infants with 

low rate of weight gain. I. A study of organic factors 

and growth patterns. Acta Paediatr Scand 

1981;70(5):655-662. Not about consequences of

testing 

Kugathasan S, Czinn S J. Gastroduodenal 

inflammation and related disorders in children. Curr 

Opin Gastroenterol 1996;12(6):537-543. Not about 

consequences of testing 

Kuitunen P, Kosnai I, Savilahti E. Morphometric 

study of the jejunal mucosa in various childhood 

enteropathies with special reference to intraepithelial 

lymphocytes. J Pediatr Gastroenterol Nutr

1982;1(4):525-531. Not about consequences of testing 

Kull K, Uibo O, Salupere R et al. High frequency of 

antigliadin antibodies and absence of antireticulin and 

antiendomysium antibodies in patients with ulcerative 

colitis. J Gastroenterol 1999;34(1):61-65. Not about 

consequences of testing 

Kumar P J, Walker-Smith J, Milla P et al. The teenage

coeliac: follow up study of 102 patients. Arch Dis

Child 1988;63(8):916-920. Not about consequences of 

testing 

Kumar P J. European and North American populations 

should be screened for coeliac disease. Gut 

2003;52(2):170-171. Not about consequences of

testing 

Kumar Rajesh, Eastwood Amy L, Brown Milton L et

al. Human genome search in celiac disease: mutated 

gliadin T-cell-like epitope in two human proteins

promotes T-cell activation. J Mol Biol 

2002;319(3):593-602. Not about consequences of

testing 

Kumar V, Jarzabek-Chorzelska M, Sulej J et al. Tissue 

transglutaminase and endomysial antibodiesdiagnostic markers of gluten-sensitive enteropathy in 

dermatitis herpetiformis. Clin Immunol 

2001;98(3):378-382. Not about consequences of

testing 

Kumar V, Rajadhyaksha M, Wortsman J. Celiac

disease-associated autoimmune endocrinopathies. Clin

Diagn Lab Immunol 2001;8(4):678-685. Not about 

consequences of testing 

Kushnir Talma, Rabinowitz Stanley, Melamed Samuel

et al. Health responsibility and workplace health 

promotion among women: Early detection of cancer. 

Health Care Women Int 1995;16(4):329-340. Not 

about consequences of testing 

La Seta F, Salerno G, Buccellato A et al. Radiographic 

indicants of adult celiac disease assessed by doublecontrast small bowel enteroclysis. Eur J Radiol

1992;15(2):157-162. Not about consequences of

testing 

Labate A, Gambardella A, Messina D et al. Silent 

celiac disease in patients with childhood localizationrelated epilepsies. Epilepsia 2001;42(9):1153-1155. 

Not about consequences of testing 

Labib M, Gama R, Marks V. Predictive value of Dxylose absorption test and erythrocyte folate in adult 

coeliac disease: a parallel approach. Ann Clin

Biochem 1990;27(Pt 1):75-77. Not about 

consequences of testing 

Lad R, Jacobson K. The changing face of celiac 

disease. Paediatr Child Health 2001;6(9):644-651. Not 

about consequences of testing 

Ladinser B, Rossipal E, Pittschieler K. Endomysium

antibodies in coeliac disease: an improved method. 

Gut 1994;35(6):776-778. Not about consequences of 

testing 

Lagerqvist C, Ivarsson A, Juto P et al. Screening for 

adult coeliac disease - which serological marker(s) to 

use?. J Intern Med 2001;250(3):241-248. Not about 

consequences of testing 

Lahat E, Broide E, Leshem M et al. Prevalence of

celiac antibodies in children with neurologic disorders. 

Pediatr Neurol 2000;22(5):393-396. Not about 

consequences of testing 

Lahteenoja H, Maki M, Viander M et al. Local 

challenge of oral mucosa with gliadin in patients with 

coeliac disease. Clin Exp Immunol 2000;120(1):38-

45. Not about consequences of testing 

Lahteenoja H, Maki M, Viander M et al. Local 

challenge on oral mucosa with an alpha-gliadin related 

synthetic peptide in patients with celiac disease. Am J 

Gastroenterol 2000;95(10):2880-2887. Not about 

consequences of testing 

Lahteenoja H, Toivanen A, Raiha I et al. Salivary 

antigliadin and antiendomysium antibodies in coeliac 

disease. Scand J Immunol 1999;50(5):528-535. Not 

about consequences of testing 

Lamabadusuriya S P, Packer S, Harries J T.

Limitations of xylose tolerance test as a screening 

procedure in childhood coeliac disease. Arch Dis 

Child 1975;50(1):34-39. Not about consequences of 

testing 

Lamabadusuriya S P, Packer S, Harries J T.

Proceedings: Limitations of xylose tolerance test as

screening procedure for coeliac disease. Arch Dis

A-627
Child 1974;49(3):244-245. Not about consequences of 

testing 

Lamontagne P, West G E, Galibois I. Quebecers with 

celiac disease: analysis of dietary problems. Canadian

Journal of Dietetic Practice and Research - a 

Publication of Dietitians of Canada = Revue 

Canadienne De La Pratique Et De La Recherche En 

Dietetique - Une Publication Des Dietetistes Du C 

2001;62(4):175-181. Not about consequences of

testing 

Lampasona V, Bazzigaluppi E, Barera G et al. Tissue 

transglutaminase and combined screening for coeliac

disease and type 1 diabetes-associated autoantibodies.

Lancet 1998;352(9135):1192-1193. Not about 

consequences of testing 

Lang-Muritano M, Molinari L, Dommann-Scherrer C

et al. Incidence of enteropathy-associated T-cell 

lymphoma in celiac disease: Implications for children 

and adolescents with type 1 diabetes. Pediatr Diabetes

2002;3(1):42-45. Not about consequences of testing 

Lankisch P G, Martinez Schramm A, Petersen F et al.

Diagnostic intervals for recognizing celiac disease. Z 

Gastroenterol 1996;34(8):473-477. Not about 

consequences of testing 

Lapini M, Lasagni D, Ferrari R. Detection of antismooth muscle antibodies in the sera of patients with 

celiac disease: Relationship with anti-endomysium 

antibodies. Eur J Lab Med 1998;6(3):174-176. Not 

about consequences of testing 

Larcher V F, Shepherd R, Francis D E et al. Protracted 

diarrhoea in infancy. Analysis of 82 cases with 

particular reference to diagnosis and management. 

Arch Dis Child 1977;52(8):597-605. Not about 

consequences of testing 

Larizza D, Calcaterra V, De Giacomo C et al. Celiac 

disease in children with autoimmune thyroid disease. 

Eur J Pediatr 2001;139(5):738-740. Not about 

consequences of testing 

Larizza D, Calcaterra V, Luinetti O et al. Evidence for

immunogenetic predisposition in children with celiac 

disease and autoimmune thyroid disease. Int J Med 

Biol Environ 2001;29(2):143-148. Not about 

consequences of testing 

Lasagni D, Ferrari R, Lapini M. Unmasking antiendomysial antibodies in coeliac subjects positive for

anti-smooth muscle antibodies. Acta Paediatr

1999;88(4):462-464. Not about consequences of

testing 

Lavy U, Bauer C H. Pathophysiology of failure to 

thrive in gastrointestinal disorders. Pediatr Ann

1978;7(11):743-749. Not about consequences of

testing 

Lazzari R, Volta U, Bianchi F B et al. R1 reticulin

antibodies: markers of celiac disease in children on a 

normal diet and on gluten challenge. J Pediatr 

Gastroenterol Nutr 1984;3(4):516-522. Not about 

consequences of testing 

Lebenthal E, Branski D. Childhood celiac disease--a 

reappraisal. Eur J Pediatr 1981;98(5):681-690. Not 

about consequences of testing 

Lebenthal E, Heitlinger L A. Gliadin antibodies in

celiac disease. Eur J Pediatr 1983;102(5):711-712. Not 

about consequences of testing 

Lebenthal Emanuel, Branski David. Celiac disease: an 

emerging global problem. J Pediatr Gastroenterol Nutr 

2002;35(4):472-474. Not about consequences of

testing 

Lebenthal Emanuel, Branski David. Serum antiendomysial and anti-tissue transglutaminase for 

screening of celiac disease. Isr Med Assoc J

2002;4(8):627-628. Not about consequences of testing 

Lee M F. The diagnosis of steatorrhoea in outpatients. 

Br J Surg 1970;57(5):387-388. Not about 

consequences of testing 

Lee Susie K, Lo Winson, Memeo Lorenzo et al. 

Duodenal histology in patients with celiac disease 

after treatment with a gluten-free diet. Gastrointest 

Endosc 2003;57(2):187-191. Not about consequences 

of testing 

Lejarraga H, Caino S, Salvador A et al. Normal

growth velocity before diagnosis of celiac disease. J 

Pediatr Gastroenterol Nutr 2000;30(5):552-556. Not 

about consequences of testing 

Lembcke B, Grimm K, Lankisch P G. Raised fecal fat 

concentration is not a valid indicator of pancreatic 

steatorrhea. Am J Gastroenterol 1987;82(6):526-531. 

Not about consequences of testing 

Lenihan Genie O, Kirk William G. Conjoint 

supervision with beginning trainees: The model and its 

effectiveness. Clinical Supervisor 1992;10(1):35-50. 

Not about consequences of testing 

Leon F, Camarero C, Pena R et al. Antitransglutaminase IgA ELISA: clinical potential and 

drawbacks in celiac disease diagnosis. Scand J

Gastroenterol 2001;36(8):849-853. Not about 

consequences of testing 

Lepore L, Martelossi S, Pennesi M et al. Prevalence of

celiac disease in patients with juvenile chronic

arthritis. Eur J Pediatr 1996;129(2):311-313. Not 

about consequences of testing 

A-628
Lepore L, Pennesi M, Ventura A et al. Anti-alphagliadin antibodies are not predictive of celiac disease 

in juvenile chronic arthritis. Acta Paediatr 1993;82(6-

7):569-573. Not about consequences of testing 

Lerman Caryn, Trock Bruce, Rimer Barbara K et al. 

Psychological side effects of breast cancer screening. 

Health Psychol 1991;10(4):259-267. Not about 

consequences of testing 

Lerner A. The race for the diagnostic autoantibody in 

celiac disease. And the winner is... Isr Med Assoc J 

2000;2(2):82-83. Not about consequences of testing 

Leshowitz Barry, Meyers Jonathan M. Application of 

decision theory to DUI assessment. Alcohol Clin Exp 

Res 1996;20(7):1148-1152. Not about consequences 

of testing 

Levine A, Bujanover Y, Reif S et al. Comparison of 

assays for anti-endomysial and anti-transglutaminase 

antibodies for diagnosis of pediatric celiac disease. Isr 

Med Assoc J 2000;2(2):122-125. Not about 

consequences of testing 

Levine A, Lahav J, Zahavi I et al. Activated protein C 

resistance in pediatric inflammatory bowel disease. J

Pediatr Gastroenterol Nutr 1998;26(2):172-174. Not 

about consequences of testing 

Levy-Gigi C, Mandelowitz N, Peled Y et al. Is the fat 

breath test effective in the diagnosis of fat

malabsorption and pancreatic disease?. Digestion

1978;18(1-2):77-85. Not about consequences of

testing 

Lewis C, Book L, Black J et al. Celiac disease and 

human leukocyte antigen genotype: Accuracy of

diagnosis in self-diagnosed individuals, dosage effect, 

and sibling risk. J Pediatr Gastroenterol Nutr

2000;31(1):22-27. Not about consequences of testing 

Li Voon, Chong J S W, Leong K S et al. Is coeliac 

disease more prevalent in young adults with coexisting 

Type 1 diabetes mellitus and autoimmune thyroid 

disease compared with those with Type 1 diabetes

mellitus alone?. Diabet Med 2002;19(4):334-337. Not 

about consequences of testing 

Lightdale C J, Winawer S J. Screening diagnosis and 

staging of esophageal cancer. Semin Oncol 

1984;11(2):101-112. Not about consequences of

testing 

Linaker B D, Calam J. Is jejunal biopsy valuable in the 

elderly?. Age Ageing 1978;7(4):244-245. Not about 

consequences of testing 

Lindgren S, Sjoberg K, Eriksson S. Unsuspected

coeliac disease in chronic 'cryptogenic' liver disease. 

Scand J Gastroenterol 1994;29(7):661-664. Not about 

consequences of testing 

Lindh E, Ljunghall S, Larsson K et al. Screening for 

antibodies against gliadin in patients with

osteoporosis. J Intern Med 1992;231(4):403-406. Not 

about consequences of testing 

Lindquist B L, Rogozinski T, Moi H et al. 

Endomysium and gliadin IgA antibodies in children 

with coeliac disease. Scand J Gastroenterol 

1994;29(5):452-456. Not about consequences of

testing 

Lindqvist U, Rudsander A, Bostrom A et al. IgA 

antibodies to gliadin and coeliac disease in psoriatic 

arthritis. Rheumatology (Oxford) 2002;41(1):31-37. 

Not about consequences of testing 

Littlewood J M. Coeliac disease in childhood. 

Bailliere's Clinical Gastroenterology 1995;9(2):295-

327. Not about consequences of testing 

Liu E, Bao F, Barriga K et al. Fluctuating 

transglutaminase autoantibodies are related to 

histologic features of celiac disease. Clin

Gastroenterol Hepatol 2003;1(5):356-362. Not about 

consequences of testing 

Ljungman G, Myrdal U. Compliance in teenagers with 

coeliac disease--a Swedish follow-up study. Acta

Paediatr 1993;82(3):235-238. Not about consequences 

of testing 

Lloyd J K. Effects and treatment of malabsorption in 

childhood. Proc Nutr Soc 1972;31(1):61-66. Not about 

consequences of testing 

Lloyd-Still J D. Chronic diarrhea of childhood and the 

misuse of elimination diets. Eur J Pediatr 

1979;95(1):10-13. Not about consequences of testing 

Lo Winson, Sano Kevin, Lebwohl Ben et al. Changing 

presentation of adult celiac disease. Dig Dis Sci

2003;48(2):395-398. Not about consequences of

testing 

Lock R J, Pitcher M C, Unsworth D J. IgA anti-tissue

transglutaminase as a diagnostic marker of gluten

sensitive enteropathy. Am J Clin Pathol 

1999;52(4):274-277. Not about consequences of

testing 

Loft D E, Marsh M N, Crowe P T. Rectal gluten 

challenge and diagnosis of coeliac disease. Lancet 

1990;335(8701):1293-1295. Not about consequences 

of testing 

Loft D E, Nwokolo C U, Ciclitira P J. The diagnosis 

of gluten sensitivity and coeliac disease--the two are 

not mutually inclusive. Eur J Gastroenterol Hepatol 

1998;10(11):911-913. Not about consequences of

testing 

A-629
Loft D E. The epidemiology and diagnosis of coeliac 

disease. Eur J Gastroenterol Hepatol 1993;5(2):69-72. 

Not about consequences of testing 

Logan A C, Wong C. Chronic fatigue syndrome: 

oxidative stress and dietary modifications. Altern Med 

Rev 2001;6(5):450-459. Not about consequences of 

testing 

Logan R F A, Howarth G F, West J et al. How often is 

a positive faecal occult blood test the result of coeliac 

disease?. Eur J Gastroenterol Hepatol 

2003;15(10):1097-1100. Not about consequences of 

testing 

Logan R F, Rifkind E A, Turner I D et al. Mortality in

celiac disease. Gastroenterology 1989;97(2):265-271. 

Not about consequences of testing 

Logan RF. Screening for coeliac disease--has the time 

come for mass screening? Acta Paediatr 1996; 

412(Suppl):15-19. Unable to obtain article 

Longstreth George F, Drossman Douglas A. New

developments in the diagnosis and treatment of 

irritable bowel syndrome. Curr Gastroenterol Rep 

2002;4(5):427-434. Not about consequences of testing 

Lorini R, Scaramuzza A, Vitali L et al. Clinical

aspects of coeliac disease in children with insulindependent diabetes mellitus. J Pediatr Endocrinol 

Metab 1996;9(Suppl 1):101-111. Not about 

consequences of testing 

Lorini R, Scotta M S, Cortona L et al. Celiac disease 

and type I (insulin-dependent) diabetes mellitus in 

childhood: follow-up study. J Diabetes Complications 

1996;10(3):154-159. Not about consequences of

testing 

Lubben James E, Chi Iris, Weiler Philip G. 

Differential health screening of the well elderly by

gender and age: Appropriate care or bias?. J Appl 

Gerontol 1989;8(3):335-354. Not about consequences 

of testing 

Ludvigsson J F, Falth-Magnusson K, Ludvigsson J. 

Tissue transglutaminase auto-antibodies in cord blood 

from children to become celiacs. Scand J

Gastroenterol 2001;36(12):1279-1283. Not about 

consequences of testing 

Lundberg A, Eriksson B O, Jansson G. Muscle 

abnormalities in coeliac disease: studies on gross 

motor development and muscle fibre composition, size

and metabolic substrates. Eur J Pediatr 

1979;130(2):93-103. Not about consequences of

testing 

Luostarinen L K, Collin P O, Peraaho M J et al. 

Coeliac disease in patients with cerebellar ataxia of 

unknown origin. Ann Med 2001;33(6):445-449. Not 

about consequences of testing 

Luostarinen L, Dastidar P, Collin P et al. Association

between coeliac disease, epilepsy and brain atrophy.

Eur Neurol 2001;46(4):187-191. Not about 

consequences of testing 

Luostarinen L, Pirttila T, Collin P. Coeliac disease 

presenting with neurological disorders. Eur Neurol 

1999;42(3):132-135. Not about consequences of

testing 

Mackey J, Treem W R, Worley G et al. Frequency of 

celiac disease in individuals with Down syndrome in 

the United States. Clin Pediatr (Phila) 2001;40(5):249-

252. Not about consequences of testing 

Mader R, Adawi M, Schonfeld S. Malabsorption in 

systemic lupus erythematosus. Clin Exp Rheumatol 

1997;15(6):659-661. Not about consequences of

testing 

Magazzu G, Bottari M, Tuccari G et al. Upper

gastrointestinal endoscopy can be a reliable screening 

tool for celiac sprue in adults. J Clin Gastroenterol

1994;19(3):255-257. Not about consequences of

testing 

Magazzu G, Bottaro G, Cataldo F et al. Increasing 

incidence of childhood celiac disease in Sicily: results 

of a multicenter study. Acta Paediatr

1994;83(10):1065-1069. Not about consequences of 

testing 

Magazzu G, Jacono G, Di Pasquale G et al. Reliability

and usefulness of random fecal alpha 1-antitrypsin

concentration: further simplification of the method. J 

Pediatr Gastroenterol Nutr 1985;4(3):402-407. Not 

about consequences of testing 

Magliocca F M, Bonamico M, Petrozza V et al. 

Usefulness of endoscopic small intestinal biopsies in 

children with coeliac disease. Ital J Anat Embryol 

2001;106(2 Suppl 1):329-335. Not about 

consequences of testing 

Mahadeva S, Wyatt J I, Howdle P D. Is a raised 

intraepithelial lymphocyte count with normal 

duodenal villous architecture clinically relevant?. Am 

J Clin Pathol 2002;55(6):424-428. Not about 

consequences of testing 

Mahoney Diane F. One simple solution to hearing

impairment. Geriatr Nurs (Minneap) 1987;8(5):242-

245. Not about consequences of testing 

Maiuri L, Ciacci C, Vacca L et al. IL-15 drives the 

specific migration of CD94+ and TCR-gammadelta+ 

intraepithelial lymphocytes in organ cultures of treated 

celiac patients. Am J Gastroenterol 2001;96(1):150-

156. Not about consequences of testing 

A-630
Maiuri L, Troncone R, Mayer M et al. In vitro 

activities of A-gliadin-related synthetic peptides: 

damaging effect on the atrophic coeliac mucosa and 

activation of mucosal immune response in the treated

coeliac mucosa. Scand J Gastroenterol

1996;31(3):247-253. Not about consequences of

testing 

Maki M, Aine L, Lipsanen V et al. Dental enamel

defects in first-degree relatives of coeliac disease

patients. Lancet 1991;337(8744):763-764. Not about 

consequences of testing 

Maki M, Hallstrom O, Huupponen T et al. Increased 

prevalence of coeliac disease in diabetes. Arch Dis

Child 1984;59(8):739-742. Not about consequences of 

testing 

Maki M, Hallstrom O, Vesikari T et al. Evaluation of 

a serum IgA-class reticulin antibody test for the 

detection of childhood celiac disease. Eur J Pediatr 

1984;105(6):901-905. Not about consequences of

testing 

Maki M, Huupponen T, Holm K et al. Seroconversion 

of reticulin autoantibodies predicts coeliac disease in 

insulin dependent diabetes mellitus. Gut 

1995;36(2):239-242. Not about consequences of

testing 

Maki M, Lahdeaho M L, Hallstrom O et al.

Postpubertal gluten challenge in coeliac disease. Arch 

Dis Child 1989;64(11):1604-1607. Not about 

consequences of testing 

Maki M, Sulkanen S, Collin P. Antibodies in relation 

to gluten intake. Dig Dis 1998;16(6):330-332. Not 

about consequences of testing 

Maki Markku, Mustalahti Kirsi, Kokkonen Jorma et 

al. Prevalence of Celiac disease among children in 

Finland. N Engl J Med 2003;348(25):2517-2524. Not 

about consequences of testing 

Maldonado J E, Gregg J A, Green P A et al. Chronic 

idiopathic intestinal pseudo-obstruction. Am J Med 

1970;49(2):203-212. Not about consequences of

testing 

Mallas E, Terry J M, Asquith P et al. Serum lysozyme

in inflammatory bowel and coeliac disease. Am J Clin 

Pathol 1976;29(7):598-600. Not about consequences 

of testing 

Malnick S D, Lurie Y, Beergabel M et al. Celiac

disease. Postgrad Med 1997;101(6):239-244. Not 

about consequences of testing 

Mamon Joyce A, Shediac Mona C, Crosby Coral B et 

al. Development and implementation of an

intervention to increase cervical cancer screening in 

inner-city women. Int Q Community Health Educ

1991;12(1):21-34. Not about consequences of testing 

Mandal A, Mayberry J. How common is celiac disease 

in South America?. Am J Gastroenterol 

2000;95(3):579-580. Not about consequences of

testing 

Mantzaris G J, Tsirogianni A, Perivolioti E et al. 

Sensitivity and specificity of serum IgA class 

endomysial antibody in the diagnosis of coeliac 

disease. Hell J Gastroenterol 1996;8(4):308-311. Not 

about consequences of testing 

Mariani P, Viti M G, Montuori M et al. The glutenfree diet: a nutritional risk factor for adolescents with 

celiac disease?. J Pediatr Gastroenterol Nutr

1998;27(5):519-523. Not about consequences of

testing 

Marien P, Molla A M, Eggermont E. Coeliac disease

in childhood. Problems in differential diagnosis. Acta 

Gastroenterol Belg 1986;49(4):387-392. Not about 

consequences of testing 

Marinello D, Rapa A, Osello R et al. Celiac disease

screening: exploring the iceberg with salivary

antigliadin antibodies. J Pediatr Gastroenterol Nutr 

2001;32(2):227-228. Not about consequences of

testing 

Marsh M N, Miller V. Studies of intestinal lymphoid 

tissue. VIII. Use of epithelial lymphocyte mitotic 

indices in differentiating untreated celiac sprue

mucosa from other childhood enteropathies. J Pediatr

Gastroenterol Nutr 1985;4(6):931-935. Not about 

consequences of testing 

Marsh MN. Screening for latent gluten sensitivity:

questions many, but answers few. Eur J Gastroenterol 

Hepatol 1996; 8(1):3-6. Unable to obtain article 

Marshall C M, Grunow J E. Emesis in infants as a 

consequence of feedings. Semin Pediatr Surg 

1995;4(3):147-151. Not about consequences of testing 

Martelossi S, Torre G, Zanatta M et al. Dental enamel 

defects and screening for coeliac disease. Pediatr Med 

Chir 1996;18(6):579-581. Not about consequences of 

testing 

Martelossi S, Zanatta E, Del Santo E et al. Dental

enamel defects and screening for coeliac disease. Acta 

Paediatr 1996;412(Suppl):47-48. Not about 

consequences of testing 

Martinelli P, Troncone R, Paparo F et al. Coeliac

disease and unfavourable outcome of pregnancy. Gut 

2000; 46(3):332-335. Not about consequences of

testing 

A-631
Martini Silvia, Mengozzi Giulio, Aimo Giuseppe et al.

Comparative evaluation of serologic tests for celiac

disease diagnosis and follow-up. Clin Chem 

2002;48(6 Pt 1):960-963. Not about consequences of 

testing 

Martucci S, Biagi F, Di Sabatino A et al. Coeliac

disease. Digestive and Liver Disease - Official Journal 

of the Italian Society of Gastroenterology and the 

Italian Association for the Study of the Liver 

2002;34(Suppl 2):150-153. Not about consequences of 

testing 

Masala S, Annibale B, Fiori R et al. DXA vs. QCT for 

subclinical celiac disease patients. Acta Diabetol Lat

2003;40(Suppl 1):S174-S176. Not about consequences 

of testing 

Mascart-Lemone F, Lambrechts A. Serology of 

coeliac disease: early diagnosis and therapeutic 

impact. Acta Gastroenterol Belg 1995;58(5-6):388-

396. Not about consequences of testing 

Mascart-Lemone F, Van den, Broeck J et al. 

Serological aspects of coeliac disease. Acta

Gastroenterol Belg 1992;55(2):200-208. Not about 

consequences of testing 

Mascart-Lemone F. Strategy for serological screening 

of celiac disease. Gastroenterol Int 1998;11(3):144-

148. Not about consequences of testing 

Matek Z, Jungvirth-Hegedus M, Kolacek S. 

Epidemiology of coeliac disease in children in one

Croatian county: possible factors that could affect the 

incidence of coeliac disease and adherence to a glutenfree diet (Part II). Coll Antropol 2000;24(2):397-404. 

Not about consequences of testing 

Mather K J, Meddings J B, Beck P L et al. Prevalence

of IgA-antiendomysial antibody in asymptomatic low 

bone mineral density. Am J Gastroenterol 

2001;96(1):120-125. Not about consequences of

testing 

Mathus-Vliegen E M. Coeliac disease and lymphoma: 

current status. Neth J Med 1996;49(5):212-220. Not 

about consequences of testing 

Matteucci E, Cinapri V, Quilici S et al. Screening for 

coeliac disease in families of adults with Type 1 

diabetes based on serological markers. Diabetes Nutr 

Metab 2001;14(1):37-42. Not about consequences of 

testing 

Mauk Gary W, White Karl R. Giving children a sound 

beginning: The promise of universal newborn hearing 

screening. Volta Review 1995;97(1):5-32. Not about 

consequences of testing 

Maurino E, Capizzano H, Niveloni S et al. Value of 

endoscopic markers in celiac disease. Dig Dis Sci 

1993;38(11):2028-2033. Not about consequences of 

testing 

Mayer M, Greco L, Troncone R et al. Compliance of 

adolescents with coeliac disease with a gluten free

diet. Gut 1991;32(8):881-885. Not about 

consequences of testing 

Mazure R M, Vazquez H, Gonzalez D et al. Early 

changes of body composition in asymptomatic celiac

disease patients. Am J Gastroenterol 1996;91(4):726-

730. Not about consequences of testing 

Mazzetti di, Pietralata Giorgetti G M, Gregori M et al.

Subclinical coeliac disease. Ital J Gastroenterol 

1992;24(6):352-354. Not about consequences of

testing 

McBee J W. The sprue syndrome. Tex Med 

1966;62(12):54-56. Not about consequences of testing 

McCaul Kevin D, Reid Patricia A, Rathge Richard W

et al. Does concern about breast cancer inhibit or

promote breast cancer screening?. Basic Appl Soc

Psych 1996;18(2):183-194. Not about consequences of 

testing 

McCrae W M, Eastwood M A, Martin M R et al. 

Neglected coeliac disease. Lancet 1975;1(7900):187-

190. Not about consequences of testing 

McElvaney N G, Duignan R, Fielding J F. Coeliac 

disease: clinical presentations, correlations of dietary 

compliance, symptomatic response and repeat biopsy

findings. Ulster Med J 1992;61(2):134-138. Not about 

consequences of testing 

McIntyre A S, Ng D P, Smith J A et al. The 

endoscopic appearance of duodenal folds is predictive 

of untreated adult celiac disease. Gastrointest Endosc

1992;38(2):148-151. Not about consequences of

testing 

McMillan S A, Haughton D J, Biggart J D et al. 

Predictive value for coeliac disease of antibodies to

gliadin, endomysium, and jejunum in patients

attending for jejunal biopsy. BMJ 

1991;303(6811):1163-1165. Not about consequences 

of testing 

McMillan S A, Johnston S D, Watson R G et al. 

Dietary intake, smoking, and transient anti-gliadin

antibodies. Scand J Gastroenterol 1998;33(5):499-503. 

Not about consequences of testing 

McNeish A S, Harms H K, Rey J et al. The diagnosis 

of coeliac disease. A commentary on the current

practices of members of the European Society for 

Paediatric Gastroenterology and Nutrition (ESPGAN). 

Arch Dis Child 1979;54(10):783-786. Not about 

consequences of testing 

A-632
McNeish A S, Willoughby M L. Whole-blood folate 

as a screening test for coeliac disease in childhood. 

Lancet 1969;1(7592):442-443. Not about 

consequences of testing 

McNeish A S. Diagnosis of coeliac disease in

retrospect. Arch Dis Child 1968;43(229):362-364. Not 

about consequences of testing 

McNicholl B, Egan-Mitchell B, Stevens F et al.

Mucosal recovery in treated childhood celiac disease 

(gluten-sensitive enteropathy). Eur J Pediatr 

1976;89(3):418-424. Not about consequences of

testing 

McNicholl B. Childhood coeliac disease. J Ir Med 

Assoc 1970;63(391):1-7. Not about consequences of 

testing 

McNicholl B. Coeliac disease: ecology, life history 

and management. Hum Nutr Appl Nutr 

1986;40(1):55-60. Not about consequences of testing 

McPhillips J. Understanding coeliac disease: 

symptoms and long-term risks. Br J Nurs 

2000;9(8):479-483. Not about consequences of testing 

Mearin M L, Polanco I, Strober W et al. B-cell

antigens recognized by maternal antisera in glutensensitive enteropathy. J Clin Nutr Gastroenterol

1986;1(1):30-36. Not about consequences of testing 

Meijer Jos W R, Wahab Peter J, Mulder Chris J J.

Small intestinal biopsies in celiac disease: duodenal or

jejunal?. Virchows Arch 2002;442(2):124-128. Not 

about consequences of testing 

Meloni G F, Dessole S, Vargiu N et al. The prevalence

of coeliac disease in infertility. Hum Reprod 

1999;14(11):2759-2761. Not about consequences of 

testing 

Meloni G F, Tomasi P A, Bertoncelli A et al.

Prevalence of silent celiac disease in patients with

autoimmune thyroiditis from Northern Sardinia. J 

Endocrinol Invest 2001;24(5):298-302. Not about 

consequences of testing 

Menendez-Corrada R. Current views on tropical sprue 

and a comparison to nontropical sprue. Med Clin

North Am 1968;52(6):1367-1385. Not about 

consequences of testing 

Menni S, Cavalli R, Prampolini R et al. Dental enamel

defects in children suffering from dermatitis

herpetiformis and in their first degree relatives. Eur J

Pediatr Dermatol 1996;6(1):33-38. Not about 

consequences of testing 

Messmann H. Squamous cell cancer of the 

oesophagus. Baillieres Best Pract Res Clin 

Gastroenterol 2001;15(2):249-265. Not about 

consequences of testing 

Metcalf J. Coeliac disease and primary biliary 

cirrhosis: a case for mutual screening. Gut

1998;42(1):9-10. Not about consequences of testing 

Meyer D, Stavropolous S, Diamond B et al. 

Osteoporosis in a north american adult population

with celiac disease. Am J Gastroenterol 

2001;96(1):112-119. Not about consequences of

testing 

Mic caron, Umek-Bradac caron, Dolins caron et al. 

Ultrasonographic assessment of celiac disease in 

children: Comparison with antiendomysium antibodies 

and histology. Wien Klin Wochenschr Suppl 

2001;113(3):27-31. Not about consequences of testing 

Michaelsson G, Gerden B, Hagforsen E et al. Psoriasis 

patients with antibodies to gliadin can be improved by

a gluten-free diet. Br J Dermatol 2000;142(1):44-51. 

Not about consequences of testing 

Michaelsson G, Gerden B, Ottosson M et al. Patients

with psoriasis often have increased serum levels of 

IgA antibodies to gliadin. Br J Dermatol 

1993;129(6):667-673. Not about consequences of

testing 

Michaelsson G, Kraaz W, Gerden B et al. Increased 

lymphocyte infiltration in duodenal mucosa from 

patients with psoriasis and serum IgA antibodies to

gliadin. Br J Dermatol 1995;133(6):896-904. Not 

about consequences of testing 

Michie S, Johnston M, Cockcroft A et al. Methods and 

impact of health screening for hospital staff. Journal of

Organizational Behavior 1995;16(1):85-92. Not about 

consequences of testing 

Miller A, Paspaliaris W, Elliott P R et al. Antitransglutaminase antibodies and coeliac disease. Aust 

N Z J Med 1999;29(2):239-242. Not about 

consequences of testing 

Mills P R, Horton P W, Watkinson G. The value of the

14C breath test in the assessment of fat absorption. 

Scand J Gastroenterol 1979;14(8):914-920. Not about 

consequences of testing 

Misra S, Ament M E. Diagnosis of coeliac sprue in 

1994. Gastroenterol Clin North Am 1995;24(1):133-

143. Not about consequences of testing 

Mitchell C J, Field H P, Simpson F G et al.

Preliminary evaluation of a single-day tubeless test of 

pancreatic function. Br Med J (Clin Res Ed) 

1981;282(6278):1751-1753. Not about consequences 

of testing 

A-633
Mohindra S, Yachha S K, Srivastava A et al. Coeliac 

disease in Indian children: assessment of clinical,

nutritional and pathologic characteristics. J Health

Popul Nutr 2001;19(3):204-208. Not about 

consequences of testing 

Molteni N, Bardella M T, Bianchi P A. Obstetric and 

gynecological problems in women with untreated

celiac sprue. J Clin Gastroenterol 1990;12(1):37-39. 

Not about consequences of testing 

Monteiro E, Menezes M L, Magalhaes Ramalho P.

Anti-reticulin antibodies: a diagnostic and monitoring 

test for childhood coeliac disease. Scand J 

Gastroenterol 1986;21(8):955-957. Not about 

consequences of testing 

Montgomery R D, Atiyeh M, Scales W R et al.

Intestinal absorption in Saudi Arabia: an evaluation of 

the one hour blood xylose test. Trans R Soc Trop Med 

Hyg 1982;76(1):25-28. Not about consequences of

testing 

Moodie S, Ciclitira P. Recent developments in celiac 

disease. Curr Opin Gastroenterol 2002;18(2):182-186. 

Not about consequences of testing 

Mooradian A D, Morley J E, Levine A S et al. 

Abnormal intestinal permeability to sugars in diabetes 

mellitus. Diabetologia 1986;29(4):221-224. Not about 

consequences of testing 

Morris M A, Ciclitira P J. Coeliac disease. J R Coll 

Physicians Lond 1997;31(6):614-618. Not about 

consequences of testing 

Mortimer P E, Stewart J S, Norman A P et al. Followup study of coeliac disease. Br Med J 1968;3(609):7-9. 

Not about consequences of testing 

Mottaleb A, Kapp F, Noguera E C et al. The Lundh 

test in the diagnosis of pancreatic disease: a review of 

five years' experience. Gut 1973;14(11):835-841. Not 

about consequences of testing 

Muench R, Ammann R. Fecal immunoreactive lipase:

a new tubeless pancreatic function test. Scand J 

Gastroenterol 1992;27(4):289-294. Not about 

consequences of testing 

Mugica F, Castiella A, Otazua P et al. Prevalence of 

coeliac disease in unexplained chronic 

hypertransaminasemia. Revista Espanola De 

Enfermedades Digestivas - Organo Oficial De La

Sociedad Espanola De Patologia Digestiva 

2001;93(11):707-714. Not about consequences of

testing 

Mulder C J, van Bergeijk J D, Jansen T L et al. 

Coeliac disease. Diagnostic and therapeutic pitfalls. 

Scand J Gastroenterol 1993;200(Suppl):42-47. Review 

article 

Mulder C J, Wahab P J, Moshaver B et al. Refractory 

coeliac disease: a window between coeliac disease and

enteropathy associated T cell lymphoma. Scand J 

Gastroenterol 2000;232(Suppl):32-37. Not about 

consequences of testing 

Mulder C J. Do we have to screen the general

population for coeliac disease instead of only patients 

with so-called associated diseases?. Digestive and 

Liver Disease - Official Journal of the Italian Society

of Gastroenterology and the Italian Association for the

Study of the Liver 2000;32(9):780-781. Not about 

consequences of testing 

Mulder Chris J J, Hadithi Mohammed M, Rostami 

Kamran et al. Coeliac disease--has the time come for 

routine mass screening? In 2002--2010--2020?. Rom J 

Gastroenterol 2002;11(3):179-182. Not about 

consequences of testing 

Munck L K, Kjeldsen J, Philipsen E et al. Incomplete

remission with short-term prednisolone treatment in 

collagenous colitis: A randomized study. Scand J

Gastroenterol 2003;38(6):606-610. Not about 

consequences of testing 

Murphy M S, Sood M, Johnson T. Use of the lactose 

H2 breath test to monitor mucosal healing in coeliac 

disease. Acta Paediatr 2002;91(2):141-144. Not about 

consequences of testing 

Murphy M S, Walker W A. Celiac disease. Pediatr 

Rev 1991;12(11):325-330. Not about consequences of 

testing 

Murray J A, Van Dyke C, Plevak M F et al. Trends in 

the identification and clinical features of celiac disease 

in a North American community, 1950-2001. Clin

Gastroenterol Hepatol 2003;1(1):19-27. Not about 

consequences of testing 

Murray J A. It's not time to put away the biopsy

forceps. Am J Gastroenterol 1999;94(4):869-871. Not 

about consequences of testing 

Murray J A. Serodiagnosis of celiac disease. Clin Lab 

Med 1997;17(3):445-464. Not about consequences of 

testing 

Murray J A. The widening spectrum of celiac disease. 

Am J Clin Nutr 1999;69(3):354-365. Not about 

consequences of testing 

Murray Michael, McMillan Carol. Health beliefs, 

locus of control, emotional control and women's 

cancer screening behaviour. Br J Clin Psychol 

1993;32(1):87-100. Not about consequences of testing 

Mustadjab I, Soeparto P, Karyadi. Floating test

(Rossipal) for screening patients with fat 

A-634
malabsorption. Paediatr Indones 1980;20(5-6):104-

110. Not about consequences of testing 

Mustalahti K, Sulkanen S, Holopainen P et al. Coeliac 

disease among healthy members of multiple case 

coeliac disease families. Scand J Gastroenterol 

2002;37(2):161-165. Not about consequences of

testing 

Mustalahti Kirsi, Lohiniemi Susanna, Collin Pekka et

al. Gluten-free diet and quality of life in patients with 

screen-detected celiac disease. Eff Clin Pract 

2002;5(3):105-113. Not about consequences of testing 

Myhre A G, Aarsetoy H, Undlien D E et al. High 

frequency of coeliac disease among patients with 

autoimmune adrenocortical failure. Scand J

Gastroenterol 2003;38(5):511-515. Not about 

consequences of testing 

Nathavitharana K A, Lloyd D R, Raafat F et al.

Urinary mannitol: lactulose excretion ratios and 

jejunal mucosal structure. Arch Dis Child 

1988;63(9):1054-1059. Not about consequences of

testing 

Nehra V. New clinical issues in celiac disease.

Gastroenterol Clin North Am 1998;27(2):453-465. 

Not about consequences of testing 

Neilson Aileen R, Whynes David K. Determinants of 

persistent compliance with screening for colorectal 

cancer. Soc Sci Med 1995;41(3):365-374. Not about 

consequences of testing 

Nelsen David A. Gluten-sensitive enteropathy (celiac

disease): more common than you think. Am Fam 

Physician 2002;66(12):2259-2266. Not about 

consequences of testing 

Neuberger J. PBC and the gut: the villi atrophy, the 

plot thickens. Gut 1999;44(5):594-595. Not about 

consequences of testing 

Neuhausen Susan L, Feolo Mike, Camp Nicola J et al. 

Genome-wide linkage analysis for celiac disease in 

North American families. Am J Med Genet

2002;111(1):1-9. Not about consequences of testing 

Newcomer A D, Hofmann A F, DiMagno E P et al. 

Triolein breath test: a sensitive and specific test for fat

malabsorption. Gastroenterology 1979;76(1):6-13. Not 

about consequences of testing 

Nielsen O H, Jacobsen O, Pedersen E R et al. Nontropical sprue. Malignant diseases and mortality rate. 

Scand J Gastroenterol 1985;20(1):13-18. Not about 

consequences of testing 

Nieminen U, Kahri A, Savilahti E et al. Duodenal 

disaccharidase activities in the follow-up of villous

atrophy in coeliac disease. Scand J Gastroenterol 

2001;36(5):507-510. Not about consequences of

testing 

Nieto A, Blanco Quiros A, Arranz E et al. Study of 

HLA-DQA1 alleles in celiac children. Journal of 

Investigational Allergology & Clinical Immunology - 

Official Organ of the International Association of

Asthmology (Interasma) and Sociedad

Latinoamericana De Alergia E Inmunologia 

1995;5(4):209-215. Not about consequences of testing 

Nilsen E M, Johansen F E, Jahnsen F L et al. Cytokine 

profiles of cultured microvascular endothelial cells 

from the human intestine. Gut 1998;42(5):635-642. 

Not about consequences of testing 

Niveloni S, Fiorini A, Dezi R et al. Usefulness of 

videoduodenoscopy and vital dye staining as 

indicators of mucosal atrophy of celiac disease: 

assessment of interobserver agreement. Gastrointest

Endosc 1998;47(3):223-229. Not about consequences 

of testing 

Niveloni S, Pedreira S, Sugai E et al. The natural 

history of gluten sensitivity: report of two new celiac

disease patients resulting from a long-term follow-up 

of nonatrophic, first-degree relatives. Am J 

Gastroenterol 2000;95(2):463-468. Not about 

consequences of testing 

Norman Paul, Fitter Mike. Intention to attend a health

screening appointment: Some implications for general

practice. Couns Psychol 1989;2(3):261-272. Not about 

consequences of testing 

Norman Paul, Fitter Mike. Predicting attendance at 

health screening: Organizational factors and patients' 

health beliefs. Couns Psychol 1991;4(2-3):143-155. 

Not about consequences of testing 

Norman Paul. Applying the health belief model to the 

prediction of attendance at health checks in general 

practice. Br J Clin Psychol 1995;34(3):461-470. Not 

about consequences of testing 

Norman Paul. Social learning theory and the 

prediction of attendance at screening. Psychol Health 

1991;5(3):231-239. Not about consequences of testing 

Nosari I, Casati A, Mora C et al. The use of IgAantiendomysial antibody test for screening coeliac 

disease in insulin-dependent diabetes mellitus.

Diabetes Nutr Metab Clin Exp 1996;9(5):267-272. 

Not about consequences of testing 

Not T, Citta A, Lucchesi A et al. Anti-endomysium 

antibody on human umbilical cord vein tissue: an

inexpensive and sensitive diagnostic tool for the 

screening of coeliac disease. Eur J Pediatr

1997;156(8):616-618. Not about consequences of

testing 

A-635
Not T, Horvath K, Hill I D et al. Celiac disease risk in 

the USA: high prevalence of antiendomysium 

antibodies in healthy blood donors. Scand J 

Gastroenterol 1998;33(5):494-498. Not about 

consequences of testing 

Not T, Tommasini A, Tonini G et al. Undiagnosed 

coeliac disease and risk of autoimmune disorders in 

subjects with Type I diabetes mellitus. Diabetologia 

2001;44(2):151-155. Not about consequences of

testing 

Not T, Ventura A, Peticarari S et al. A new, rapid, 

noninvasive screening test for celiac disease. Eur J 

Pediatr 1993;123(3):425-427. Not about consequences 

of testing 

Not Tarcisio, Faleschini Elena, Tommasini Alberto et 

al. Celiac disease in patients with sporadic and

inherited cardiomyopathies and in their relatives. Eur 

Heart J 2003;24(15):1455-1461. Not about 

consequences of testing 

Nuti R, Martini G, Valenti R et al. Prevalence of 

undiagnosed coeliac syndrome in osteoporotic women. 

J Intern Med 2001;250(4):361-366. Not about 

consequences of testing 

Nyren O, Adami H O, Gustavsson S et al. The 

"epigastric distress syndrome". A possible disease

entity identified by history and endoscopy in patients 

with nonulcer dyspepsia. J Clin Gastroenterol 

1987;9(3):303-309. Not about consequences of testing 

Oberhuber G, Granditsch G, Vogelsang H. The 

histopathology of coeliac disease: time for a 

standardized report scheme for pathologists. Eur J 

Gastroenterol Hepatol 1999;11(10):1185-1194. Not 

about consequences of testing 

O'Brien C J, Saverymuttu S, Hodgson H J F et al. 

Coeliac disease, adenocarcinoma of jejunum and in 

situ squamous carcinoma of oesophagus. J Clin Pathol 

1983;36(1):62-67. Not about consequences of testing 

O'Farrelly C, Feighery C, O'Briain D S et al. Humoral 

response to wheat protein in patients with coeliac 

disease and enteropathy associated T cell lymphoma. 

Br Med J (Clin Res Ed) 1986;293(6552):908-910. Not 

about consequences of testing 

O'Farrelly C, Kelly J, Hekkens W et al. Alpha gliadin

antibody levels: a serological test for coeliac disease. 

Br Med J (Clin Res Ed) 1983;286(6383):2007-2010. 

Not about consequences of testing 

Olden Kevin W. Diagnosis of irritable bowel 

syndrome. Gastroenterology 2002;122(6):1701-1714. 

Not about consequences of testing 

O'Leary C, Walsh C H, Wieneke P et al. Coeliac 

disease and autoimmune Addison's disease: a clinical 

pitfall. QJM 2002;95(2):79-82. Not about 

consequences of testing 

O'Leary Clare, Quigley Eamonn M M. Small bowel 

bacterial overgrowth, celiac disease, and IBS: what are 

the real associations?. Am J Gastroenterol 

2003;98(4):720-722. Not about consequences of

testing 

Olsen W A. A practical approach to diagnosis of 

disorders of intestinal absorption. N Engl J Med 

1971;285(24):1358-1361. Not about consequences of 

testing 

Onstad G R, Zieve L. Carotene absorption. A

screening test for steatorrhea. JAMA 

1972;221(7):677-679. Not about consequences of

testing 

Osman A A, Gunnel T, Dietl A et al. B cell epitopes 

of gliadin. Clin Exp Immunol 2000;121(2):248-254. 

Not about consequences of testing 

Osman A A, Uhlig H H, Valdes I et al. A monoclonal 

antibody that recognizes a potential coeliac-toxic 

repetitive pentapeptide epitope in gliadins. Eur J

Gastroenterol Hepatol 2001;13(10):1189-1193. Not 

about consequences of testing 

Osman A A, Uhlig H, Thamm B et al. Use of the 

phage display technique for detection of epitopes 

recognized by polyclonal rabbit gliadin antibodies. 

FEBS Lett 1998;433(1-2):103-107. Not about 

consequences of testing 

Oxentenko Amy S, Grisolano Scott W, Murray Joseph 

A et al. The insensitivity of endoscopic markers in

celiac disease. Am J Gastroenterol 2002;97(4):933-

938. Not about consequences of testing 

Pacht A, Sinai N, Hornstein L et al. The diagnostic 

reliability of anti-endomysial antibody in celiac 

disease: the north Israel experience. Isr J Med Sci

1995;31(4):218-220. Not about consequences of

testing 

Packer S, Rowlatt R J, Harries J T. Proceedings: 

Reappraisal of a past diagnosis of "coeliac disease". 

Arch Dis Child 1974;49(10):819Not about 

consequences of testing 

Paerregaard A, Vilien M, Krasilnikoff P A et al. 

Supposed coeliac disease during childhood and its 

presentation 14-38 years later. Scand J Gastroenterol 

1988;23(1):65-70. Not about consequences of testing 

Page S R, Lloyd C A, Hill P G et al. The prevalence of

coeliac disease in adult diabetes mellitus. QJM 

1994;87(10):631-637. Not about consequences of

testing 

A-636
Paimela L, Kurki P, Leirisalo-Repo M et al. Gliadin 

immune reactivity in patients with rheumatoid

arthritis. Clin Exp Rheumatol 1995;13(5):603-607. 

Not about consequences of testing 

Palosuo K, Alenius H, Varjonen E et al. A novel 

wheat gliadin as a cause of exercise-induced

anaphylaxis. J Allergy Clin Immunol 1999;103(5 Pt 

1):912-917. Not about consequences of testing 

Papadatou B, Crino A, Giannotti A et al. 

Antiendomysial and antigliadin antibodies in patients 

with Down syndrome. Dev Brain Dysfunct 1996;9(2-

3):129-132. Not about consequences of testing 

Pare P, Douville P, Caron D et al. Adult celiac sprue: 

changes in the pattern of clinical recognition. J Clin 

Gastroenterol 1988;10(4):395-400. Not about 

consequences of testing 

Parker S L, Sussman G L, Krondl M. Dietary aspects

of adverse reactions to foods in adults. Cmaj - 

Canadian Medical Association Journal = Journal De 

L'association Medicale Canadienne 1988;139(8):711-

718. Not about consequences of testing 

Parnell N D, Ciclitira P J. Review article: coeliac 

disease and its management. Aliment Pharmacol Ther

1999;13(1):1-13. Not about consequences of testing 

Parnell N, Ciclitira P J. Celiac disease. Curr Opin

Gastroenterol 1999;15(2):120-124. Not about 

consequences of testing 

Partanen J, Milner C, Campbell R D et al. HLA-linked 

heat-shock protein 70 (HSP70-2) gene polymorphism 

and celiac disease. Tissue Antigens 1993;41(1):15-19. 

Not about consequences of testing 

Patinen P, Bjorksten F, Malmstrom M et al. Salivary

and serum IgA antigliadin antibodies in dermatitis 

herpetiformis. Eur J Oral Sci 1995;103(5):280-284. 

Not about consequences of testing 

Patterson R N, Johnston S D. Iron deficiency anaemia: 

are the British Society of Gastroenterology guidelines 

being adhered to?. Postgrad Med J 2003;79(930):226-

228. Not about consequences of testing 

Patwari A K, Anand V K, Kapur Gaurav et al. Clinical

and nutritional profile of children with celiac disease. 

Indian Pediatr 2003;40(4):337-342. Not about 

consequences of testing 

Pearce Allum B, Sinclair David, Duncan Hamish D et 

al. Use of the anti-endomysial antibody test to

diagnose coeliac disease in clinical practice. Clin Lab 

2002;48(5-6):319-325. Not about consequences of

testing 

Pecsi G. Genetic associations and

immunopathogenesis of coeliac disease. Acta Physiol 

Hung 2000;87(4):339-353. Not about consequences of 

testing 

Pellecchia M T, Ambrosio G, Salvatore E et al.

Possible gluten sensitivity in multiple system atrophy. 

Neurology 2002;59(7):1114-1115. Not about 

consequences of testing 

Pellecchia M T, Scala R, Filla A et al. Idiopathic

cerebellar ataxia associated with celiac disease: lack of 

distinctive neurological features. J Neurol Neurosurg 

Psychiatry 1999;66(1):32-35. Not about consequences 

of testing 

Pelli M A, Capodicasa E, De Angelis V et al. Sorbitol 

Hinf 2-breath test in celiac disease. Importance of

early positivity. Gastroenterol Int 1998;11(2):65-68. 

Not about consequences of testing 

Pena A S, Garrote J A, Crusius J B. Advances in the 

immunogenetics of coeliac disease. Clues for

understanding the pathogenesis and disease 

heterogeneity. Scand J Gastroenterol 

1998;255(Suppl):56-58. Not about consequences of

testing 

Pena A S, Wijmenga C. Genetic factors underlying 

gluten-sensitive enteropathy. Curr Allergy Asthma

Rep 2001;1(6):526-533. Not about consequences of 

testing 

Pengiran Tengah D S N A, Wills A J, Holmes G K T.

Neurological complications of coeliac disease. 

Postgrad Med J 2002;78(921):393-398. Not about 

consequences of testing 

Peracchi Maddalena, Trovato Cristina, Longhi

Massimo et al. Tissue transglutaminase antibodies in 

patients with end-stage heart failure. Am J

Gastroenterol 2002;97(11):2850-2854. Not about 

consequences of testing 

Perera D R, Weinstein W M, Rubin C E. Symposium 

on pathology of the gastrointestinal tract-Part II. Small 

intestinal biopsy. Hum Pathol 1975;6(2):157-217. Not 

about consequences of testing 

Perri F, Andriulli A. "Mixed" triglyceride breath test: 

methodological problems and clinical applications. 

Rev Med Univ Navarra 1998;42(2):99-103. Not about 

consequences of testing 

Perticarari S, Presani G, Trevisan M et al. Serum IgA 

and IgG antibodies to alpha-gliadin: comparison 

between two ELISA methods. Ric Clin Lab 

1987;17(4):323-329. Not about consequences of

testing 

Petaros P, Martelossi S, Tommasini A et al. 

Prevalence of autoimmune disorders in relatives of

patients with celiac disease. Dig Dis Sci 

A-637
2002;47(7):1427-1431. Not about consequences of

testing 

Peters Ulrike, Askling Johan, Gridley Gloria et al. 

Causes of death in patients with celiac disease in a 

population-based Swedish cohort. Arch Intern Med 

2003;163(13):1566-1572. Not about consequences of 

testing 

Petersen J, Drasche A, Raithel M et al. Analysis of 

genetic polymorphisms of enzymes involved in 

histamine metabolism. Inflamm Res 2003;52(Suppl 

1):S69-S70. Not about consequences of testing 

Pham T H, Barr G D. Coeliac disease in adults.

Presentation and management. Aust Fam Physician 

1996;25(1):62-65. Not about consequences of testing 

Piattella L, Zamponi N, Cardinali C et al. Endocranial 

calcifications, infantile celiac disease, and epilepsy.

Child's Nervous System - Chns - Official Journal of 

the International Society for Pediatric Neurosurgery

1993;9(3):172-175. Not about consequences of testing 

Picarelli A, di Tola M, Sabbatella L et al.

Identification of a new coeliac disease subgroup: 

antiendomysial and anti-transglutaminase antibodies 

of IgG class in the absence of selective IgA

deficiency. J Intern Med 2001;249(2):181-188. Not 

about consequences of testing 

Picarelli A, Sabbatella L, di Tola M et al. Celiac

disease diagnosis in misdiagnosed children. Pediatr 

Res 2000;48(5):590-592. Not about consequences of 

testing 

Picarelli A, Sabbatella L, di Tola M et al. Forty-eight 

hours of biopsy culture improve the sensitivity of the 

in vitro gliadin challenge in the diagnosis of celiac 

disease. Clin Chem 2001;47(10):1841-1843. Not 

about consequences of testing 

Picarelli A, Triglione P, Mariani P et al. Use of a

threshold serum level of anti-gliadin antibodies 

improves diagnostic efficiency of the test in adult 

coeliac disease but is unreliable as a screening test. Ital

J Gastroenterol 1996;28(2):70-75. Not about 

consequences of testing 

Picarelli Antonio, Sabbatella Luigi, Di Tola et al. 

Antiendomysial antibody detection in fecal 

supernatants: in vivo proof that small bowel mucosa is 

the site of antiendomysial antibody production. Am J 

Gastroenterol 2002;97(1):95-98. Not about 

consequences of testing 

Pittschieler K, Gentili L, Niederhofer H. Onset of

coeliac disease: A prospective longitudinal study. Acta 

Paediatr 2003;92(10):1149-1152. Not about 

consequences of testing 

Pittschieler K, Ladinser B. Coeliac disease: screened 

by a new strategy. Acta Paediatr 1996;412(Suppl):42-

45. Not about consequences of testing 

Polvi A, Arranz E, Fernandez-Arquero M et al. HLADQ2-negative celiac disease in Finland and Spain. 

Hum Immunol 1998;59(3):169-175. Not about 

consequences of testing 

Polvi A, Garden O A, Elwood C M et al. Canine major 

histocompatibility complex genes DQA and DQB in 

Irish setter dogs. Tissue Antigens 1997;49(3 Pt 1):236-

243. Not about consequences of testing 

Popat S, Hearle N, Bevan S et al. Mutational analysis

of CD28 in coeliac disease. Scand J Gastroenterol 

2002;37(5):536-539. Not about consequences of

testing 

Popat S, Hearle N, Wixey J et al. Analysis of the

CTLA4 gene in Swedish coeliac disease patients.

Scand J Gastroenterol 2002;37(1):28-31. Not about 

consequences of testing 

Popat S, Hogberg L, McGuire S et al. Germline 

mutations in TGM2 do not contribute to coeliac 

disease susceptibility in the Swedish population. Eur J 

Gastroenterol Hepatol 2001;13(12):1477-1479. Not 

about consequences of testing 

Popper Stephen E, Morris Charles E, Briggs Jeffrey. 

Human subject screening: A dynamic process. Aviat 

Space Environ Med 1997;68(10):939-942. Not about 

consequences of testing 

Pozler O, Parizek J, Chylkova V et al. Immunological 

aspects of diagnosis of celiac sprue in children. Sb

Ved Pr Lek Fak Karlovy Univerzity Hradci Kralove 

1989;32(2):169-233. Not about consequences of

testing 

Prasad S, Thomas P, Nicholas D S et al. Adult

endomysial antibody-negative coeliac disease and 

cigarette smoking. Eur J Gastroenterol Hepatol 

2001;13(6):667-671. Not about consequences of

testing 

Pratesi R, Gandolfi L, Garcia S G et al. Prevalence of 

coeliac disease: Unexplained age-related variation in 

the same population. Scand J Gastroenterol 

2003;38(7):747-750. Not about consequences of

testing 

Pratesi R, Modelli I C, Martins R C et al. Celiac 

disease and epilepsy: Favorable outcome in a child 

with difficult to control seizures. Acta Neurol Scand 

2003;108(4):290-293. Not about consequences of

testing 

Pratesi Riccardo, Gandolfi Lenora, Martins Rita C et 

al. Is the prevalence of celiac disease increased among 

epileptic patients?. Arq Neuropsiquiatr

A-638
2003;61(2b):330-334. Not about consequences of

testing 

Presani G, Perticarari S, Mangiarotti M A. Flow 

cytometric detection of anti-gliadin antibodies. J 

Immunol Methods 1989;119(2):197-202. Not about 

consequences of testing 

Pringle E M, Young W F, Mortimer P E et al. Coeliac 

syndrome. Proc R Soc Med 1968;61(8):775-776. Not 

about consequences of testing 

Pruessner H T. Detecting celiac disease in your

patients. Am Fam Physician 1998;57(5):1023-34, 

1039. Not about consequences of testing 

Pynnonen P, Isometsa E, Aalberg V et al. Is coeliac 

disease prevalent among adolescent psychiatric 

patients?. Acta Paediatr 2002;91(6):657-659. Not 

about consequences of testing 

Quaglino D, Corazza G R. Anaemias and other 

haematological changes due to disease of the 

alimentary tract. Recenti Prog Med 1993;84(9):624-

633. Not about consequences of testing 

Quisel Anna, Gill James M, Westerberg Dyanne. 

Guideline for diagnosis of celiac disease. Del Med J 

2002;74(5):229-241. Not about consequences of

testing 

Ralston S H, Willocks L, Pitkeathly D A et al. High 

prevalence of unrecognized osteomalacia in hospital 

patients with rheumatoid arthritis. Br J Rheumatol

1988;27(3):202-205. Not about consequences of

testing 

Rampton D S, Kasidas G P, Rose G A et al. Oxalate 

loading test. A screening test for steatorrhoea. Gut 

1979;20(5):A456Not about consequences of testing 

Rampton D S, McCullough A D, Sabbat J S et al. 

Screening for steatorrhoea with an oxalate loading 

test. Br Med J (Clin Res Ed) 1984;288(6428):1419Not 

about consequences of testing 

Ransford Rupert A J, Hayes Mark, Palmer Martin et

al. A controlled, prospective screening study of celiac 

disease presenting as iron deficiency anemia. J Clin 

Gastroenterol 2002;35(3):228-233. Not about 

consequences of testing 

Rasanen L, Lehto M, Turjanmaa K et al. Allergy to

ingested cereals in atopic children. Allergy

1994;49(10):871-876. Not about consequences of

testing 

Rasmusson C G, Eriksson M A. Celiac disease and 

mineralisation disturbances of permanent teeth. 

International Journal of Paediatric Dentistry / the 

British Paedodontic Society and the International

Association of Dentistry for Children 2001;11(3):179-

183. Not about consequences of testing 

Rastogi A, Malhotra V, Uppal B et al. Aetiology of 

chronic diarrhoea in tropical children. Trop 

Gastroenterol 1999;20(1):45-49. Not about 

consequences of testing 

Rautonen J, Rautonen N, Savilahti E. Antibodies to 

gliadin in children with coeliac disease. Acta Paediatr

Scand 1991;80(12):1200-1206. Not about 

consequences of testing 

Ravaglia Giovanni, Forti Paola, Maioli Fabiola et al.

Increased prevalence of coeliac disease in autoimmune 

thyroiditis is restricted to aged patients. Exp Gerontol 

2003;38(5):589-595. Not about consequences of

testing 

Ravelli A M, Tobanelli P, Minelli L et al. Endoscopic 

features of celiac disease in children. Gastrointest

Endosc 2001;54(6):736-742. Not about consequences 

of testing 

Read M, O'Halloran ET, O'Sullivan C. Coeliac disease 

in adolescents/young adults: difficulties in monitoring. 

Br J Biomed Sci 2000; 57(3):217-221. Not about 

consequences of testing 

Reeves G E, Burns C, Hall S T et al. The measurement 

of IgA and IgG transglutaminase antibodies in celiac 

disease: a comparison with current diagnostic 

methods. Pathology 2000;32(3):181-185. Not about 

consequences of testing 

Rensch M J, Merenich J A, Lieberman M et al. 

Gluten-sensitive enteropathy in patients with insulindependent diabetes mellitus. Ann Intern Med

1996;124(6):564-567. Not about consequences of

testing 

Ribes C, Pena A S, Pereda A et al. IGA gliadin 

antibodies, a useful screening test for coeliac disease 

in family members of children with coeliac disease. J

Clin Nutr Gastroenterol 1991;6(4):196-202. Not about 

consequences of testing 

Ribes-Koninckx C, Alfonso P, Ortigosa L et al. A 

beta-turn rich oats peptide as an antigen in an ELISA

method for the screening of coeliac disease in a 

paediatric population. Eur J Clin Invest 

2000;30(8):702-708. Not about consequences of

testing 

Riccabona M, Rossipal E. Sonographic findings in 

celiac disease. J Pediatr Gastroenterol Nutr 

1993;17(2):198-200. Not about consequences of

testing 

Rich E J, Christie D L. Anti-gliadin antibody panel

and xylose absorption test in screening for celiac 

A-639
disease. J Pediatr Gastroenterol Nutr 1990;10(2):174-

178. Not about consequences of testing 

Riestra S, Fernandez E, Rodrigo L et al. Prevalence of

Coeliac disease in the general population of northern 

Spain. Strategies of serologic screening. Scand J

Gastroenterol 2000;35(4):398-402. Not about 

consequences of testing 

Robert M E, Ament M E, Weinstein W M. The

histologic spectrum and clinical outcome of refractory

and unclassified sprue. Am J Surg Pathol 

2000;24(5):676-687. Not about consequences of

testing 

Roberts I M, Poturich C, Wald A. Utility of fecal fat 

concentrations as screening test in pancreatic

insufficiency. Dig Dis Sci 1986;31(10):1021-1024. 

Not about consequences of testing 

Roberts R K, Campbell C B, Bryant S J et al. Xylose1-14C absorption test: the use of urine, serum and

breath analysis, and comparison with a colorimetric 

assay. Aust N Z J Med 1976;6(6):532-536. Not about 

consequences of testing 

Robins Robert S, Post Jerrold M. Choosing a healthy

president. Political Psychology 1995;16(4):841-860. 

Not about consequences of testing 

Robinson T J, Nelson S D, Haire M. Jejunal villous 

changes associated with farmer's lung. Postgrad Med J 

1981;57(673):697-701. Not about consequences of

testing 

Robinson T J. Coeliac disease with farmers' lung. Br 

Med J 1976;1(6012):745-746. Not about consequences 

of testing 

Rogers A I. Steatorrhea. Postgrad Med 

1971;50(6):123-129. Not about consequences of

testing 

Roizen N J. Down syndrome: Progress in research. 

Ment Retard Dev Disabil Res Rev 2001;7(1):38-44. 

Not about consequences of testing 

Roizen Nancy J, Patterson David. Down Syndrome. 

Lancet 2003;361(9365):1281-1289. Not about 

consequences of testing 

Roldan M B, Barrio R, Roy G et al. Diagnostic value 

of serological markers for celiac disease in diabetic 

children and adolescents. J Pediatr Endocrinol Metab 

1998;11(6):751-756. Not about consequences of

testing 

Rolles C J, Kendall M J. One hour blood D-xylose as 

a screening test for malabsorption in infants and young 

children. Arch Dis Child 1972;47(254):673Not about 

consequences of testing 

Rolles C J, Nutter S, Kendall M J et al. One-hour

blood-xylose screening-test for coeliac disease in

infants and young children. Lancet 

1973;2(7837):1043-1045. Not about consequences of 

testing 

Rona R J, Tanner J M. Aetiology of idiopathic growth 

hormone deficiency in England and Wales. Arch Dis 

Child 1977;52(3):197-208. Not about consequences of 

testing 

Rosa Utiyama S R, Silva Kotze L M, Nisihara R M et 

al. Spectrum of autoantibodies in celiac patients and 

relatives. Dig Dis Sci 2001;46(12):2624-2630. Not 

about consequences of testing 

Rosenman Kenneth D, Gardiner Joseph, Swanson G et 

al. Use of skin-cancer prevention strategies among 

farmers and their spouses. Am J Prev Med 

1995;11(5):342-347. Not about consequences of

testing 

Rosenthal E, Golan D T, Benderly A.

Immunofluorescent antigluten antibody test. Titer and 

profile of gluten antibodies in celiac disease. Am J Dis 

Child 1984;138(7):659-662. Not about consequences 

of testing 

Rossipal E, Mlekusch W. Steatorrhea, a simple and 

rapid method of diagnosis. Eur J Pediatr

1976;122(4):297-302. Not about consequences of

testing 

Rostami K, Kerckhaert J P, Tiemessen R et al. The 

relationship between anti-endomysium antibodies and 

villous atrophy in coeliac disease using both monkey

and human substrate. Eur J Gastroenterol Hepatol 

1999;11(4):439-442. Not about consequences of

testing 

Rostami K, Kerckhaert J, Tiemessen R et al. 

Sensitivity of antiendomysium and antigliadin

antibodies in untreated celiac disease: disappointing in 

clinical practice. Am J Gastroenterol 1999;94(4):888-

894. Not about consequences of testing 

Rostami K, Kerckhaert J, von Blomberg B M et al. 

SAT and serology in adult coeliacs, seronegative 

coeliac disease seems a reality. Neth J Med

1998;53(1):15-19. Not about consequences of testing 

Rostami K, Mulder C J J, Stapell S et al.

Autoantibodies and histogenesis of celiac disease. 

Rom J Gastroenterol 2003;12(2):101-106. Not about 

consequences of testing 

Rostami K, Mulder C J, van Overbeek F M et al.

Should relatives of coeliacs with mild clinical 

complaints undergo a small-bowel biopsy despite 

negative serology?. Eur J Gastroenterol Hepatol 

2000;12(1):51-55. Not about consequences of testing 

A-640
Rostami K, Mulder C J, Werre J M et al. High 

prevalence of celiac disease in apparently healthy 

blood donors suggests a high prevalence of 

undiagnosed celiac disease in the Dutch population. 

Scand J Gastroenterol 1999;34(3):276-279. Not about 

consequences of testing 

Rostami K, Steegers E A, Wong W Y et al. Coeliac 

disease and reproductive disorders: a neglected 

association. Eur J Obstet Gynecol Reprod Biol 

2001;96(2):146-149. Not about consequences of

testing 

Rubin C E, Brandborg L L, Phelps P C et al. Studies 

of celiac disease. I. The apparent identical and specific

nature of the duodenal and proximal jejunal lesion in 

celiac disease and idiopathic sprue. Gastroenterology

1968;54(4):Suppl:800-802. Not about consequences of 

testing 

Rubin C E, Eidelman S, Weinstein W M. Sprue by

any other name. Gastroenterology 1970;58(3):409-

413. Not about consequences of testing 

Rude R K, Olerich M. Magnesium deficiency: 

possible role in osteoporosis associated with glutensensitive enteropathy. Osteoporosis International - a 

Journal Established as Result of Cooperation Between 

the European Foundation for Osteoporosis and the 

National Osteoporosis Foundation of the Usa 

1996;6(6):453-461. Not about consequences of testing 

Rujner J, Brett-Chrusciel J, Piontek E et al. Negative

results for serum antiendomysial antibodies do not 

exclude late developing jejunal mucosal atrophy - A 

case of latent coeliac disease in a 12-year old boy with 

type 1 diabetes mellitus. Pediatr Wspolczesna 

2002;4(3):331-333. Not about consequences of testing 

Rujner J, Socha J, Barra E et al. Serum and salivary

antigliadin antibodies and serum IgA antiendomysium antibodies as a screening test for coeliac 

disease. Acta Paediatr 1996;85(7):814-817. Not about 

consequences of testing 

Rumbo M, Chirdo F G, Ben R et al. Evaluation of

coeliac disease serological markers in Down syndrome

patients. Digestive and Liver Disease - Official

Journal of the Italian Society of Gastroenterology and 

the Italian Association for the Study of the Liver 

2002;34(2):116-121. Not about consequences of

testing 

Ruokonen J. Reactions in the cytotoxic leucocyte test. 

Allergol Immunopathol (Madr) 1981;9(4):281-288. 

Not about consequences of testing 

Ruskone-Fourmestraux A, Rambaud J C.

Gastrointestinal lymphoma: prevention and treatment 

of early lesions. Baillieres Best Pract Res Clin 

Gastroenterol 2001;15(2):337-354. Not about 

consequences of testing 

Russo P A, Chartrand L J, Seidman E. Comparative 

analysis of serologic screening tests for the initial

diagnosis of celiac disease. Pediatrics 1999;104(1 Pt 

1):75-78. Not about consequences of testing 

Ryan J. Coeliac disease. Update 2000. Aust Fam 

Physician 2000;29(9):835-838. Not about 

consequences of testing 

Sacchetti L, Calcagno G, Ferrajolo A et al. 

Discrimination between celiac and other

gastrointestinal disorders in childhood by rapid human 

lymphocyte antigen typing. Clin Chem 1998;44(8 Pt 

1):1755-1757. Not about consequences of testing 

Sacchetti L, Ferrajolo A, Salerno G et al. Diagnostic 

value of various serum antibodies detected by diverse 

methods in childhood celiac disease. Clin Chem 

1996;42(11):1838-1842. Not about consequences of 

testing 

Salmaso C, Ocmant A, Pesce G et al. Comparison of 

ELISA for tissue transglutaminase autoantibodies with 

antiendomysium antibodies in pediatric and adult 

patients with celiac disease. Allergy 2001;56(6):544-

547. Not about consequences of testing 

Salur L, Uibo O, Talvik I et al. The high frequency of 

coeliac disease among children with neurological 

disorders. European Journal of Neurology - the 

Official Journal of the European Federation of

Neurological Societies 2000;7(6):707-711. Not about 

consequences of testing 

Sandberg-Bennich S, Dahlquist G, Kallen B. Coeliac 

disease is associated with intrauterine growth and

neonatal infections. Acta Paediatr 2002;91(1):30-33. 

Not about consequences of testing 

Sanders D S. Coeliac disease. Br J Surg 

2002;89(6):676-677. Not about consequences of

testing 

Sanders David S, Patel Dina, Stephenson Timothy J et 

al. A primary care cross-sectional study of

undiagnosed adult coeliac disease. Eur J Gastroenterol 

Hepatol 2003;15(4):407-413. Not about consequences 

of testing 

Sardy M, Karpati S, Peterfy F et al. Comparison of a 

tissue transglutaminase ELISA with the endomysium 

antibody test in the diagnosis of gluten-sensitive 

enteropathy. Z Gastroenterol 2000;38(5):357-364. Not 

about consequences of testing 

Sardy M, Odenthal U, Karpati S et al. Recombinant 

human tissue transglutaminase ELISA for the 

diagnosis of gluten-sensitive enteropathy. Clin Chem

1999;45(12):2142-2149. Not about consequences of 

testing 

A-641
Sategna Guidetti C, Solerio E, Scaglione N et al. 

Duration of gluten exposure in adult coeliac disease 

does not correlate with the risk for autoimmune 

disorders. Gut 2001;49(4):502-505. Not about 

consequences of testing 

Sategna Guidetti, Carla Scaglione, Nadia Martini et al.

Red cell distribution width as a marker of coeliac 

disease: a prospective study. Eur J Gastroenterol 

Hepatol 2002;14(2):177-181. Not about consequences 

of testing 

Sategna-Guidetti C, Bruno M, Mazza E et al. 

Autoimmune thyroid diseases and coeliac disease. Eur

J Gastroenterol Hepatol 1998;10(11):927-931. Not 

about consequences of testing 

Sategna-Guidetti C, Grosso S B, Bruno M et al. 

Indirect immunofluorescence for of anti-jejunum 

antibody detection in celiac disease: comparison 

among different antigenic substrates. Panminerva Med 

1998;40(4):261-263. Not about consequences of

testing 

Sategna-Guidetti C, Grosso S B, Bruno M et al. Is 

human umbilical cord the most suitable substrate for 

the detection of endomysium antibodies in the 

screening and follow-up of coeliac disease?. Eur J

Gastroenterol Hepatol 1997;9(7):657-660. Not about 

consequences of testing 

Sategna-Guidetti C, Grosso S, Bruno M et al. 

Comparison of serum anti-gliadin, anti-endomysium, 

and anti-jejunum antibodies in adult celiac sprue. J 

Clin Gastroenterol 1995;20(1):17-21. Not about 

consequences of testing 

Sategna-Guidetti C, Grosso S, Pulitano R et al. Celiac 

disease and insulin-dependent diabetes mellitus.

Screening in an adult population. Dig Dis Sci 

1994;39(8):1633-1637. Not about consequences of

testing 

Sategna-Guidetti C, Grosso S. Changing pattern in

adult coeliac disease: A 24-year survey. Eur J

Gastroenterol Hepatol 1994;6(1):15-19. Not about 

consequences of testing 

Sategna-Guidetti C, Pulitano R, Grosso S et al. Serum 

IgA antiendomysium antibody titers as a marker of

intestinal involvement and diet compliance in adult 

celiac sprue. J Clin Gastroenterol 1993;17(2):123-127. 

Not about consequences of testing 

Saukkonen T, Ilonen J, Akerblom H K et al. 

Prevalence of coeliac disease in siblings of patients

with Type I diabetes is related to the prevalence of

DQB1*02 allele. Diabetologia 2001;44(8):1051-1053. 

Not about consequences of testing 

Saukkonen T, Savilahti E, Reijonen H et al. Coeliac 

disease: frequent occurrence after clinical onset of

insulin-dependent diabetes mellitus. Childhood 

Diabetes in Finland Study Group. Diabet Med 

1996;13(5):464-470. Not about consequences of

testing 

Saverymuttu S H, Sabbat J, Burke M et al. Impact of

endoscopic duodenal biopsy on the detection of small 

intestinal villous atrophy. Postgrad Med J 

1991;67(783):47-49. Not about consequences of

testing 

Sblattero D, Berti I, Trevisiol C et al. Human 

recombinant tissue transglutaminase ELISA: an

innovative diagnostic assay for celiac disease. Am J 

Gastroenterol 2000;95(5):1253-1257. Not about 

consequences of testing 

Schaad U, Gaze H, Hadorn B. Value of 1-hour bloodxylose test in diagnosis of childhood coeliac disease. 

Arch Dis Child 1978;53(5):420-422. Not about 

consequences of testing 

Schenk E A, Samloff I M, Klipstein F A. Morphologic 

characteristics of jejunal biopsy in celiac disease and 

tropical sprue. Am J Pathol 1965;47(5):765-781. Not 

about consequences of testing 

Schmitz J. Is celiac disease a lifelong disorder?. Clin 

Invest Med 1996;19(5):352-356. Not about 

consequences of testing 

Schober E, Bittmann B, Granditsch G et al. Screening 

by anti-endomysium antibody for celiac disease in

diabetic children and adolescents in Austria. J Pediatr

Gastroenterol Nutr 2000;30(4):391-396. Not about 

consequences of testing 

Schober Edith, Rami Birgit, Granditsch Gerhard et al. 

Coeliac disease in children and adolescents with type

1 diabetes mellitus: to screen or not, to treat or not?.

Horm Res 2002;57(Suppl 1):97-100. Not about 

consequences of testing 

Schuppan D, Hahn E G. IgA anti-tissue 

transglutaminase: setting the stage for coeliac disease 

screening. Eur J Gastroenterol Hepatol 

2001;13(6):635-637. Not about consequences of

testing 

Schwartz F C M, Lunat M, Wolfsdorf J. Blood xylose 

concentrations in protein energy malnutrition.

Relationship to serum albumin and jejunal histology. S 

Afr Med J 1974;48(58):2387-2390. Not about 

consequences of testing 

Scoglio Riccardo, Di Pasquale, Giuseppe Pagano et al. 

Is intestinal biopsy always needed for diagnosis of

celiac disease?. Am J Gastroenterol 2003;98(6):1325-

1331. Not about consequences of testing 

Scott E M, Scott B B. A strategy for osteoporosis in 

gastroenterology. Eur J Gastroenterol Hepatol 

A-642
1998;10(8):689-696. Not about consequences of

testing 

Scott H, Ek J, Havnen J et al. Serum antibodies to

dietary antigens: a prospective study of the diagnostic 

usefulness in celiac disease of children. J Pediatr

Gastroenterol Nutr 1990;11(2):215-220. Not about 

consequences of testing 

Scott H, Fausa O, Ek J et al. Measurements of serum

IgA and IgG activities to dietary antigens. A 

prospective study of the diagnostic usefulness in adult 

coeliac disease. Scand J Gastroenterol

1990;25(3):287-292. Not about consequences of

testing 

Seah P P, Fry L, Holborow E J et al. Antireticulin

antibody: incidence and diagnostic significance. Gut 

1973;14(4):311-315. Not about consequences of

testing 

Sedghizadeh Parish P, Shuler Charles F, Allen Carl M 

et al. Celiac disease and recurrent aphthous stomatitis:

a report and review of the literature. Oral Surg Oral 

Med Oral Pathol Oral Radiol Endod 2002;94(4):474-

478. Not about consequences of testing 

Seissler J, Boms S, Wohlrab U et al. Antibodies to 

human recombinant tissue transglutaminase measured 

by radioligand assay: evidence for high diagnostic 

sensitivity for celiac disease. Horm Metab Res 

1999;31(6):375-379. Not about consequences of

testing 

Selby W S, Gallagher N D. Malignancy in a 19-year 

experience of adult celiac disease. Dig Dis Sci 

1979;24(9):684-688. Not about consequences of

testing 

Selby W S, Painter D, Collins A et al. Persistent

mucosal abnormalities in coeliac disease are not 

related to the ingestion of trace amounts of gluten. 

Scand J Gastroenterol 1999;34(9):909-914. Not about 

consequences of testing 

Selby W. Gluten enteropathy. Aust Prescr 

2001;24(2):38-40+47. Not about consequences of

testing 

Semrad C E. Bone mass and gastrointestinal disease.

Ann N Y Acad Sci 2000;904564-570. Not about 

consequences of testing 

Seraphin P, Mobarhan S. Mortality in patients with

celiac disease. Nutr Rev 2002; 60(4):116-118. Not 

about consequences of testing 

Shafer R B, Onstad G R. Measurement of fat

absorption utilizing 131iodine-triolein and

nonabsorbable radioactive markers. Am J Med Sci 

1975;269(3):327-331. Not about consequences of

testing 

Shahbazkhani Bijan, Malekzadeh Reza, Sotoudeh

Masoud et al. High prevalence of coeliac disease in 

apparently healthy Iranian blood donors. Eur J 

Gastroenterol Hepatol 2003;15(5):475-478. Not about 

consequences of testing 

Shaker J L, Brickner R C, Findling J W et al. 

Hypocalcemia and skeletal disease as presenting

features of celiac disease. Arch Intern Med

1997;157(9):1013-1016. Not about consequences of 

testing 

Shamir Raanan, Lerner Aaron, Shinar Eilat et al. The 

use of a single serological marker underestimates the 

prevalence of celiac disease in Israel: a study of blood 

donors. Am J Gastroenterol 2002;97(10):2589-2594. 

Not about consequences of testing 

Sheldon W. Prognosis in early adult life of coeliac 

children treated with a gluten-free diet. Br Med J 

1969; 2(654):401-404. Unable to obtain article 

Shelley J M, Irwig L M, Simpson J M et al. Evaluation 

of a mass-media-led campaign to increase Pap smear 

screening. Health Educ Res 1991;6(3):267-277. Not 

about consequences of testing 

Sher K S, Mayberry J F. Female fertility, obstetric and 

gynaecological history in coeliac disease. A case

control study. Digestion 1994;55(4):243-246. Not 

about consequences of testing 

Sherr H P, Sasaki Y, Newman A et al. Detection of 

bacterial deconjugation of bile salts by a convenient 

breath-analysis technic. N Engl J Med 

1971;285(12):656-661. Not about consequences of

testing 

Shidrawi R G, Przemioslo R, Davies D R et al. Pitfalls

in diagnosing coeliac disease. Am J Clin Pathol

1994;47(8):693-694. Not about consequences of

testing 

Shmerling DH, Franckx J. Childhood celiac disease: a 

long-term analysis of relapses in 91 patients. J Pediatr

Gastroenterol Nutr 1986; 5(4):565-569. Not about 

consequences of testing 

Signer E, Burgin-Wolff A, Berger R et al. Antibodies 

to gliadin as a screening test for coeliac disease. A

prospective study. Helv Paediatr Acta 1979;34(1):41-

52. Not about consequences of testing 

Signore A, Chianelli M, Annovazzi A et al. Imaging 

active lymphocytic infiltration in coeliac disease with 

iodine-123-interleukin-2 and the response to diet. Eur 

J Nucl Med 2000;27(1):18-24. Not about 

consequences of testing 

Sigurs N, Hattevig G, Kjellman B et al. Appearance of

atopic disease in relation to serum IgE antibodies in 

A-643
children followed up from birth for 4 to 15 years. J 

Allergy Clin Immunol 1994;94(4):757-763. Not about 

consequences of testing 

Sikora K, Anand B S, Truelove S C et al. Stimulation 

of lymphocytes from patients with coeliac disease by a 

subfraction of gluten. Lancet 1976;2(7982):389-391. 

Not about consequences of testing 

Silano M, De Vincenzi M. In vitro screening of food 

peptides toxic for coeliac and other gluten-sensitive 

patients: a review. Toxicology 1999;132(2-3):99-110. 

Not about consequences of testing 

Simko V. Fecal fat microscopy. Acceptable predictive 

value in screening for steatorrhea. Am J Gastroenterol 

1981;75(3):204-208. Not about consequences of

testing 

Sinclair D, Pearce C B, Saas M S L et al. A 

comparative study of tissue transglutaminase

antibodies and endomysium antibody

immunofluorescence in routine clinical laboratory

practice. Ann Clin Biochem 2003;40(4):411-416. Not 

about consequences of testing 

Sjoberg K, Alm R, Ivarsson S A et al. Prevalence and 

clinical significance of gliadin antibodies in healthy

children and adults. Scand J Gastroenterol 

1994;29(3):248-254. Not about consequences of

testing 

Sjoberg K, Eriksson K F, Bredberg A et al. Screening 

for coeliac disease in adult insulin-dependent diabetes

mellitus. J Intern Med 1998;243(2):133-140. Not

about consequences of testing 

Sjoberg K, Eriksson S, Tenngart B et al. Factor XIII 

and tissue transglutaminase antibodies in coeliac and 

inflammatory bowel disease. Autoimmunity

2002;35(5):357-364. Not about consequences of

testing 

Sjoberg K, Eriksson S. Regional differences in coeliac 

disease prevalence in Scandinavia?. Scand J

Gastroenterol 1999;34(1):41-45. Not about 

consequences of testing 

Sjoberg K, Lindgren S, Eriksson S. Frequent 

occurrence of non-specific gliadin antibodies in 

chronic liver disease. Endomysial but not gliadin 

antibodies predict coeliac disease in patients with 

chronic liver disease. Scand J Gastroenterol 

1997;32(11):1162-1167. Not about consequences of 

testing 

Sjoberg K, Wassmuth R, Reichstetter S et al. Gliadin 

antibodies in adult insulin-dependent diabetes--

autoimmune and immunogenetic correlates.

Autoimmunity 2000;32(4):217-228. Not about 

consequences of testing 

Skala I, Krondl A, Vulterinova M et al. Composition 

of feces in steatorrhea of different etiology: mutual 

relationship between the volume of feces, water, dry

matter, nitrogen, and fat content. Am J Dig Dis 

1968;13(3):204-212. Not about consequences of

testing 

Skovbjerg H, Sjostrom H, Noren O B. Coeliac disease 

- A diagnostic and scientific challenge. Ugeskr Laeg 

2002;164(25):3329-3333. Not about consequences of 

testing 

Smecuol E, Vazquez H, Sugai E et al. Sugar tests 

detect celiac disease among first-degree relatives. Am 

J Gastroenterol 1999;94(12):3547-3552. Not about 

consequences of testing 

Smith S E, Littlewood J M. The two-film barium meal 

in the exclusion of coeliac disease. Clin Radiol

1977;28(6):629-634. Not about consequences of

testing 

Smith S. Jejunal biopsy--seeking an alternative.

Paediatr Nurs 1996;8(4):17-19. Not about 

consequences of testing 

Sobel Judith, Curtin Ann, Fell Deborah. The Oregon 

Breast Cancer Detection and Awareness Project: The 

legacy of a mammogram screening campaign. Health

Values 1991;15(1):3-8. Not about consequences of

testing 

Sollid L M, Scott H. New tool to predict celiac disease 

on its way to the clinics. Gastroenterology

1998;115(6):1584-1586. Not about consequences of 

testing 

Somech R, Spirer Z. Celiac disease: extraintestinal

manifestations, associated diseases, and

complications. Adv Pediatr 2002; 49:191-201. Not 

about consequences of testing 

Sorell L, Garrote J A, Acevedo B et al. One-step

immunochromatographic assay for screening of

coeliac disease. Lancet 2002;359(9310):945-946. Not 

about consequences of testing 

Sorensen H T, Fonager K. Risk estimation of disorders 

associated with coeliac disease. A 16-year Danish

nationwide follow-up study based on hospital 

discharge data. Implications for screening. Int J Risk 

Saf Med 1996;8(2):137-140. Not about consequences 

of testing 

Soresi M, Amplo M, Agliastro R et al. Screening for 

autoantibodies to tissue transglutaminase reveals a low 

prevalence of celiac disease in blood donors with

cryptogenic hypertransaminasemia. Digestion

2001;64(2):87-91. Not about consequences of testing 

Spiekerkoetter U, Seissler J, Wendel U. General 

screening for celiac disease is advisable in children 

A-644
with type 1 diabetes. Horm Metab Res

2002;34(4):192-195. Not about consequences of

testing 

Stahlberg M R, Savilahti E, Viander M. Antibodies to

gliadin by ELISA as a screening test for childhood 

celiac disease. J Pediatr Gastroenterol Nutr 

1986;5(5):726-729. Not about consequences of testing 

Stazi A V, Mantovani A. A risk factor for female 

fertility and pregnancy: celiac disease. Gynecological 

Endocrinology - the Official Journal of the 

International Society of Gynecological Endocrinology

2000;14(6):454-463. Not about consequences of

testing 

Stenhammar L, Ascher H, Danielsson L et al. Small

bowel biopsy in Swedish paediatric clinics. Acta 

Paediatr 2002;91(10):1126-1129. Not about 

consequences of testing 

Stenhammar L. Transient gastro-intestinal disorders

during infancy and early childhood. A follow-up study

with special reference to coeliac disease. Acta Paediatr 

Scand 1981;70(3):383-387. Not about consequences 

of testing 

Stern M, Ciclitira P J, van Eckert R et al. Analysis and 

clinical effects of gluten in coeliac disease. Eur J

Gastroenterol Hepatol 2001;13(6):741-747. Not about 

consequences of testing 

Stern M, Fischer K, Gruettner R. Gliadin antibodies in 

coeliac disease. Acta Paediatr Belg 1977;30(4):252Not 

about consequences of testing 

Stern M, Teuscher M, Wechmann T. Serological 

screening for coeliac disease: methodological 

standards and quality control. Acta Paediatr

1996;412(Suppl):49-51. Not about consequences of

testing 

Stern M. Comparative evaluation of serologic tests for 

celiac disease: a European initiative toward

standardization. J Pediatr Gastroenterol Nutr

2000;31(5):513-519. Not about consequences of

testing 

Stevens F M, Lloyd R S, Geraghty S M et al.

Schizophrenia and coeliac disease--the nature of the 

relationship. Psychol Med 1977;7(2):259-263. Not 

about consequences of testing 

Stevens F M, Lloyd R, Egan-Mitchell B et al. 

Reticulin antibodies in patients with coeliac disease 

and their relatives. Gut 1975;16(8):598-602. Not about 

consequences of testing 

Stewart J. Child coeliacs in adult life. Ir Med J

1974;67(15):411-414. Not about consequences of

testing 

Stockbrugger R W, Armbrecht U, Muller E et al. 

Determination of faecal chymotrypsin concentration 

and 72-hour faecal chymotrypsin output in the 

detection of pancreatic steatorrhoea. Scand J 

Gastroenterol 1991;188(Suppl):13-19. Not about 

consequences of testing 

Stocker W, Otte M, Ulrich S et al. Autoimmunity to 

pancreatic juice in Crohn's disease. Results of an

autoantibody screening in patients with chronic

inflammatory bowel disease. Scand J Gastroenterol 

1987;139(Suppl):41-52. Not about consequences of

testing 

Storm W. Celiac disease and alopecia areata in a child 

with Down Syndrome. J Intellect Disabil Res 

2000;44(5):621-623. Not about consequences of

testing 

Storsrud S, Olsson M, Arvidsson Lenner R et al. Adult 

coeliac patients do tolerate large amounts of oats. Eur 

J Clin Nutr 2003;57(1):163-169. Not about 

consequences of testing 

Storsrud Stine, Hulthen Lena R, Lenner Ragnhild A. 

Beneficial effects of oats in the gluten-free diet of

adults with special reference to nutrient status, 

symptoms and subjective experiences. Br J Nutr 

2003;90(1):101-107. Not about consequences of

testing 

Straughan P T, Seow A. Barriers to mammography

among Chinese women in Singapore: A focus group 

approach. Health Educ Res 1995;10(4):431-441. Not 

about consequences of testing 

Strobel S, Brydon W G, Ferguson A. 

Cellobiose/mannitol sugar permeability test 

complements biopsy histopathology in clinical 

investigation of the jejunum. Gut 1984;25(11):1241-

1246. Not about consequences of testing 

Stulik J, Hernychova L, Porkertova S et al. 

Identification of new celiac disease autoantigens using 

proteomic analysis. Proteomics 2003;3(6):951-956. 

Not about consequences of testing 

Sugai E, Selvaggio G, Vazquez H et al. Tissue 

transglutaminase antibodies in celiac disease: 

assessment of a commercial kit. Am J Gastroenterol 

2000;95(9):2318-2322. Not about consequences of

testing 

Sugai E, Srur G, Vazquez H et al. Steatocrit: a reliable

semiquantitative method for detection of steatorrhea. J 

Clin Gastroenterol 1994;19(3):206-209. Not about 

consequences of testing 

Sugai Emilia, Chernavsky Alejandra, Pedreira Silvia

et al. Bone-specific antibodies in sera from patients

with celiac disease: characterization and implications 

A-645
in osteoporosis. J Clin Immunol 2002;22(6):353-362. 

Not about consequences of testing 

Suharjono. Intestinal biopsy and coeliac disease. 

Paediatr Indones 1971;11(3):116-134. Not about 

consequences of testing 

Sulkanen S, Halttunen T, Laurila K et al. Tissue 

transglutaminase autoantibody enzyme-linked

immunosorbent assay in detecting celiac disease. 

Gastroenterology 1998;115(6):1322-1328. Not about 

consequences of testing 

Sumnik Z, Kolouskova S, Cinek O et al. HLADQA1*05-DQB1*0201 positivity predisposes to

coeliac disease in Czech diabetic children. Acta

Paediatr 2000;89(12):1426-1430. Not about 

consequences of testing 

Swain V A, Young W F, Pringle E M. Hypertrophy of 

the appendices epiploicae and lipomatous polyposis of 

the colon. Gut 1969;10(7):587-589. Not about 

consequences of testing 

Swinson C M, Slavin G, Coles E C et al. Coeliac 

disease and malignancy. Lancet 1983;1(8316):111-

115. Not about consequences of testing 

Szaflarska-Szczepanik A, Czerwionka-Szaflarska M. 

The frequency of occurrence and clinical picture of 

celiac disease in the parents of children with the

disease. Medical Science Monitor - International 

Medical Journal of Experimental and Clinical 

Research 2001;7(5):971-976. Not about consequences 

of testing 

Tai V, Crowe M, O'Keefe S. Celiac disease in older 

people. J Am Geriatr Soc 2000;48(12):1690-1696. Not 

about consequences of testing 

Talal A H, Murray J A, Goeken J A et al. Celiac

disease in an adult population with insulin-dependent 

diabetes mellitus: use of endomysial antibody testing. 

Am J Gastroenterol 1997;92(8):1280-1284. Not about 

consequences of testing 

Talstad I, Fretheim B, Myren J et al. Graded 

gastrectomy for duodenal ulcer -- a five-year

prospective study. Scand J Gastroenterol 

1975;33(Suppl):1-27. Not about consequences of

testing 

Tandon B N, Iyenger K P, Deo M G et al. A study of 

"sprue syndrome in adults" in northern India. J Assoc 

Physicians India 1966;14(4):197-202. Not about 

consequences of testing 

Tandon B N, Tandon R K, Satpathy B K et al. 

Mechanism of malabsorption in giardiasis: a study of 

bacterial flora and bile salt deconjugation in upper 

jejunum. Gut 1977;18(3):176-181. Not about 

consequences of testing 

Tarmure Simina, Grigorescu Mircea, Cristea Anca et

al. Antiendomysial and antitissue transglutaminase

antibodies in gluten-induced enteropathy. Rom J 

Gastroenterol 2002;11(2):91-95. Not about 

consequences of testing 

Taylor C J. Predictive value of intraepithelial 

lymphocyte counts in childhood coeliac disease. J 

Pediatr Gastroenterol Nutr 1988;7(4):532-536. Not 

about consequences of testing 

Tesei N, Sugai E, Vazquez H et al. Antibodies to 

human recombinant tissue transglutaminase may 

detect coeliac disease patients undiagnosed by

endomysial antibodies. Aliment Pharmacol Ther 

2003;17(11):1415-1423. Not about consequences of 

testing 

Thapa B R. Celiac disease in India. Indian J Pediatr 

1999;66(1 Suppl):S16-S20. Not about consequences 

of testing 

Thomas A G, Phillips A D, Walker-Smith J A. The 

value of proximal small intestinal biopsy in the 

differential diagnosis of chronic diarrhoea. Arch Dis 

Child 1992;67(6):741-743. Not about consequences of 

testing 

Thomas D W, Sinatra F R, Merritt R J. Random fecal 

alpha-1-antitrypsin concentration in children with 

gastrointestinal disease. Gastroenterology

1981;80(4):776-782. Not about consequences of

testing 

Thomas P D, Forbes A, Green J et al. Guidelines for 

the investigation of chronic diarrhoea, 2nd edition. 

Gut 2003;52(Suppl 5):v1-v15. Not about 

consequences of testing 

Thompson H. Necropsy studies on adult coeliac 

disease. Am J Clin Pathol 1974;27(9):710-721. Not 

about consequences of testing 

Thompson J B, Su C K, Ringrose R E et al. Fecal 

triglycerides. II. Digestive versus absorptive 

steatorrhea. J Lab Clin Med 1969;73(3):521-530. Not 

about consequences of testing 

Thornquist H, Jacobsen GS, Dahl LB et al. Coeliac 

disease and gluten-free diet: a following-up study of 

fifteen young adults. Ann Nutr Metab 1993; 

37(6):295-301. Not about consequences of testing 

Tonutti E, Visentini D, Bizzaro N et al. The role of 

antitissue transglutaminase assay for the diagnosis and 

monitoring of coeliac disease: a French-Italian 

multicentre study. Am J Clin Pathol 2003;56(5):389-

393. Not about consequences of testing 

Tovey F I, Godfrey J E, Lewin M R. A gastrectomy

population: 25-30 years on. Postgrad Med J 

A-646
1990;66(776):450-456. Not about consequences of

testing 

Townley R R, Anderson C M. Coeliac disease. A

review. Ergeb Inn Med Kinderheilkd 1967;261-44. 

Not about consequences of testing 

Tran M, Forget P, Van den et al. Improved steatocrit 

results obtained by acidification of fecal homogenates 

are due to improved fat extraction. J Pediatr

Gastroenterol Nutr 1996;22(2):157-160. Not about 

consequences of testing 

Tran M, Forget P, Van den et al. The acid steatocrit: a 

much improved method. J Pediatr Gastroenterol Nutr 

1994;19(3):299-303. Not about consequences of

testing 

Trevisiol C, Not T, Berti I et al. Screening for coeliac

disease in healthy blood donors at two immunotransfusion centres in north-east Italy. Ital J

Gastroenterol Hepatol 1999;31(7):584-586. Not about 

consequences of testing 

Trevisiol C, Ventura A, Baldas V et al. A reliable

screening procedure for coeliac disease in clinical

practice. Scand J Gastroenterol 2002;37(6):679-684. 

Not about consequences of testing 

Trewby P N, Chipping P M, Palmer S J et al. Splenic 

atrophy in adult coeliac disease: is it reversible?. Gut 

1981;22(8):628-632. Not about consequences of

testing 

Trier J S. Diagnostic value of peroral biopsy of the 

proximal small intestine. N Engl J Med 

1971;285(26):1470-1473. Not about consequences of 

testing 

Troncone R, Greco L, Auricchio S. Gluten-sensitive 

enteropathy. Pediatr Clin North Am 1996;43(2):355-

373. Not about consequences of testing 

Troncone R, Maurano F, Rossi M et al. IgA antibodies 

to tissue transglutaminase: An effective diagnostic test 

for celiac disease. Eur J Pediatr 1999;134(2):166-171. 

Not about consequences of testing 

Troncone R, Starita A, Coletta S et al. Antigliadin

antibody, D-xylose, and cellobiose/mannitol

permeability tests as indicators of mucosal damage in

children with coeliac disease. Scand J Gastroenterol 

1992;27(8):703-706. Not about consequences of

testing 

Tucker N T, Barghuthy F S, Prihoda T J et al. 

Antigliadin antibodies detected by enzyme-linked

immunosorbent assay as a marker of childhood celiac 

disease. Eur J Pediatr 1988;113(2):286-289. Not about 

consequences of testing 

Tumer L, Hasanoglu A, Aybay C. Endomysium 

antibodies in the diagnosis of celiac disease in shortstatured children with no gastrointestinal symptoms. 

Pediatr Int 2001;43(1):71-73. Not about consequences 

of testing 

Tursi A, Brandimarte G, Giorgetti G et al. Low 

prevalence of antigliadin and anti-endomysium 

antibodies in subclinical/silent celiac disease. Am J 

Gastroenterol 2001;96(5):1507-1510. Not about 

consequences of testing 

Tursi A, Brandimarte G, Giorgetti G M et al. 

Effectiveness of the sorbitol HSUB2 breath test in

detecting histological damage among relatives of

coeliacs. Scand J Gastroenterol 2003;38(7):727-731. 

Not about consequences of testing 

Tursi A, Brandimarte G, Giorgetti G M. Sorbitol H2-

breath test versus anti-endomysium antibodies for the 

diagnosis of subclinical/silent coeliac disease. Scand J 

Gastroenterol 2001;36(11):1170-1172. Not about 

consequences of testing 

Tursi A, Giorgetti G, Brandimarte G et al. Prevalence

and clinical presentation of subclinical/silent celiac

disease in adults: an analysis on a 12-year observation.

Hepatogastroenterology 2001;48(38):462-464. Not 

about consequences of testing 

Tursi Antonio, Brandimarte Giovanni, Giorgetti Gian 

et al. Prevalence of antitissue transglutaminase

antibodies in different degrees of intestinal damage in

celiac disease. J Clin Gastroenterol 2003;36(3):219-

221. Not about consequences of testing 

Tursi Antonio, Brandimarte Giovanni. The 

symptomatic and histologic response to a gluten-free 

diet in patients with borderline enteropathy. J Clin 

Gastroenterol 2003;36(1):13-17. Not about 

consequences of testing 

Uibo O, Lambrechts A, Mascart-Lemone F. Human 

oesophagus: a convenient antigenic substrate for the 

determination of anti-endomysium antibodies in the 

serological diagnosis of coeliac disease. Eur J 

Gastroenterol Hepatol 1995;7(1):37-40. Not about 

consequences of testing 

Uibo O, Maaroos H I. Hospital screening of coeliac 

disease in Estonian children by anti-gliadin antibodies

of IgA class. Acta Paediatr 1993;82(3):233-234. Not 

about consequences of testing 

Uibo O, Metskula K, Kukk T et al. Results of coeliac 

disease screening in Estonia in 1990-1994. Acta 

Paediatr 1996;412(Suppl):39-41. Not about 

consequences of testing 

Uibo O, Uibo R, Kleimola V et al. Serum IgA antigliadin antibodies in an adult population sample. High 

prevalence without celiac disease. Dig Dis Sci

A-647
1993;38(11):2034-2037. Not about consequences of 

testing 

Uibo O. Childhood celiac disease in Estonia: efficacy

of the IgA-class antigliadin antibody test in the search 

for new cases. J Pediatr Gastroenterol Nutr 

1994;18(1):53-55. Not about consequences of testing 

Uil J J, van Elburg R M, Janssens P M et al.

Sensitivity of a hyperosmolar or "low"-osmolar test 

solution for sugar absorption in recognizing small 

intestinal mucosal damage in coeliac disease.

Digestive and Liver Disease - Official Journal of the 

Italian Society of Gastroenterology and the Italian 

Association for the Study of the Liver 2000;32(3):195-

200. Not about consequences of testing 

Uil J J, van Elburg R M, van Overbeek F M et al. 

Clinical implications of the sugar absorption test: 

intestinal permeability test to assess mucosal barrier 

function. Scand J Gastroenterol 1997;233(Suppl):70-

78. Not about consequences of testing 

Uil J J, van Elburg R M, van Overbeek F M et al. 

Follow-up of treated coeliac patients: sugar absorption 

test and intestinal biopsies compared. Eur J

Gastroenterol Hepatol 1996;8(3):219-223. Not about 

consequences of testing 

Unsworth D J, Brown D L. Serological screening

suggests that adult coeliac disease is underdiagnosed 

in the UK and increases the incidence by up to 12%. 

Gut 1994;35(1):61-64. Not about consequences of

testing 

Unsworth D J, Johnson G D, Haffenden G et al. 

Binding of wheat gliadin in vitro to reticulum in 

normal and dermatitis herpetiformis skin. J Invest 

Dermatol 1981;76(2):88-93. Not about consequences 

of testing 

Unsworth D J, Lock R J, Harvey R F. Improving the 

diagnosis of coeliac disease in anaemic women. Br J 

Haematol 2000;111(3):898-901. Not about 

consequences of testing 

Usai P, Boi M F, Piga M et al. Adult celiac disease is

frequently associated with sacroiliitis. Dig Dis Sci

1995;40(9):1906-1908. Not about consequences of

testing 

Usai P, Minerba L, Marini B et al. Case control study 

on health-related quality of life in adult coeliac 

disease. Digestive and Liver Disease - Official Journal 

of the Italian Society of Gastroenterology and the 

Italian Association for the Study of the Liver 

2002;34(8):547-552. Not about consequences of

testing 

Usselmann B, Loft D E. An easy test for coeliac 

disease using human umbilical vein endothelial cells. 

Eur J Gastroenterol Hepatol 1996;8(10):947-950. Not 

about consequences of testing 

Ussher R, Yeong M L, Stace N. Coeliac disease:

incidence and prevalence in Wellington 1985-92. N Z 

Med J 1994;107(978):195-197. Not about 

consequences of testing 

Vahedi Kouroche, Mascart Francoise, Mary Jean et al. 

Reliability of antitransglutaminase antibodies as 

predictors of gluten-free diet compliance in adult 

celiac disease. Am J Gastroenterol 2003;98(5):1079-

1087. Not about consequences of testing 

Valdimarsson T, Franzen L, Grodzinsky E et al. Is

small bowel biopsy necessary in adults with suspected 

celiac disease and IgA anti-endomysium antibodies?

100% positive predictive value for celiac disease in 

adults. Dig Dis Sci 1996;41(1):83-87. Not about 

consequences of testing 

Valdimarsson T, Toss G, Ross I et al. Bone mineral 

density in coeliac disease. Scand J Gastroenterol 

1994;29(5):457-461. Not about consequences of

testing 

Valentini R A, Andreani M L, Corazza G R et al. IgA 

endomysium antibody: a valuable tool in the screening 

of coeliac disease but not its follow-up. Ital J

Gastroenterol 1994;26(6):279-282. Not about 

consequences of testing 

Valentino R, Savastano S, Tommaselli A P et al. 

Prevalence of coeliac disease in patients with thyroid 

autoimmunity. Horm Res 1999;51(3):124-127. Not 

about consequences of testing 

Valletta E A, Trevisiol D, Mastella G. IgA anti-gliadin

antibodies in the monitoring of gluten challenge in 

celiac disease. J Pediatr Gastroenterol Nutr 

1990;10(2):169-173. Not about consequences of

testing 

Van Belzen M J, Meijer J W R, Sandkuijl L A et al. A

major non-HLA locus in celiac disease maps to

chromosome 19. Gastroenterology 2003;125(4):1032-

1041. Not about consequences of testing 

van den, Bosch H C, Tham R T et al. Celiac disease: 

small-bowel enteroclysis findings in adult patients

treated with a gluten-free diet. Radiology

1996;201(3):803-808. Not about consequences of

testing 

Van den, Neucker A M, Kerkvliet E M et al. Acid 

steatocrit: a reliable screening tool for steatorrhoea.

Acta Paediatr 2001;90(8):873-875. Not about 

consequences of testing 

Van den, Neucker A, Pestel N et al. Clinical use of 

acid steatocrit. Acta Paediatr 1997;86(5):466-469. Not 

about consequences of testing 

A-648
van Lith, Marcel van, Ham Marieke et al. Novel 

polymorphisms in HLA-DOA and HLA-DOB in Bcell malignancies. Immunogenetics 2002;54(8):591-

595. Not about consequences of testing 

van Overbeek F M, Uil-Dieterman I G, Mol I W et al. 

The daily gluten intake in relatives of patients with

coeliac disease compared with that of the general 

Dutch population. Eur J Gastroenterol Hepatol 

1997;9(11):1097-1099. Not about consequences of

testing 

Van Wouwe J P. Clinical and laboratory diagnosis of 

acrodermatitis enteropathica. Eur J Pediatr 

1989;149(1):2-8. Not about consequences of testing 

Vancikova Z, Chlumecky V, Sokol D et al. The 

serologic screening for celiac disease in the general 

population (blood donors) and in some high-risk 

groups of adults (patients with autoimmune diseases, 

osteoporosis and infertility) in the Czech republic. 

Folia Microbiol (Praha) 2002;47(6):753-758. Not 

about consequences of testing 

Vanderschueren-Lodeweyckx M, Wolter R, Malvaux 

P et al. The glucagon stimulation test: effect of plasma 

growth hormone and on immunoreactive insulin, 

cortisol, and glucose in children. Eur J Pediatr 

1974;85(2):182-187. Not about consequences of

testing 

Varjonen E, Vainio E, Kalimo K. Antigliadin IgE--

indicator of wheat allergy in atopic dermatitis. Allergy 

2000;55(4):386-391. Not about consequences of

testing 

Varkonyi A, Boda M, Endreffy E et al. Coeliac 

disease: always something to discover. Scand J

Gastroenterol 1998;228(Suppl):122-129. Not about 

consequences of testing 

Varma S, Malhotra P, Kochhar R et al. Celiac disease 

presenting as iron-deficiency anemia in northern India. 

Indian Journal of Gastroenterology - Official Journal 

of the Indian Society of Gastroenterology

2001;20(6):234-236. Not about consequences of

testing 

Vazquez H, Cabanne A, Sugai E et al. Serological

markers identify histologically latent coeliac disease 

among first-degree relatives. Eur J Gastroenterol 

Hepatol 1996;8(1):15-21. Not about consequences of 

testing 

Vazquez H, Sugai E, Pedreira S et al. Screening for 

asymptomatic celiac sprue in families. J Clin 

Gastroenterol 1995;21(2):130-133. Not about 

consequences of testing 

Ventrucci M, Cipolla A, Di Stefano M et al.

Determination of fecal fat concentration by near

infrared spectrometry for the screening of pancreatic

steatorrhea. International Journal of Pancreatology - 

Official Journal of the International Association of 

Pancreatology 1998;23(1):17-23. Not about 

consequences of testing 

Ventura A, Magazzu G, Greco L. Duration of

exposure to gluten and risk for autoimmune disorders 

in patients with celiac disease. SIGEP Study Group for 

Autoimmune Disorders in Celiac Disease.

Gastroenterology 1999;117(2):297-303. Not about 

consequences of testing 

Ventura A, Martelossi S. The old and new coeliac 

disease. Eur J Pediatr Dermatol 1995;5(2):87-94. Not 

about consequences of testing 

Verhulst M L, Dur A H M, Driessen W M M. Two 

sisters with coeliac disease and jejunal cancer: Just a

coincidence?. Neth J Med 1993;42(1):16-20. Not 

about consequences of testing 

Vermeer B J, Lindeman J, Harst-Oostveen C J et al.

The immunoglobulin-bearing cells in the lamina 

propria and the clinical response to a gluten-free diet 

in dermatitis herpetiformis. Arch Dermatol Res 

1977;258(3):223-230. Not about consequences of

testing 

Vesy C J, Greenson J K, Papp A C et al. Evaluation of 

celiac disease biopsies for adenovirus 12 DNA using a 

multiplex polymerase chain reaction. Modern

Pathology - an Official Journal of the United States 

and Canadian Academy of Pathology, Inc 

1993;6(1):61-64. Not about consequences of testing 

Viner Mark W, Waite John, Thienhaus Ole J. 

Comorbidity and the need for physical examinations

among patients seen in the psychiatric emergency

service. Psychiatr Serv 1996;47(9):947-948. Not about 

consequences of testing 

Visakorpi J K, Kuitunen P, Pelkonen P. Intestinal

malabsorption: a clinical study of 22 children over 2 

years of age. Acta Paediatr Scand 1970;59(3):273-280. 

Not about consequences of testing 

Visakorpi J K, Kuitunen P, Savilahti E. Frequency and 

nature of relapses in children suffering from the 

malabsorption syndrome with gluten intolerance. Acta

Paediatr Scand 1970;59(5):481-486. Not about 

consequences of testing 

Visakorpi J K, Maki M. Changing clinical features of 

coeliac disease. Acta Paediatr Suppl 1994;83(395):10-

13. Not about consequences of testing 

Vitoria J C, Arrieta A, Arranz C et al. Antibodies to 

gliadin, endomysium, and tissue transglutaminase for 

the diagnosis of celiac disease. J Pediatr Gastroenterol 

A-649
Nutr 1999;29(5):571-574. Not about consequences of 

testing 

Vitoria J C, Arrieta A, Astigarraga I et al. Use of

serological markers as a screening test in family

members of patients with celiac disease. J Pediatr 

Gastroenterol Nutr 1994;19(3):304-309. Not about 

consequences of testing 

Vitoria J C, Arrieta A, Ortiz L et al. Antibodies to

human tissue transglutaminase for the diagnosis of

celiac disease. J Pediatr Gastroenterol Nutr 

2001;33(3):349-350. Not about consequences of

testing 

Vitoria J C, Castano L, Rica I et al. Association of

insulin-dependent diabetes mellitus and celiac disease: 

a study based on serologic markers. J Pediatr 

Gastroenterol Nutr 1998;27(1):47-52. Not about 

consequences of testing 

Vivas Santiago, Ruiz de, Morales Jose M et al. Human 

recombinant anti-transglutaminase antibody testing is

useful in the diagnosis of silent coeliac disease in a 

selected group of at-risk patients. Eur J Gastroenterol 

Hepatol 2003;15(5):479-483. Not about consequences 

of testing 

Vjero Katerina, Martucci Susi, Alvisi Costanza et al.

Defining a proper setting for endoscopy in coeliac 

disease. Eur J Gastroenterol Hepatol 2003;15(6):675-

678. Not about consequences of testing 

Vogelsang H, Genser D, Wyatt J et al. Screening for 

celiac disease: a prospective study on the value of

noninvasive tests. Am J Gastroenterol 1995;90(3):394-

398. Not about consequences of testing 

Vogelsang H, Schwarzenhofer M, Oberhuber G. 

Changes in gastrointestinal permeability in celiac

disease. Dig Dis 1998;16(6):333-336. Not about 

consequences of testing 

Vogelsang H, Wyatt J, Penner E et al. Screening for 

celiac disease in first-degree relatives of patients with 

celiac disease by lactulose/mannitol test. Am J

Gastroenterol 1995;90(10):1838-1842. Not about 

consequences of testing 

Vogelsang H. The changing features of celiac disease.

Preface. Dig Dis 1998;16(6):328-329. Not about 

consequences of testing 

Volta U, De Franceschi L, Lari F et al. Coeliac disease 

hidden by cryptogenic hypertransaminasaemia. Lancet

1998;352(9121):26-29. Not about consequences of

testing 

Volta U, De Franceschi L, Molinaro N et al. 

Frequency and significance of anti-gliadin and antiendomysial antibodies in autoimmune hepatitis. Dig 

Dis Sci 1998;43(10):2190-2195. Not about 

consequences of testing 

Volta U, Granito A, De Franceschi L et al. Anti tissue

transglutaminase antibodies as predictors of silent 

coeliac disease in patients with 

hypertransaminasaemia of unknown origin. Digestive 

and Liver Disease - Official Journal of the Italian

Society of Gastroenterology and the Italian

Association for the Study of the Liver 2001;33(5):420-

425. Not about consequences of testing 

Volta U, Lazzari R, Guidetti C S et al. Multicenter 

study on the reproducibility of antigliadin (AGA) and 

antiendomysial antibodies (EmA) in celiac sprue 

screening. The Tenue Club Group. J Clin 

Gastroenterol 1994;19(1):81-82. Not about 

consequences of testing 

Volta U, Lenzi M, Lazzari R et al. Antibodies to

gliadin detected by immunofluorescence and a microELISA method: markers of active childhood and adult 

coeliac disease. Gut 1985;26(7):667-671. Not about 

consequences of testing 

Volta U, Molinaro N, De Franceschi L et al. Human 

umbilical cord as substrate for IgA antiendomysial 

antibodies allows large scale screening for celiac 

sprue. J Clin Gastroenterol 1996;23(1):18-20. Not 

about consequences of testing 

Volta U, Molinaro N, De Franceschi L et al. IgA antiendomysial antibodies on human umbilical cord tissue 

for celiac disease screening. Save both money and 

monkeys. Dig Dis Sci 1995;40(9):1902-1905. Not 

about consequences of testing 

Volta U, Molinaro N, De Franchis R et al. Correlation 

between IgA antiendomysial antibodies and subtotal 

villous atrophy in dermatitis herpetiformis. J Clin

Gastroenterol 1992;14(4):298-301. Not about 

consequences of testing 

Volta U, Molinaro N, Fratangelo D et al. IgA 

antibodies to jejunum. Specific immunity directed 

against target organ of gluten-sensitive enteropathy. 

Dig Dis Sci 1994;39(9):1924-1929. Not about 

consequences of testing 

Volta U, Molinaro N, Fusconi M et al. IgA 

antiendomysial antibody test. A step forward in celiac 

disease screening. Dig Dis Sci 1991;36(6):752-756. 

Not about consequences of testing 

Volta U, Ravaglia G, Granito A et al. Coeliac disease

in patients with autoimmune thyroiditis. Digestion 

2001;64(1):61-65. Not about consequences of testing 

Volta Umberto, Rodrigo Luis, Granito Alessandro et 

al. Celiac disease in autoimmune cholestatic liver

disorders. Am J Gastroenterol 2002;97(10):2609-

2613. Not about consequences of testing 

A-650
Vuoristo M, Tilvis R, Miettinen T A. Serum plant 

sterols and lathosterol related to cholesterol absorption 

in coeliac disease. Clin Chim Acta 1988;174(2):213-

224. Not about consequences of testing 

Wagner Mary H, Bowser Ellen K, Sherman James M 

et al. Comparison of steatocrit and fat absorption in

persons with cystic fibrosis. J Pediatr Gastroenterol 

Nutr 2002;35(2):202-205. Not about consequences of 

testing 

Wahab P J, Meijer J W R, Goerres M S et al. Coeliac

disease: changing views on gluten-sensitive

enteropathy. Scand J Gastroenterol 

2002;236(Suppl):60-65. Not about consequences of

testing 

Wahab P J, Meijer Jos W R, Dumitra D et al. Coeliac 

disease: more than villous atrophy. Rom J 

Gastroenterol 2002;11(2):121-127. Not about 

consequences of testing 

Wahab PJ, Meijer Jos WR, Mulder CJJ. Histologic

follow-up of people with celiac disease on a glutenfree diet: slow and incomplete recovery. Am J Clin 

Pathol 2002; 118(3):459-463. Not about consequences 

of testing 

Walker-Smith J A. Celiac disease and Down 

syndrome. Eur J Pediatr 2000;137(6):743-744. Not 

about consequences of testing 

Walker-Smith J A. Diabetes and coeliac disease.

Lancet 1969;2(7634):1366Not about consequences of 

testing 

Walker-Smith J A. Transient gluten intolerance. Arch 

Dis Child 1972;47(251):155Not about consequences 

of testing 

Walker-Smith J. Cow's milk protein intolerance.

Transient food intolerance of infancy. Arch Dis Child 

1975;50(5):347-350. Not about consequences of

testing 

Walker-Smith J. Transient gluten intolerance. Arch

Dis Child 1970;45(242):523-526. Not about 

consequences of testing 

Walkowiak J, Herzig K H. Fecal elastase-1 is 

decreased in villous atrophy regardless of the 

underlying disease. Eur J Clin Invest 2001;31(5):425-

430. Not about consequences of testing 

Walkowiak Jaroslaw, Herzig Karl, Strzykala Krystyna

et al. Fecal elastase-1 is superior to fecal chymotrypsin 

in the assessment of pancreatic involvement in cystic 

fibrosis. Pediatrics 2002;110(1 Pt 1):E7Not about 

consequences of testing 

Waller S L, Mottaleb A, Wiggins H S et al. Further 

observations on the Lundh test meal in the diagnosis 

of pancreatic disease. Gut 1971;12(10):869Not about 

consequences of testing 

Ward Jeanette E, Boyle Kate, Redman Selina et al.

Increasing women's compliance with opportunistic 

cervical cancer screening: A randomized trial. Am J

Prev Med 1991;7(5):285-291. Not about consequences 

of testing 

Watson R G, McMillan S A, Dickey W et al.

Detection of undiagnosed coeliac disease with atypical 

features using antireticulin and antigliadin antibodies. 

Q J Med 1992;84(305):713-718. Not about 

consequences of testing 

Wauters E A, Jansen J, Houwen R H et al. Serum IgG 

and IgA anti-gliadin antibodies as markers of mucosal 

damage in children with suspected celiac disease upon 

gluten challenge. J Pediatr Gastroenterol Nutr

1991;13(2):192-196. Not about consequences of

testing 

Weile B, Grodzinsky E, Skogh T et al. Screening 

Danish blood donors for antigliadin and

antiendomysium antibodies. Acta Paediatr

1996;412(Suppl):46Not about consequences of testing 

Weile B. Aspects of classic symptomatic childhood 

coeliac disease in Denmark: Retrospectively 

illustrated by local, regional, and national studies.

APMIS Suppl 2003;111(113):5-46. Not about 

consequences of testing 

Weile I, Grodzinsky E, Skogh T et al. High prevalence 

rates of adult silent coeliac disease, as seen in Sweden,

must be expected in Denmark. APMIS

2001;109(11):745-750. Not about consequences of

testing 

Weinstein W M, Brow J R, Parker F et al. The small 

intestinal mucosa in dermatitis herpetiformis. II. 

Relationship of the small intestinal lesion to gluten. 

Gastroenterology 1971;60(3):362-369. Not about 

consequences of testing 

Weinstein W M. Latent celiac sprue. Gastroenterology

1974;66(4):489-493. Not about consequences of

testing 

Weir D G, Hourihane D O. Coeliac disease during the

teenage period: the value of serial serum folate 

estimations. Gut 1974;15(6):450-457. Not about 

consequences of testing 

Weizman Z, Forstner G G, Gaskin K J et al. 

Bentiromide test for assessing pancreatic dysfunction 

using analysis of para-aminobenzoic acid in plasma 

and urine. Studies in cystic fibrosis and Shwachman's

syndrome. Gastroenterology 1985;89(3):596-604. Not 

about consequences of testing 

Weizman Z, Hamilton J R, Kopelman H R et al.

Treatment failure in celiac disease due to coexistent 

A-651
exocrine pancreatic insufficiency. Pediatrics

1987;80(6):924-926. Not about consequences of

testing 

West J, Lloyd C A, Hill P G et al. IgA-antitissue 

transglutaminase: validation of a commercial assay for 

diagnosing coeliac disease. Clin Lab 2002;48(5-

6):241-246. Not about consequences of testing 

Whitfield C R. Obstetric sprue. J Obstet Gynaecol Br 

Commonw 1970;77(7):577-586. Not about 

consequences of testing 

Whorwell P J, Alderson M R, Foster K J et al. Death 

from ischaemic heart-disease and malignancy in adult

patients with coeliac disease. Lancet

1976;2(7977):113-114. Not about consequences of

testing 

Williams A J, Annis P, Lock R J et al. Evaluation of a

high-throughput second antibody radiobinding assay

for measuring IgA antibodies to human tissue 

transglutaminase. J Immunol Methods 1999;228(1-

2):81-85. Not about consequences of testing 

Williams A J, Norcross A J, Lock R J et al. The high 

prevalence of autoantibodies to tissue 

transglutaminase in first-degree relatives of patients 

with type 1 diabetes is not associated with islet 

autoimmunity. Diabetes Care 2001;24(3):504-509. 

Not about consequences of testing 

Wills A J, Turner B, Lock R J et al. Dermatitis 

herpetiformis and neurological dysfunction. J Neurol 

Neurosurg Psychiatry 2002;72(2):259-261. Not about 

consequences of testing 

Wills A J. The neurology and neuropathology of 

coeliac disease. Neuropathol Appl Neurobiol

2000;26(6):493-496. Not about consequences of

testing 

Wilson C, Eade O E, Elstein M et al. Subclinical

coeliac disease and infertility. Br Med J 

1976;2(6029):215-216. Not about consequences of

testing 

Wilson F A, Dietschy J M. Differential diagnostic 

approach to clinical problems of malabsorption. 

Gastroenterology 1971;61(6):911-931. Not about 

consequences of testing 

Winston A P. Physical assessment of the eating

disordered patient. European Eating Disorders Review 

2000;8(2):188-191. Not about consequences of testing 

Wolford George L, Rosenberg Stanley D, Drake 

Robert E et al. Evaluation of methods for detecting 

substance use disorder in persons with severe mental 

illness. Psychol Addict Behav 1999;13(4):313-326. 

Not about consequences of testing 

Wolters Victorien, Vooijs-Moulaert Anne, Burger

Huib et al. Human tissue transglutaminase enzyme

linked immunosorbent assay outperforms both the 

guinea pig based tissue transglutaminase assay and 

anti-endomysium antibodies when screening for 

coeliac disease. Eur J Pediatr 2002;161(5):284-287. 

Not about consequences of testing 

Wong R C W, Wilson R J, Steele R H et al. A 

comparison of 13 guinea pig and human anti-tissue 

transglutaminase antibody ELISA kits. Am J Clin 

Pathol 2002;55(7):488-494. Not about consequences 

of testing 

Woolley Niina, Holopainen Paivi, Ollikainen Vesa et

al. A new locus for coeliac disease mapped to 

chromosome 15 in a population isolate. Hum Genet 

2002;111(1):40-45. Not about consequences of testing 

Worden John K, Mickey Ruth M, Flynn Brian S et al. 

Development of a community breast screening

promotion program using baseline data. Am J Prev

Med 1994;23(3):267-275. Not about consequences of 

testing 

Wray D, Ferguson M M, Mason D K et al. Recurrent 

aphthae: treatment with vitamin B12, folic acid, and 

iron. Br Med J 1975;2(5969):490-493. Not about 

consequences of testing 

Yeboah F A, White D. AlphaB-crystallin expression 

in celiac disease - a preliminary study. Croat Med J

2001;42(5):523-526. Not about consequences of

testing 

Yiannakou J Y, Dell'Olio D, Saaka M et al. Detection

and characterisation of anti-endomysial antibody in 

coeliac disease using human umbilical cord. Int Arch 

Allergy Immunol 1997;112(2):140-144. Not about 

consequences of testing 

Young G P, Hebbard G S. Diagnostic techniques for 

small intestinal disease. Curr Opin Gastroenterol 

1992;8(2):232-238. Not about consequences of testing 

Zachor D A, Mroczek-Musulman E, Brown P.

Prevalence of celiac disease in Down syndrome in the

United States. J Pediatr Gastroenterol Nutr 

2000;31(3):275-279. Not about consequences of

testing 

Zadik Z, Kowarski A. Incidence of neurosecretory

dysfunction among children aged 6-14 years in

Rehovot, Israel. Acta Paediatr Scand Suppl 

1989;34977-83. Not about consequences of testing 

Zalev A H, Gardiner G W, Warren R E. NSAID injury

to the small intestine. Abdom Imaging 1998;23(1):40-

44. Not about consequences of testing 

Zauli D, Grassi A, Granito A et al. Prevalence of silent

coeliac disease in atopics. Digestive and Liver Disease 

- Official Journal of the Italian Society of 

A-652
Gastroenterology and the Italian Association for the 

Study of the Liver 2000;32(9):775-779. Not about 

consequences of testing 

Zhong F, McCombs C C, Olson J M et 

al. An autosomal screen for genes that 

predispose to celiac disease in the 

western counties of Ireland. Nat Genet 

1996;14(3):329-333. Not about 

consequences of testing 

Zipser Robert D, Patel Sunil, Yahya Kareem Z et al.

Presentations of adult celiac disease in a nationwide 

patient support group. Dig Dis Sci 2003;48(4):761-

764. Not about consequences of testing 

Zouganelis S, Priest M. Impact of dietary compliance 

on nutritional status in adult coeliac disease. Gut 2001; 

48(Suppl 1):A42. Unable to obtain article 

Zwolak R M. Can duplex ultrasound replace 

arteriography in screening for mesenteric ischemia?.

Semin Vasc Surg 1999;12(4):252-260. Not about 

consequences of testing 

Objective 5 – Promoting or Monitoring Adherence to a GFD 

Abdulkarim A S, Murray J A. Celiac disease. Curr

Treat Options Gastroenterol. 2002;5(1):27-38. Not 

relevant to adherence 

Addolorato G, Capristo E, Ghittoni G et al. Anxiety

but not depression decreases in coeliac patients after 

one-year gluten-free diet: a longitudinal study. Scand 

J Gastroenterol 2001;36(5):502-506. Not relevant to

adherence 

Addolorato G, Stefanini G F, Capristo E et al. Anxiety

and depression in adult untreated celiac subjects and 

in patients affected by inflammatory bowel disease: A 

personality 'trait' or a reactive illness?. 

Hepatogastroenterology 1996;43(12):1513-1517. Not 

relevant to adherence 

Al Bayaty HF, Aldred MJ, Walker DM et al. Salivary and

serum antibodies to gliadin in the diagnosis of celiac 

disease. J Oral Pathol Med 1989; 18(10):578-581. No 

correlations with other measures 

Amari A, Grace N C, Fisher W W. Achieving and 

Maintaining Compliance With the Ketogenic Diet. J Appl 

Behav Anal 1995;28(3):341-342. Not relevant to adherence 

Amin Rakesh, Murphy Nuala, Edge Julie et al. A 

longitudinal study of the effects of a gluten-free diet on

glycemic control and weight gain in subjects with type 1

diabetes and celiac disease. Diabetes Care

2002;25(7):1117-1122. Not relevant to adherence 

Anderson R P, Degano P, Godkin A J et al. In vivo antigen

challenge in celiac disease identifies a single 

transglutaminase-modified peptide as the dominant Agliadin T-cell epitope. Nat Med 2000;6(3):337-342. Not 

relevant to adherence 

Andersson H, Bjorkman A C, Gillberg R et al. Influence of

the amount of dietary gluten on gastrointestinal 

morphology and function in dermatitis herpetiformis. 

Human Nutrition.Clinical Nutrition 1984;38(4):279-285. 

Not relevant to adherence 

Andersson H, Mobacken H. Dietary treatment of dermatitis

herpetiformis. Eur J Clin Nutr 1992;46(5):309-315. Not 

relevant to adherence 

Andre F, Andre C, Colin L et al. Role of new allergens and

of allergens consumption in the increased incidence of food 

sensitizations in France. Toxicology 1994;93(1):77-83. Not

relevant to adherence 

Andrews A. Coeliac disease: new aspects. BNF Nutrition

Bulletin 1999;24(87):66-70. Not relevant to adherence 

Annibale B, Severi C, Chistolini A et al. Efficacy of glutenfree diet alone on recovery from iron deficiency anemia in

adult celiac patients. Am J Gastroenterol 2001;96(1):132-

137. Not relevant to adherence 

Anonymous. A long-term survey of coeliac disease. Med J 

Aust 1971;2(20):992Not relevant to adherence 

Anonymous. Catch-up growth in celiac disease. Nutr Rev

1973;31(1):13-14. Not relevant to adherence 

Anonymous. Celiac disease and how to live with it. 

Harvard Women's Health Watch 2001;8(9):3-4. Not 

relevant to adherence 

Anonymous. Celiac disease. Am Fam Phys

1998;57(5):1039-1041. Not relevant to adherence 

Anonymous. Growing up with coeliac disease. Lancet

1988;2(8622):1231-1232. Not relevant to adherence 

Anonymous. Oats safe for coeliac disease patients. Pharm J

2002;268(7185):200Not relevant to adherence 

Ansaldi N, Dell'Olio D, Tavassoli K et al. Dietary habits 

and social aspects of patients with coeliac disease. Minerva 

Med 1992;83(7-8):439-443. Not relevant to adherence 

Ansaldi-Balocco N, Malorgio E, Faussone D et al. 

Hydrogen breath-test in coeliac disease. Hydrogen 

A-653
excretion is related to jejunal histological changes. Minerva 

Pediatr 1994;46(12):569-574. No monitoring measure of 

interest 

Ascher H. Paediatric aspects of coeliac disease: old 

challenges and new ones... Digestive and Liver Disease -

Official Journal of the Italian Society of Gastroenterology

and the Italian Association for the Study of the Liver 

2002;34(3):216-224. Not relevant to adherence 

Ashkenazi A, Levin S, Idar D et al. Cellular immunity in

children with coeliac disease. Eur J Pediatr 

1982;138(3):250-253. Not relevant to adherence 

Ashkenazi A. Living with celiac disease. Child Hosp Q 

1989;1(3):265-271. Not relevant to adherence 

Asquith P. Adult coeliac disease and malignancy. Ir Med J 

1974;67(15):417-420. Not relevant to adherence 

Atkinson K, Tokmakajian S, Watson W et al. Evaluation of 

the endomysial antibody for celiac disease: operating 

properties and associated cost implications in clinical

practice. Can J Gastroenterol 1997;11(8):673-677. Not 

relevant to adherence 

Auricchio S, Greco L, Troncone R. Gluten-sensitive 

enteropathy in childhood. Pediatr Clin North Am 

1988;35(1):157-187. Not relevant to adherence 

Auricchio S, Troncone R. Effects of small amounts of 

gluten in the diet of coeliac patients. Panminerva Med 

1991;33(2):83-85. Not relevant to adherence 

Austin A S, Logan R F A, Thomason K et al. Cigarette 

smoking and adult coeliac disease. Scand J Gastroenterol 

2002;37(8):978-982. Not relevant to adherence 

Bachle T, Ruhl U, Ott G et al. Enteropathy-associated Tcell lymphoma, presenting as diet-refractory coeliac 

disease. Dtsch Med Wochenschr 2001;126(51-52):1460-

1463. Not relevant to adherence 

Bai J C, Gonzalez D, Mautalen C et al. Long-term effect of 

gluten restriction on bone mineral density of patients with 

coeliac disease. Aliment Pharmacol Ther 1997;11(1):157-

164. Not relevant to adherence 

Bai J, Moran C, Martinez C et al. Celiac sprue after surgery

of the upper gastrointestinal tract. Report of 10 patients 

with special attention to diagnosis, clinical behavior, and

follow-up. J Clin Gastroenterol 1991;13(5):521-524. Not 

relevant to adherence 

Bardella M T, Fraquelli M, Quatrini M et al. Prevalence of 

hypertransaminasemia in adult celiac patients and effect of

gluten-free diet. J Gastroenterol Hepatol 1995;22(3):833-

836. Not relevant to adherence 

Bardella M T, Fredella C, Prampolini L et al. Body

composition and dietary intakes in adult celiac disease 

patients consuming a strict gluten-free diet. Am J Clin Nutr

2000;72(4):937-939. Not relevant to adherence 

Bardella M T, Molteni N, Prampolini L et al. Need for 

follow up in coeliac disease. Arch Dis Child

1994;70(3):211-213. Not relevant to adherence 

Bardella M T, Molteni N, Quatrini M et al. Clinical, 

biochemical and histological abnormalities in adult celiac 

patients on gluten-free diet. Gastroenterol Clin Biol 

1985;9(11):787-789. Not relevant to adherence 

Barera G, Mora S, Brambilla P et al. Body composition in

children with celiac disease and the effects of a gluten-free 

diet: a prospective case-control study. Am J Clin Nutr 

2000;72(1):71-75. Not relevant to adherence 

Barna M, Pinter E. Anti-gliadin and anti-endomysium 

antibodies in children with celiac disease consuming a 

gluten free diet. Z Ernahrungswiss 1998;37(Suppl 1):103-

105. Monitoring not serology, EMA, tTG or biopsy based, 

or not promoting GFD adherence 

Bentley A C. A survey of celiac-sprue patients: effect of 

dietary restrictions on religious practices. J Gen Psychol 

1988;115(1):7-14. Not relevant to adherence 

Berger R, Schmidt G. Evaluation of six anti-gliadin 

antibody assays. J Immunol Methods 1996; 191(1):77-86. 

Not relevant to adherence 

Bhatia K P, Brown P, Gregory R et al. Progressive 

myoclonic ataxia associated with coeliac disease: The 

myoclonus is of cortical origin, but the pathology is in the 

cerebellum. Brain Dev 1995;118(5):1087-1093. Not 

relevant to adherence 

Biagi F, Corazza G R. A review on ulcerative jejunoileitis: 

LA JEJUNO-ILEITE ULCEREUSE: REVUE DE LA 

LITTERATURE. Acta Endoscopica 2001;31(3):265-269. 

Not relevant to adherence 

Biagi F, Parnell N D, Ellis H J et al. Endomysial antibody

production is not related to histological damage after in 

vitro gluten challenge. Eur J Gastroenterol Hepatol 

2000;12(1):57-60. Not relevant to adherence 

Bjornsson E, Janson C, Plaschke P et al. Prevalence of

sensitization to food allergens in adult Swedes. Ann 

Allergy Asthma Immunol 1996;77(4):327-332. Not 

relevant to adherence 

Blazer S, Naveh Y, Berant M et al. Serum IgG antibodies 

to gliadin in children with celiac disease as measured by an 

immunofluorescence method. J Pediatr Gastroenterol Nutr

1984; 3(2):205-209. Not relevant to adherence 

Boersma B, Houwen R H J, Blum W F et al. Catch-up 

growth and endocrine changes in childhood celiac disease. 

Endocrine changes during catch-up growth. Horm Res 

2002;58(Suppl 1):57-65. Not relevant to adherence 
Bonamico M, Mariani P, Mazzilli M C et al. Frequency and 

clinical pattern of celiac disease among siblings of celiac 

children. J Pediatr Gastroenterol Nutr 1996;23(2):159-163. 

Not relevant to adherence 

Bonamico M, Morellini M, Mariani P et al. HLA antigens 

and antigliadin antibodies in coeliac disease. Dis Markers 

1991;9(6):313-317. Not relevant to adherence 

Booth I W. The nutritional consequences of gastrointestinal

disease in adolescence. Acta Paediatrica

Scandinavica.Supplement; 1991;37391-102. Not relevant to 

adherence 

Bottaro G, Failla P, Rotolo N et al. Changes in coeliac 

disease behaviour over the years. Acta Paediatr 1993;82(6-

7):566-568. Not relevant to adherence 

Brink S J. Pediatric, adolescent, and young-adult nutrition

issues in IDDM. Diabetes Care 1988;11(2):192-200. Not 

relevant to adherence 

Broberg A, Engstrom I, Kalimo K et al. Elimination diet in 

young children with atopic dermatitis. Acta Derm-Venereol 

1992;72(5):365-369. Not relevant to adherence 

Burrows R, Leiva L, Burgueno M et al. Bone mineral

density (BMD) in children with celiac disease (CD): Its

relation to puberty and calcium intake. Nutr Res 

1999;19(4):493-499. Not relevant to adherence 

Butterfield J H, Murray J A. Eosinophilic gastroenteritis 

and gluten-sensitive enteropathy in the same patient. J Clin

Gastroenterol 2002;34(5):552-553. Not relevant to 

adherence 

Butterworth JR, Banfield L, Iqbal TH et al. What factors 

influence compliance with a gluten-free diet? A

comparison of white caucasian and South Asian coeliac 

patients. Gut 2002; 50(Suppl 2):A18. No correlations with 

other measures 

Byrne M F, Razak A R A, Leader M B et al. Disabling 

osteomalacic myopathy as the only presenting feature of

coeliac disease. Eur J Gastroenterol Hepatol

2002;14(11):1271-1274. Not relevant to adherence 

Campbell J A, Molloy M K, Davidson A G F et al. Dietary

aspects from national survey of persons with celiac disease 

and dermatitis herpetiformis. J Can Diet Assoc 

1991;52(3):161-165. Not relevant to adherence 

Campbell J A. Diet therapy of celiac disease and dermatitis

herpetiformis. World Rev Nutr Diet 1987;51189-233. Not 

relevant to adherence 

Campbell J A. Dietary management of celiac disease: 

variations in the gluten-free diet. J Can Diet Assoc 

1992;53(1):15-18. Not relevant to adherence 

Capristo E, Addolorato G, Mingrone G et al. Changes in 

body composition, substrate oxidation, and resting 

metabolic rate in adult celiac disease patients after a 1-y 

gluten-free diet treatment. Am J Clin Nutr 2000;72(1):76-

81. Not relevant to adherence 

Capristo E, Mingrone G, Addolorato G et al. Differences in

metabolic variables between adult coeliac patients at

diagnosis and patients on a gluten-free diet. Scand J 

Gastroenterol 1997;32(12):1222-1229. Not relevant to

adherence 

Cardenas A, Kelly C P. Celiac sprue. Semin Gastrointest

Dis 2002;13(4):232-244. Not relevant to adherence 

Carpino F, Ceccamea A, Magliocca FM et al. Scanning 

electron microscopy of jejunal biopsies in patients with 

untreated and treated coeliac disease. Acta Paediatr Scand

1985; 74(5):775-781. Not relevant to adherence 

Carroccio A, Iacono G, Montalto G et al. Pancreatic 

enzyme therapy in childhood celiac disease. A double-blind

prospective randomized study. Dig Dis Sci 

1995;40(12):2555-2560. Not relevant to adherence 

Casellas F, De Torres I, Malagelada J-R. Follow-up of 

celiac disease with D-xylose breath test. Dig Dis Sci 

1996;41(10):2106-2111. Not relevant to adherence 

Cataldo F, Lio D, Marino V et al. IgG(1) antiendomysium 

and IgG antitissue transglutaminase (anti-tTG) antibodies

in coeliac patients with selective IgA deficiency. Working 

Groups on Celiac Disease of SIGEP and Club del Tenue. 

Gut 2000;47(3):366-369. Not relevant to adherence 

Catassi C, Doloretta Macis M, Ratsch I-M et al. The

distribution of DQ genes in the Saharawi population 

provides only a partial explanation for the high celiac 

disease prevalence. Tissue Antigens 2001;58(6):402-406. 

Not relevant to adherence 

Catassi C, Rossini M, Ratsch I M et al. Dose dependent 

effects of protracted ingestion of small amounts of gliadin 

in coeliac disease children: a clinical and jejunal 

morphometric study. Gut 1993;34(11):1515-1519. Not 

relevant to adherence 

Catassi C. Intestinal permeability tests: Research or

diagnosis?. Pediatric Reviews and Communications 

1993;7(3):202-205. Not relevant to adherence 

Cellier C, Cervoni J P, Patey N et al. Gluten-free diet

induces regression of T-cell activation in the rectal mucosa

of patients with celiac disease. Am J Gastroenterol 

1998;93(9):1527-1530. Not relevant to adherence 

Chapman BL, Henry K, Paice F et al. Measuring the 

response of the jejunal mucosa in adult coeliac disease to 

treatment with a gluten-free diet. Gut 1974; 15(11):870-

874. Not relevant to adherence 

Chartrand L J, Russo P A, Duhaime A G et al. Wheat

starch intolerance in patients with celiac disease. J Am Diet 

Assoc 1997;97(6):612-618. Not relevant to adherence 
Ciacci C, Cirillo M, Mellone M et al. Hypocalciuria in 

overt and subclinical celiac disease. Am J Gastroenterol 

1995;90(9):1480-1484. Not relevant to adherence 

Ciacci C, De Rosa A, de Michele G et al. Sexual behaviour

in untreated and treated coeliac patients. Eur J

Gastroenterol Hepatol 1998;10(8):649-651. Not relevant to 

adherence 

Ciacci C, Di Vizio D, Seth R et al. Selective reduction of 

intestinal trefoil factor in untreated coeliac disease. Clin

Exp Immunol 2002;130(3):526-531. Not relevant to 

adherence 

Ciacci C, Iavarone A, Mazzacca G et al. Depressive 

symptoms in adult coeliac disease. Scand J Gastroenterol 

1998;33(3):247-250. Not relevant to adherence 

Ciacci C, Maurelli L, Klain M et al. Effects of dietary 

treatment on bone mineral density in adults with celiac

disease: factors predicting response. Am J Gastroenterol 

1997;92(6):992-996. Not relevant to adherence 

Ciacci Carolina, Iavarone Alessandro, Siniscalchi Monica 

et al. Psychological dimensions of celiac disease: toward an

integrated approach. Dig Dis Sci 2002;47(9):2082-2087. 

Not relevant to adherence 

Ciampolini M, Bini S. Serum lipids in celiac children. J

Pediatr Gastroenterol Nutr 1991; 12(4):459-460. No 

correlations with other measures 

Ciclitira P J, Ellis H J, Evans D J et al. A 

radioimmunoassay for wheat gliadin to assess the 

suitability of gluten free foods for patients with coeliac 

disease. Clin Exp Immunol 1985;59(3):703-708. Not 

relevant to adherence 

Ciclitira P J. Recent advances in coeliac disease. Clin Med

2003;3(2):166-169. Not relevant to adherence 

Cinquetti M, Trabucchi C, Menegazzi N et al. 

Psychological problems connected to the dietary

restrictions in the adolescent with coeliac disease. La

Pediatria Medica E Chirurgica - Medical and Surgical

Pediatrics 1999;21(6):279-283. Not relevant to adherence 

Cocchi Renato. Toilet habits in drugs treated downs: A 

survey on 209 subjects. Italian Journal of Intellective 

Impairment 1997;10(1):13-17. Not relevant to adherence 

Colaco J, Egan-Mitchell B, Stevens FM et al. Compliance

with gluten free diet in coeliac disease. Arch Dis Child 

1987; 62(7):706-708. Not relevant to adherence 

Collin P, Hallstrom O, Maki M et al. Atypical coeliac 

disease found with serologic screening. Scand J 

Gastroenterol 1990;25(3):245-250. Not relevant to 

adherence 

Collin P, Pirttilae T, Nurmikko T et al. Celiac Disease, 

Brain Atrophy, and Dementia. Neurology 1991;41(3):372-

375. Not relevant to adherence 

Collin P, Reunala T. Recognition and management of the 

cutaneous manifestations of celiac disease: A guide for

dermatologists. Am J Clin Dermatol 2003;4(1):13-20. Not 

relevant to adherence 

Collins B J, Bell P M, Boyd S et al. Endocrine and exocrine

pancreatic function in treated coeliac disease. Pancreas

1986;1(2):143-147. Not relevant to adherence 

Collins B J, Bell P M, Thomson J M et al. Dietary history 

and nutritional state in treated coeliac patients. J R Soc 

Med 1986;79(4):206-209. Not relevant to adherence 

Congdon P, Mason MK, Smith S et al. Small-bowel 

mucosa in asymptomatic children with celiac disease.

Mucosal changes with gluten-free diets. Am J Dis Child 

1981; 135(2):118-121. Not relevant to adherence 

Corazza G R, Di Sario A, Sacco G et al. Subclinical coeliac

disease: an anthropometric assessment. J Intern Med 

1994;236(2):183-187. No monitoring measure of interest 

Corazza G R, Di Stefano M, Jorizzo R A et al. Propeptide 

of type I procollagen is predictive of posttreatment bone 

mass gain in adult celiac disease. Gastroenterology

1997;113(1):67-71. Not relevant to adherence 

Corrao G, Corazza G R, Bagnardi V et al. Mortality in

patients with coeliac disease and their relatives: a cohort 

study. Lancet 2001;358(9279):356-361. Not relevant to 

adherence 

Corvaglia L, Catamo R, Pepe G et al. Depression in adult 

untreated celiac subjects: Diagnosis by the pediatrician. Am

J Gastroenterol 1999;94(3):839-843. Not relevant to

adherence 

Crofton R W, Glover S C, Ewen S W et al. Zinc absorption 

in celiac disease and dermatitis herpetiformis: a test of 

small intestinal function. Am J Clin Nutr 1983;38(5):706-

712. No monitoring measure of interest 

Cronin C C, Feighery A, Ferriss J B et al. High prevalence

of celiac disease among patients with insulin-dependent 

(type I) diabetes mellitus. Am J Gastroenterol 

1997;92(12):2210-2212. Not relevant to adherence 

Cronin Cornelius C, Shanahan Fergus. Exploring the 

iceberg--the spectrum of celiac disease. Am J Gastroenterol 

2003;98(3):518-520. Not relevant to adherence 

Cummins A G, Thompson F M, Butler R N et al. 

Improvement in intestinal permeability precedes

morphometric recovery of the small intestine in coeliac 

disease. Clinical Science (London, England - 1979) 

2001;100(4):379-386. Not relevant to adherence 
Cuoco L, Cammarota G, Tursi A et al. Disappearance of

gastric mucosa-associated lymphoid tissue in coeliac

patients after gluten withdrawal. Scand J Gastroenterol

1998;33(4):401-405. Not relevant to adherence 

Cuomo A, Romano M, Rocco A et al. Reflux oesophagitis

in adult coeliac disease: beneficial effect of a gluten free

diet. Gut 2003;52(4):514-517. Not relevant to adherence 

Curione M, Barbato M, Viola F et al. Idiopathic dilated 

cardiomyopathy associated with coeliac disease: The effect

of a gluten-free diet on cardiac performance. Dig Dis Sci 

2002;34(12):866-869. Not relevant to adherence 

Dahele A, V, Aldhous MC, Humphreys K et al. Serum IgA 

tissue transglutaminase antibodies in coeliac disease and 

other gastrointestinal diseases. Q J Med 2001; 94(4):195-

205. Not relevant to adherence 

Damen G M, Boersma B, Wit J M et al. Catch-up growth in

60 children with celiac disease. J Pediatr Gastroenterol

Nutr 1994;19(4):394-400. Not relevant to adherence 

Damoiseaux J G M C, Tervaert J W C. Celiac disease: the

role of (auto)antibody detection in diagnosis and follow-up. 

Neth J Med 2002;60(7):303-304. Review article 

Daniels D E, Rene A A, Daniels V R. Race: an Explanation 

of Patient Compliance: Fact or Fiction?. J Natl Med Assoc 

1994;86(1):20-25. Not relevant to adherence 

Davis M K. Breastfeeding and chronic disease in childhood 

and adolescence. Pediatr Clin North Am 2001;48(1):125-

141. Not relevant to adherence 

De Lorenzo A, Di Campli C, Andreoli A et al. Assessment 

of body composition by bioelectrical impedance in 

adolescent patients with celiac disease. Am J Gastroenterol 

1999;94(10):2951-2955. Not relevant to adherence 

de Vries T W, Wierdsma N, van Ede J et al. Dieting in 

children referred to the paediatric outpatient clinic. Eur J 

Pediatr 2001;160(10):595-598. Not relevant to adherence 

Denman A M. Nature and diagnosis of food allergy. Proc 

Nutr Soc 1979;38(3):391-402. Not relevant to adherence 

Devine PL, Birrell GW, Golder JP et al. Screening and 

monitoring coeliac disease: multicentre trial of a new serum

antibody test kit. Dis Markers 1994; 12(1):71-80. Not 

relevant to adherence 

Di Sabatino A, Bertrandi E, Casadei Maldini M et al. 

Phenotyping of peripheral blood lymphocytes in adult 

coeliac disease. Immunology 1998;95(4):572-576. Not 

relevant to adherence 

Di Stefano M, Veneto G, Corrao G et al. Role of lifestyle 

factors in the pathogenesis of osteopenia in adult coeliac 

disease: A multivariate analysis. Eur J Gastroenterol 

Hepatol 2000;12(11):1195-1199. Not relevant to adherence 

Diamanti A, Maino C, Niveloni S et al. Characterization of

gastric mucosal lesions in patients with celiac disease: a

prospective controlled study. Am J Gastroenterol 

1999;94(5):1313-1319. Not relevant to adherence 

Dickey W, Bodkin S. Prospective study of body mass index 

in patients with coeliac disease. BMJ 

1998;317(7168):1290Not relevant to adherence 

Dimatteo M R, Giordani P J, Lepper H S et al. Patient 

Adherence and Medical Treatment Outcomes - a MetaAnalysis. Med Care 2002;40(9):794-811. Not relevant to 

adherence 

Dimatteo M R, Lepper H S, Croghan T W. Depression Is a 

Risk Factor for Noncompliance With Medical Treatment - 

Meta-Analysis of the Effects of Anxiety and Depression on 

Patient Adherence. Arch Intern Med 2000;160(14):2101-

2107. Not relevant to adherence 

Dinari G, Rosenbach Y, Marcus H et al. IgA antigliadin

antibodies in childhood celiac disease. Isr J Med Sci 

1988;24(6):286-290. Not relevant to adherence 

Dissanayake AS, Truelove SC, Whitehead R. Jejunal 

mucosal recovery in coeliac disease in relation to the

degree of adherence to a gluten-free diet. Q J Med 1974; 

43(170):161-185. Not relevant to adherence 

Dohan F C. Is celiac disease a clue to the pathogenesis of 

schizophrenia?. Ment Hyg 1969;53(4):525-529. Not 

relevant to adherence 

Donat Aliaga E, Polo Miquel B, Ribes-Koninckx C. 

Serological markers of celiac disease. Acta Pediatr Esp 

2003;61(1):24-32. Not relevant to adherence 

Dubel L, Absalon Y B, Baudon J J et al. Screening of 

coeliac disease: Optimal technique and serological marker.

Ann Biol Clin (Paris) 1996;54(7):303-306. Not relevant to

adherence 

Elsborg L, Mosbech J. Sprue: a follow-up study of an old 

series. Dan Med Bull 1978;25(5):205-206. Not relevant to

adherence 

Erdman John W. Factors that limit or enhance 

bioavailability of minerals from food. Nutrition & the Md 

1983;9(2):1-2. Not relevant to adherence 

Falth-Magnusson K, Franzen L, Jansson G et al. Infant 

feeding history shows distinct differences between Swedish 

celiac and reference children. Pediatric Allergy and 

Immunology - Official Publication of the European Society

of Pediatric Allergy and Immunology 1996;7(1):1-5. Not 

relevant to adherence 

Falzon L. Topic: Gluten-free diet of coeliac disease. J Clin 

Excellence 2001;3(4):209-211. Not relevant to adherence 

Fasano A, Catassi C. Current approaches to diagnosis and 

treatment of celiac disease: an evolving spectrum.
Gastroenterology 2001;120(3):636-651. Not relevant to 

adherence 

Fasano Alessio. Celiac disease--how to handle a clinical 

chameleon. N Engl J Med 2003;348(25):2568-2570. Not 

relevant to adherence 

Faulkner-Hogg K B, Selby W S, Loblay R H. Dietary

analysis in symptomatic patients with coeliac disease on a 

gluten-free diet: the role of trace amounts of gluten and 

non-gluten food intolerances. Scand J Gastroenterol 

1999;34(8):784-789. Not relevant to adherence 

Feighery C F. Coeliac disease: How much of what is toxic

to whom?. Gut 1998;43(2):164-165. Not relevant to 

adherence 

Ferfoglia G, Pulitano R, Sategna-Guidetti C. Do dietary

antibodies still play a role in the diagnosis and follow-up of 

coeliac disease? A comparison among different serological 

tests. Panminerva Med 1995; 37(2):55-59. Not relevant to

adherence 

Ferguson A, Denton-Miller P, Lai C L. Coeliac disease--

objectives of life-long follow-up. Health Bull (Edinb) 

1977;35(2):78-80. Not relevant to adherence 

Ferguson A. Symptoms and manifestations of food allergy,

with particular relevance to the gut. Environ Toxicol 

Pharmacol 1997;4(1-2):33-38. Not relevant to adherence 

Fernandez-Calle P, Codoceo R, Polanco I et al. Is an 

intestinal permeability test a valid marker for slight dietary 

transgressions in adolescents with coeliac disease?. Gut

1993;34(6):774-777. No monitoring measure of interest 

Fine K D, Meyer R L, Lee E L. The prevalence and causes

of chronic diarrhea in patients with celiac sprue treated

with a gluten-free diet. Gastroenterology

1997;112(6):1830-1838. Not relevant to adherence 

Finkel M, Gelb A M, Cohen N et al. Long-term follow-up 

study in idiopathic steatorrhea. Am J Gastroenterol 

1967;47(1):35-40. Not relevant to adherence 

Finn R. Food allergy - fact or fiction: A review. J R Soc 

Med 1992;85(9):560-564. Not relevant to adherence 

Flanagan D A, Wagner H L. Expressed Emotion and 

Panic^Fear in the Prediction of Diet Treatment 

Compliance. Br J Clin Psychol 1991;30(3):231-240. Not 

relevant to adherence 

Fois A, Vascotto M, Di Bartolo R M et al. Celiac disease 

and epilepsy in pediatric patients. Child's Nerv Syst 

1994;10(7):450-454. Not relevant to adherence 

Fox L A. Diabetes therapy in children: Setting ageappropriate goals. Drug Benefit Trends 2002;14(Suppl 

D):30-35+44. Not relevant to adherence 

Francesco Stefanini G, Resta F, Marsigli L et al. Prurigo 

nodularis (Hyde's prurigo) disclosing celiac disease. 

Hepatogastroenterology 1999;46(28):2281-2284. Not 

relevant to adherence 

Francis Dorothy E M. Inborn errors of metabolism: The 

need for sugar. J Hum Nutr 1979;33(2):146-154. Not 

relevant to adherence 

Freeman H J. Free perforation due to intestinal lymphoma 

in biopsy-defined or suspected celiac disease. J Clin 

Gastroenterol 2003;37(4):299-302. Not relevant to 

adherence 

Fried M W. Side effects of therapy of hepatitis C and their

management. J Gastroenterol Hepatol 2002;36(5 I):S237-

S244. Not relevant to adherence 

Friis S U. Enzyme-linked immunosorbent assay for 

quantitation of cereal proteins toxic in coeliac disease. Clin 

Chim Acta 1988;178(3):261-270. Not relevant to adherence 

Fry L, Seah P P, Riches D J et al. Clearance of skin lesions

in dermatitis herpetiformis after gluten withdrawal. Lancet

1973;1(7798):288-291. Not relevant to adherence 

Fuhrmann A, Kuhl J. Maintaining a Healthy Diet: Effects

of Personality and Self-Reward Versus Self-Punishment on 

Commitment to and Enactment of Self-Chosen and 

Assigned Goals. Psychol Health 1998;13(4):651-686. Not 

relevant to adherence 

Gabel L L, Latanick M R. Nutrition-related prevention: An

interdisciplinary strategy. J Fam Pract 1993;37(4):396-398. 

Not relevant to adherence 

Galli-Tsinopoulou A, Nousia-Arvanitakis S, Dracoulacos D 

et al. Autoantibodies predicting diabetes mellitus type I in 

celiac disease. Horm Res 1999;52(3):119-124. Not relevant

to adherence 

Garioch J J, Lewis H M, Sargent S A et al. 25 years'

experience of a gluten-free diet in the treatment of

dermatitis herpetiformis. Br J Dermatol 1994;131(4):541-

545. Not relevant to adherence 

Gawkrodger D J, Vestey J P, O'Mahony S et al. Dermatitis 

herpetiformis and established coeliac disease. Br J

Dermatol 1993;129(6):694-695. Not relevant to adherence 

Gemme G, Vignolo M, Naselli A et al. Linear growth and 

skeletal maturation in subjects with treated celiac disease. J

Pediatr Gastroenterol Nutr 1999;29(3):339-342. Not 

relevant to adherence 

Gillberg R, Ahren C. Coeliac disease diagnosed by means 

of duodenoscopy and endoscopic duodenal biopsy. Scand J 

Gastroenterol 1977; 12(8):911-916. Not relevant to 

adherence 

Gillett H R, Arnott I D R, McIntyre M et al. Successful 

infliximab treatment for steroid-refractory celiac disease: A 
case report. Gastroenterology 2002;122(3):800-805. Not 

relevant to adherence 

Gillett PM, Gillett HR, Israel DM et al. High prevalence of 

celaic disease in patients with type 1 diabetes detected by

antibodies to endomysium and tissue transglutaminase. Can

J Gastroenterol 2001; 15(5):297-301. Not relevant to

adherence 

Giomi B, Cardinali C, Caproni M et al. Immunological 

markers in dermatitis herpetiformis: Anti-endomysium and

anti-transglutaminase in association with increased

myeloperoxidase and eosinophil cationic protein serum 

levels. Int J Med Biol Environ 2001;29(2):149-153. Not 

relevant to adherence 

Gonczi J, Skerritt JH, Mitchell JD. A reliable screening test

for coeliac disease: enzyme-linked immunosorbent assay to 

detect anti-gliadin antibodies in serum. Aust N Z J Med 

1991; 21(5):723-731. Not relevant to adherence 

Greco L, Mayer M, Ciccarelli G et al. Compliance to a

gluten-free diet in adolescents, or "what do 300 coeliac 

adolescents eat every day?". Ital J Gastroenterol Hepatol 

1997;29(4):305-310. Not relevant to adherence 

Greco L, Mayer M, Grimaldi M et al. The Effects of early 

feeding on the onset of Symptoms in celiac disease. J

Pediatr Gastroenterol Nutr 1985;4(1):52-59. Not relevant to 

adherence 

Greco L, Percopo S. The coeliac disease task force " Free

from Gluten," " Improved knowledge to cure coeliac 

disease". Acta Paediatrica.Supplement 1996;4225-28. Not 

relevant to adherence 

Greco L, Tipo V, Di Donato F et al. Pulsatile growth 

pattern during catch-up growth in childhood coeliac 

disease. Acta Paediatr 1994;83(7):724-729. Not relevant to 

adherence 

Green P H R, Fleischauer A T, Bhagat G et al. Risk of 

malignancy in patients with celiac disease. Am J Med 

2003;115(3):191-195. Not relevant to adherence 

Green P H R, Stavropoulos S N, Panagi S G et al. 

Characteristics of adult celiac disease in the USA: results of

a national survey. Am J Gastroenterol 2001;96(1):126-131. 

Not relevant to adherence 

Grefte J M, Bouman J G, Grond J et al. Slow and

incomplete histological and functional recovery in adult 

gluten sensitive enteropathy. J Clin Pathol 1988;41(8):886-

891. Not relevant to adherence 

Grehn S, Fridell K, Lilliecreutz M et al. Dietary habits of

Swedish adult coeliac patients treated by a gluten-free diet 

for 10 years. Scand J Nutr Naringsforsk 2001;45(4):178-

182. Not relevant to adherence 

Gryboski J. False security of a gluten-free diet. Am J Dis 

Child 1981; 135(2):110-111. Not relevant to adherence 

Guandalini S, Ventura A, Ansaldi N et al. Diagnosis of 

coeliac disease: time for a change?. Arch Dis Child 

1989;64(9):1320-1325. Not relevant to adherence 

Guandalini S. Celiac disease in the new world. J Pediatr

Gastroenterol Nutr 2000;31(4):362-364. Not relevant to 

adherence 

Hadjivassiliou M, Davies-Jones G A B, Sanders D S et al. 

Dietary treatment of gluten ataxia. J Neurol Neurosurg 

Psychiatry 2003;74(9):1221-1224. Not relevant to

adherence 

Hallert C, Granno C, Grant C et al. Quality of life of adult 

coeliac patients treated for 10 years. Scand J Gastroenterol 

1998;33(9):933-938. Not relevant to adherence 

Hallert C, Granno C, Hulten S et al. Living with coeliac 

disease: controlled study of the burden of illness. Scand J

Gastroenterol 2002;37(1):39-42. Not relevant to adherence 

Hallert C, Grant C, Grehn S et al. Evidence of poor vitamin 

status in coeliac patients on a gluten-free diet for 10 years.

Aliment Pharmacol Ther 2002;16(7):1333-1339. Not 

relevant to adherence 

Hallert C, Lohiniemi S. Quality of life of celiac patients 

living on a gluten-free diet. Nutrition 1999;15(10):795-797. 

Not relevant to adherence 

Hallert C, Tobiasson P, Walan A. Serum folate

determinations in tracing adult coeliacs. Scand J 

Gastroenterol 1981;16(2):263-267. Not relevant to 

adherence 

Hallstrom O, Reunala T. IgA class reticulin antibodies in

dermatitis herpetiformis: a good indicator of jejunal 

damage. Acta Derm Venereol 1985;65(4):330-332. Not 

relevant to adherence 

Hamilton J R, McNeill L K. Childhood celiac disease: 

response of treated patients to a small uniform daily dose of

wheat gluten. Eur J Pediatr 1972;81(5):885-893. Not 

relevant to adherence 

Hankey G L, Holmes G K. Coeliac disease in the elderly.

Gut 1994;35(1):65-67. Not relevant to adherence 

Hansson T, Dahlbom I, Rogberg S et al. Recombinant 

human tissue transglutaminase for diagnosis and follow-up 

of childhood coeliac disease. Pediatr Res 2002; 51(6):700-

705. Not relevant to adherence 

Hansson T, Dannaeus A, Kraaz W et al. Production of 

antibodies to gliadin by peripheral blood lymphocytes in 

children with celiac disease: the use of an enzyme-linked

immunospot technique for screening and follow-up. Pediatr

Res 1997; 41(4 Pt 1):554-559. Not relevant to adherence 
Harris O D, Warner M, Cooke W T. Serum alkaline 

phosphatase in adult coeliac disease. Gut 

1969;10(11):951Not relevant to adherence 

Hawkes N D, Swift G L, Smith P M et al. Incidence and 

presentation of coeliac disease in South Glamorgan. Eur J 

Gastroenterol Hepatol 2000;12(3):345-349. Not relevant to 

adherence 

Henry C L. Patients' view of a gluten-free diet. J Hum Nutr 

1980;34(1):50-51. Not relevant to adherence 

Hernandez M A, Colina G, Ortigosa L. Epilepsy, cerebral

calcifications and clinical or subclinical coeliac disease.

Course and follow up with gluten-free diet. Seizure - the 

Journal of the British Epilepsy Association 1998;7(1):49-

54. Not relevant to adherence 

Hetzel P A S, Labrooy J T, Bellon M. The sup 5sup 1Cr 

EDTA absorption test in coeliac patients treated with a

gluten free diet. Ircs Med Sci 1986;14(12):1183-1184. Not 

relevant to adherence 

Hill PG, Thompson SP, Holmes GK. IgA anti-gliadin 

antibodies in adult celiac disease. Clin Chem 1991; 

37(5):647-650. Not relevant to adherence 

Hjelt K, Krasilnikoff P A. The impact of gluten on

haematological status, dietary intakes of haemopoietic 

nutrients and vitamin B12 and folic acid absorption in 

children with coeliac disease. Acta Paediatr Scand 

1990;79(10):911-919. Not relevant to adherence 

Holmes G K T. Coeliac disease and malignancy. Dig Dis 

Sci 2002;34(3):229-237. Not relevant to adherence 

Holmes G K, Asquith P, Stokes P L et al. Cellular infiltrate

of jejunal biopsies in adult coeliac disease (ACD) in 

relation to gluten withdrawal. Gut 1973;14(5):429Not 

relevant to adherence 

Holmes G K, Asquith P, Stokes P L et al. Cellular infiltrate

of jejunal biopsies in adult coeliac disease in relation to

gluten withdrawal. Gut 1974;15(4):278-283. Not relevant 

to adherence 

Holmes G K, Prior P, Lane M R et al. Malignancy in 

coeliac disease--effect of a gluten free diet. Gut

1989;30(3):333-338. Not relevant to adherence 

Holmes G K, Stokes P L, Sorahan T M et al. Coeliac 

disease, gluten-free diet, and malignancy. Gut

1976;17(8):612-619. Not relevant to adherence 

Holmes G K. Non-malignant complications of coeliac 

disease. Acta Paediatrica.Supplement 1996;41268-75. Not 

relevant to adherence 

Horvath K, Horn G. Tardyferon therapy in hyposiderosis of 

infancy and childhood. Ther Hung 1992;40(1):40-43. Not 

relevant to adherence 

Horvath-Stolarczyk A, Sidor K, Dziechciarz P et al.

Assessment of emotional status, selected personality traits 

and depression in young adults with celiac disease. Pediatr

Wspolczesna 2002;4(3):241-246. Not relevant to adherence 

Huff C. Celiac disease: helping families adapt.

Gastroenterology Nursing - the Official Journal of the

Society of Gastroenterology Nurses and Associates

1997;20(3):79-81. Not relevant to adherence 

Hussain G, Ali S, Iqbal M M et al. Study of coeliac disease 

in children. J Coll Phys Surg Pak 1999;9(2):81-84. Not 

relevant to adherence 

Ibbotson M. Gluten-free diets--helping patients to cope. 

Prof Nurse 1986;1(8):219-220. Not relevant to adherence 

Ibbotson M. Living with a gluten-free diet. Prof Nurse 

1986;1(8):221-222. Not relevant to adherence 

Iliffe G D, Owen D A. An association between primary 

biliary cirrhosis and jejunal villous atrophy resembling 

celiac disease. Dig Dis Sci 1979;24(10):802-806. Not 

relevant to adherence 

Iovino P, Ciacci C, Sabbatini F et al. Esophageal 

impairment in adult celiac disease with steatorrhea. Am J 

Gastroenterol 1998;93(8):1243-1249. Not relevant to

adherence 

Ivarsson A, Persson L A, Hernell O. Does breast-feeding

affect the risk for coeliac disease?. Adv Exp Med Biol

2000;478139-149. Not relevant to adherence 

Ivarsson A, Persson L A, Nystrom L et al. The Swedish 

coeliac disease epidemic with a prevailing twofold higher

risk in girls compared to boys may reflect gender specific

risk factors. Eur J Epidemiol 2003;18(7):677-684. Not 

relevant to adherence 

Janatuinen E K, Kemppainen T A, Julkunen R J K et al. No 

harm from five year ingestion of oats in coeliac disease.

Gut 2002;50(3):332-335. Not relevant to adherence 

Janatuinen E K, Kemppainen T A, Pikkarainen P H et al. 

Lack of cellular and humoral immunological responses to 

oats in adults with coeliac disease. Gut 2000;46(3):327-

331. Not relevant to adherence 

Janatuinen E K, Pikkarainen P H, Kemppainen T A et al. A 

comparison of diets with and without oats in adults with 

celiac disease. N Engl J Med 1995;333(16):1033-1037. Not 

relevant to adherence 

Jansson U H, Gudjonsdottir A H, Ryd W et al. Two 

different doses of gluten show a dose-dependent response 

of enteropathy but not of serological markers during gluten 

challenge in children with coeliac disease. Acta Paediatr 

2001;90(3):255-259. Not relevant to adherence 
Jarvinen T T, Kaukinen K, Laurila K et al. Intraepithelial

lymphocytes in celiac disease. Am J Gastroenterol 

2003;98(6):1332-1337. Not relevant to adherence 

Jessernigg G, Goriup U, Deutsch J et al. The importance of

antibodies in the guidance of coeliac patients. Jpgn 2000; 

31(Suppl 2):S65-S66. No correlations with other measures 

Jewell D P. Celiac disease. Can J Gastroenterol

2000;14(8):665-666. Not relevant to adherence 

Jodl J, Stepan J, Lojda Z. Diagnostic significance of 

determination of serum alkaline phosphatase intestinal 

isoenzyme activity in coeliac sprue in childhood. Acta 

Universitatis Carolinae.Medica.Monographia 1977;(78 Pt 

2):65-70. Not relevant to adherence 

Johnston S D, Peter Watson R G, McMillan S A. Soda 

bread provocation test for subjects with transient serology

for coeliac disease 3 years after a population screening 

survey. Eur J Gastroenterol Hepatol 2000;12(9):1013-1015. 

Not relevant to adherence 

Johnston S D, Smye M, Watson R P. Intestinal 

permeability tests in coeliac disease. Clin Lab 2001;47(3-

4):143-150. Not relevant to adherence 

Johnston S D, Watson R G, McMillan S A et al. Coeliac 

disease detected by screening is not silent--simply 

unrecognized. Q J Med 1998;91(12):853-860. Not relevant

to adherence 

Johnston S D, Watson R G, Middleton D et al. Genetic, 

morphometric and immunohistochemical markers of latent

coeliac disease. Eur J Gastroenterol Hepatol

1999;11(11):1283-1288. Not relevant to adherence 

Jones P E, Peters T J. DNA synthesis by jejunal mucosa in 

responsive and non-responsive coeliac disease. Br Med J 

1977;1(6069):1130-1131. Not relevant to adherence 

Joshi Preeti, Mofidi Shideh, Sicherer Scott H. Interpretation

of commercial food ingredient labels by parents of foodallergic children. J Allergy Clin Immunol 

2002;109(6):1019-1021. Not relevant to adherence 

Junqueira JC, Calcado AC, Percope S. Compliance of 

coeliac pediatric patients in Rio De Janeiro Brazil. J Pediatr 

Gastroenterol Nutr 2000; 31(Suppl 2). No correlations with

other measures 

Juto P, Fredrikzon B, Hernell O. Gliadin-specific serum 

immunoglobulins A, E, G, and M in childhood: Relation of

small intestine mucosal morphology. J Pediatr 

Gastroenterol Nutr 1985;4(5):723-729. Monitoring not 

serology, EMA, tTG or biopsy based, or not promoting 

GFD adherence 

Kalayci A G, Kansu A, Girgin N et al. Bone mineral 

density and importance of a gluten-free diet in patients with 

celiac disease in childhood. Pediatrics 2001;108(5):E89Not 

relevant to adherence 

Kalra K K, Jain N, Mittal S K. Management of celiac

disease. Indian J Pediatr 1999;66(1 Suppl):S32-S36. Not 

relevant to adherence 

Kapuscinska A, Zalewski T, Chorzelski TP et al. Disease 

specificity and dynamics of changes in IgA class antiendomysial antibodies in celiac disease. J Pediatr 

Gastroenterol Nutr 1987; 6(4):529-534. Not relevant to 

adherence 

Kastrup W, Andersson H, Gillberg R et al. Influence of

gluten-free diet on the gastric condition in dermatitis 

herpetiformis. Scand J Gastroenterol 1985;20(1):39-45. Not 

relevant to adherence 

Katz K D. Celiac Disease - Current Clinical Considerations

in Treatment and Avoidance of Nutritional Deficiencies.

Today's Ther Trends 2003;21(4):379-389. Not relevant to

adherence 

Kaukinen K, Collin P, Holm K et al. Wheat starchcontaining gluten-free flour products in the treatment of 

coeliac disease and dermatitis herpetiformis. A long-term

follow-up study. Scand J Gastroenterol 1999;34(2):163-

169. Not relevant to adherence 

Kaukinen K, Salmi J, Lahtela J et al. No effect of glutenfree diet on the metabolic control of type 1 diabetes in 

patients with diabetes and celiac disease. Diabetes Care 

1999;22(10):1747-1748. Not relevant to adherence 

Kelly CP, Feighery CF, Gallagher RB et al. Mucosal and

systemic IgA anti-gliadin antibody in celiac disease. 

Contrasting patterns of response in serum, saliva, and 

intestinal secretions. Dig Dis Sci 1991; 36(6):743-751. Not 

relevant to adherence 

Kemppainen T A, Kosma V M, Janatuinen E K et al.

Nutritional status of newly diagnosed celiac disease 

patients before and after the institution of a celiac disease 

diet--association with the grade of mucosal villous atrophy.

Am J Clin Nutr 1998;67(3):482-487. Not relevant to

adherence 

Kemppainen T, Kroger H, Janatuinen E et al. Bone 

recovery after a gluten-free diet: a 5-year follow-up study.

Bone 1999;25(3):355-360. Not relevant to adherence 

Kemppainen T, Kroger H, Janatuinen E et al. Osteoporosis 

in adult patients with celiac disease. Bone 1999;24(3):249-

255. Not relevant to adherence 

Kemppainen T, Uusitupa M, Janatuinen E et al. Intakes of

nutrients and nutritional status in coeliac patients. Scand J 

Gastroenterol 1995;30(6):575-579. Not relevant to 

adherence 

Kennedy N P, Feighery C. Clinical features of coeliac 

disease today. Biomed Pharmacother 2000;54(7):373-380. 

Not relevant to adherence 
Khoshoo V, Bhan M K, Puri S et al. Serum anti-gliadin

antibody profile in childhood protracted diarrhoea due to 

coeliac disease and other causes in a developing country. 

Scand J Gastroenterol 1989;24(10):1212-1216. Not 

relevant to adherence 

Khuffash F A, Barakat M H, Shaltout A A et al. Coeliac 

disease among children in Kuwait: difficulties in diagnosis 

and management. Gut 1987;28(12):1595-1599. Not 

relevant to adherence 

Kieffer M, Barnetson RS, Blackwell JN. Sequential studies 

of gliadin antibodies in patients with dermatitis

herpetiformis. Arch Dermatol Res 1984; 276(2):74-77. No 

correlations with other measures 

Kieffer M. Serum antibodies to gliadin and other cereal 

proteins in patients with coeliac disease and dermatitis 

herpetiformis. Dan Med Bull 1985;32(5):251-262. Not 

relevant to adherence 

Kieslich M, Errazuriz G, Posselt H G et al. Brain whitematter lesions in celiac disease: a prospective study of 75

diet-treated patients. Pediatrics 2001;108(2):E21Not 

relevant to adherence 

Kilander A F, Nilsson L A, Gillberg R. Serum antibodies to 

gliadin in coeliac disease after gluten withdrawal. Scand J

Gastroenterol 1987;22(1):29-34. Monitoring not serology, 

EMA, tTG or biopsy based, or not promoting GFD 

adherence 

King David S. Psychological and behavioral effects of food

and chemical exposure in sensitive individuals. Nutr Health 

1984;3(3):137-151. Not relevant to adherence 

Kitts D, Yuan Y, Joneja J et al. Adverse reactions to food 

constituents: allergy, intolerance, and autoimmunity. Can J 

Physiol Pharmacol 1997;75(4):241-254. Not relevant to 

adherence 

Kjeldsen-Kragh J. Rheumatoid arthritis treated with 

vegetarian diets. Am J Clin Nutr 1999;70(3 Suppl):594S600S. Not relevant to adherence 

Kleiner S M. Sense and food sensitivity: Coping wit 

allergies and food intolerance. Phys Sportsmed 

1998;26(5):105-106. Not relevant to adherence 

Kluge F, Koch HK, Grosse-Wilde H et al. Follow-up of 

treated adult celiac disease: clinical and morphological 

studies. Hepatogastroenterology 1982; 29(1):17-23. Not 

relevant to adherence 

Kohout P. Small bowel permeability in diagnosis of celiac 

disease and monitoring of compliance of a gluten-free diet

(gut permeability in celiac disease). Acta Medica (Hradec

Kralove) 2001;44(3):101-104. No monitoring measure of

interest 

Kokkonen J, Viitanen A, Simila S. Coping with a coeliac 

diet after adolescence. Helv Paediatr Acta 1989;43(4):261-

265. Not relevant to adherence 

Kolsteren M M, Koopman H M, Schalekamp G et al. 

Health-related quality of life in children with celiac disease.

Eur J Pediatr 2001;138(4):593-595. Not relevant to 

adherence 

Korponay-Szabo I R, Kovacs J B, Lorincz M et al. 

Prospective significance of antiendomysium antibody

positivity in subsequently verified celiac disease. J Pediatr

Gastroenterol Nutr 1997;25(1):56-63. Not relevant to

adherence 

Kuitunen M, Savilahti E. Gut permeability to human alphalactalbumin, beta-lactoglobulin, mannitol, and lactulose in 

celiac disease. J Pediatr Gastroenterol Nutr 

1996;22(2):197-204. Not relevant to adherence 

Kumar P J, Walker-Smith J, Milla P et al. The teenage

coeliac: follow up study of 102 patients. Arch Dis Child

1988;63(8):916-920. Not relevant to adherence 

Kumar P J. Commentary: are patients any better at adhering 

to a gluten-free diet?. Ital J Gastroenterol Hepatol 

1997;29(4):310-311. Not relevant to adherence 

Kumar V, Jarzabek-Chorzelska M, Sulej J et al. Celiac 

disease and immunoglobulin A deficiency: How effective 

are the serological methods of diagnosis? Clin Diagn Lab 

Immunol 2002; 9(6):1295-1300. Not relevant to adherence 

Kumar V, Lerner A, Valeski J E et al. Endomysial 

antibodies in the diagnosis of celiac disease and the effect 

of gluten on antibody titers. Immunol Invest 1989;18(1-

4):533-544. Not relevant to adherence 

Kutlu T, Brousse N, Rambaud C et al. Numbers of T cell 

receptor (TCR) alpha beta+ but not of TcR gamma delta+

intraepithelial lymphocytes correlate with the grade of 

villous atrophy in coeliac patients on a long term normal 

diet. Gut 1993;34(2):208-214. Not relevant to adherence 

Labrooy JT, Hohmann AW, Davidson GP et al. Intestinal 

and serum antibody in coeliac disease: a comparison using 

ELISA. Clinical and Experimental Immunology 1986; 

66(3):661-668. Not relevant to adherence 

Lahteenoja H, Toivanen A, Viander M et al. Increase in Tcell subsets of oral mucosa: a late immune response in 

patients with treated coeliac disease?. Scand J Immunol 

2000;52(6):602-608. Not relevant to adherence 

Lahteenoja H, Toivanen A, Viander M et al. Oral mucosal 

changes in coeliac patients on a gluten-free diet. Eur J Oral

Sci 1998;106(5):899-906. Not relevant to adherence 

Lancaster-Smith M, Joyce S, Kumar P. Immunoglobulins 

in the jejunal mucosa in adult coeliac disease and dermatitis 

herpetiformis after the reintroduction of dietary gluten. Gut 

1977;18(11):887-891. Not relevant to adherence 
Lancaster-Smith M, Kumar P, Clark M L et al.

Antireticulin antibodies in dermatitis herpetiformis and 

adult coeliac disease. Their relationship to a gluten free diet

and jejunal histology. Br J Dermatol 1975;92(1):37-42. Not 

relevant to adherence 

Lancaster-Smith M, Packer S, Kumar P J et al.

Immunological phenomena in the jejunum and serum after

reintroduction of dietary gluten in children with treated 

coeliac disease. J Clin Pathol 1976;29(7):592-597. Not 

relevant to adherence 

Langman M J. Can epidemiology help us prevent celiac

disease?. Gastroenterology 1986;90(2):489-491. Not 

relevant to adherence 

Lankisch P G, Martinez Schramm A, Petersen F et al.

Diagnostic intervals for recognizing celiac disease. Z 

Gastroenterol 1996;34(8):473-477. Not relevant to 

adherence 

Laurin P, Falth-Magnusson K, Sundqvist T. Increase in 

nitric oxide urinary products during gluten challenge in

children with coeliac disease. Scand J Gastroenterol 

2003;38(1):55-60. Not relevant to adherence 

Laurin P, Wolving M, Falth-Magnusson K. Even small 

amounts of gluten cause relapse in children with celiac 

disease. J Pediatr Gastroenterol Nutr 2002; 34(1):26-30. 

Not relevant to adherence 

Layer P, Keller J. Lipase supplementation therapy:

Standards, alternatives, and perspectives. Pancreas

2003;26(1):1-7. Not relevant to adherence 

Le Quellec A, Clapie M, Callamand P et al. Circulating

oxyntomodulin-like immunoreactivity in healthy children

and children with celiac disease. J Pediatr Gastroenterol 

Nutr 1998;27(5):513-518. Not relevant to adherence 

Lehmann F G, Hillert U. Fecal intestinal alkaline 

phosphatase in coeliac disease. Z Gastroenterol 

1980;18(7):381-388. Not relevant to adherence 

Lemieux B, Boivin M, Brossard J H et al. Normal 

parathyroid function with decreased bone mineral density

in treated celiac disease. Can J Gastroenterol 

2001;15(5):302-307. Not relevant to adherence 

Leonard S. No grain, no pain. Nurs Times 1999;95(8):69-

70. Not relevant to adherence 

Levi S, Bjarnason I, Swinson C M et al. Malignant 

pancreatic somatostatinoma in a patient with dermatitis 

herpetiformis and coeliac disease. Digestion 1988;39(1):1-

6. Not relevant to adherence 

Lewis C, Book L, Black J et al. Celiac disease and human 

leukocyte antigen genotype: Accuracy of diagnosis in selfdiagnosed individuals, dosage effect, and sibling risk. J 

Pediatr Gastroenterol Nutr 2000;31(1):22-27. Not relevant 

to adherence 

Lifschitz C H, Polanco I, Lobb K. The urinary excretion of

polyethylene glycol as a test for mucosal integrity in 

children with celiac disease: comparison with other 

noninvasive tests. J Pediatr Gastroenterol Nutr

1989;9(1):49-57. No monitoring measure of interest 

Lindberg T, Nilsson LA, Borulf S et al. Serum IgA and IgG 

gliadin antibodies and small intestinal mucosal damage in

children. J Pediatr Gastroenterol Nutr 1985; 4(6):917-922. 

Not relevant to adherence 

Littlewood J M. Coeliac disease in childhood. Bailliere's

Clinical Gastroenterology 1995;9(2):295-327. Not relevant

to adherence 

Lloyd-Still J D. Chronic diarrhea of childhood and the 

misuse of elimination diets. Eur J Pediatr 1979;95(1):10-

13. Not relevant to adherence 

Lohiniemi S, Maki M, Kaukinen K et al. Gastrointestinal

symptoms rating scale in coeliac disease patients on wheat

starch-based gluten-free diets. Scand J Gastroenterol 

2000;35(9):947-949. Not relevant to adherence 

Lohiniemi S. Coeliac disease. Tricky to find, hard to treat,

impossible to cure. Lancet 2001;358(Suppl):14Not relevant

to adherence 

Londei M, Quaratino S, Maiuri L. Celiac disease: A model 

autoimmune disease with gene therapy applications. Hum 

Gene Ther 2003;10(10):835-843. Not relevant to adherence 

Lorini R, Scotta M S, Cortona L et al. Celiac disease and

type I (insulin-dependent) diabetes mellitus in childhood: 

follow-up study. J Diabetes Complications 1996;10(3):154-

159. Not relevant to adherence 

Lovik A, Fluge Holsdal E R, Ek J et al. Dietary Treatment

of Coeliac Disease. Tidsskr Nor Laegeforen

1999;119(13):1888-1891. Not relevant to adherence 

Lynch D A, Thornton J R, Axon A T. Acute fatty liver

complicating coeliac disease. Eur J Gastroenterol Hepatol 

1994;6(8):745-747. Not relevant to adherence 

Mackner L M, McGrath A M, Stark L J. Dietary

recommendations to prevent and manage chronic pediatric 

health conditions: Adherence, intervention, and future 

directions. J Dev Behav Pediatr 2001;22(2):130-143. Not 

relevant to adherence 

Maffei H V, Kingston D, Hill I D et al. Histopathologic 

changes and the immune response within the jejunal 

mucosa in infants and children. Pediatr Res

1979;13(6):733-736. Not relevant to adherence 

Magliocca F M, Bonamico M, Petrozza V et al. A new 

morphological classification during follow-up in patients 

with celiac disease: a three-dimensional observation by
scanning electron microscopy. Histol Histopathol 

1996;11(2):343-350. Not relevant to adherence 

Magrath G, Hartland B V. Dietary recommendations for 

children and adolescents with diabetes: An implementation

paper. J Hum Nutr Diet 1993;6(6):491-507. Not relevant to 

adherence 

Mainardi E, Montanelli A, Dotti M et al. Thyroid-related

autoantibodies and celiac disease: A role for a gluten-free 

diet?. J Clin Gastroenterol 2002;35(3):245-248. Not 

relevant to adherence 

Maki M, Lahdeaho ML, Hallstrom O et al. Postpubertal

gluten challenge in coeliac disease. Arch Dis Child 1989; 

64(11):1604-1607. Not relevant to adherence 

Maki M, Sulkanen S, Collin P. Antibodies in relation to

gluten intake. Dig Dis 1998;16(6):330-332. Review article 

Mariani P, Viti M G, Montuori M et al. The gluten-free 

diet: a nutritional risk factor for adolescents with celiac

disease?. J Pediatr Gastroenterol Nutr 1998;27(5):519-523. 

Not relevant to adherence 

Matek Z, Jungvirth-Hegedus M, Kolacek S. Epidemiology

of coeliac disease in children in one Croatian county: 

possible factors that could affect the incidence of coeliac 

disease and adherence to a gluten-free diet (Part II). Coll 

Antropol 2000;24(2):397-404. Not relevant to adherence 

Mauro A, Orsi L, Mortara P et al. Cerebellar Syndrome in 

Adult Celiac Disease With Vitamin E Deficiency. Acta 

Neurol Scand 1991;84(2):167-170. Not relevant to 

adherence 

Mautalen C, Gonzalez D, Mazure R et al. Effect of 

treatment on bone mass, mineral metabolism, and body 

composition in untreated celiac disease patients. Am J 

Gastroenterol 1997;92(2):313-318. Not relevant to 

adherence 

McCarthy D M, Coleman M. Response of intestinal 

mucosa to gluten challenge in autistic subjects. Lancet

1979;2(8148):877-878. Not relevant to adherence 

McCrae W M, Eastwood M A, Martin M R et al. Neglected

coeliac disease. Lancet 1975;1(7900):187-190. Not relevant

to adherence 

McElvaney NG, Duignan R, Fielding JF. Coeliac disease:

clinical presentations, correlations of dietary compliance,

symptomatic response and repeat biopsy findings. Ulster 

Med J 1992; 61(2):134-138. No correlations with other

measures

McFarlane X A, Bhalla A K, Robertson D A. Effect of a 

gluten free diet on osteopenia in adults with newly 

diagnosed coeliac disease. Gut 1996;39(2):180-184. Not 

relevant to adherence 

McLoughlin R, Sebastian S S, Qasim A et al. Coeliac 

disease in Europe. Aliment Pharmacol Ther Suppl 

2003;18(3):45-48. Not relevant to adherence 

McMillan SA, Dickey W, Douglas JP et al. Transthyretin

values correlate with mucosal recovery in patients with 

coeliac disease taking a gluten free diet. J Clin Pathol 2001; 

54(10):783-786. Not relevant to adherence 

McNeish A S, Harms H K, Rey J et al. The diagnosis of 

coeliac disease. A commentary on the current practices of

members of the European Society for Paediatric

Gastroenterology and Nutrition (ESPGAN). Arch Dis Child

1979;54(10):783-786. Not relevant to adherence 

McNeish A S. Coeliac disease: Duration of gluten-free diet. 

Arch Dis Child 1980;55(2):110-111. Not relevant to

adherence 

McNicholl B. Coeliac disease: ecology, life history and 

management. Human Nutrition.Applied Nutrition 

1986;40(Suppl 1):55-60. Not relevant to adherence 

McNicholl B. Management of coeliac disease. Midwife 

Health Visit Community Nurse 1986;22(10):361-364. Not 

relevant to adherence 

McPhillips J. Understanding coeliac disease: symptoms and 

long-term risks. Br J Nurs 2000;9(8):479-483. Not relevant

to adherence 

Mearin M L, Koninckx C R, Biemond I et al. Influence of 

genetic factors on the serum levels of antigliadin antibodies 

in celiac disease. J Pediatr Gastroenterol Nutr

1984;3(3):373-377. Not relevant to adherence 

Meyer D, Stavropolous S, Diamond B et al. Osteoporosis in 

a north american adult population with celiac disease. Am J 

Gastroenterol 2001;96(1):112-119. Not relevant to 

adherence 

Michalski J P, McCombs C C. Celiac disease: Clinical

features and pathogenesis. Am J Med Sci 1994;307(3):204-

211. Not relevant to adherence 

Mitchell R M S, Robinson T J. Monitoring dietary 

compliance in coeliac disease using red cell distribution 

width. Int J Clin Pract 2002;56(4):249-250. No monitoring

measure of interest

Mitchison H C, al Mardini H, Gillespie S et al. A pilot

study of fluticasone propionate in untreated coeliac disease.

Gut 1991;32(3):260-265. Not relevant to adherence 

Mitt K, Uibo O. Low cereal intake in Estonian infants: The

possible explanation for the low frequency of coeliac 

disease in Estonia. Eur J Clin Nutr 1998;52(2):85-88. Not 

relevant to adherence 

Mobacken H, Andersson H, Gillberg R. Gluten-free diet in

clinical practice: a Scandinavian perspective. Clin

Dermatol 1991;9(3):415-419. Not relevant to adherence 
Mokhallalaty M, Debek A, Naja Z et al. Celiac disease at 

Makassed General Hospital (8 years of experience). Revue 

Medicale Libanaise 2002;14(2-3):49-53. Not relevant to 

adherence 

Moll-Kotowski M, Stern M. Dietary attitude and follow-up 

in coeliac patients diagnosed 1964-1986. Monatsschr 

Kinderheilkd 1995; 143(2):142-148. Not relevant to 

adherence 

Molteni N, Bardella M T, Vezzoli G et al. Intestinal 

calcium absorption as shown by stable strontium test in 

celiac disease before and after gluten-free diet. Am J 

Gastroenterol 1995;90(11):2025-2028. Not relevant to

adherence 

Monteiro E, Menezes M L, Magalhaes Ramalho P. Antireticulin antibodies: a diagnostic and monitoring test for 

childhood coeliac disease. Scand J Gastroenterol 

1986;21(8):955-957. Monitoring not serology, EMA, tTG 

or biopsy based, or not promoting GFD adherence 

Mora S, Barera G, Beccio S et al. A prospective, 

longitudinal study of the long-term effect of treatment on 

bone density in children with celiac disease. Eur J Pediatr 

2001;139(4):516-521. Not relevant to adherence 

Mora S, Barera G, Beccio S et al. Bone density and bone 

metabolism are normal after long-term gluten-free diet in

young celiac patients. Am J Gastroenterol 1999;94(2):398-

403. Not relevant to adherence 

Mora S, Barera G, Ricotti A et al. Reversal of low bone 

density with a gluten-free diet in children and adolescents 

with celiac disease. Am J Clin Nutr 1998;67(3):477-481. 

Not relevant to adherence 

Mora S, Weber G, Barera G et al. Effect of gluten-free diet 

on bone mineral content in growing patients with celiac 

disease. Am J Clin Nutr 1993;57(2):224-228. Not relevant 

to adherence 

Morley J E. Pathophysiology of anorexia. Clin Geriatr Med 

2002;18(4):661-673. Not relevant to adherence 

Morris M A, Ciclitira P J. Coeliac disease. J R Coll 

Physicians Lond 1997;31(6):614-618. Not relevant to

adherence 

Morroni M, Sbarbati A, D'Angelo G et al. Scanning

electron microscopy of the small intestine mucosa in 

children with celiac disease after long-term dietary

treatment. Scanning Microsc 1989;3(4):1161-1166. Not 

relevant to adherence 

Mortimer P E, Stewart J S, Norman A P et al. Follow-up 

study of coeliac disease. Br Med J 1968;3(609):7-9. Not 

relevant to adherence 

Mowat A M. Coeliac disease - A future for peptide 

therapy?. Lancet 2000;356(9226):270-271. Not relevant to

adherence 

Mulder C J J, Wahab P J, Moshaver B et al. Refractory 

coeliac disease: A window between coeliac disease and 

enteropathy associated T cell lymphoma. Scandinavian

Journal of Gastroenterology.Supplement 2000;35(232):32-

37. Not relevant to adherence 

Murphy D. Celiac sprue. Gastroenterology Nursing - the 

Official Journal of the Society of Gastroenterology Nurses

and Associates 1995;18(4):133-137. Not relevant to 

adherence 

Murphy M S, Sood M, Johnson T. Use of the lactose H2 

breath test to monitor mucosal healing in coeliac disease.

Acta Paediatr 2002;91(2):141-144. No monitoring measure 

of interest 

Murray J A. The widening spectrum of celiac disease. Am J

Clin Nutr 1999;69(3):354-365. Not relevant to adherence 

Mustalahti Kirsi, Lohiniemi Susanna, Collin Pekka et al.

Gluten-free diet and quality of life in patients with screendetected celiac disease. Effective Clinical Practice - Ecp 

2002;5(3):105-113. Not relevant to adherence 

Muzzo S, Burrows R, Burgueno M et al. Effect of calcium

and vitamin D supplementation on bone mineral density of

celiac children. Nutr Res 2000;20(9):1241-1247. Not 

relevant to adherence 

Naeslund G K, Fredrikson M, Hellenius M L et al. 

Determinants of Compliance in Men Enrolled in a Diet and 

Exercise Intervention Trial: a Randomized, Controlled

Study. Patient Education & Counseling 1996;29(3):247-

256. Not relevant to adherence 

Nash Samantha. Does exclusive breast-feeding reduce the

risk of coeliac disease in children?. Br J Community Nurs

2003;8(3):127-132. Not relevant to adherence 

Naveh Y, Ken-Dror A, Zinder O et al. Comparative 

reliability of D-xylose absorption and serum beta-carotene 

measurements in small intestinal disease. J Pediatr 

Gastroenterol Nutr 1986;5(2):210-213. Not relevant to 

adherence 

Nehra V. New clinical issues in celiac disease.

Gastroenterol Clin North Am 1998;27(2):453-465. Not 

relevant to adherence 

Nieminen U, Kahri A, Savilahti E et al. Duodenal 

disaccharidase activities in the follow-up of villous atrophy 

in coeliac disease. Scand J Gastroenterol 2001;36(5):507-

510. Not relevant to adherence 

Norgard B, Fonager K, Sorensen H T et al. Birth outcomes 

of women with celiac disease: A nationwide historical 

cohort study. Am J Gastroenterol 1999;94(9):2435-2440. 

Not relevant to adherence 
not found, in reference. Nutritional problems and 

controversies in gastrointestinal diseases. Nutrition in 

Practice 1982;2(1):3-32. Not relevant to adherence 

Not relevant to adherence 

Not T, Tommasini A, Tonini G et al. Undiagnosed coeliac 

disease and risk of autoimmune disorders in subjects with 

type I diabetes mellitus. Diabetologia 2001;44(2):151-155. 

Not relevant to adherence 

Novacek G, Miehsler W, Wrba F et al. Prevalence and

clinical importance of hypertransaminasaemia in coeliac

disease. Eur J Gastroenterol Hepatol 1999;11(3):283-288. 

Not relevant to adherence 

Nowowiejska B, Kaczmarski M, Dabrowska E J. A longterm study in children with a recognized gluten intolerance.

Rocz Akad Med Bialymst 1995;40(3):580-587. No 

monitoring measure of interest 

Ogborn A D. Pregnancy in patients with coeliac disease. Br 

J Obstet Gynaecol 1975;82(4):293-296. Not relevant to 

adherence 

O'Halloran E T, Read M, Morrissey-Walsh E M. Coeliac

disease in children: Problems in diagnosis and

management. Ir Med J 1985;78(7):188-191. Not relevant to 

adherence 

O'Leary Clare, Wieneke Peter, Buckley Sarah et al. Celiac

disease and irritable bowel-type symptoms. Am J 

Gastroenterol 2002;97(6):1463-1467. Not relevant to

adherence 

Olives PrJ. Coeliac disease and gluten intolerance: New 

data for a new method of treatment. Rev Med Liban 

2000;12(3):127-128. Not relevant to adherence 

O'Mahony S, Nawroz I M, Ferguson A. Coeliac disease 

and collagenous colitis. Postgrad Med J 1990;66(773):238-

241. Not relevant to adherence 

Ott D J. Celiac disease: biopsy or enteroclysis better for

evaluating response to a gluten-free diet?. Am J

Gastroenterol 1997;92(4):715-716. Review article 

Packer S, Rowlatt R J, Harries J T. Proceedings: 

Reappraisal of a past diagnosis of "coeliac disease". Arch 

Dis Child 1974;49(10):819Not relevant to adherence 

Paerregaard A, Vilien M, Krasilnikoff P A et al. Supposed 

coeliac disease during childhood and its presentation 14-38 

years later. Scand J Gastroenterol 1988;23(1):65-70. Not 

relevant to adherence 

Page S R, Lloyd C A, Hill P G et al. The prevalence of

coeliac disease in adult diabetes mellitus. Q J Med 

1994;87(10):631-637. Not relevant to adherence 

Parker S L, Sussman G L, Krondl M. Dietary aspects of

adverse reactions to foods in adults. Cmaj - Canadian 

Medical Association Journal = Journal De L'association 

Medicale Canadienne 1988;139(8):711-718. Not relevant to 

adherence 

Paterson Heather. Plant foods for coeliacs. Food Nutr Notes 

Rev 1975;32(11-12):205-209. Not relevant to adherence 

Patin NM, Johnson F, Kirks BA. Promoting dietary

compliance in gluten-intolerant children. J Nutr Educ 1989; 

21(2):100D. Not relevant to adherence 

Patwari A K, Anand V K, Kapur Gaurav et al. Clinical and

nutritional profile of children with celiac disease. Indian 

Pediatr 2003;40(4):337-342. Not relevant to adherence 

Peraaho M, Kaukinen K, Paasikivi K et al. Wheat-starchbased gluten-free products in the treatment of newly

detected coeliac disease: prospective and randomized 

study. Aliment Pharmacol Ther 2003;17(4):587-594. Not 

relevant to adherence 

Peters Ulrike, Askling Johan, Gridley Gloria et al. Causes

of death in patients with celiac disease in a populationbased Swedish cohort. Arch Intern Med 

2003;163(13):1566-1572. Not relevant to adherence 

Pistorius L R, Sweidan W H, Purdie D W et al. Coeliac 

disease and bone mineral density in adult female patients. 

Gut 1995;37(5):639-642. Not relevant to adherence 

Polito C, Olivieri A N, Marchese L et al. Weight 

overgrowth of coeliac children on gluten-free diet. Nutr

Res 1992;12(3):353-358. Not relevant to adherence 

Pruessner H T. Detecting celiac disease in your patients. 

Am Fam Physician 1998;57(5):1023-1034. Not relevant to 

adherence 

Pueschel S M. Gastrointestinal concerns and nutritional

issues in persons with Down syndrome. Down Syndrome 

Quarterly 1999;4(4):1-11. Not relevant to adherence 

Pynnoenen P, Isometsae E T, Verkasalo M A et al. 

Untreated Celiac Disease and Development of Mental

Disorders in Children and Adolescents. Psychosomatics: 

Journal of Consultation Liaison Psychiatry 2002;43(4):331-

334. Not relevant to adherence 

Radzikowski A, Kulus M, Krauze A et al. Growth, bone 

age and nutritional status in neglected coeliac disease. 

Materia Medica Polona.Polish Journal of Medicine and

Pharmacy 1991;23(2):146-150. Not relevant to adherence 

Rautonen J, Rautonen N, Savilahti E. Antibodies to gliadin

in children with coeliac disease. Acta Paediatr Scand 

1991;80(12):1200-1206. Monitoring not serology, EMA, 

tTG or biopsy based, or not promoting GFD adherence 

Rea F, Polito C, Marotta A et al. Restoration of body

composition in celiac children after one year of gluten-free 
diet. J Pediatr Gastroenterol Nutr 1996;23(4):408-412. Not 

relevant to adherence 

Read M, O'Halloran ET, O'Sullivan C. Coeliac disease in

adolescents/young adults: difficulties in monitoring. Br J 

Biomed Sci 2000; 57(3):217-221. No correlations with 

other measures 

Reeves G E M, Burns C, Hall S T et al. The measurement 

of IgA and IgG transglutaminase antibodies in celiac 

disease: A comparison with current diagnostic methods. 

Pathology 2000;32(3):181-185. Monitoring not serology, 

EMA, tTG or biopsy based, or not promoting GFD 

adherence 

Reifen R, Reif S, Buskila D et al. Transthyretin: a marker 

for celiac disease activity. J Med 1998;29(1-2):30-36. No 

monitoring measure of interest 

Reunala T, Chorzelski T P, Viander M et al. IgA antiendomysial antibodies in dermatitis herpetiformis: 

correlation with jejunal morphology, gluten-free diet and

anti-gliadin antibodies. Br J Dermatol 1987;117(2):185-

191. Not relevant to adherence 

Ricart E, Bouma G, Salvador Pen et al. The therapeutic 

spectrum of infliximab and tumor necrosis factor 

immunomodulation in chronic inflammatory diseases. 

Drugs Today 2002;38(11):725-744. Not relevant to 

adherence 

Robert M E, Ament M E, Weinstein W M. The histologic 

spectrum and clinical outcome of refractory and

unclassified sprue. Am J Surg Pathol 2000;24(5):676-687. 

Not relevant to adherence 

Roizen N J, Patterson D. Down Syndrome. Lancet 

2003;361(9365):1281-1289. Not relevant to adherence 

Rolles C J, Anderson M, McNeish A S. Confirming 

persistence of gluten intolerance in children diagnosed as

having coeliac disease in infancy. Arch Dis Child

1975;50(4):259-263. Not relevant to adherence 

Rolles C J. Proceedings: Usefulness of a modified D-xylose 

absorption test in the preliminary diagnosis of coeliac 

disease and its later confirmation. Arch Dis Child 

1973;48(10):825Not relevant to adherence 

Romaldini Ceres C, Barbieri Dorina, Okay Thelma S et al. 

Serum soluble interleukin-2 receptor, interleukin-6, and

tumor necrosis factor-alpha levels in children with celiac 

disease: response to treatment. J Pediatr Gastroenterol Nutr 

2002;35(4):513-517. Monitoring not serology, EMA, tTG 

or biopsy based, or not promoting GFD adherence 

Rosekrans P C, Meijer C J, Polanco I et al. Long-term 

morphological and immunohistochemical observations on

biopsy specimens of small intestine from children with 

gluten-sensitive enteropathy. J Clin Pathol 1981;34(2):138-

144. Not relevant to adherence 

Roter D L, Hall J A, Merisca R et al. Effectiveness of 

Interventions to Improve Patient Compliance - a MetaAnalysis. Med Care 1998;36(8):1138-1161. Not relevant to 

adherence 

Russell J A. Osteomalacic myopathy. Muscle Nerve

1994;17(6):578-580. Not relevant to adherence 

Ryan J. Coeliac disease. Update 2000. Aust Fam Physician 

2000;29(9):835-838. Not relevant to adherence 

Sampson H A. 9. Food allergy. J Allergy Clin Immunol 

2003;111(2 Suppl 2):S540-S547. Not relevant to adherence 

Sanders S W, Zone J J. The relationship between dapsone 

dose, serum concentration and disease severity in dermatitis

herpetiformis. Arzneim-Forsch Drug Res 1986;36(1):146-

149. Not relevant to adherence 

Sategna Guidetti C, Solerio E, Scaglione N et al. Duration 

of gluten exposure in adult coeliac disease does not 

correlate with the risk for autoimmune disorders. Gut 

2001;49(4):502-505. Not relevant to adherence 

Sategna Guidetti, Carla Scaglione, Nadia Martini et al. Red 

cell distribution width as a marker of coeliac disease: a

prospective study. Eur J Gastroenterol Hepatol 

2002;14(2):177-181. Not relevant to adherence 

Sategna-Guidetti C, Grosso SB, Bruno M et al. Is human 

umbilical cord the most suitable substrate for the detection

of endomysium antibodies in the screening and follow-up 

of coeliac disease? Eur J Gastroenterol Hepatol 1997; 

9(7):657-660. Not relevant to adherence 

Sategna-Guidetti C, Grosso SB, Grosso S et al. The effects

of 1-year gluten withdrawal on bone mass, bone 

metabolism and nutritional status in newly-diagnosed adult 

coeliac disease patients. Alimentary Pharmacology & 

Therapeutics 2000; 14(1):35-43. No correlations with other 

measures

Sategna-Guidetti C, Volta U, Ciacci C et al. Prevalence of

thyroid disorders in untreated adult celiac disease patients 

and effect of gluten withdrawal: an Italian multicenter

study. Am J Gastroenterol 2001;96(3):751-757. Not 

relevant to adherence 

Scalici C, Manzoni D, Licastro G et al. Celiac disease in

the pediatric age, psychological difficulties experienced on 

the gluten-free diet. A preliminary investigation at the 

Clinic for Celiac Disease of the "G. Di Cristina" Hospital 

ARNAS, Palermo, Italy. Arch Mediterr Med 

2003;19(1):63-66. Not relevant to adherence 

Schenk E A, Samloff I M. Clinical and morphologic 

changes following gluten administration to patients with 

treated celiac dsease. Am J Pathol 1968;52(3):579-593. Not 

relevant to adherence 

Schmitz J. Is celiac disease a lifelong disorder?. Clinical 

and Investigative Medicine.Medecine Clinique Et
Experimentale 1996;19(5):352-356. Not relevant to 

adherence 

Schutz S M, Stroebel J, Schutz E M et al. Celiac sprue.

Diagnosis and diet: keys to recovery. N C Med J 

1994;55(1):32-36. Not relevant to adherence 

Schwartz M K, Sleisenger M H, Pert J H et al. The effect of

a gluten-free diet on fat, nitrogen, and mineral metabolism

in patients with sprue. Gastroenterology

1968;54(4):SupplNot relevant to adherence 

Scott E M, Gaywood I, Scott B B. Guidelines for 

osteoporosis in coeliac disease and inflammatory bowel 

disease. British Society of Gastroenterology. Gut

2000;46(Suppl 1):-1. Not relevant to adherence 

Scott H, Brandtzaeg P. Pathogenesis of food protein 

intolerance. Acta Paediatr Scand 1989;(Suppl 351):48-52. 

Not relevant to adherence 

Sdepanian V L, Morais M B, Scaletsky I C A et al.

Evaluation of theoretical knowledge of celiac disease and 

practical knowledge in preparing gluten-free foods by

celiac patients. Pediatrika 2001;21(8):39-44. Not relevant 

to adherence 

Secker-Walker R H, MorrowAL Kresnow M J, Flynn B S. 

Family Physician's Attitudes About Dietary Advice. Fam 

Pract Res J 1991;11(2):161-170. Not relevant to adherence 

Seraphin P, Mobarhan S. Mortality in patients with celiac 

disease. Nutr Rev 2002;60(4):116-118. Not relevant to 

adherence 

Shamir R, Levine A, Yalon-Hacohen M et al. Faecal occult

blood in children with coeliac disease. Eur J Pediatr 

2000;159(11):832-834. Not relevant to adherence 

Sheldon W. Prognosis in early adult life of coeliac children 

treated with a gluten-free diet. Br Med J 1969;2(654):401-

404. Not relevant to adherence 

Sher K S, Mayberry J F. Female fertility, obstetric and 

gynaecological history in coeliac disease: a case control 

study. Acta Paediatrica.Supplement 1996;41276-77. Not 

relevant to adherence 

Shmerling DH, Franckx J. Childhood celiac disease: a 

long-term analysis of relapses in 91 patients. J Pediatr

Gastroenterol Nutr 1986; 5(4):565-569. Not relevant to 

adherence 

Sicherer S H, Sampson H A. Food hypersensitivity and 

atopic dermatitis: Pathophysiology, epidemiology,

diagnosis, and management. J Allergy Clin Immunol 

1999;104(3 II):S114-S122. Not relevant to adherence 

Signore A, Chianelli M, Annovazzi A et al. Imaging active 

lymphocytic infiltration in coeliac disease with iodine-123-

interleukin-2 and the response to diet. European Journal of

Nuclear Medicine 2000; 27(1):18-24. No correlations with 

other measures 

Silink M. How should we manage celiac disease in 

childhood diabetes?. Pediatr Diabetes 2001;2(3):95-97. Not 

relevant to adherence 

Sklar M, Kirsner J B. Assessing and interviewing the

elderly: Interpretation of signs and symptoms. Bailliere's 

Best Pract Res Clin Gastroenterol 2001;15(6):851-867. Not 

relevant to adherence 

Smecuol E, Gonzalez D, Mautalen C et al. Longitudinal

study on the effect of treatment on body composition and

anthropometry of celiac disease patients. Am J 

Gastroenterol 1997;92(4):639-643. Not relevant to 

adherence 

Spiller R C. Postinfectious irritable bowel syndrome. 

Gastroenterology 2003;124(6):1662-1671. Not relevant to 

adherence 

Spollett G R. Nutritional management of common 

gastrointestinal problems. Nurse Pract Forum 1994;5(1):24-

27. Not relevant to adherence 

Srinivasan U, Jones E, Weir D G et al. Lactase enzyme, 

detected immunohistochemically, is lost in active celiac 

disease, but unaffected by oats challenge. Am J

Gastroenterol 1999;94(10):2936-2941. Not relevant to

adherence 

Stahlberg MR, Savilahti E, Siimes MA. Iron deficiency in

coeliac disease is mild and it is detected and corrected by

gluten-free diet. Acta Paediatr Scand 1991; 80(2):190-193. 

Not relevant to adherence 

Stenhammar L, Brandt A, Wagermark J. A family study of

coeliac disease. Acta Paediatr Scand 1982;71(4):625-628. 

Not relevant to adherence 

Stenhammar L, Kilander A F, Nilsson L A et al. Serum 

gliadin antibodies for detection and control of childhood 

coeliac disease. Acta Paediatr Scand 1984;73(5):657-663. 

Monitoring not serology, EMA, tTG or biopsy based, or not 

promoting GFD adherence 

Stenhammar L, Stromberg L, Kilander A F et al. Plasma 

enteroglucagon in the control of childhood celiac disease. J 

Pediatr Gastroenterol Nutr 1985;4(2):325-330. Not relevant

to adherence 

Stenhammar L. Transient gastro-intestinal disorders during 

infancy and early childhood. A follow-up study with 

special reference to coeliac disease. Acta Paediatr Scand 

1981;70(3):383-387. Not relevant to adherence 

Stern M, Ciclitira P J, van Eckert R et al. Analysis and 

clinical effects of gluten in coeliac disease. Eur J

Gastroenterol Hepatol 2001;13(6):741-747. Not relevant to 

adherence 
Stern M, Fischer K, Gruettner R. Gliadin antibodies in 

coeliac disease. Acta Paediatr Belg 

1977;30(4):252Monitoring not serology, EMA, tTG or 

biopsy based, or not promoting GFD adherence 

Stewart J S. Clinical and morphologic response to gluten

withdrawal. Clin Gastroenterol 1974;3(1):109-126. Not 

relevant to adherence 

Stewart Truswell A. Therapeutic diets. Br Med J

1985;291(6498):807-811. Not relevant to adherence 

Storsrud S, Olsson M, Arvidsson Lenner R et al. Adult 

coeliac patients do tolerate large amounts of oats. Eur J

Clin Nutr 2003;57(1):163-169. Not relevant to adherence 

Storsrud Stine, Hulthen Lena R, Lenner Ragnhild A. 

Beneficial effects of oats in the gluten-free diet of adults 

with special reference to nutrient status, symptoms and 

subjective experiences. Br J Nutr 2003;90(1):101-107. Not 

relevant to adherence 

Sullivan A. Coeliac disease. Nursing Standard (Royal

College of Nursing (Great Britain) - 1987) 1999;14(11):48-

52. Not relevant to adherence 

Sutton G. Coeliac disease: Testing the New Zealand 

iceberg. N Z J Med Lab Sci 2000; 54(2):46-48. No

correlations with other measures 

Szathmari M, Tulassay T, Arato A et al. Bone mineral

content and density in asymptomatic children with coeliac 

disease on a gluten-free diet. Eur J Gastroenterol Hepatol 

2001;13(4):419-424. Not relevant to adherence 

Tai V, Crowe M, O'Keefe S. Celiac disease in older people. 

J Am Geriatr Soc 2000;48(12):1690-1696. Not relevant to 

adherence 

Taylor S L, Hefle S L. Ingredient and labeling issues 

associated with allergenic foods. Allergy 2001;56(Suppl 

67):64-69. Not relevant to adherence 

Teeffelen-Heithoff A. Dietetic treatment of celiac disease.

Monatsschr Kinderheilkd 2003;151(7):719-725. Not 

relevant to adherence 

Thalayasingam B. Coeliac disease as a cause of

osteomalacia and rickets in the Asian immigrant

population. Br Med J 1985;290(6475):1146-1147. Not 

relevant to adherence 

Thomas T. Helping coeliac disease patients adapt to a 

gluten-free diet. Community Nurse 2000;6(6):19-22. Not 

relevant to adherence 

Thompson T. Do oats belong in a gluten-free diet?. J Am

Diet Assoc 1997;97(12):1413-1416. Not relevant to 

adherence 

Thompson T. Questionable foods and the gluten-free diet: 

survey of current recommendations. J Am Diet Assoc 

2000;100(4):463-465. Not relevant to adherence 

Thompson T. Wheat starch, gliadin, and the gluten-free 

diet. J Am Diet Assoc 2001;101(12):1456-1459. Not 

relevant to adherence 

Thornquist H, Jacobsen GS, Dahl LB et al. Coeliac disease 

and gluten-free diet: a following-up study of fifteen young 

adults. Ann Nutr Metab 1993; 37(6):295-301. Not relevant 

to adherence 

Tonder M, Sorlie D, Kearney M S. Adult coeliac disease: a 

case with ulceration, dermatitis herpetiformis and

reticulosarcoma. Scand J Gastroenterol 1976;11(1):107-

111. Not relevant to adherence 

Tonutti E, Visentini D, Bizzaro N et al. The role of 

antitissue transglutaminase assay for the diagnosis and 

monitoring of coeliac disease: a French-Italian multicentre 

study. J Clin Pathol 2003;56(5):389-393. Not relevant to 

adherence 

Trewby P N, Chipping P M, Palmer S J et al. Splenic 

atrophy in adult coeliac disease: is it reversible?. Gut 

1981;22(8):628-632. Not relevant to adherence 

Troncone R, Caputo N, Micillo M et al. Immunologic and

intestinal permeability tests as predictors of relapse during 

gluten challenge in childhood coeliac disease. Scand J 

Gastroenterol 1994;29(2):144-147. Not relevant to 

adherence 

Troncone R, Greco L, Mayer M et al. In siblings of celiac 

children, rectal gluten challenge reveals gluten sensitization

not restricted to celiac HLA. Gastroenterology

1996;111(2):318-324. Not relevant to adherence 

Troncone R, Starita A, Coletta S et al. Antigliadin

antibody, D-xylose, and cellobiose/mannitol permeability 

tests as indicators of mucosal damage in children with 

coeliac disease. Scand J Gastroenterol 1992;27(8):703-706. 

No monitoring measure of interest 

Troncone Riccardo, Franzese Adriana, Mazzarella

Giuseppe et al. Gluten sensitivity in a subset of children

with insulin dependent diabetes mellitus. Am J 

Gastroenterol 2003;98(3):590-595. Not relevant to 

adherence 

Tursi A, Brandimarte G, Giorgetti GM. Sorbitol H2-breath 

test versus anti-endomysium antibodies to assess 

histological recovery after gluten-free diet in coeliac 

disease. Digestive and Liver Disease - Official Journal of

the Italian Society of Gastroenterology and the Italian

Association for the Study of the Liver 2002; 34(12):846-

850. No correlations with other measures 

Tursi Antonio, Brandimarte Giovanni, Giorgetti 

GianMarco. High prevalence of small intestinal bacterial 

overgrowth in celiac patients with persistence of 
gastrointestinal symptoms after gluten withdrawal. Am J 

Gastroenterol 2003;98(4):839-843. Not relevant to 

adherence 

Tursi Antonio, Brandimarte Giovanni. The symptomatic

and histologic response to a gluten-free diet in patients with 

borderline enteropathy. J Clin Gastroenterol 2003;36(1):13-

17. Not relevant to adherence 

Twist S R, Hackett A F. An investigation of some

implications of coeliac disease. J Hum Nutr Diet 

1992;5(6):343-350. Not relevant to adherence 

Uil J J, van Elburg R M, van Overbeek F M et al. Followup of treated coeliac patients: sugar absorption test and

intestinal biopsies compared. Eur J Gastroenterol Hepatol

1996;8(3):219-223. No monitoring measure of interest 

Usai P, Minerba L, Marini B et al. Case control study on 

health-related quality of life in adult coeliac disease. 

Digestive and Liver Disease - Official Journal of the Italian

Society of Gastroenterology and the Italian Association for

the Study of the Liver 2002;34(8):547-552. Not relevant to 

adherence 

Vainio E, Kosnai I, Hallstrom O et al. Antigliadin and 

antireticulin antibodies in children with dermatitis

herpetiformis. J Pediatr Gastroenterol Nutr 1986;5(5):735-

739. Not relevant to adherence 

Valdimarsson T, Lofman O, Toss G et al. Reversal of 

osteopenia with diet in adult coeliac disease. Gut 

1996;38(3):322-327. Not relevant to adherence 

Valdimarsson T, Toss G, Lofman O et al. Three years'

follow-up of bone density in adult coeliac disease: 

significance of secondary hyperparathyroidism. Scand J 

Gastroenterol 2000;35(3):274-280. Not relevant to 

adherence 

van den, Bosch H C, Tham R T et al. Celiac disease: smallbowel enteroclysis findings in adult patients treated with a

gluten-free diet. Radiology 1996;201(3):803-808. Not 

relevant to adherence 

Varkonyi A, Boda M, Endreffy E et al. Coeliac disease:

always something to discover. Scandinavian Journal of

Gastroenterology.Supplement 1998;228122-129. Not 

relevant to adherence 

Vazquez H, Smecuol E, Flores D et al. Relation between 

cigarette smoking and celiac disease: evidence from a casecontrol study. Am J Gastroenterol 2001;96(3):798-802. Not 

relevant to adherence 

Vermeer B J, Lindeman J, Harst-Oostveen C J et al. The 

immunoglobulin-bearing cells in the lamina propria and the 

clinical response to a gluten-free diet in dermatitis

herpetiformis. Archives for Dermatological 

Research.Archiv Fur Dermatologische Forschung

1977;258(3):223-230. Not relevant to adherence 

Vermeire E, Hearnshaw H, Van Royen P et al. Patient

Adherence to Treatment: Three Decades of Research. A 

Comprehensive Review. J Clin Pharm Ther

2001;26(5):331-342. Not relevant to adherence 

Visakorpi J K, Kuitunen P, Savilahti E. Frequency and 

nature of relapses in children suffering from the 

malabsorption syndrome with gluten intolerance. Acta

Paediatr Scand 1970;59(5):481-486. Not relevant to 

adherence 

Vogelsang H, Propst A, Dragosics B et al. Diagnosis and 

therapy of celiac disease in adolescence and adulthood. Z 

Gastroenterol 2002;40(7):1-7. Not relevant to adherence 

Vogelsang H, Schwarzenhofer M, Oberhuber G. Changes 

in gastrointestinal permeability in celiac disease. Dig Dis 

1998;16(6):333-336. Review article 

Volta U, Cassani F, De Franchis R et al. Antibodies to 

gliadin in adult coeliac disease and dermatitis

herpetiformis. Digestion 1984;30(4):263-270. Monitoring

not serology, EMA, tTG or biopsy based, or not promoting 

GFD adherence 

Volta U, De Giorgio R, Petrolini N et al. Clinical findings

and anti-neuronal antibodies in coeliac disease with 

neurological disorders. Scand J Gastroenterol 

2002;37(11):1276-1281. Not relevant to adherence 

Vuoristo M, Tilvis R, Miettinen T A. Serum plant sterols 

and lathosterol related to cholesterol absorption in coeliac 

disease. Clinica Chimica Acta - International Journal of

Clinical Chemistry 1988;174(2):213-224. No monitoring

measure of interest

Wahab PJ, Meijer Jos WR, Mulder Chris JJ. Histologic 

follow-up of people with celiac disease on a gluten-free 

diet: slow and incomplete recovery. American Journal of

Clinical Pathology 2002; 118(3):459-463. No correlations 

with other measures

Walton C, Walton S. Primary biliary cirrhosis in a diabetic

male with dermatitis herpetiformis. Clin Exp Dermatol 

1987;12(1):46-47. Not relevant to adherence 

Wauters E A, Jansen J, Houwen R H et al. Serum IgG and

IgA anti-gliadin antibodies as markers of mucosal damage 

in children with suspected celiac disease upon gluten 

challenge. J Pediatr Gastroenterol Nutr 1991;13(2):192-

196. Not relevant to adherence 

Weile B. Aspects of classic symptomatic childhood coeliac 

disease in Denmark: Retrospectively illustrated by local,

regional, and national studies. APMIS Suppl 

2003;111(113):5-46. Not relevant to adherence 

Weir D G, Hourihane D O. Coeliac disease during the

teenage period: the value of serial serum folate estimations.

Gut 1974;15(6):450-457. Not relevant to adherence 
Weizman Z, Ben Zion Y Z, Binsztok M et al. Correlation 

of clinical characteristics and small bowel histopathology

in celiac disease. J Pediatr Gastroenterol Nutr

1997;24(5):555-558. Not relevant to adherence 

Westman E, Ambler G R, Royle M et al. Children with 

coeliac disease and insulin dependent diabetes mellitus--

growth, diabetes control and dietary intake. Journal of

Pediatric Endocrinology & Metabolism - Jpem 

1999;12(3):433-442. Not relevant to adherence 

Wharton B, Wharton P. Nutrition in adolescence. Nutr 

Health 1987;4(4):195-203. Not relevant to adherence 

Willis J. Coeliac disease: maintaining a gluten-free diet. 

Nurs Times 1996;92(17):44, 46Not relevant to adherence 

Young W F, Pringle E M. 110 children with coeliac 

disease, 1950-1969. Arch Dis Child 1971;46(248):421-436. 

Not relevant to adherence 

Ziegler Anette, Schmid Sandra, Huber Doris et al. Early

Infant Feeding and Risk of Developing Type 1 DiabetesAssociated Autoantibodies. JAMA 2003;290(13):1721-

1728. Not relevant to adherence 

Zouganelis S, Priest M. Impact of dietary compliance on 

nutritional status in adult coeliac disease. Gut 2001; 

48(Suppl 1):A42. No correlations with other measur