title: Amiodarone-induced thyrotoxicosis: clinical course and predictors of outcome.
abstract: OBJECTIVE
  This study sought to determine the clinical course and predictors of long-term outcome in patients with documented amiodarone-induced thyrotoxicosis (AIT).
  
  
  BACKGROUND
  Amiodarone-induced thyrotoxicosis is a condition that is difficult to manage, in particular because of the long half-life of amiodarone. Data on optimal treatment for AIT are scarce.
  
  
  METHODS
  We performed a retrospective review among patients with documented AIT at a tertiary care center. Baseline characteristics, treatment received, laboratory parameters, and events during follow-up were evaluated. The predefined composite end point consisted of the following AIT-associated complications: death, heart transplantation, hospitalization for heart failure, myocardial infarction, stroke, hospitalization for arrhythmia management, or hospitalization for treatment complications.
  
  
  RESULTS
  Eighty-four patients were included in the present analysis; 27 patients received prednisone for AIT. There was no difference in time to normalization of free thyroxine between those receiving and those not receiving prednisone. Long-term follow-up showed high morbidity and mortality; 47 patients (56%) reached the primary end point. Patients receiving prednisone had a worse outcome than those not receiving prednisone (p = 0.003). Although patients received prednisone for 84 +/- 65 days, curves started to separate only 12 months after the initial diagnosis.
  
  
  CONCLUSIONS
  Patients with AIT have a high event rate during follow-up. Prednisone had no effect on time to normalization of thyroxine levels and was associated with an increased event rate. Importantly, AIT-related problems must be expected late, at a time when thyroid function is under control.
authors.affiliation: Department of Cardiology, University Hospital, Basel, Switzerland.
authors.forename: David
authors.initials: D
authors.lastname: Conen
authors.forename: Ludovic
authors.initials: L
authors.lastname: Melly
authors.forename: Christoph
authors.initials: C
authors.lastname: Kaufmann
authors.forename: Stefan
authors.initials: S
authors.lastname: Bilz
authors.forename: Peter
authors.initials: P
authors.lastname: Ammann
authors.forename: Beat
authors.initials: B
authors.lastname: Schaer
authors.forename: Christian
authors.initials: C
authors.lastname: Sticherling
authors.forename: Beat
authors.initials: B
authors.lastname: Muller
authors.forename: Stefan
authors.initials: S
authors.lastname: Osswald
mesh_terms: D000368:Aged; D000638:Amiodarone / Q000009:adverse effects*; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects*; D003937:Diagnosis, Differential; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology; D006801:Humans; D006980:Hyperthyroidism / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D011241:Prednisone / Q000494:pharmacology; D011379:Prognosis; D012189:Retrospective Studies; D013963:Thyroid Hormones / Q000097:blood; D013971:Thyrotoxicosis / Q000139:chemically induced* / Q000175:diagnosis / Q000188:drug therapy
chemical_list: D000889:Anti-Arrhythmia Agents; D005938:Glucocorticoids; D013963:Thyroid Hormones; D000638:Amiodarone; D011241:Prednisone