Limited information suggests the existence of a high prevalence of hepatitis B (HBV) and C virus (HCV) infection in infl ammatory bowel disease (IBD). This knowledge is relevant because the viruses may reactivate under immunosuppressive therapy. The objectives of this study are to assess the prevalence of HBV and HCV infection in IBD, in a nationwide study, and to evaluate associated risk factors. This cross-sectional multicenter study included 2,076 IBD patients, consecutively recruited in 17 Spanish hospitals. Factors related to IBD (severity, invasive procedures, etc.) and to infection (transfusions, drug abuse, etc.) were registered. Independent risk factors for viral infection were evaluated using logistic regression analysis. Present and/or past HBV and HCV infection was found in 9.7% of patients of both ulcerative colitis (UC) and Crohn's disease (CD) (UC: HBsAg 0.8%, anti-HBc 8%, anti-HCV 1.3%; CD: HBsAg 0.6%, anti-HBc 7.1%, anti-HCV 2.3 %). Effective vaccination (anti-HBs, without anti-HBc) was present in 12% of patients. In multivariate analysis, age (odds ratio (OR) 1.04; 95% confidence interval (CI) 1.02–1.06; P=0.000), family history of hepatitis (OR 2.48; 95% CI 1.3–4.74; P=0.006) and moderate-to-severe IBD disease (OR 2.5; 95% CI 1.02–6.15; P=0.046) were significantly related to HBV, whereas transfusions (OR 2.66; 95% CI 1.2–5.87; P=0.015) and antibiotic use (OR 2.66; 95% CI 1.1–6.3; P=0.03) were significantly related to HCV. The significance for transfusions was lost if they were administered after 1991, when HCV markers became mandatory in blood banks. Prevalence of HBV and HCV infection in IBD is similar to that of the general population of reference and lower than that in previously published series. This fact, in addition to the lack of association with invasive procedures, suggests the existence of adequate preventive measures in centers attending to these patients. The low percentage of effective vaccination makes it mandatory to intensify B virus vaccination in IBD.

Background Some limited studies of coeliac disease have shown higher frequency of coeliac disease in infancy and adolescence than in adulthood. This finding has remained unnoticed and not adequately demonstrated. Aim To assess whether there are age and gender differences in coeliac disease prevalence. Methods A total of 4230 subjects were included consecutively (1 to ≥80 years old) reproducing the reference population by age and gender. Sample size was calculated assuming a population‐based coeliac disease prevalence of 1:250. After an interim analysis, the paediatric sample was expanded (2010 children) due to high prevalence in this group. Anti‐transglutaminase and antiendomysial antibodies were determined and duodenal biopsy was performed if positive. Log‐linear models were fitted to coeliac disease prevalence by age allowing calculation of percentage change of prevalence. Differences between groups were compared using Chi‐squared test. Results Twenty‐one subjects had coeliac disease (male/female 1:2.5). Coeliac disease prevalence in the total population was 1:204. Coeliac disease prevalence was higher in children (1:71) than in adults (1:357) (P = 0.00005). A significant decrease of prevalence in older generations was observed [change of prevalence by age of −5% (95% CI: −7.58 to −2.42%)]. In the paediatric expanded group (1–14 years), a decrease of coeliac disease prevalence was also observed [prevalence change: −17% (95% CI: −25.02 to −6.10)]. Conclusions The prevalence of coeliac disease in childhood was five times higher than in adults. Whether this difference is due to environmental factors influencing infancy, or latency of coeliac disease in adulthood, remains to be demonstrated in prospective longitudinal studies.

It has been suggested that paucicellular lymphocytic colitis (PLC) should be considered to be part of the morphological spectrum of microscopic colitis. The aim of the study was to evaluate whether PLC may be considered to be a true microscopic colitis, and in this case, whether it is a minor form of lymphocytic colitis (LC) or a different entity. All incident cases of PLC, LC, and collagenous colitis (CC) during the period 2004–2006 were included. The incidence rate and the clinical, histopathological, and immunological features of PLC were assessed and compared with those of both LC and CC. Immunoreactivities to CD25, c-Kit, and FOXP3 in lamina propria were assessed. In all, 19 patients with CC, 19 with LC, and 26 with PLC were identified. CD25⁺FOXP3⁺ expression was seen only in classical forms of microscopic colitis: 12 of 19 LC, 14 of 20 CC, and none of 20 PLC cases (P<0.0001). Diarrhea ceased in 21 of the 26 patients, with a decrease in the daily stool number from 5.08±0.44 to 1.7±0.2 (P<0.005). The five patients with no response to therapy fulfilled the Rome II criteria of irritable bowel syndrome (IBS). The incidence rate of PLC, identified using objective histological criteria, was higher than those of CC and LC. The lack of expression of CD25⁺FOXP3⁺ cells in PLC, in contrast to those seen in both LC and CC, would suggest the existence of different pathophysiological mechanisms and does not support that PLC is a minor form of LC.