Islet cell and thyroid antibody prevalence in patients with hepatitis C virus infection: Effect of treatment with interferon

Citation
S. Piquer et al., Islet cell and thyroid antibody prevalence in patients with hepatitis C virus infection: Effect of treatment with interferon, J LA CL MED, 137(1), 2001, pp. 38-42
Citations number
39
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Medical Research General Topics
Journal title
JOURNAL OF LABORATORY AND CLINICAL MEDICINE
ISSN journal
00222143 → ACNP
Volume
137
Issue
1
Year of publication
2001
Pages
38 - 42
Database
ISI
SICI code
0022-2143(200101)137:1<38:ICATAP>2.0.ZU;2-#
Abstract
An increased prevalence of hepatitis C virus (HCV) infection in patients wi th diabetes and a higher prevalence of diabetes in HCV-infected patients ha ve been reported. However, the relationship between these two conditions re mains controversial. In addition, although the effect of interferon treatme nt on thyroid autoimmunity has been extensively reported, its influence on beta -cell autoantibodies has not been investigated. The aims of the study were (1) to evaluate whether autoimmune beta -cell damage could be involved in the development of diabetes mellitus in HCV-infected patients and (2) t o determine whether interferon treatment influences the appearance of beta -cell and thyroid autoantibodies. The prevalence of islet cell autoantibodi es (glutamic acid decarboxylase antibodies (GADAs), tyrosine phosphatase an tibodies (IA-2s), islet cell antibodies (ICAs)) was assessed in 303 nan-sel ected HCV-infected patients (277 non-diabetic and 26 type 2 diabetic patien ts) and in 273 sex- and age-matched control subjects, ICAs and thyroid auto antibodies were also determined before and 6 and 12 months after treatment with interferon for 24 weeks in a subgroup of 46 HCV-infected patients. GAD As were detected in 4 of 277 (1.4%) HCV-infected non-diabetic patients, 1 o f 273 (0.3%) control subjects, and 0 of 26 (0%) HCV-infected patients with diabetes. Anti-IA2s and ICAs were negative in all subjects. Both GADAs and anti-IA2s were negative in all HCV-infected patients treated with interfero n. After therapy, only thyroid antibodies became positive in 5 of 46 (10.9% ) treated patients, disappearing in all but 1 of these at the 12-month foll ow-up. Our results suggest that beta -cell autoimmunity is not associated w ith HCV infection, thus making it unlikely that the increased diabetes mell itus prevalence among HCV-infected patients could be mediated by autoimmune mechanisms. In addition, interferon treatment induces a transient increase in thyroid autoantibodies but does not influence the appearance of beta -c ell autoantibodies.