bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antibodies to human recombinant tissue transglutaminase may detect coeliac disease patients undiagnosed by endomysial antibodies
Authors: Tesei N. , Sugai E. , Vázquez H. , Smecuol E. , Niveloni S. , Mazure R. , Moreno M. L. , Gomez J. C. , Mauriño E. , Bai J. C. 
Published: June 2003

SummaryBackground:The screening and diagnosis of coeliac disease have been simplified by the advent of new serological tools.Aim:To assess the clinical utility of a newly developed kit for antibodies to human recombinant tissue transglutaminase (hu‐anti‐tTG) in a large population of patients undergoing intestinal biopsy for suspected intestinal disorders.Methods:We evaluated 426 serum samples from consecutive adult patients (250 from untreated coeliac disease patients and 176 from individuals in whom a diagnosis of coeliac disease had been excluded), obtained at the time of intestinal biopsy. Samples were tested for immunoglobulin A (IgA) hu‐anti‐tTG by enzyme‐linked immunoabsorbent assay, IgA endomysial antibodies (EmA) by indirect immunofluorescence and IgA and IgG antigliadin antibodies by enzyme‐linked immunoabsorbent assay. A sub‐group of samples was also assessed for a guinea‐pig‐based anti‐tissue transglutaminase.Results:According to the cut‐off for hu‐anti‐tTG, the sensitivity, specificity and positive and negative predictive values were 91%, 96%, 97% and 87%, respectively. Simultaneous determination of EmA showed values of 86%, 100%, 100% and 83% for the same parameters. Although 19 coeliac disease patients (7.6%) were negative for EmA and hu‐anti‐tTG, both tests rendered superior statistical values to antigliadin antibody tests. At diagnosis, IgA deficiency was detected in 11 patients, but both assays were able to detect samples with mild to moderate deficiency. The comparison of hu‐anti‐tTG with EmA showed excellent concordance between the tests (κstatistic, 0.85). Discordance was observed in 20 samples from coeliac disease patients (8%) and in nine samples from controls (5%). Fifteen samples had an EmA‐negative but hu‐anti‐tTG‐positive serology, and five showed the converse pattern. Comparison of human recombinant and guinea‐pig tests showed concordant results in 96% of cases.Conclusions:The quantitative determination of hu‐anti‐tTG type IgA using a commercial enzyme‐linked immunoabsorbent assay kit was highly sensitive and specific for the detection of coeliac disease. Our results in a large population of patients with a clinical condition suggestive of the disorder demonstrated that the test can be used to detect a substantial number of patients otherwise unrecognized by IgA EmA.
A practical method for the detection of macroprolactinaemia using ultrafiltration
Authors: Prazeres Susana , Santos M. Amparo , Ferreira H. Gil , Sobrinho Luís G. 
Published: June 2003

Summaryobjective The aim of this study was to evaluate a method for the estimation of the percentage of big‐big prolactin (bb‐PRL) in serum, based on centrifugal ultrafiltration (UF) and to be used for the detection of macroprolactinaemia.design Serum samples were submitted to gel filtration chromatography (GFC), UF and precipitation with polyethylene glycol (PEG).patients Serum samples obtained from 13 patients with macroprolactinaemia (Group 1) and from 15 hyperprolactinaemic patients without macroprolactinaemia (Group 2) were studied by the three methods.measurements PRL was measured in serum, fractions from GFC, filtrate and retentate obtained after UF (this last measurement was used only to study the ‘recovery’ of PRL after UF and was not necessary for clinical purposes), and supernatant obtained after PEG precipitation. The calculation of the percentage of bb‐PRL, by UF, was made using a simple algorithm.results In Group 1 the percentages (mean and SD) of bb‐PRL as determined by GFC, UF and PEG were, respectively, 73 ± 16, 83 ± 5·3 and 78 ± 7·0. In Group 2, the percentages of bb‐PRL were, in the same order as above, 4·3 ± 8·2, 16 ± 19 and 3·7 ± 11. The difference of the means between Groups 1 and 2 was highly significant (P << 0·001) for all the three methods. In Group 1 the percentages of bb‐PRL were widely scattered when measured by GFC but closely clustered when measured by either UF or PEG. The opposite occurred in Group 2.conclusions The centrifugal ultrafiltration method for the detection of macroprolactinaemia is simple, inexpensive, requires only two prolactin assays and yields the same results as the polyethylene glycol precipitation method.
The correlation between the response to progestogen treatment and the expression of progesterone receptor B and 17β‐hydroxysteroid dehydrogenase type 2 in human endometrial carcinoma
Authors: Utsunomiya Hiroki , Suzuki Takashi , Ito Kiyoshi , Moriya Takuya , Konno Ryo , Sato Shinji , Yaegashi Nobuo , Okamura Kunihiro , Sasano Hironobu 
Published: June 2003

Summaryobjective  In situ metabolism and synthesis of oestrogens are considered to play important roles in the pathogenesis and development of human endometrial endometrioid adenocarcinoma. Approximately 3–5% of patients with these neoplasms are under age 40, some of whom have been treated with progestogen alone as a primary therapy for both atypical endometrial hyperplasia and adenocarcinoma in order to preserve their fertility. Medroxyprogesterone acetate (MPA) has been used extensively in the treatment of both breast and endometrial disorders as an endocrine therapy. However, details of the alterations of in situ oestrogen metabolism following progestogen treatment have yet to be fully elucidated.design, patients and measurements  In this study we examined the immunolocalization of 17β‐hydroxysteroid dehydrogenase (17β‐HSD) types 1 and 2, oestrogen receptor (ER), progesterone receptor (PR)A + PRB, PRB, and Ki67 in progestogen‐treated endometrial endometrioid adenocarcinoma (16 cases). We compared our findings both prior to and following treatment. These findings were then correlated with the treatment outcome of individual patients in order to elucidate factors associated with the response to treatment.results  17β‐HSD type 2 immunoreactivity was detected in 8/16 cases examined, whereas 17β‐HSD type 1 immunoreactivity was undetected in all cases examined. 17β‐HSD type 2 positive immunostaining, PRA + PRB labelling index (LI), and PRB/PRA + PRB ratio were all significantly higher in cases responding to the treatment than in those not responding. There were no significant correlations between responsive and nonresponsive cases for positive 17β‐HSD type 1 immunostaining, Ki67 LI, ER LI and age. There were no significant differences in the positive immunostaining for 17β‐HSD types 1 and 2, Ki67 LI, ER LI, PRA + PRB LI, age and PRB/PRA + PRB ratio between specimens taken prior to and following progestogen treatment.conclusion  These results suggest that in situ abundance of 17β‐HSD type 2 and PR, especially PRB, can predict the possible response of patients with endometrial carcinoma to progestogen treatment.
The effects of soy protein containing isoflavones on lipids and indices of bone resorption in postmenopausal women
Authors: Dalais Fabien S. , Ebeling Peter R. , Kotsopoulos Dimitra , McGrath Barry P. , Teede Helena J. 
Published: June 2003

Summaryobjective To assess the effect of a dietary soy protein supplement containing isoflavones on lipids and indices of bone resorption in postmenopausal women.design Placebo‐controlled, double‐blind, randomized study.patients One hundred and six postmenopausal women were randomized to dietary soy supplementation (n = 51) or placebo (n = 55) for 3 months, of which 78 were included in the final analysis.measurements Lipid profiles including total, low‐density lipoprotein (LDL) and HDL cholesterol as well as triacylglycerol were measured. Pyridinoline and deoxypyridinoline were used as markers of bone resorption. Urinary isoflavone excretion was measured to assess compliance.results There was a significantly greater increase in urinary isoflavone excretion detected in the soy group compared to placebo. Lipid profiles improved with significant decreases in LDL cholesterol (−0·60 ± 0·10 vs.–0·29 ± 0·09 mmol/l, P < 0·05), triacylglycerol (−0·22 ± 0·07 vs. +0·01 ± 0·05 mmol/l, P < 0·005) and the LDL : HDL ratio (−0·32 ± 0·10 vs. +0·20 ± 0·10, P < 0·005) in the soy group compared to placebo. There were no significant differences between the soy and placebo groups for urinary excretion of pyridinoline (−3·8 ± 3·1 vs.−0·8 ± 3·1 nmol/mmolCr, P = 0·4) or deoxypyridinoline (−0·8 ± 0·9 vs.–0·3 ± 0·7 nmol/mmolCr, P = 0·4).conclusions In postmenopausal women, dietary supplementation with soy protein containing isoflavones does not appear to have oestrogenic effects on markers of bone resorption. Soy protein favourably affected lipids; however, these effects (fall in triacylglycerol and no change in HDL) differ from those observed with oral oestrogen. These findings suggest that soy may not have biologically significant oestrogenic effects on bone resorption and we hypothesize that the lipid effects may be mediated, at least in part, through nonoestrogenic mechanisms.
CTLA4 gene and Graves’ disease: association of Graves’ disease with the CTLA4 exon 1 and intron 1 polymorphisms, but not with the promoter polymorphism
Authors: Vaidya B. , Oakes E. J. C. , Imrie H. , Dickinson A. J. , Perros P. , Kendall‐Taylor P. , Pearce S. H. S. 
Published: June 2003

Summaryobjective Recent studies have shown that Graves’ disease (GD) is linked to and associated with alleles of the cytotoxic T lymphocyte antigen‐4 (CTLA4) locus. However, the true pathogenic polymorphism(s) at this locus remains uncertain. Moreover, the association studies of the promoter CTLA4(−318)C/T polymorphism in white GD populations have produced conflicting results. Therefore, we have analysed three CTLA4 single nucleotide polymorphisms, including promoter CTLA4(−318)C/T, exon 1 CTLA4(49)A/G and intron 1 CTLA4(1822)C/T in our GD cohort from the UK.patients and methods We studied 301 white patients with GD and 349 healthy ethnically matched local controls. Amongst GD probands, 129 had significant thyroid‐associated orbitopathy (TAO; NOSPECS class III or worse). The CTLA4(−318)C/T, CTLA4(49)A/G and CTLA4(1822)C/T polymorphisms were genotyped by using the restriction enzymes MseI, Bst71I and HaeIII, respectively.results We found no association between GD and alleles of CTLA4(−318)C/T. GD was found to be associated with the G allele of CTLA4(49)A/G[P = 5·9 × 10−6, odds ratio (OR) 1·65] and the T allele of CTLA4(1822)C/T (P = 7·7 × 10−6, OR 1·64). The frequencies of these alleles were significantly higher in GD probands with significant TAO than in those without TAO (G allele: P = 0·001, OR 1·68; T allele: P = 0·001, OR 1·70).conclusions The promoter CTLA4(−318)C/T polymorphism is not in linkage disequilibrium with the pathogenic polymorphism(s) at the CTLA4 locus. The alleles of both the exon 1 CTLA4(49)A/G and the intron 1 CTLA4(1822)C/T polymorphisms are associated with GD, which is stronger in patients with TAO.
Combined pituitary hormone deficiency in Australian children: clinical and genetic correlates
Authors: McLennan Kim , Jeske Yvette , Cotterill Andrew , Cowley David , Penfold James , Jones Tim , Howard Neville , Thomsett Michael , Choong Catherine 
Published: June 2003

Summaryobjective Mutations in the gene for the POU domain transcription factor POU1F1 (human Pit‐1) have been reported in patients with GH, TSH and PRL deficiencies. PROP1 (Prophet of Pit‐1) gene mutations also cause gonadotrophin deficiencies and in some cases partial ACTH deficiency. This study analyses the POU1F1 and PROP1 genes in a cohort of Australian children with combined pituitary hormone deficiency (CPHD) and correlates results with patient phenotype.patients and design Genomic analysis was carried out on 33 patients with CPHD referred from centres around Australia. Clinical data were collected from medical records and referring physicans.results POU1F1 mutations were identified in two of four patients with a suggestive phenotype. In a female patient, novel compound heterozygous POU1F1 mutations were identified: Arg143Leu in exon 3 and Leu194Gln in exon 4. This patient presented with failure to thrive at 6 weeks of age and has deficiencies of TSH and GH. A previously described heterozygous Arg271Trp mutation in exon 6 of the POU1F1 gene was identified in a female infant who presented with growth failure and was diagnosed with TSH then GH deficiencies. No PROP1 mutations were identified; however, we describe a number of previously unreported PROP1 polymorphisms. No patients presenting with deficiencies of all anterior pituitary hormones early in life had POU1F1 or PROP1 gene mutations.conclusions In 33 Australian children with CPHD we have identified POU1F1 mutations in two patients and no PROP1 mutations. We speculate that in the majority of children other genes must be responsible for the CPHD phenotype.
Postoperative surveillance of clinically nonfunctioning pituitary macroadenomas: markers of tumour quiescence and regrowth
Authors: Greenman Y. , Ouaknine G. , Veshchev I. , Reider‐Groswasser I. I. , Segev Y. , Stern N. 
Published: June 2003

Summarybackground Postoperative management of clinically nonfunctioning pituitary adenomas (NFPA) presents difficult challenges. There are no good serum markers for presence or growth of the tumour, medical treatment is not effective and radiotherapy carries the risk of significant side‐effects.objective The purpose of this study was to investigate the natural history and biological behaviour of surgically treated NFPA, with a special effort to identify characteristics indicative of a more aggressive course that could assist in the clinical decision‐making process.study design Patients operated on at our institution for NFPA undergo uniform routine clinical follow‐up at the endocrine clinic. Magnetic resonance imaging (MRI) studies are performed 3, 6 and 12 months after transsphenoidal surgery and yearly thereafter for the first 5 years. Subsequently, imaging is performed once every 2 years or as clinically indicated. From 1992 onwards, no patient received immediate postoperative radiation therapy.patients One hundred and twenty‐two patients (78M/45F) operated on at our institution since 1989 and with a minimal follow‐up of 1 year comprised the study group.measurements Tumour size and characteristics were determined by MRI using a modification of Hardy's and Wilson's classifications. Maximal tumour height was also recorded and the information was routinely stored in a computerized database.results Mean (± SD) follow‐up was 51 ± 31 months. Fourteen patients received postoperative radiation therapy. Subsequent tumour growth was observed in five of them, reduction in tumour size in four and no size changes in five. One hundred and eight patients did not receive postoperative radiation. Tumour enlargement occurred in 41 of 78 and in six of 30 patients with and without residual tumour after operation (P = 0·0024). The presence of cavernous sinus invasion before surgery [P = 0·02, odds ratio (OR) 2·72; confidence interval (CI) 1·1–6·43] and the extent of suprasellar extension in the postoperative tumour remnant (P = 0·0054 for presence of stage A, OR 4·4; 95% CI 1·5–12·5; and P = 0·012 for presence of stages B or C, OR 16·2; CI 1·8–144) were strong independent predictors of tumour enlargement.conclusion Our data may ease the selection of patients in whom radiation therapy is likely to be necessary for tumour control, and confirms that close postoperative follow‐up is an adequate primary approach in low‐risk patients.
Hypothalamic growth hormone‐releasing hormone (GHRH) cell number is increased in human illness, but is not reduced in Prader–Willi syndrome or obesity
Authors: Goldstone Anthony P. , Unmehopa Unga A. , Swaab Dick F. 
Published: June 2003

SummarybackgroundAcute illness leads to increased GH, but reduced IGF‐I secretion, while both are reduced in chronic illness. Prader–Willi syndrome (PWS) is a genetic obesity syndrome, with GH deficiency a feature independent of obesity. Reduced GH secretion may result from decreased hypothalamic release of GH‐releasing hormone (GHRH).objectiveTo quantify hypothalamic GHRH neurone cell number in control subjects with various lengths of premorbid illness duration, PWS and non‐PWS obese subjects.designWe examined GHRH neurones in the infundibular nucleus/median eminence complex of control subjects (n = 26, including four children), PWS (n = 6) and non‐PWS (n = 4) obese adults and PWS children (n = 2), by quantitative immunocytochemistry, using postmortem material.resultsWe found: (i) higher GHRH cell number during prolonged illness prior to death in both control adults (r = +0·62,P = 0·002, cell numbervs.premorbid illness duration) and PWS adults (r = +0·90,P = 0·02); (ii) higher GHRH cell number in female than male adults [by 53% (95% confidence interval 28–83%) in controls,P = 0·005, correcting for premorbid illness duration]; (iii) no difference in GHRH cell number between PWS adults and control or non‐PWS obese adults (P = 0·7 andP = 0·4, adjusting for sex and illness duration); and (iv) low GHRH cell number in only one PWS child (who had been receiving exogenous GH therapy).conclusionsThese findings suggest continued activation of GHRH neurones during prolonged illness. There is no evidence that the GH deficiency in PWS results from reduced GHRH cell number, and GHRH neuronal reponses to illness and exogenous GH treatment appear normal in PWS.
The circulating IGF system and its relationship with 24‐h glucose regulation and insulin sensitivity in healthy subjects
Authors: Frystyk Jan , Nyholm Birgit , Skjærbæk Christian , Baxter Robert C. , Schmitz Ole , Ørskov Hans 
Published: June 2003

Summaryobjective and design It has been suggested that circulating free IGF‐I participates in glucose homeostasis and that IGFBP‐1 reflects changes in insulin sensitivity. To study this further, we examined 10 healthy, nonobese subjects under standardized conditions for 24 h with and without an intravenous infusion of glucose, the latter in order to augment insulin sensitivity. Serum was collected every 2 h for analysis of free and total IGFs, IGFBP‐1, − 2 and − 3 and the acid labile subunit (ALS). Insulin sensitivity was estimated at the end of each 24‐h study period by use of the hyperinsulinaemic euglycaemic clamp technique.results Glucose infusion resulted in mild hyperglycaemia (P < 0·0001), a reduction in IGFBP‐1 by approximately 40% (P < 0·0003), and increased insulin and C‐peptide levels (P < 0·0001). Glucose infusion also increased insulin sensitivity (P < 0·003). However, despite the reduction in IGFBP‐1, glucose infusion did not increase free IGF‐I over the control level, and free IGF‐II was slightly reduced (P < 0·02). Irrespective of glucose infusion, free IGF‐I and ‐II remained stable during daytime (i.e. they were unresponsive to meal‐related changes in plasma glucose), but both free fractions decreased during the night, reaching nadir at 04·00 h. None of the other members of the IGF system showed any relationship with plasma glucose levels. Finally, we failed to observe any relationship between changes in insulin sensitivity and the circulating IGF system.conclusion We found no evidence that the circulating IGF system is involved in meal‐related blood glucose regulation or that it reflects short‐term changes in insulin sensitivity in healthy, nonobese subjects. However, we cannot preclude that the observed changes in circulating IGFBP‐1 may affect the glucose‐lowering effect of IGF‐I and ‐II at the local tissue level.
Constructions of spirituality in contemporary nursing theory
Authors: Henery Neil 
Published: June 2003

Background. The nursing literature on spirituality tends to agree that modern science is relatively powerless to address the loss of personal meaning experienced by people facing death, suffering and loss. As a remedy, the literature recommends addressing patients' spirituality. The typical analytical move is to distinguish spirituality from religion and consider it a part, dimension or property of the patient. Aim and method. This paper uses discourse analysis to identify the formal properties of scientific and religious discourses and their social and political implications. The nursing literature is then investigated to detect the use of such discourses in constructing the object spirituality and to consider any implications for nursing as a social practice. Findings. Far from escaping science and religion, the literature constructs spirituality by means of scientific and religious discourses. These discourses have characteristic strengths and weaknesses that the nursing literature seems to miss. Accordingly, its use of religious discourse lacks coherence and depth, and risks merging human with transcendent authority. Its use of scientific discourse lacks precision and clarity and risks intensifying those features of modernity which contribute to a loss of personal meaning in the face of death, suffering and loss. Conclusion. Nursing literature on spirituality raises important questions but is limited in its capacity to address them. This paper provides an alternative perspective. First, it draws on an analysis of the modern institutional environment and its existential dimension. Secondly, it applies discourse analysis to the task of helping people experiencing illness and injury. This approach respects the strengths and limitations of both scientific and religious discourses.