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Background: Abdominal complaints after ingestion of cereals are not uncommon. We assessed how reliable such a history is as a marker for the presence of overt coeliac disease, and whether we should also take into account latent coeliac disease and cereal allergy. Methods: The study group comprised 93 consecutive adults from health centres spontaneously reporting abdominal symptoms after consumption of cereals. Small bowel mucosal morphology, CD3+, αβ+ and γδ+ intraepithelial lymphocytes (IELs), HLA DQ alleles and serum IgA-class endomysial (EmA), tissue transglutaminase (tTg) and gliadin (AGA) antibodies were determined. Skin prick and patch tests and serum radioallergosorbent tests for cereals were carried out. Thirty non-coeliac adults served as biopsy controls. Results: Eight (9%) patients had coeliac disease and one mild partial villous atrophy. Altogether 17 had an increased density of γδ+ IELs without atrophy. However, only seven (8%) showed evidence of latent coeliac disease, i.e. both an increase in γδ+ IELs and the presence of coeliac disease-type HLA. One or more of the allergy tests for cereals was positive in 19; 9 adopted a gluten-free diet and abdominal symptoms were alleviated in all. In non-coeliac patients, serum EmA and tTg tests were negative in all, whereas AGA was seen in 40%. Conclusions: Intolerance to cereals is not a specific sign of overt or latent coeliac disease. All experimental dietary interventions before proper diagnosis of coeliac disease are therefore to be discouraged. Allergy to cereals, on the other hand, should be considered even in adults. [ABSTRACT FROM AUTHOR]

Background: Recent epidemiologic studies in Europe using antigliadin (AGA) and anti-endomysium antibodies (AEA) for initial screening have shown that the overall prevalence of celiac disease (CD) is about 1:300. There are no comparable scientific data for the USA, where CD is considered rare. The main aim of this study was to determine the prevalence of increased AEA in healthy blood donors in the USA. Methods: Sera from 2000 healthy blood donors were screened for IgG AGA and IgA AGA with an enzyme-linked immunosorbent assay test. All those with increased AGA levels, those with intermediate levels, and random samples with low levels were tested for AEA, using both monkey esophagus (ME) and human umbilical cord (HUC) cryosections as substrates. Results: The mean age of the blood donors was 39 years, with 52% being men, 85.2% being Caucasian, 11.8% African-American, 1.5% Asian, and 1.5% Hispanic. Eight healthy blood donors had positive AEA tests on both monkey esophagus and human umbilical cord. Among the eight subjects with increased AEA levels seven were Caucasian and one was African-American. All the four examined AEA-positive donors carried the known susceptibility alleles for CD. Conclusions: The prevalence of increased AEA levels in healthy blood donors in the USA is 1:250 (8:2000). This is similar to that reported in countries in Europe, where subsequent small-intestinal biopsies have confirmed CD in all those with AEA positivity. On the basis of a high positive predictive value of the AEA antibody test, it is likely that the eight blood donors identified in this study have CD. These data suggest that CD is not rare in the USA and that there is need for a large-scale epidemiologic study to determine the precise prevalence of the disease in the USA. [ABSTRACT FROM AUTHOR]

Objective: Circulating antibodies against naive, whole gliadin have been replaced by more accurate endomysial and tissue transglutaminase antibody tests in the diagnosis of coeliac disease. The purpose of this study was to compare these serological tests with a new test recognizing antibodies against deamidated and defined gliadin peptides., Material and Methods: The study population comprised selected coeliac disease patients in a tertiary clinic: newly detected patients before and after a gluten-free diet, patients with persistent small-bowel mucosal villous atrophy despite a strict gluten-free diet and non-coeliac controls reporting abdominal symptoms after ingestion of cereals. Comparisons were made between serum IgA-class gliadin peptide, endomysial, tissue transglutaminase and conventional gliadin antibodies., Results: The deamidated gliadin peptide antibody test showed a sensitivity of 91% and a specificity of 98% in coeliac disease. The tissue transglutaminase antibody test performed equally well. The specificity of endomysial antibody was just as high, but its sensitivity was lower, 80%. The conventional gliadin antibody test showed poor sensitivity and specificity. Combination of the deamidated gliadin peptide and tissue transglutaminase tests offered the best sensitivity without loss of specificity in the diagnosis of coeliac disease. All antibody levels declined in line with mucosal recovery. The deamidated gliadin peptide antibody test showed six of the nine cases with small-bowel mucosal damage persisting on a gluten-free diet, whereas tissue transglutaminase detected only two cases and endomysial antibody none., Conclusions: The new gliadin peptide antibody test proved highly accurate in the diagnostic work-up and follow-up of coeliac disease and can be endorsed in combination with the tissue transglutaminase test.

Objective: In coeliac disease, autoantibodies directed against transglutaminase 2 are produced in small-bowel mucosa, and they have been found to be deposited extracellularly. The aim of this study was to investigate whether such mucosal IgA deposits are important in the diagnostic work-up of early-stage coeliac disease without small-bowel mucosal villous atrophy., Material and Methods: Forty-one adults suspected of coeliac disease owing to increased density of mucosal gamma(delta)+ intraepithelial lymphocytes but normal villous morphology were randomized to gluten challenge or a gluten-free diet for 6 months. Clinically and histologically verified gluten dependency was compared with existence of small-bowel mucosal transglutaminase 2-specific extracellular IgA deposits and (coeliac disease-type) HLA DQ2 and DQ8; 34 non-coeliac subjects and 18 patients with classical coeliac disease served as controls., Results: Of the 41 patients, 5 in the challenge group and 6 in the gluten-free diet group were clinically gluten sensitive; all 11 had HLA DQ2 or DQ8. Ten of these 11 patients showed transglutaminase 2-targeted mucosal IgA deposits, which were dependent on gluten consumption. Minimal IgA deposits were seen in only 3 out of 30 patients with suspected coeliac disease without any clinically detected gluten dependency. The deposits were found in all classical coeliac patients and in none of the non-coeliac control subjects., Conclusions: Clinically pertinent coeliac disease exists despite normal small-bowel mucosal villous architecture. Mucosal transglutaminase 2-specific IgA deposits can be utilized in detecting such patients with genetic gluten intolerance.