title: Long-term outcome of interferon-alpha-induced autoimmune thyroid disorders in chronic hepatitis C.
abstract: BACKGROUND
  Autoimmune thyroid disorders are among the well-known adverse effects of interferon-alpha (IFN-alpha) therapy in patients with chronic hepatitis C. However, there are few reports regarding the long-term outcome of this complication. We aimed to evaluate the natural history of IFN-alpha-induced autoimmune thyroid disorders with long-term follow-up.
  
  
  METHODS
  Four hundred and thirty-nine patients with chronic hepatitis C were treated with IFN-alpha for 24 weeks between March 1993 and April 1998. Seventeen of 439 (3.9%) patients developed symptomatic autoimmune thyroid disorders including nine cases of hyperthyroidism and eight cases of hypothyroidism. The patients with hypothyroidism were all women. These 17 patients were followed up for 71.1 +/- 17.8 months (48-120 months) and were evaluated for long-term outcome.
  
  
  RESULTS
  Eight patients could discontinue the thyroid medication (2-36 months, median 10 months). Nine patients needed the thyroid medication at the follow-up period. The patients with hyperthyroidism who needed long-term thyroid medication had a significantly high titer of TSH receptor antibody on onset compared with the patients who could discontinue the thyroid medication. There were no significant differences in age, type of IFN, duration from IFN administration to onset, cessation of IFN, genotype of hepatitis C virus and thyroid hormone levels on onset between the patients who needed long-term thyroid medication and the patients who could discontinue the thyroid medication.
  
  
  CONCLUSIONS
  All patients with IFN-alpha-induced thyroid disorders could be controlled with medication. However, the IFN-alpha-induced thyroid disorders are not always reversible. One must be careful about not only the development of autoimmune thyroid disorders during IFN-alpha therapy but also the outcome of the thyroid disease.
authors.affiliation: Department of Medicine and Molecular Science, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
authors.forename: Fumina
authors.initials: F
authors.lastname: Doi
authors.forename: Satoru
authors.initials: S
authors.lastname: Kakizaki
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Takagi
authors.forename: Masami
authors.initials: M
authors.lastname: Murakami
authors.forename: Naondo
authors.initials: N
authors.lastname: Sohara
authors.forename: Toshiyuki
authors.initials: T
authors.lastname: Otsuka
authors.forename: Takehiko
authors.initials: T
authors.lastname: Abe
authors.forename: Masatomo
authors.initials: M
authors.lastname: Mori
mesh_terms: D000328:Adult; D017677:Age Distribution; D000368:Aged; D001323:Autoantibodies / Q000032:analysis / Q000276:immunology; D015331:Cohort Studies; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D005260:Female; D005500:Follow-Up Studies; D019698:Hepatitis C, Chronic / Q000175:diagnosis / Q000188:drug therapy*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000009:adverse effects* / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D011336:Probability; D011994:Recombinant Proteins; D012189:Retrospective Studies; D018570:Risk Assessment; D012720:Severity of Illness Index; D017678:Sex Distribution; D013960:Thyroid Function Tests; D013967:Thyroiditis, Autoimmune / Q000139:chemically induced* / Q000453:epidemiology* / Q000503:physiopathology
chemical_list: D001323:Autoantibodies; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins