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An 11-year prospective study was carried out in 226 patients with organ-specific autoimmune disease (OSAD) coming from northern Italy and southern England. Patients were investigated for diabetes-related autoantibodies (ICAs, GADAbs, and IA2Abs) in order to evaluate the best immunological combination in predicting type 1 DM. One hundred twenty-eight patients were ICA positive (77 Italian and 51 English), and 98 were ICA negative. ICAs were detected by immunofluorescence technique on human pancreas, whereas GADAbs and IA2Abs were found by immunoprecipitation assay. During follow-up, 33 of 128 (25.8%) ICA(+) (26% of Italian and 25.5% of English) and 2 of 98 (2%) ICA(-) patients developed type 1 DM (17 with acute-onset, and 18 with non-acute-onset disease). Among ICA(+) patients, three subgroups were considered: ICA(+) alone; ICA and GADAb(+); ICA, GADAb, and IA2Ab(+). Patients who were only ICA(+) had a predictive value for type 1 DM of 4.7%, with an annual incidence of 0.7%, and a cumulative risk of 6%. ICA and GADAb(+) patients had a predictive value of 17.5%, with an annual incidence of 2%, and a cumulative risk of 20%. ICA, GADAb, and IA2Ab(+) patients had a predictive value of 72, with an annual incidence of 13%, and a cumulative risk of 87%. Patients having three immunological markers revealed a prevalence increased in HLA-DR3 and/or -DR4, but reduced in HLA-DR2 haplotypes. The risk for type 1 DM increased proportionally with the number of diabetes-related antibodies, which were also related to the presence of genetic markers of disease susceptibility.

Background Several studies have suggested a link between coeliac disease and other autoimmune diseases. Aim To compare the presence of autoimmune disease in children with coeliac disease and in controls. Methods When coeliac disease was diagnosed, 267 children were evaluated for clinical autoimmune disease (with signs/symptoms), subclinical autoimmune disease (with autoantibodies and subclinical impairment of the target organ) or potential autoimmune disease (with autoantibodies only) and compared with 220 healthy controls. 170 coeliac disease patients were followed up for a mean 47 ± 31 months, in complete remission on a gluten-free diet. Ninety-nine controls were followed up for 45 ± 33 months. Results When coeliac disease was diagnosed, 71 (27%) children had autoimmune disease vs. 1% among the controls ( P < 0.001): 31 had clinical autoimmune disease and 40 had subclinical or potential autoimmune disease. During the follow-up, the clinical autoimmune disease cases slightly decreased from 12% to 11%, while the potential autoimmune disease cases increased from 14% to 21%. Of the 99 controls, none had any variation in their autoantibody profile. Conclusions Gluten-free diet does not modify the natural history of autoimmunity in patients with coeliac disease. However, gluten-free diet seems to produce a favourable effect on the previously present clinical autoimmune disease and to prevent the development of new clinical autoimmune disease, but does not affect the onset of potential autoimmunity, which tends to increase with time. [ABSTRACT FROM AUTHOR]

The role of hepatitis C virus (HCV) in inducing thyroid autoimmunity is still under discussion and to assess the prevalence of thyroid autoantibodies and thyroid disease in the general population and to analyse the role of HCV in inducing thyroid autoimmunity. We studied 697 subjects residing in Arsita (a small town in central Italy). Thyroid autoantibodies and nonorgan-specific autoantibodies (NOSAs) were tested in each subject, who were also screened for anti-HCV antibodies; all subjects found positive to HCV–RNA were considered as being HCV-infected. Thyroid function tests were performed in all subjects positive for thyroid autoantibody. Seventy-one subjects were found HCV-positive; four of these (5.6%) were positive for at least one thyroid autoantibody, as opposed to 7 (4.9%) of the 142 sex- and age-matched controls of the same population ( P = n.s.). Thyroid dysfunction was found in 2/4 HCV-positive, and in 1/7 HCV-negative subjects with thyroid autoantibodies ( P = n.s.). NOSAs were significantly more common in HCV-positive than in HCV-negative subjects ( P < 0.0001). Hence HCV per se is not responsible for thyroid autoimmune dysfunction, whereas HCV does seem to induce NOSAs. It should be taken into account, however, that the phenotypic expression of autoimmune diseases is obviously influenced by a number of risk factors, including genetic predisposition, female sex and infectious agents, that could trigger the onset of the disease. [ABSTRACT FROM AUTHOR]