title: Thyroid autoantibodies and thyroid dysfunction during treatment with interferon-alpha for chronic hepatitis C.
abstract: Interferon-alpha (2a or 2b) is increasingly used for treatment of chronic hepatitis C virus (HCV) infection. Recent reports suggested a correlation between increases in thyroid autoantibodies and the development of thyroid dysfunction during interferon-alpha therapy. In this study, we analyzed thyroid hormones and antithyroid antibodies at monthly intervals in 53 patients who received interferon alpha for chronic active hepatitis C infection. Of five patients with initially elevated levels of antithyroid peroxydase antibodies (anti-TPO), the antibodies increased further in two of them. Ten patients, who started interferon therapy with normal antibody levels, developed elevated anti-TPO antibodies for limited times during treatment. Levels of anti-TPO antibodies showed a marked fluctuation, and only three patients had increased anti-TPO antibodies persisting for longer than 3 mo. Antithyroglobulin antibodies appeared in four patients, all of whom were also positive for anti-TPO antibodies. No changes in TRAB levels were observed. All of these patients with elevated antithyroid antibodies remained in an euthyroid state. One patient with normal antithyroid antibodies developed thyroiditis with severe thyrotoxicosis after 9 wk of interferon therapy. These findings suggest that the induction of antithyroid antibodies during treatment with interferon-alpha does not indicate clinical relevant thyroid dysfunction. Routine measurement of antithyroid antibodies during interferon-alpha therapy does not seem to be mandatory.
authors.affiliation: Medizinische Klinik, Christian-Albrechts Universität Kiel, Germany.
authors.forename: K
authors.initials: K
authors.lastname: Kiehne
authors.forename: S
authors.initials: S
authors.lastname: Kloehn
authors.forename: H
authors.initials: H
authors.lastname: Hinrichsen
authors.forename: B
authors.initials: B
authors.lastname: Gallwitz
authors.forename: H
authors.initials: H
authors.lastname: Mönig
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000008:administration & dosage / Q000627:therapeutic use*; D001323:Autoantibodies / Q000097:blood* / Q000187:drug effects / Q000276:immunology; D005260:Female; D006526:Hepatitis C / Q000188:drug therapy* / Q000276:immunology; D006801:Humans; D007279:Injections, Subcutaneous; D007370:Interferon Type I / Q000008:administration & dosage / Q000627:therapeutic use*; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000008:administration & dosage / Q000627:therapeutic use; D007453:Iodide Peroxidase / Q000276:immunology; D008297:Male; D011994:Recombinant Proteins; D012016:Reference Values; D013954:Thyroglobulin / Q000276:immunology; D013961:Thyroid Gland / Q000201:enzymology / Q000276:immunology*; D013997:Time Factors
chemical_list: D000998:Antiviral Agents; D001323:Autoantibodies; D007370:Interferon Type I; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D013954:Thyroglobulin; D007453:Iodide Peroxidase