title: Interferon-alpha therapy may induce insulin autoantibody development in patients with chronic viral hepatitis.
abstract: Development of type 1 insulin-dependent diabetes mellitus has been recently reported in patients who underwent interferon-alpha (IFN-alpha) therapy because of chronic viral hepatitis. Furthermore IFN-alpha seems to be involved in the immunological events that lead to beta-cell destruction and development of type 1 diabetes. To evaluate whether IFN-alpha treatment could elicit an autoimmune response against beta-cell antigens, we determined the occurrence of islet cell antibodies and insulin autoantibodies in the sera of 60 patients with HCV- or HBV-related chronic hepatitis who had been treated with IFN-alpha for 6 or 12 months. The presence of antibodies against thyroglobulin, thyroid microsomal antigen, gastric parietal cells, and non-organ-specific antigens was also investigated. Insulin autoantibody positivity was observed in 2/60 (3.3%), 8/60 (13.3%), and 4/30 (13.3%) patients, before IFN-alpha treatment, and after 6 months and 12 months of therapy, respectively. None of the studied patients developed islet cell antibodies or type 1 diabetes. Before IFN-alpha therapy four patients showed thyroid autoantibodies and four others developed antibodies against thyroglobulin and/or thyroid microsomal antigen during the treatment. Coexistence of insulin autoantibodies and thyroid autoantibodies was observed in only two patients. Our results showed that IFN-alpha therapy in patients with chronic viral hepatitis is capable of inducing development of autoantibodies against insulin. This event seems to be not related to other autoimmune disorders.
authors.affiliation: Department of Internal Medicine, University of Messina, Italy.
authors.forename: E
authors.initials: E
authors.lastname: di Cesare
authors.forename: M
authors.initials: M
authors.lastname: Previti
authors.forename: F
authors.initials: F
authors.lastname: Russo
authors.forename: S
authors.initials: S
authors.lastname: Brancatelli
authors.forename: M C
authors.initials: MC
authors.lastname: Ingemi
authors.forename: R
authors.initials: R
authors.lastname: Scoglio
authors.forename: N
authors.initials: N
authors.lastname: Mazzù
authors.forename: D
authors.initials: D
authors.lastname: Cucinotta
authors.forename: G
authors.initials: G
authors.lastname: Raimondo
mesh_terms: D000293:Adolescent; D000328:Adult; D001323:Autoantibodies / Q000032:analysis; D002908:Chronic Disease; D003922:Diabetes Mellitus, Type 1 / Q000209:etiology; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D006509:Hepatitis B / Q000276:immunology / Q000628:therapy*; D006526:Hepatitis C / Q000276:immunology / Q000628:therapy*; D006801:Humans; D007330:Insulin Antibodies / Q000096:biosynthesis*; D007370:Interferon Type I / Q000009:adverse effects* / Q000627:therapeutic use; D007515:Islets of Langerhans / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011994:Recombinant Proteins; D012189:Retrospective Studies
chemical_list: D001323:Autoantibodies; D007330:Insulin Antibodies; D007370:Interferon Type I; D011994:Recombinant Proteins