Expression of endocrine autoantibodies in chronic hepatitis C, before and after interferon-alpha therapy.

Interferon-alpha (IFN-alpha) treatment for chronic hepatitis C (CHC) has been associated with thyroid autoimmunity and/or dysfunction. Only a few data concerning the prevalence of islet-cell or adrenal cortex autoantibodies in IFN-alpha-treated subjects are currently available. The aims of our study were to evaluate in CHC, 1) the prevalence and association of thyroid, islet-cell and adrenal autoantibodies, and 2) the appearance of endocrine dysfunction, before and after a 6 month IFN-alpha treatment. We analyzed serum samples from 203 adult patients at the time of clinical diagnosis of CHC and showed that the prevalence of thyroperoxidase (TPOAb), thyroglobulin (TGAb), TSH-receptor (TRAb), glutamic acid decarboxylase (GAD65Ab), IA-2/ICA512 (IA-2/ICA512Ab) and 21-hydroxylase (21OHAb) autoantibodies was similar to that observed among healthy control subjects of similar age and sex distribution. Among 99 patients with follow-up serum samples, 83 accepted and 16 refused IFN-alpha treatment. The IFN-alpha treatment was associated with increase of TPOAb levels in 3 subjects already positive at baseline, with progression to overt hypothyroidism in 2 of them. The de novo appearance of autoantibodies was observed in 5/80 (6%) cases for TPOAb, 1/81 (1.2%) for GAD65Ab and 2/81 (2.5%) for IA-2/ICA512Ab. Clinical or subclinical signs of either hyperthyroidism or hypothyroidism were demonstrated in 3/5 cases with de novo appearance of TPOAb. Four subjects, initially positive for either GAD65Ab or IA2/ICA512Ab, were all found negative after IFN-alpha-treatment. No subjects showed positivity for 21OHAb either at baseline or after the follow-up period. Our study suggests that, in CHC untreated patients, the prevalence of endocrine autoantibodies is similar to that observed in the general population. Furthermore, we demonstrate that IFN-alpha treatment is associated with the induction or enhancement of thyroid, but not of islet-cell or adrenal cortex autoimmunity.