title: Continuation of amiodarone delays restoration of euthyroidism in patients with type 2 amiodarone-induced thyrotoxicosis treated with prednisone: a pilot study.
abstract: BACKGROUND
  Type 2 amiodarone-induced thyrotoxicosis (AIT) is a destructive thyroiditis usually responsive to glucocorticoids. Whether continuation of amiodarone affects treatment outcome is unsettled.
  
  
  OBJECTIVE
  The objective of the study was to compare the outcome of glucocorticoid treatment in type 2 AIT patients who continued or withdrew amiodarone.
  
  
  METHODS
  This was a matched retrospective cohort study.
  
  
  METHODS
  The study was conducted at a university center.
  
  
  METHODS
  Eighty-three consecutive patients with untreated type 2 AIT participated in the study. After matching with patients continuing amiodarone (AMIO-ON, n = 8), patients interrupting amiodarone were randomly selected in a 4:1 ratio (AMIO-OFF, n = 32).
  
  
  METHODS
  All patients were treated with oral prednisone. Patients whose thyrotoxicosis recurred after glucocorticoid withdrawal were treated with a second course of prednisone.
  
  
  METHODS
  Time and rate of cure were measured.
  
  
  RESULTS
  Median time to the first normalization of serum thyroid hormone levels did not significantly differ in AMIO-ON and AMIO-OFF patients (24 and 31 d, respectively; P = 0.326). Conversely, median time for stably restoring euthyroidism was 140 d in AMIO-ON patients and 47 d in AMIO-OFF patients (log rank, P = 0.011). In fact, AIT recurred in five of seven AMIO-ON patients (71.4%) and in only three of 32 AMIO-OFF patients (9.4%, P = 0.002), requiring readministration of prednisone. One AMIO-ON patient never reached thyroid hormone normalization during the study period. Factors associated with glucocorticoid failure were thyroid volume and amiodarone continuation.
  
  
  CONCLUSIONS
  Prednisone restores euthyroidism in most type 2 AIT patients, irrespective of amiodarone continuation or withdrawal. However, continuing amiodarone increases the recurrence rate of thyrotoxicosis, causing a delay in the stable restoration of euthyroidism and a longer exposure of the heart to thyroid hormone excess.
authors.affiliation: Department of Endocrinology and Metabolism, University of Pisa, Ospedale Cisanello, Via Paradisa, 2, 56124 Pisa, Italy. fausto.bogazzi@med.unipi.it
authors.forename: Fausto
authors.initials: F
authors.lastname: Bogazzi
authors.forename: Luigi
authors.initials: L
authors.lastname: Bartalena
authors.forename: Luca
authors.initials: L
authors.lastname: Tomisti
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Rossi
authors.forename: Sandra
authors.initials: S
authors.lastname: Brogioni
authors.forename: Enio
authors.initials: E
authors.lastname: Martino
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000638:Amiodarone / Q000009:adverse effects*; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects*; D015331:Cohort Studies; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010865:Pilot Projects; D011241:Prednisone / Q000627:therapeutic use*; D012189:Retrospective Studies; D013971:Thyrotoxicosis / Q000139:chemically induced* / Q000188:drug therapy*; D016896:Treatment Outcome
chemical_list: D000889:Anti-Arrhythmia Agents; D005938:Glucocorticoids; D000638:Amiodarone; D011241:Prednisone