title: Reversibility of thyroid dysfunction induced by recombinant alpha interferon in chronic hepatitis C.
abstract: OBJECTIVE
  Thyroid dysfunction has been reported as a complication of interferon therapy. The aim of our study was to assess the risk factors and reversibility of thyroid disorders induced by interferon therapy.
  
  
  METHODS
  Prospective study.
  
  
  METHODS
  A series of 68 patients with chronic hepatitis C completed a therapeutic trial of interferon alpha 2b (IFN), randomized for dose adaptation, lasting for 24 weeks.
  
  
  METHODS
  TSH and autoantibodies against thyroid were looked for at (-2) weeks and 24 weeks in all patients. Blood samples obtained at (-2), 12, and 24 weeks were stored for additional hormonal studies in patients who developed thyroid dysfunction. Such patients with thyroid dysfunction were followed up for at least one year.
  
  
  RESULTS
  Only one out of 68 patients had abnormal TSH levels, and two had thyroid autoantibodies prior to interferon therapy. Eight patients (12%) developed thyroid dysfunction (five hypothyroidism and three hyperthyroidism) during treatment. In four patients (all of them with thyroid dysfunction, P < 0.001) antimicrosomal, antithyroglobulin, and/or anti-TSH receptor antibodies appeared during interferon therapy. All patients recovered normal thyroid function within 1.5 years after interferon withdrawal. No pretreatment risk factor was identified. The patients with thyroid dysfunction did not significantly differ from the others as regards the dose of interferon they received or the rate of normalization of transaminases.
  
  
  CONCLUSIONS
  (i) A 12% incidence of thyroid dysfunction was observed under interferon therapy; (ii) secondary appearance under interferon therapy of elevated thyroid autoantibodies was a risk factor; (iii) the thyroid disorders induced by interferon were reversible.
authors.affiliation: Service de Médecine Nucléaire, Hôpital Beaujon, Université Paris 7, Clichy, France.
authors.forename: E
authors.initials: E
authors.lastname: Baudin
authors.forename: P
authors.initials: P
authors.lastname: Marcellin
authors.forename: M
authors.initials: M
authors.lastname: Pouteau
authors.forename: N
authors.initials: N
authors.lastname: Colas-Linhart
authors.forename: J P
authors.initials: JP
authors.lastname: Le Floch
authors.forename: C
authors.initials: C
authors.lastname: Lemmonier
authors.forename: J P
authors.initials: JP
authors.lastname: Benhamou
authors.forename: B
authors.initials: B
authors.lastname: Bok
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D002908:Chronic Disease; D004334:Drug Administration Schedule; D005260:Female; D005500:Follow-Up Studies; D006526:Hepatitis C / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D007370:Interferon Type I / Q000008:administration & dosage / Q000009:adverse effects*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011994:Recombinant Proteins; D012307:Risk Factors; D013961:Thyroid Gland / Q000503:physiopathology*
chemical_list: D007370:Interferon Type I; D011994:Recombinant Proteins