title: Thyroid dysfunction in patients with chronic hepatitis C: virus- or therapy-related?
abstract: OBJECTIVE
  Thyroid dysfunction (TD) represents an extrahepatic manifestation of chronic hepatitis C (CHC). Moreover, the currently approved treatment of CHC is often associated with TD. However, it remains debatable if TD is mainly virus- or treatment-related. The aim of this study was to assess the incidence and features of TD, and to identify its predictors in treated and untreated CHC patients.
  
  
  METHODS
  Ninety-four patients with CHC and normal thyroid function were evaluated long-term for TD: 33 were untreated (control group) and 61 were treated with pegylated interferon alpha (PEG-IFN-alpha) plus ribavirin (treatment group). Mean follow up was 80.1 and 39.4 months, respectively.
  
  
  RESULTS
  All patients in the control group remained euthyroid, while 13 treated patients (21.3%) developed TD (P < 0.001). Eleven of these were diagnosed with hypothyroidism and two with hyperthyroidism, which then converted to hypothyroidism. In the majority of cases (9/13, 69.2%) TD did not reverse after treatment discontinuation and required hormone replacement therapy. Pretreatment virological parameters did not predict TD, according to multiple logistic regression analysis. TD was not associated with total dose of PEG-IFN-alpha or ribavirin, viral kinetics or with virological outcome, but it was linked to development of other therapy-related autoimmune disorders (odds ratio, 8.29).
  
  
  CONCLUSIONS
  Antiviral therapy of CHC possibly induces de novo or exacerbates pre-existing silent TD. TD does not seem to correlate with any pretreatment virological parameter; it is probably not related to dose or treatment duration, nor linked to viral kinetics or virological outcome. The role of chronic hepatitis C per se in TD remains to be determined.
authors.affiliation: University Department of Internal Medicine, Hepatology Unit, Elena Venizelou Hospital, Athens, Greece. avezalis@otenet.gr
authors.forename: Elena
authors.initials: E
authors.lastname: Vezali
authors.forename: Ioannis
authors.initials: I
authors.lastname: Elefsiniotis
authors.forename: Constantinos
authors.initials: C
authors.lastname: Mihas
authors.forename: Evangelos
authors.initials: E
authors.lastname: Konstantinou
authors.forename: George
authors.initials: G
authors.lastname: Saroglou
mesh_terms: D000328:Adult; D000998:Antiviral Agents / Q000009:adverse effects* / Q000627:therapeutic use; D016009:Chi-Square Distribution; D004359:Drug Therapy, Combination; D005260:Female; D019698:Hepatitis C, Chronic / Q000188:drug therapy*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000009:adverse effects* / Q000627:therapeutic use; D016015:Logistic Models; D008297:Male; D011092:Polyethylene Glycols / Q000009:adverse effects* / Q000627:therapeutic use; D012367:RNA, Viral / Q000097:blood; D011994:Recombinant Proteins; D012254:Ribavirin / Q000009:adverse effects* / Q000627:therapeutic use; D013959:Thyroid Diseases / Q000139:chemically induced*; D013960:Thyroid Function Tests
chemical_list: D000998:Antiviral Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; C100416:peginterferon alfa-2a