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## Complete Summary

#### GUIDELINE TITLE

Eosinophilic esophagitis in children and adults: a systematic review and
consensus recommendations for diagnosis and treatment.

#### BIBLIOGRAPHIC SOURCE(S)

Furuta GT, Liacouras CA, Collins MH, Gupta SK, Justinich C, Putnam PE,
Bonis P, Hassall E, Straumann A, Rothenberg ME, First International
Gastrointestinal Eosinophil Research Symposium (FIGERS). Eosinophilic
esophagitis in children and adults: a systematic review and consensus
recommendations for diagnosis and treatment. Gastroenterology 2007
Oct;133(4):1342-63. \[121 references\]
[PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17919504)

#### GUIDELINE STATUS

This is the current release of the guideline.

According to the guideline developer, the Clinical Practice Committee
meets three times a year to review all American Gastroenterological
Association Institute (AGA Institute) guidelines. This review includes
new literature searches of electronic databases followed by expert
committee review of new evidence that has emerged since the original
publication date.

### COMPLETE SUMMARY CONTENT

 SCOPE\
 METHODOLOGY - including Rating Scheme and Cost Analysis\
 RECOMMENDATIONS\
 EVIDENCE SUPPORTING THE RECOMMENDATIONS\
 BENEFITS/HARMS OF IMPLEMENTING THE GUIDELINE RECOMMENDATIONS\
 IMPLEMENTATION OF THE GUIDELINE\
 INSTITUTE OF MEDICINE (IOM) NATIONAL HEALTHCARE QUALITY REPORT
CATEGORIES\
 IDENTIFYING INFORMATION AND AVAILABILITY\
 DISCLAIMER

### SCOPE

#### DISEASE/CONDITION(S)

Eosinophilic esophagitis

#### GUIDELINE CATEGORY

Diagnosis\
Evaluation\
Management\
Treatment

#### CLINICAL SPECIALTY

Allergy and Immunology\
Family Practice\
Gastroenterology\
Internal Medicine\
Nutrition\
Pathology\
Pediatrics

#### INTENDED USERS

Dietitians\
Physicians

#### GUIDELINE OBJECTIVE(S)

-   To document the current state of knowledge in eosinophilic
    esophagitis

-   To determine diagnostic criteria and make recommendations for
    evaluation and treatment of children and adults with suspected
    eosinophilic esophagitis

-   To determine how to advance the field by expanding knowledge and
    defining priorities and strategies for future research

#### TARGET POPULATION

Adults and children with eosinophilic esophagitis

#### INTERVENTIONS AND PRACTICES CONSIDERED

**[Diagnosis/Evaluation/Monitoring]{.underline}**

1.  Endoscopy

2.  Biopsy

3.  Intraesophageal pH testing

4.  Esophageal manometry (not recommended)

5.  Endoscopic ultrasound

6.  Radiography (upper gastrointestinal contrast study)

7.  Histopathology

    -   Quantitation of eosinophils

    -   Observation of eosinophil morphology

    -   Evaluation of other inflammatory cell types (lymphocytes,
        polymorphonuclear leukocytes, mast cells)

8.  Monitoring via regular clinic visits

**[Management]{.underline}**

**Allergic Evaluation**

1.  History, physical examination, and testing for other atopic
    diatheses

2.  Evaluation of peripheral blood eosinophil count and granule proteins

3.  Evaluation of total circulating immunoglobulin E (IgE),
    aeroallergen-specific IgE, and food-specific IgE

4.  Evaluation of peripheral cytokines and gene expression

5.  Skin prick testing

6.  Atopy patch testing (not yet recommended)

**[Treatment]{.underline}**

1.  Acid suppression using proton pump inhibitors

2.  Esophageal dilatation

3.  Corticosteroids (systemic and topical)

4.  Cromolyn sodium (not recommended)

5.  Leukotriene receptor antagonists (not recommended)

6.  Dietary treatment

7.  Biologics (anti-interleukin 5) (not recommended)

#### MAJOR OUTCOMES CONSIDERED

-   Morbidity and comorbidity

-   Relapse rate

-   Quality of life

-   Incidence of treatment side effects

-   Sensitivity, specificity, and positive and negative predictive
    values of laboratory tests

-   Correlation of laboratory signs with symptoms

### METHODOLOGY

#### METHODS USED TO COLLECT/SELECT EVIDENCE

Searches of Electronic Databases

#### DESCRIPTION OF METHODS USED TO COLLECT/SELECT THE EVIDENCE

A systematic review of the English language medical literature through
September 2006 was performed using electronic databases (MEDLINE,
PubMed, and Ovid), with the key words \"eosinophilic esophagitis,\"
\"allergic esophagitis,\" and \"eosinophilic oesophagitis.\" Review
articles, letters to the editor, most case reports of \<3 patients, and
abstracts were excluded.

A total of 80 studies met the inclusion criteria and served as the basis
of this report. They include a total of 754 children (age range, 4
months to 20 years) and 323 adults (age range, 22 to 89 years). The
sample sizes varied from 7 to 381 patients (mean, 37 years). The studies
were published between 1977 and September 2006. Most were conducted in
academic centers in the United States, Canada , Europe, and Australia.

#### NUMBER OF SOURCE DOCUMENTS

A total of 80 studies met the inclusion criteria and served as the basis
of this report.

#### METHODS USED TO ASSESS THE QUALITY AND STRENGTH OF THE EVIDENCE

Weighting According to a Rating Scheme (Scheme Given)

#### RATING SCHEME FOR THE STRENGTH OF THE EVIDENCE

The quality of evidence supporting the recommendations contained in this
review was assessed as follows:

**Grade A**: Homogeneous evidence from multiple, well-designed,
randomized (therapeutic) or cohort (descriptive) controlled trials, each
involving a number of participants to be of sufficient statistical power

**Grade B**: Evidence from at least 1, large, well-designed clinical
trial with or without randomization from cohort or case-control analytic
studies or well-designed meta-analysis

**Grade C**: Evidence based on clinical experience, descriptive studies,
or reports of expert committees

#### METHODS USED TO ANALYZE THE EVIDENCE

Review of Published Meta-Analyses\
Systematic Review

#### DESCRIPTION OF THE METHODS USED TO ANALYZE THE EVIDENCE

Relevant data were discussed among committee members in conference
calls. Critical evaluations included study design, numbers of patients,
definitions used, outcomes reported, and potential biases. The chair of
each committee synthesized the data, and inconsistencies were resolved
by discussion until consensus was achieved.

#### METHODS USED TO FORMULATE THE RECOMMENDATIONS

Expert Consensus

#### DESCRIPTION OF METHODS USED TO FORMULATE THE RECOMMENDATIONS

A task force of 31 physicians who participated in the First
International Gastrointestinal Eosinophil Research Symposium (FIGERS)
performed the review. The reviewers were divided into subcommittees
along the lines of their recognized expertise in clinical evaluation,
endoscopy, histopathology, allergy, and treatment.

Relevant data were discussed among committee members in conference
calls. Critical evaluations included study design, numbers of patients,
definitions used, outcomes reported, and potential biases. The chair of
each committee synthesized the data, and inconsistencies were resolved
by discussion until consensus was achieved.

#### RATING SCHEME FOR THE STRENGTH OF THE RECOMMENDATIONS

Not applicable

#### COST ANALYSIS

A formal cost analysis was not performed and published cost analyses
were not reviewed.

#### METHOD OF GUIDELINE VALIDATION

Peer Review

#### DESCRIPTION OF METHOD OF GUIDELINE VALIDATION

Not stated

### RECOMMENDATIONS

#### MAJOR RECOMMENDATIONS

The level of evidence supporting the recommendations (A--C) is defined
at the end of the \"Major Recommendations\" field.

**[Clinical Manifestations]{.underline}**

Eosinophilic esophagitis (EE) should be considered in young children
with gastroesophageal reflux disease (GERD)-like symptoms, including
feeding problems, and in older children and adults with GERD-like
symptoms, especially in those with dysphagia or esophageal food
impaction. When the primary diagnosis is EE, symptoms are unresponsive
or only partially responsive to acid blockade (**Grade B**).

**[Natural History]{.underline}**

EE tends to be a chronic disease with persistent or relapsing symptoms.
To date, esophageal strictures and small caliber esophagus, often
resulting in food impaction, have been the major complications
identified. When these findings are encountered, either radiologically
or at endoscopy, a high index of suspicion should be raised for EE, and
mucosal biopsy specimens should be obtained (**Grade B**). Although
esophageal metaplasia (Barrett\'s esophagus or cardia-type metaplasia)
has not been described as an associated finding in patients with EE,
careful long-term follow-up is advised. Other chronic problems include
failure to thrive and feeding intolerance in children. At present, it is
unclear whether persistent esophageal eosinophilia is always accompanied
by symptoms. See \"Monitoring\" section below.

**[Diagnostic Testing]{.underline}**

**Biopsy Procurement and Evaluation**

The rationale for histological assessment of EE is provided in the
original guideline document. Endoscopic appearances should be documented
and photographed. Mucosal pinch biopsy specimens should be obtained from
all patients in whom EE is in the differential diagnosis. Biopsy
specimens should be obtained *regardless of the gross appearance of the
mucosa*, and multiple biopsy specimens should be obtained from different
esophageal locations along the length of the esophagus. Biopsy specimens
should also be obtained from stomach and duodenum to rule out other
diseases such as eosinophilic gastroenteritis and, when appropriate,
inflammatory bowel disease. Optimal fixation is accomplished by using
fixative such as formalin or paraformaldehyde (**Grade C**). The
cost-effectiveness of these recommendations has not been evaluated but
deserves further study.

**Endoscopic Ultrasound**

When the diagnosis of GERD vs EE is not apparent despite endoscopy and
biopsy, intraesophageal pH monitoring may be of use in excluding
pathologic reflux as either the primary or a concomitant cause for
esophageal eosinophilia (**Grade B**). Alternatively, an upper endoscopy
after 6 to 8 weeks of high-dose proton pump inhibitor (PPI) treatment
can help determine the etiology of esophageal eosinophilia (see
Treatment section). Esophageal manometry does not provide diagnostic
value in patients with EE.

**Radiography**

In patients with dysphagia, an upper gastrointestinal (GI) contrast
study may identify the presence of a stricture, as well as its caliber
and length. A contrast study may be beneficial for children who present
with vomiting to rule out anatomic etiologies such as malrotation
(**Grade C**). This information is also potentially helpful for a
subsequent upper endoscopy because it may alert the endoscopist to use a
smaller caliber endoscope or to proceed particularly cautiously with
passage of the instrument so as to lessen the likelihood of a mucosal
tear. In addition, it prepares the endoscopist for the possible need for
a dilatation. An upper GI contrast study is generally not useful in
patients presenting with symptoms typical of GERD, e.g., heartburn.

**[Histopathology]{.underline}**

EE is a clinicopathologic disease defined by esophageal symptoms
associated with a severe isolated esophageal eosinophilia and absence of
pathologic GERD as evidenced by normal pH monitoring of the distal
esophagus or lack of response to high-dose PPI treatment.
Intraepithelial eosinophils should be counted in the most intensely
inflamed high-power field (HPF) of the biopsy (x400) to generate a peak
count. Setting a fixed number of eosinophils as the sole cut-off
criterion to distinguish EE from GERD is contentious, possibly
misleading, and probably unwise based on current knowledge. On the basis
of this literature review and collective clinical experience, the
guideline authors conclude that a peak count of at least 15
intraepithelial eos/HPF is an absolute minimum number to make the
diagnosis of EE *in the proper clinical context* (**Grade B**). If all
HPFs are counted, the mean eosinophil number may be less than 15 because
of focal inflammation in the biopsy specimens, but at least 1 HPF must
contain at least 15 intraepithelial eosinophils. For research purposes,
defining EE with a higher threshold of peak eosinophils may be advisable
to increase the specificity of the diagnosis.

Additional features that are not pathognomonic but may be helpful to the
pathologist in recognizing EE include eosinophil microabscesses
(correlate of endoscopic mucosal with specks and plaques), surface
layering of eosinophils, basal layer hyperplasia, papillary lengthening,
degranulating eosinophils, and lamina propria fibrosis and inflammation.
These features should be assessed in all biopsy specimens and included
in pathology reports in addition to the number of eosinophils. The
diagnostic criteria for adults are the same as for children.
Gastroenterologists treating adults and children with symptoms of
esophageal dysfunction and numerous intraepithelial eosinophils in
esophageal biopsy specimens should ensure that the disease cannot be
attributed solely to GERD before making a diagnosis of EE.

**[Allergic Evaluation]{.underline}**

**History, Physical Examination, and Testing for Other Atopic
Diatheses**

Because of the high rate of allergic rhinitis, asthma, and/or eczema in
EE patients, a complete evaluation by a well-informed allergist for
other atopic diatheses is recommended (**Grade C**).

**Assessment of Atopy by Analysis of Blood Samples**

*Peripheral Eosinophil Count and Eosinophil Granule Proteins*

Evaluation of peripheral blood eosinophils may provide supportive
evidence for the presence of EE and the degree of tissue involvement but
are not diagnostic, and correlation with disease activity is unknown
(**Grade C**). In future studies, if eosinophil levels are to be
followed, it is important that (1) blood eosinophil levels be drawn at
diagnosis and again at each evaluation for response to treatment
(dietary or medical) and (2) notation is made regarding the control of
concurrent atopic diatheses and the extent of aeroallergen exposure at
each time when eosinophil count is evaluated. Absolute eosinophil counts
and defining criteria for \"blood eosinophilia\" should be reported in
publications that document peripheral eosinophilia. Further studies are
needed to evaluate whether eosinophils constitute an adequate surrogate
disease marker either alone or in combination with other surrogate
disease markers such as eosinophil-derived neurotoxin (EDN).

*Total Immunoglobulin E (IgE)*

No published studies document whether or not total IgE can serve as a
surrogate marker for disease progression or resolution. If total IgE
levels are to be followed, it is imperative that (1) an evaluation is
done regarding whether or not the patient has adequate aeroallergen
avoidance and the pollen season at each time when the total IgE level is
evaluated and (2) an evaluation is done regarding whether or not
concurrent atopic diatheses are adequately controlled at the time that
the total IgE is evaluated. If IgE levels are followed, it is
recommended that levels be checked at diagnosis and at each endoscopic
evaluation of disease response to intervention (**Grade C**). It is
important that total IgE levels be interpreted within the context of
age-defined normal values and that the total IgE level that is
considered \"normal\" be clearly stated in any publication.

*Aeroallergen-Specific IgE*

Given the high rate of other allergic diatheses (50% to 80%) in EE
patients and the potential of aeroallergens to have a role in the
instigation of EE, it may be important to evaluate EE patients for
aeroallergen sensitivity (**Grade C**). Allergy testing may predict the
response to pharmacotherapy or dietary avoidance in EE patients and thus
warrants evaluation.

*Food-Specific IgE*

There are no positive or negative predictive values for food-specific
IgE level testing in EE. In vitro food allergy testing is not supported
in the evaluation of EE patients at this time, and empiric food testing
should utilize skin prick tests (see below; **Grade B**).

*Peripheral Cytokines*

Eotaxin-3 expression and its genetic variation are promising markers of
distinguishing EE from other causes of esophagitis (**Grade B**). Future
research concerning the reversibility of eotaxin-3 levels with therapy
and their prognostic significance deserve further investigation.

*Gene Expression*

Although the results of eotaxin-3 expression in EE vs non-EE patients
are highly promising, assessment of eotaxin-3 remains a research tool,
and correlations with disease severity and activity remain to be
evaluated (**Grade B**). The identified EE transcriptome may indeed have
promising value for disease diagnosis, assessment of therapeutic
responsiveness, and prognosis.

*Skin Prick Testing for Antigen Sensitization*

Skin prick testing for foods and environmental allergens should be
considered so that potential allergens and the atopic status of EE
patients are identified (**Grade C**).

**Application of Atopy Patch Testing (APT) in EE**

The combination of prick skin tests and APT has been successful in one
center and is being examined at other centers to verify these results.
In addition, APT has shown promise in atopic dermatitis with good
predictive values, high specificity, and low sensitivity, and APT has
shown highly promising results with regard to food elimination diet and
food reintroduction in patients with EE. However, its use should be
reserved until additional data from multiple research teams emerge that
clearly establish its value for diagnosing and/or managing EE (**Grade
B**). In addition, further data regarding the types of cells and immune
response that is occurring at the site of patch testing are needed
(e.g., skin biopsy studies).

**[Treatment of EE]{.underline}**

**Acid Suppression**

Acid suppression is useful as a part of fulfilling the diagnostic
criteria for EE. In addition, it may be used in lieu of esophageal pH
monitoring for patients with established EE who have symptoms secondary
to concomitant GERD. PPI therapy should not be considered as a primary
treatment for patients with EE. Rather, it may be considered as
co-therapy because it sometimes alleviates symptoms in part (**Grade
C**). It is interesting to speculate that the esophagus of EE patients
may have enhanced sensitivity to acid, even in the absence of pathologic
reflux.

**Esophageal Dilatation**

Esophageal dilatation is useful for symptomatic patients who present
with symptomatic esophageal narrowing secondary to fixed strictures
causing food impaction (**Grade C**). However, because of the risk of
mucosal tearing and perforation, whenever possible, a diagnostic
endoscopy with biopsy followed by medical or dietary therapy for EE
should be attempted prior to performing esophageal dilatation.
Inspection of the esophageal mucosa (radiographic or very gentle
endoscopic examination) should be considered following esophageal
dilation to assess for laceration injury prior to the performance of
sequential, larger caliber dilation.

**Corticosteroids**

Systemic and topical corticosteroids effectively resolve acute
clinicopathologic features of EE; however, when discontinued, the
disease generally recurs. Systemic corticosteroids may be utilized in
emergent cases such as dysphagia requiring hospitalization, dehydration
because of swallowing difficulties, and weight loss. However, because of
the potential for significant toxicity, their long-term use is not
recommended (**Grade B**). For many patients, topical corticosteroids
are also effective in inducing EE remission. Although the incidence of
adverse effects with this form of administration has not been formally
studied, several studies have documented its safety, except for local
fungal infections.

The use of topical corticosteroids for maintenance treatment has not
been studied. Age adjusted doses and administration frequency of topical
corticosteroids, i.e., fluticasone, budesonide, for children and adults
with EE have not been established and these formulations were not
designed for esophageal administration. One study extrapolated doses
from those utilized in the treatment of asthma. Since then, others have
utilized higher doses without significant complications. On the basis of
expert opinion and the current literature, suggested starting doses
range from 440 to 880 micrograms per day for children and 880 to 1760
per day for adolescents/adults. Drug has been administered by mouth and
can be split into twice or 4 times daily doses. Equally important is the
method of administration; patients should be instructed to administer
the metered dose inhaler (MDI) without the use of a spacer. The MDI
should be inserted into the mouth, sprayed with lips sealed around the
device. The powder should then be swallowed and not rinsed. Patients
should not eat or drink for at least 30 minutes. This regimen is
continued for 6 to 8 weeks and then patients followed as described in
Monitoring section (**Grade B**). More studies are needed to clarify
specifics of topical steroid treatment plans. Also see Update section in
the original guideline document for information on alternative method of
administration.

**Leukotriene Receptor Antagonists and Mast Cell Stabilizers**

Although cromolyn sodium has no significant adverse effects, it has no
apparent therapeutic effect for patients with EE. Leukotriene receptor
antagonists have been shown to induce symptomatic relief at high
dosages; however, its use has not been shown to have any effect on
esophageal eosinophilia. Measurements of mucosal leukotriene levels do
not suggest potential for a therapeutic benefit. The use of these drugs
for the treatment of EE is not supported by the current literature
(**Grade C**).

**Dietary Treatment**

Dietary therapy (the specific antigens removal or elemental formula)
should be considered as an effective therapy in all children diagnosed
with EE (**Grade B**). When deciding on the use of a specific dietary
therapy, the patient\'s lifestyle and family resources also need to be
considered. Consultation with a registered dietitian is strongly
encouraged to ensure that proper calories, vitamins, and micronutrients
are maintained. The use of dietary therapy in adults requires further
study.

**Biologics**

Novel biologic agents present a unique opportunity for certain patients
with EE. These molecules await clinical trials and cannot be recommended
for routine use at the present time (**Grade C**).

**Monitoring**

In children and adults with EE, the guideline authors suggest regular
clinic visits during which the patient and parents should be questioned
about symptoms, compliance with therapy, and adverse effects (**Grade
C**). This suggestion is based on improving the recognition of long-term
complications associated with chronic esophageal eosinophilia;
presently, the incidence of complications is unknown.

In children, options for endoscopic and radiographic monitoring should
be discussed considering the issues above. One approach might be to
perform repeated upper endoscopies until settling on a treatment regimen
that has controlled symptoms and ideally resolved esophageal
eosinophilia. Repeat examinations can be based on change in symptoms or
compliance with therapy. If repeat endoscopy with biopsy is planned, it
should be performed no sooner than 4 weeks after the last therapeutic
intervention. These suggestions are based on improving the recognition
of long-term complications associated with chronic esophageal
eosinophilia; currently, data are not available to determine the optimal
method to follow patients.

In asymptomatic patients with persistent esophageal eosinophilia, a
repeat upper endoscopy can be performed following institution of
additional treatment. For those in whom additional treatment is
deferred, a repeat upper endoscopy and/or barium swallow can be obtained
every 2 to 3 years to evaluate for progressive disease, but the risks of
this approach outside of a clinical research protocol need to be weighed
against the unknown benefits; this is especially important because the
accuracy of histologic and radiologic predictors of disease progression
is unclear.

The approach to adults with EE should consider similar principles as
described above for children. However, clinical experience suggests that
adults may be inclined to guide treatment based mainly on symptoms.
Thus, the need for surveillance should also consider willingness to
accept more aggressive treatment based on the results.

**[Definitions]{.underline}**:

**Levels of Evidence**

**Grade A**: Homogeneous evidence from multiple, well-designed,
randomized (therapeutic) or cohort (descriptive) controlled trials, each
involving a number of participants to be of sufficient statistical power

**Grade B**: Evidence from at least 1, large, well-designed clinical
trial with or without randomization from cohort or case-control analytic
studies or well-designed meta-analysis

**Grade C**: Evidence based on clinical experience, descriptive studies,
or reports of expert committees

#### CLINICAL ALGORITHM(S)

None provided

### EVIDENCE SUPPORTING THE RECOMMENDATIONS

#### TYPE OF EVIDENCE SUPPORTING THE RECOMMENDATIONS

The type of supporting evidence is graded and identified for each
recommendation (see \"Major Recommendations\").

The quality of evidence fell primarily into the grade C category
(evidence based on clinical experience, descriptive studies, or reports
of expert committees).

### BENEFITS/HARMS OF IMPLEMENTING THE GUIDELINE RECOMMENDATIONS

#### POTENTIAL BENEFITS

Accurate diagnosis and appropriate treatment of eosinophilic esophagitis

#### POTENTIAL HARMS

-   Esophageal dilation carries the risk of mucosal tearing and
    perforation.

-   Systemic corticosteroids are associated with significant adverse
    effects.

-   Drug treatments are less restrictive \[than dietary treatments\],
    placing no compromises on the patient\'s diet, but carry potential
    adverse effects and unknown duration of treatment.

-   Dietary treatments give the prospect of prolonged remission but
    entail significant lifestyle modification.

-   Corticosteroids, even if given topically, have been associated with
    esophageal candidiasis, and the long-term safety of strategies
    involving such treatment is unknown.

### IMPLEMENTATION OF THE GUIDELINE

#### DESCRIPTION OF IMPLEMENTATION STRATEGY

An implementation strategy was not provided.

### INSTITUTE OF MEDICINE (IOM) NATIONAL HEALTHCARE QUALITY REPORT CATEGORIES

#### IOM CARE NEED

Getting Better\
Living with Illness

#### IOM DOMAIN

Effectiveness\
Patient-centeredness

### IDENTIFYING INFORMATION AND AVAILABILITY

#### BIBLIOGRAPHIC SOURCE(S)

Furuta GT, Liacouras CA, Collins MH, Gupta SK, Justinich C, Putnam PE,
Bonis P, Hassall E, Straumann A, Rothenberg ME, First International
Gastrointestinal Eosinophil Research Symposium (FIGERS). Eosinophilic
esophagitis in children and adults: a systematic review and consensus
recommendations for diagnosis and treatment. Gastroenterology 2007
Oct;133(4):1342-63. \[121 references\]
[PubMed](http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=17919504)

#### ADAPTATION

Not applicable: The guideline was not adapted from another source.

#### DATE RELEASED

2007 Aug

#### GUIDELINE DEVELOPER(S)

American Gastroenterological Association Institute - Medical Specialty
Society\
North American Society for Pediatric Gastroenterology, Hepatology, and
Nutrition - Professional Association

#### SOURCE(S) OF FUNDING

American Gastroenterological Association Institute

Supported by a small conference grant R13 DK076672 from the National
Institutes of Health to The First International Gastrointestinal
Eosinophil Research (FIGER) Symposium; North American Society of
Pediatric Gastroenterology, Hepatology; the American Academy of Allergy,
Asthma, and Immunology; The American Partnership for Eosinophilic
Diseases; a philanthropic contribution from a grateful family; and
educational grants (AstraZeneca, Abbot Laboratories, Nutricia, TAP,
Ception, GlaxoSmithKline).

#### GUIDELINE COMMITTEE

First International Gastrointestinal Eosinophil Research Symposium
(FIGERS) Subcommittee

#### COMPOSITION OF GROUP THAT AUTHORED THE GUIDELINE

*Authors*: Glenn T. Furuta; Chris A. Liacouras; Margaret H. Collins;
Sandeep K. Gupta; Chris Justinich; Phil E. Putnam; Peter Bonis; Eric
Hassall; Alex Straumann; Marc E. Rothenberg

**FIGERS Subcommittees**

*Clinical Features and Diagnostic Testing*

Sandeep K. Gupta, MD, (*Chair*), Division of Pediatric Gastroenterology,
Hepatology, and Nutrition, Riley Hospital for Children, Indiana
University School of Medicine, Indianapolis, Indiana; Samuel Nurko, MD,
MPH, Division of Gastroenterology, Hepatology, and Nutrition,
Children\'s Hospital Boston, Harvard Medical School, Boston,
Massachusetts; Nirmala Gonsalves, MD, Division of Gastroenterology,
Northwestern University, Feinberg School of Medicine, Chicago, Illinois;
Peter Bonis, MD, Division of Gastroenterology, Tufts University School
of Medicine, Boston, Massachusetts; Alex Straumann, MD, Department of
Gastroenterology, University Hospital Basel, University Basel, Basel,
Switzerland; Jonathan Markowitz, MD, MSCE, Pediatric Gastroenterology
and Nutrition, Greenville Hospital System, University Medical Center,
Greenville, South Carolina

*Histopathology*

Margaret H. Collins, MD, (*Chair*), Division of Pathology, University of
Cincinnati, Cincinnati Children\'s Hospital Medical Center, Cincinnati,
Ohio; Simon P. Hogan, PhD, Division of Allergy and Immunology,
Cincinnati Children\'s Hospital Medical Center, University of Cincinnati
College of Medicine, Cincinnati, Ohio; Glenn T. Furuta, MD, Section of
Pediatric Gastroenterology, Hepatology, and Nutrition, The Children\'s
Hospital, Denver, University of Colorado Medical School, Denver,
Colorado; Don Antonioli, MD, Department of Pathology, Beth Israel
Deaconess Hospital, Harvard Medical School, Boston, Massachusetts;
Eduardo Ruchelli, MD, University of Pennsylvania School of Medicine,
Department of Pathology, The Children\'s Hospital of Philadelphia,
Philadelphia, Pennsylvania; Hector Melin-Aldana, MD, Northwestern
University, Feinberg School of Medicine, Pathology and Laboratory
Medicine, Children\'s Memorial Hospital, Chicago, Illinois; Margret S.
Magid, MD, Department of Pathology, Mount Sinai School of Medicine, New
York, New York

*Endoscopy*

Chris Justinich, MD, FRCPC, (*Chair*), Division of Pediatric
Gastroenterology, Queen\'s University, Kingston General Hospital,
Kingston, Ontario, Canada; Ikuo Hirano, MD, Division of
Gastroenterology, Northwestern University, Feinberg School of Medicine,
Chicago, Illinois; Victor Fox, MD, Division of Gastroenterology,
Hepatology, and Nutrition, Children\'s Hospital Boston, Harvard Medical
School, Boston, Massachusetts; David Katzka, MD, University of
Pennsylvania School of Medicine, Division of Gastroenterology,
Philadelphia, Pennsylvania; Susan R. Orenstein, MD, Division of
Pediatric Gastroenterology, University of Pittsburgh Medical School,
Pittsburgh, Pennsylvania; Eric Hassall, MBChB, FRCPC, Division of
Gastroenterology, BC Children\'s Hospital, University of British
Columbia, Vancouver, British Columbia, Canada

*Allergy*

Marc E. Rothenberg, MD, PhD, (*Chair*), Division of Allergy and
Immunology, Cincinnati Children\'s Hospital Medical Center, University
of Cincinnati College of Medicine, Cincinnati, Ohio; Jonathan Spergel,
MD, Division of Allergy and Immunology, The Children\'s Hospital of
Philadelphia, University of Pennsylvania School of Medicine,
Philadelphia, Pennsylvania; Amal Assa\'ad, MD, Division of Allergy and
Immunology, Cincinnati Children\'s Hospital Medical Center, University
of Cincinnati College of Medicine, Cincinnati, Ohio; Seema Aceves, MD,
PhD, Allergy Immunology Division, Rady Children\'s Hospital, San Diego,
University of California, San Diego, San Diego, California; Barry K.
Wershil, MD, Division of Pediatric GI and Nutrition, Albert Einstein
College of Medicine, The Children\'s Hospital at Montefiore, Bronx, New
York; Thomas Platts-Mills, MD, PhD, Division of Allergy and Clinical
Immunology, University of Virginia, Charlottesville, VA

*Treatment*

Chris Liacouras, MD, (*Chair*), Division of Gastroenterology,
Hepatology, and Nutrition, University of Pennsylvania School of
Medicine, The Children\'s Hospital of Philadelphia, Philadelphia,
Pennsylvania; Chair: Phil E. Putnam, MD, FAAP, Division of Pediatric
Gastroenterology, Hepatology, and Nutrition, Cincinnati Children\'s
Hospital Medical Center, University of Cincinnati College of Medicine,
Cincinnati, Ohio; Tusar Desai, MD, William Beaumont Hospital, Department
of Internal Medicine, Royal Oak Michigan, Bloomfield Hills, Michigan;
Seema Khan, MD, Thomas Jefferson University, Philadelphia, Pennsylvania;
and Division of Gastroenterology and Nutrition, Alfred I duPont Hospital
for Children, Wilmington, Delaware; B UK Li, MD, Division of Pediatric
Gastroenterology, Medical College of Wisconsin, Milwaukee, Wisconsin;
Amir F. Kagalwalla, MD, Division of Pediatric Gastroenterology,
University of Illinois, Chicago, Chicago, Illinois; Richard J. Noel, MD,
Division of Pediatric Gastroenterology, Medical College of Wisconsin,
Milwaukee, Wisconsin

#### FINANCIAL DISCLOSURES/CONFLICTS OF INTEREST

Conflict of interest disclosures: Glenn T. Furuta, consultant, Ception
Therapeutics; speaker\'s bureau, TAP; Chris A. Liacouras, consultant,
SHS, Nutricia, Ception, Ross; grant/research support, Wyeth; speaker\'s
bureau, TAP, Merck; Margaret H. Collins, consultant, GlaxoSmithKline,
Ception Therapeutics; Sandeep K. Gupta, consultant, GlaxoSmithKline,
TAP, AstraZeneca, Salix; speaker\'s bureau, Ross Products, TAP,
AstraZeneca; educational grant, Ross Products; Christopher Justinich, no
disclosures; Phil E. Putnam, no disclosures; Peter A Bonis, no
disclosures; Eric Hassall, consultant, TAP Pharmaceuticals, Abbott
Canada, Altana Pharma; clinical research grant, AstraZeneca; Alex
Straumann, no disclosures; Marc E. Rothenberg, consultant, Merck,
Ception Therapeutics, GlaxoSmithKline, MedaCorp; speaker\'s bureau,
Merck; Samuel Nurko, grant/research support, Wyeth pharmaceutica, TAP,
Sucampo; Nirmala Gonsalves, consultant, Medacorp, Ception Therapeutics;
Jonathan Markowitz, consultant, Ception Therapeutics; Don Antonioli, no
disclosures; Eduardo Ruchelli, no disclosures; Hector Melin-Aldana, no
disclosures; Margret Magid, no disclosures; Ikuo Hirano, no disclosures;
David Katzka, no disclosures; Susan R. Orenstein, consultant, Ception
Therapeutics, TAP, Braintree, AstraZeneca, Wyeth, Bristol Myers Squibb,
McNeil; grant/research support, Braintree; Jonathan M. Spergel,
consultant, Novartis, GlaxoSmithKline; grant/research support, Novartis,
Nutricia; speaker\'s bureau, AstraZeneca, GlaxoSmith-Kline; Amal
Assa\'ad, no disclosures; Seema Aceves, no disclosures; Barry K.
Wershil, consultant, AP Pharmaceuticals, AstraZeneca; speaker\'s bureau,
Shire; educational grant, TAP Pharmaceuticals; Thomas Platts-Mills, no
disclosures; Tusar Desai, no disclosures; Seema Khan, no disclosures; B
Li, no disclosures; Amir F. Kagalwalla, no disclosures

#### GUIDELINE STATUS

This is the current release of the guideline.

According to the guideline developer, the Clinical Practice Committee
meets three times a year to review all American Gastroenterological
Association Institute (AGA Institute) guidelines. This review includes
new literature searches of electronic databases followed by expert
committee review of new evidence that has emerged since the original
publication date.

#### GUIDELINE AVAILABILITY

Electronic copies: Available from the American Gastroenterological
Association Institute (AGA Institute) [*[Gastroenterology]{.underline}*
journal Web
site](http://www.gastrojournal.org/article/PIIS0016508507014746/fulltext).

Print copies: Available from the American Gastroenterological
Association Institute, 4930 Del Ray Avenue, Bethesda, MD 20814.

#### AVAILABILITY OF COMPANION DOCUMENTS

None available

#### PATIENT RESOURCES

None available

#### NGC STATUS

This summary was completed by ECRI Institute on December 14, 2007.

#### COPYRIGHT STATEMENT

This NGC summary is based on the original guideline, which is subject to
the guideline developer\'s copyright restrictions.

### DISCLAIMER

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Date Modified: 11/3/2008