Celiac disease: predictors of compliance with a gluten-free diet in adolescents and young adults.

AIMS: To identify risk as well as protective factors related to compliance with the gluten-free diet in a cohort of teenagers with celiac disease (CD). PATIENTS AND METHODS: Two hundred four patients with CD (European Society for Pediatric Gastroenterology, Hepatology, and Nutrition criteria) older than or equal to 13 years and residents of Campania (southern Italy) were enrolled in the study. Patients underwent clinical examination and blood sampling, and were interviewed about school performance, social relationships, family integration, smoking habit, and compliance with a gluten-free diet. Anti-tissue transglutaminase antibodies were assayed with an enzyme-linked immunosorbent assay. RESULTS: One hundred fifty of 204 (73.5%) reported no dietary transgressions, and 54 of 204 (26.5%) reported occasional or frequent transgressions. During the previous month 29 of 54 (53.7%) poor compliers ate from 0.001 to 1 g of gluten per day, 14 (25.9%) from 1 to 5 g, and 11 (20.4%) more than 5 g. The daily intake of gluten was significantly related to anti-tissue transglutaminase antibodies (chi2 = 38.872, P = 0.000). Height was below the third percentile in 19 of 204 (9.3%), and weight was above the 97th percentile in 20 of 204 (9.8%). Diet compliance did not seem to influence the weight and height. One hundred eleven of 150 good compliers (74%) and 31 of 54 (57.4%) poor compliers were asymptomatic. Most patients reported good family relationships (88.7%), social relationships (91.2%), and school integration (88.2%). Alternatively, 54% of patients reported some limitation in their social life. Compliance was good in patients who reported excellent school integration (83%) and social relationships (81%). CONCLUSION: Optimal school integration significantly contributes to the likelihood of good compliance. A better understanding within the school environment about CD-related issues could improve motivation to adhere to a gluten-free diet.

Gliadin activates HLA class I-restricted CD8+ T cells in celiac disease intestinal mucosa and induces the enterocyte apoptosis.

BACKGROUND & AIMS: The extensive infiltration of CD8(+) T cells in the intestinal mucosa of celiac disease (CD) patients is a hallmark of the disease. We identified a gliadin peptide (pA2) that is selectively recognized by CD8(+) T cells infiltrating intestinal mucosa of HLA-A2(+) CD patients. Herein, we investigated the phenotype, the tissue localization, and the effector mechanism of cells responsive to pA2 by using the organ culture of CD intestinal mucosa. The target of pA2-mediated cytotoxicity was also investigated by using the intestinal epithelial cell lines Caco2 and HT29, A2(+) and A2(-), respectively, as target cells. METHODS: Jejunal biopsy specimens from CD patients were cultured in vitro with pA2, and cellular activation was evaluated by immunohistochemistry and cytofluorimetric analysis. Cytotoxicity of pA2-specific, intestinal CD8(+) T cells was assayed by granzyme-B and interferon-gamma release and by apoptosis of target cells. RESULTS: pA2 challenge of A2(+) CD mucosa increased the percentage of CD8(+)CD25(+) and of CD80(+) cells in the lamina propria, the former mainly localized beneath the epithelium, as well as the number of terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling-positive cells (TUNEL(+)) in the epithelium. Intraepithelial CD3(+) cells and enterocyte expression of Fas were also increased. CD8(+)CD25(+) and CD8(+)FASL(+) T cells were significantly increased in cell preparations from biopsy specimens cultured with pA2. CD8(+) T-cell lines released both granzyme-B and interferon-gamma following recognition of pA2 when presented by Caco2 and not by HT29. CONCLUSIONS: These data indicate that gliadins contain peptides able to activate, through a TCR/HLA class I interaction, CD8-mediated response in intestinal CD mucosa and to induce the enterocyte apoptosis.

HLA related genetic risk for coeliac disease.

BACKGROUND: Several studies have shown an elevated prevalence of coeliac disease (CD) in sibs of coeliac patients (risk 8-12%). AIM AND METHOD: We evaluated the risk that sibs of children with CD will also develop CD. This cohort of 188 Italian families was composed of probands with CD, at least one sib and both parents. CD status was determined and human leucocyte antigen (HLA)-DQ genotyping performed in all family members. The study also used a dataset of Italian triads (127 probands and both their parents) also genotyped for HLA-DQ. RESULTS: The overall risk that a sib of a CD patient will develop the disease was estimated at 10% in this sample. The risk estimate ranged from 0.1% to 29% when HLA-DQ information of the proband, parents and sib was considered. We found a negligible risk (lower than 1%) for 40% of the sibs of probands, a risk greater than 1% but less than 10% for 30%, and finally a high or very high risk (above 25%) in one-third of families. CONCLUSION: These results make it possible to provide more accurate information to parents with a child with CD about the real risk for another child. An antenatal estimate of the order of risk of CD is now possible. Specific follow-up can thus be offered for babies at high risk.