The prevalence of these antibodies in MC has been only little examined. The aim of this study was to further examine the prevalence of auto-antibodies in a larger cohort of MC patients, and if present, to examine the association between the presence of antibodies to concomitant diseases and clinical findings. Methods Ethics Statement The study protocol was approved by the Ethics Committee of Lund University, and all participants gave their written, informed consent when taking part in the study (LU 2009/565 and 2011/209). Patients Women who had been treated for MC at any outpatient clinic of the Departments of Gastroenterology, throughout the district of Sk?ne, between 2002 and 2010, were identified by a search for the ICD-10 classification for CC and LC (K52.8) in outpatient records and the local register at the Department of Pathology, Sk?ne University Hospital, Malm?. Blood samples were collected. Anti-nuclear antibodies (ANA), anti-neutrophil cytoplasmic antibodies (ANCA), anti-Saccharomyces cerevisiae Vigabatrin antibodies (ASCA), and antibodies against glutamic acid decarboxylase (anti-GAD), islet antigens-like insulin 2 (anti-IA2), thyroid peroxidase (anti-TPO), and thyrotropin receptor (TRAK) were analysed. Of 240 women identified, 133 were finally included in the study, median age 63 (59C67) years. Apart from the MC diagnosis, 52% also suffered from irritable bowel syndrome, 31% from hypertension and 31% from allergy. The prevalence of ANA (14%), ASCA IgG (13%), and anti-TPO antibodies (14%) for these patients was slightly higher than for the general population, and were found together with other concomitant diseases. Patients had more of all gastrointestinal symptoms compared with norm values, irrespective of antibody expression. Conclusions Women with MC have a slightly increased prevalence of some auto-antibodies. These antibodies are not associated with symptoms, but are expressed in patients with concomitant diseases, obscuring the pathophysiology and clinical picture of MC. Introduction Microscopic colitis (MC) is a disease with watery diarrhoea without endoscopically inflamed colonic mucosa, and is divided into two different entities, collagenous colitis (CC) and lymphocytic colitis (LC). The diagnostic criterion for LC is >20 intraepithelial lymphocytes/100 enterocytes, reactive surface epithelium and mixed inflammatory infiltrate in the lamina propria. When also the subepithelial collagen band is >10 m thick, the diagnosis CC is set [1]. The aetiology is unknown, but an auto-immune process has been proposed due to the responsiveness to corticosteroids, and a high frequency of a HLA haplotype and TNF alpha gene polymorphism (-308) associated with susceptibility to several auto-immune diseases [2]. Furthermore, other auto-immune diseases are found in 40% of these patients, thyroid diseases, rheumatologic diseases, diabetes mellitus, and coeliac disease being the most common [3], [4]. Microscopic colitis may be a different entity in younger than in older patients, where drug treatment may be a considerable aetiology of the colitis, and therefore should in these cases rather be classified as a secondary disease [1]. A high prevalence of several auto-antibodies is found in patients with auto-immune diseases [5], [6]. Antibodies against anti-neutrophil cytoplasmic antibodies (ANCA) are found in 40%C70% of patients with ulcerative colitis, and anti-Saccharomyces cerevisiae antibodies (ASCA) are found in 30%C70% of patients with Crohs disease [7], [8]. Although MC is categorised as an Vigabatrin inflammatory bowel disease (IBD) of auto-immune origin [9], only a few, small studies have been performed to examine the prevalence of auto-antibodies in this entity. No increased levels of rheumatoid factor or antibodies against thyroglobulin, microsomal antigen, endomysium and transglutaminase were found [3], [4]. In CC, a tendency to increased anti-nuclear antibodies (ANA) was seen in one study, whereas increased levels of ANA, ANCA, and ASCA were seen in others [3], [4], [7]. One confounding factor may be that the level of auto-antibodies correlates with disease activity, and high values may only be detected in the active disease [10]. Type 1 diabetes mellitus is an auto-immune disease associated with MC [3], [4]. Auto-antibodies that develop against islet antigens-like insulin 2 (IA2) and glutamic acid decarboxylase (GAD) are the markers of the disease, and are present in 70%C80% of cases [11], [12]. In the majority of diabetes cases, immune reaction against islet antigens and consequent formation of auto-antibodies begins long before the disease is diagnosed Vigabatrin clinically [13]. The prevalence of these antibodies in MC has been only little analyzed. The purpose of Vigabatrin this research was to help expand examine the prevalence of auto-antibodies Rabbit Polyclonal to SH3GLB2 in a more substantial cohort of MC individuals, and if present, to examine the association between your existence of antibodies to concomitant illnesses and clinical results. Methods Ethics Declaration.