In coeliac disease, gluten‐containing diet challenges over many years are sometimes required for diagnosis, especially if the initial diagnosis was equivocal. The rectal gluten challenge has been proposed to simplify coeliac disease diagnosis. We were interested in studying whether the oral mucosa could be used for local challenge with gliadin as an aid in finalizing the diagnosis of coeliac disease. The study groups consisted of 37 treated coeliac disease patients and 10 controls. The challenges on the oral mucosa were performed either supramucosally with gliadin powder (coeliac disease patients) or by submucosal injection of dissolved gliadin (10 μg/ml) (coeliac disease patients and controls). A control challenge with submucosal gliadin solvent was made in the coeliac disease patients. B and T cells, mast cells and T cell subsets were counted and HLA‐DR expression was determined. Biopsies were taken from each provoked area 24 h post‐challenge. A significant increase in the number of CD4+ lymphocytes in the lamina propria (observed in 27/37 patients), but a decrease in the number of mast cells was observed in treated coeliac disease patients after submucosal challenge with gliadin. Following supramucosal challenge with gliadin the counts of intraepithelial CD4+ (in 25/37 patients) and CD8+ T cells (in 27/37 patients) increased significantly and the number of CD4+ T cells in the lamina propria was also significantly increased. Control subjects were tested by submucosal gliadin challenge and no significant changes in the number of cells were observed. HLA‐DR expression did not show increased positivity in coeliac disease patients on submucosal challenge. For the first time the oral mucosa has been used for immunological testing and shown to react to gliadin challenge in coeliac disease patients. Recruitment of T cells upon submucosal gliadin challenge occurred towards the lamina propria, whereas it occurred towards the epithelium in supramucosal gliadin challenge. The numbers of T cells increased in the lamina propria after submucosal challenge. The results suggest that local oral challenge with gliadin may be used as a diagnostic method in coeliac disease; however, further studies in untreated coeliac disease patients are needed to evaluate the usefulness of this method.
surrounding the SCD itself regarding the mechanism of action, its long-term efficacy, best populations for its effective use, and the possibility of narrowing the restrictions.Despite these obvious limitations and the questions raised, lessons can be learned from both the authors' efforts and their findings. In many ways, the lessons can be grouped under the broad umbrella of caution, both for physicians and the families who opt for sustained dietary therapy instead of medication. First, the SCD is very restrictive and young patients often find it difficult to perpetuate; hence, the patients and families often modify their adherence (to say it kindly). They often start the diet on their own and, as seen in this study, they follow their own dictates as they chose what foods they want to add back and when. Second, the patients and their families are often presumptive about how well they are doing. Significant signs of malnutrition and lack of weight gain may be ignored, especially when laboratory measures are falsely reassuring. Our own experience suggests that the patients, particularly those on the diet, underreport their symptoms and overreport their adherence so as not to disappoint their parents, at least in the beginning. As these young patients tire of dietary restrictions, those strategies may reverse as they try to persuade their families to let them ''cheat'' and consume normally restricted foods.Lastly, to use a Southern homily, our surrogate markers ''ain't all they're cracked up to be.'' As clinicians, we have become devoted to laboratory tests and their numbers to explore less observable conditions or to confirm our impressions. In following pediatric patients with inflammatory bowel disease, we even incorporate hemoglobins, albumins, and sedimentation rates into the Pediatric Crohn's Disease Activity Index as evidence of the degree of activity, to imperfect effect (4,5). We do know that these markers and the CRPs are not always reliable. The CRP, with a halflife of 19 hours, is considered the most reliable and hence, the most widely used. But single nucleotide polymorphisms in the gene affect hepatocyte production in 20% to 30% of patients with active CD (6,7). Thus, they are useful when they are interpretable for the individual patient and for their aggregate, in studies. The problem is knowing when they are not (which is one of the reasons why results in some studies or their post-hoc analyses are stratified by CRP results) (8). Fortunately, Wabbeh et al all but ignored the biomarkers and again demonstrated how unreliable surrogates, and patient/family-reported symptoms can be (while they also instructed us on how unreliable a modified diet can be). Calprotectins were more useful in the present study, primarily by using a low threshold (>50 mg/g) to enhance detection (whereas other studies use considerably higher levels (3,9) and commercial laboratories report values to be abnormal at 120-150 mg/g) (10,11).The sad truth here is that the same situation may exist with medication use and nutritional t...
The relationship between adenovirus type 12 (Ad12), celiac disease (CD) and dermatitis herpetiformis (DH) was evaluated by enzyme-linked immunosorbent assay (ELISA). Diagnostic phase serum samples from 44 children with CD, 16 children with DH and 60 matched controls were studied for serum antibodies to synthetic peptides derived from an early E1b protein of Ad12 and A gliadin. Both the patient groups had significantly (p < 0.01) higher IgG antibody levels to the Ad12 E1b peptide than the controls. The difference was especially pronounced for girls (p < 0.005). Antipeptide IgG antibodies to Ad12 E1b and A gliadin posed a synergistic increase in the CD and DH risk suggesting that infection with Ad12 is associated with CD and DH.
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