Thereafter, to investigate the effect of gluten intake, we followed up some sero-positive IBD patients clinically, serologically and histologically with or without gluten containing diet prospectively. Materials and methods Study population This cohort study was prospectively conducted in a single university institute between 2009 and 2012. of both serum antibodies was significantly higher in IBD and correlated with disease activity. However, no biopsy-defined or HLA-defined true celiac disease was found. A decrease in serum antibody titers was observed with a gluten-restricted Biapenem diet. Conclusions Despite the increased incidence of IBD and high positivity for serum celiac antibody in Japanese IBD patients, no true-positive celiac disease was noted, suggesting the presence of gluten intolerance in these populations. Keywords: Celiac disease, Japanese, Inflammatory bowel diseases, Gluten Introduction The prevalence of celiac disease has significantly risen over the past years in European countries. More recently, comparable prevalence has been Biapenem reported from some Asian and Mid-eastern countries. Eastern Asia has a low prevalence of celiac disease due to both a lack of genetic predisposition and a low consumption of wheat. However, the potential for rising incidence of celiac disease has been explained in Japan [1C3], because in the past decades the traditional rice-based diet has been replaced by a western-style diet, and now wheat consumption is as much Biapenem as in India. The prevalence of HLA-DQ2 and DQ8, the two major haplotypes that play a major role in the development of celiac disease, have been reported to be Biapenem as high as 30C40?% in some Western countries. The prevalence of HLA-DQ2 and DQ8 in the general Japanese population is usually estimated to be around 10C20?%, substantially lower than in Western countries, but not absent. However, the precise prevalence of celiac disease in Japan remains unknown. Diagnostic laboratory assessments for celiac disease are not commonly used in Japan and there is a possibility of underdiagnosis or misdiagnosis as other inflammatory disorders of the gastrointestinal tract sharing similar clinical symptoms such as inflammatory bowel disease (IBD). Celiac disease, Crohns disease, and ulcerative colitis are categorized as inflammatory disorders of the gastrointestinal tract of unknown etiology, although genetic, immunological and E2F1 environmental factors are involved in their pathogenesis. Since the incidence of IBD has increased continuously in Japan, and as exposure to gluten containing food has become more common, it is possible that there is confusion in discriminating between celiac disease and IBD. The most reliable serological marker of celiac disease, anti-tissue transglutaminase (tTG), appears to be seen in IBD patients as a result of immunological phenomena [4C6]. A wide range of anti-tTG concentrations has been exhibited in IBD patients and their positive anti-tTG results are related to disease activity [4, 7]. However, a high rate of false positives has previously been reported, when guinea pig liver extracts were used as a source of tTG [8C10], and the more specific human recombinant tTG antigen is now widely used. Histological evaluation followed by serology and small intestinal biopsy with villous atrophy is the platinum standard for celiac disease diagnosis. However, villous atrophy and increased intraepithelial lymphocytosis has also been reported in Crohns disease and other intestinal disorders [11], and IBD and celiac disease can superimpose each other. These serological and histological aspects make it hard to evaluate the comorbidity of these two diseases. The anti-endomysial antibodies (EMA) blood test is considered the most specific to celiac disease, but EMA lacks sensitivity especially in the early disease stage with moderate villous atrophy [12, 13]. More recent work has led to the development of serological assessments that can identify antibody to deamidated gliadin peptides (DGP), the product of intestinal tTG action on dietary gluten peptide [14]. These peptides bind with high affinity to human leukocyte antigen (HLA) DQ2 or DQ8 on celiac patient antigen-presenting cells to potently stimulate the inflammatory T cell response [15]. This account for the antibody response for DGP is usually more highly specific for celiac disease than the historically used antibodies to native gluten (AGAs), so measurement of anti-DGP is reasonably specific [16], especially in children, in patients with early stage celiac disease and almost normal villous morphology [17], or to monitor diet compliance [18]. However, no study has evaluated this new.