The serum autoantibodies, antinuclear antibody, anti-DNA antibody, anti-smooth muscle antibody, antithyroglobulin antibody, antimicrosomal antibody, antimitochondrial antibody, rheumatoid factor and antibody to deoxyribonucleoprotein were measured at the baseline and on completion of interferon-a2a (IFN-oc2a) treatment in chronic hepatitis C (CHC) patients who did not present with any autoimmune disease prior to treatment. Of the 57 patients examined, 27 spontaneously manifested at least one autoantibody. Only the prevalence of rheumatoid factor (26%) was significantly higher in the CHCpatients than in the control subjects. There were no differences in the prevalence of the 8 autoantibodies examined between hepatitis C virus (HCV) genotypes, lb and 2a/2b. Twenty-six patients responded to IFN-oc2a. Subclinical hypothyroidism developed in two patients with elevated antithyroid antibody titers during treatment. Norelation-ship was observed betweenchanges in the status of autoantibodies and either response to IFN-a2a or HCVgenotype. Irrespective of the HCVgenotype, autoantibodies might be present in CHC patients before and during the IFN-oc2a treatment. The presence of such antibodies does not represent a contraindication to the use of IFN-a2a in CHCpatients not complicated by auto-immune diseases. Careful observations are necessary for CHCpatients positive for antithyroid antibodies during the IFN-oc2a treatment. Preexisting or newly developed autoantibodies do not necessarily predict a poor response to IFN-oc2a.

The present report describes a patient who developed Graves' disease 3 months after inception of retreatment with higher doses of interferon-oc2a for chronic hepatitis C, although the initial 6-month treatment caused no serious adverse reactions. Severe hyperthyroidism continued despite discontinuation of interferon-oc2a, and the patient was subsequently treated with 131I. This case suggests careful evaluation of the safety of retreatment to prevent manifestation of such a complication in the retreatment of chronic hepatitis C with interferon.

Twenty chronic hepatitis C patients with baseline levels of thyroid hormones, antithyroglobulin, and antimicrosomal antibodies within the normal range were monitored by thyroid testing during a 26-week treatment with interferon-alpha2a (IFN-alpha2a). The present study was aimed at retrospectively analyzing thyroid-stimulating hormone (TSH) receptor antibodies, employing stored serum samples obtained from these patients at baseline, at 12 weeks, and at the end of IFN-alpha2a treatment. Ten patients (group A) received IFN-alpha2a at a total dose of 474 million units (MU), and 10 patients (group B) at a total dose of 774 MU. None of the patients produced antithyroglobulin and antimicrosomal antibodies. Two patients in group A exhibited elevated TSH levels without free thyroid hormone alterations while on the treatment. At baseline, 1 patient in group A had a positive TSH binding inhibitory immunoglobulin, and 1 patient in group B was positive for thyroid-stimulating antibody at the end of treatment. Both patients remained euthyroid throughout the treatment. Treatment with IFN-alpha2a may infrequently induce the production of TSH receptor antibodies in chronic hepatitis C patients provided preexisting autoimmune thyroid disease is precluded.

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