The presence of celiac disease in a non-clinical Japanese population was low at 0.05% and was rarely found in patients with unexplained chronic abdominal symptoms.

Background and Aim Celiac disease (CD) is a chronic autoimmune enteropathy triggered by ingested gluten in genetically predisposed individuals. Although common in Europe and the United States, cases of CD are rarely encountered in East Asia, including Japan, and its prevalence remains to be fully evaluated in a large‐scale study. We previously investigated the presence of CD in adults in Japan, which revealed a low prevalence of 1 (0.05%) of 2008 nonclinical subjects, while 1 (2.1%) of 47 symptomatic patients was diagnosed based on serology and duodenal histopathology results. To confirm those results, we conducted an additional retrospective serological screening study of adults in Japan. Methods Serum samples were collected from 2055 adults who underwent a health examination in four local areas of Shimane prefecture in Japan from July 2008 to August 2013. As a screening test for CD, the antitissue transglutaminase IgA antibody (TTG) titer was determined in all subjects, and a value greater than 10 U/mL was considered to be evidence of CD. Results Of the 2055 subjects, 4 (0.19%) showed a high concentration of TTG. Although two of the four who were seropositive had died at the time of this retrospective study, none reported prominent digestive symptoms such as diarrhea or weight loss in a follow‐up survey. Conclusions Among a general population in Japan, a positive rate of serological tests for CD was noted in 0.19%, indicating quite a low presence, consistent with our previous results.

Background Consensus regarding the cutoff value of fecal calprotectin (FC) for predicting histological healing (HH) in ulcerative colitis (UC) is lacking. This study aimed to determine an optimal FC cutoff value for predicting HH in patients with UC with clinical and endoscopic remission. Furthermore, FC’s predictability for prolonged clinical remission (CR) was investigated. Methods Patients with UC in clinical and endoscopic remission, defined as a partial Mayo score (PMS) ≤ 2 points and a Mayo endoscopic subscore 0–1, were prospectively enrolled. Biopsy samples were evaluated by Geboes score (GS), with HH defined as a GS < 2.0. Patients were followed for 2 years or until relapse, defined as a PMS > 2 or medication escalation. Results Seventy-six patients with UC were included. The median FC value in patients with HH (n = 40) was 56.2 µg/g, significantly lower than that in those with histological activity (118.1 µg/g; P < .01). The area under the curve (AUC) in a receiver operating characteristic (ROC) curve analysis to predict HH for FC was 0.71 (95% confidence interval [CI], 0.59–0.83), with an optimal cutoff value of 82.7 µg/g (73% sensitivity; 64% specificity; P < .01). Of 74 patients observed for 2 years, 54 (73%) had prolonged CR. In the ROC curve analysis, the AUC to predict prolonged CR for FC was 0.79 (95% CI, 0.68–0.90), equivalent to that for HH (0.73; 95% CI, 0.64–0.86; P = .40). The optimal FC cutoff value to predict prolonged CR was 84.6 µg/g (72% sensitivity; 85% specificity; P < .01). Conclusions Fecal calprotectin < 82 µg/g predicts HH in patients with UC with clinical and endoscopic remission. Low FC leads to prolonged CR, equivalent to HH.

Oxaliplatin, widely used as a chemotherapy drug for colorectal cancer, is known to cause various adverse reactions. In particular, special attention for the development of portal hypertension associated with portosinusoidal vascular disease is necessary, as it is a serious adverse life-threating reaction, although rare. We herein report a case of oxaliplatin-related portal hypertension that developed several years after oxaliplatin administration and led to esophageal varices and refractory massive ascites. Clinical physicians should be aware of the possibility of oxaliplatin-induced portal hypertension and its possible development over a long period after discontinuation of the drug.

Anti-tumor necrosis factor (TNF) α agents, widely used for the treatment of Crohn's disease (CD), can sometimes induce skin-associated adverse events, which mainly include psoriasis-like eruptions, eczema, and cutaneous infections. In contrast, purpura caused by vasculitis is rarely seen. We herein report a unique case of leukocytoclastic vasculitis induced by infliximab administered for CD in which intermittent purpura development was noted. Fluorescent immunostaining showed no immunoglobulin A deposition on the vessel walls. No purpura was initially seen after starting infliximab, but it appeared approximately 10 months later; however, administration did not have to be discontinued, and the condition was later resolved. The present findings provide important details regarding vasculitis induced by anti-tumor necrosis factor-α agent administration.