2001;9:767C8. the rate of AGAAb was 132% in comparison with 35% (= 0035). The prevalence of EMAb was very low in both groups (15% and 0). The two groups differed significantly in the TPOAb rate: 221% in LADA compared to 94% in T2DM (= 004), whereas no significant difference was found in the presence of TGAb (88% and 35%, = 0187). In comparison with T2DM patients, LADA patients were found to express higher antibody activity against gluten-related antigens and against TPO. Keywords: anti-gliadin, coeliac, latent autoimmune diabetes of adults, thyroidal INTRODUCTION Type 1 diabetes mellitus (T1DM) is the result of an autoimmune destruction of beta cells of the pancreatic Langerhans islets with consequent insulin deficiency. Both humoral and cellular components participate in pathogenic autoimmune reactions. Humoral markers of the autoimmune reaction to beta cells of the pancreas include islet cell antibodies (ICAb), antibodies to insulin (IAb), antibodies to glutamic acid decarboxylase (GADAb) and antibodies to tyrosine phosphatase-like protein (IA-2Ab) [1]. The presence of these markers before the development of overt disease can identify patients at risk. In adults, the onset of diabetes-specific autoantibodies is useful E 2012 in diabetes classification and appropriate treatment; these antibodies can distinguish between diabetes mellitus Type 2 and slowly progressing T1DM (LADA: latent autoimmune diabetes of the adults) [2]. Immunologically mediated diabetes occurs commonly at any age, even in the 8th and 9th decades of life. T1DM occurs often in association with other autoimmune diseases, both organ-specific and organ-non-specific (thyroid disease, Addison’s disease, coeliac disease, rheumatic disease and others). The presence of various circulating autoantibodies has been reported frequently. The co-existence of coeliac disease (CD) and T1DM has been shown in several studies; the rates of co-existence are 1C7%[3][4], much higher than E 2012 rates in the normal population. The diagnosis of coeliac disease is based on typical antibody presence, clinical history and jejunal biopsy. Several reports show the presence of clinically milder, less symptomatic forms of CD in diabetic patients. Anti-gliadin antibodies (AGAb) have been used widely as a screening tool for CD, E 2012 with sensitivity of approximately 75% and specificity of approximately 95%[5]. Apart from anti-gliadin antibodies and antibodies to endomysium, tissue transglutaminase and calreticulin are found in the sera of coeliac patients [6]. Endomysial antibodies (EMAb-IgA) have higher sensitivity and specificity than AGAb [7]. It was shown that the prevalence E 2012 of AGAb may be high in patients with T1DM without symptoms of CD [8]. Most of the E 2012 studies have focused on the association of childhood diabetes and coeliac disease, but the patterns of antibodies and the clinical course of the two diseases in adults seem to be different. To date, no studies related to the association of autoimmune diabetes with delayed onset and coeliac disease have been published. Autoimmune thyroiditis (AT) is also a common autoimmune disease associated with T1DM, characterized by the presence of specific thyroid autoantibodies, thyroid peroxidase antibodies (TPOAb) and thyroglobulin antibodies (TGAb). The prevalence of thyroid antibodies in T1DM adult patients has been reported to be between 20% and 30%[9C12]. TPOAb occur more often than TGAb. The prevalence of autoimmune thyroiditis seems to increase with age [13]. The association of autoimmune diseases in both human patients and animal models of autoimmunity is explained by the spreading of T cell response to new determinants during the course of autoimmunity development. This phenomenon of recruitment of additional T cell epitopes has been reported during the course of experimental autoimmune encephalomyelitis (reaction to myelin basic protein and subsequently to other myelin proteins). In NOD Rabbit Polyclonal to ERI1 mice, the initial response to GAD determinants was spread to mycobacterial hsp 65 peptide, carboxypeptidase H and insulin. As proposed, the explanation can be in an up-regulated determinant presentation, the down-regulation of CD4 molecules or the presence of antibodies that bind to these epitopes on the same antigen [14]. To.