title: Amiodarone-induced thyrotoxicosis in adults with congenital heart disease--clinical presentation and response to therapy.
abstract: OBJECTIVE
  The development of amiodarone-induced thyrotoxicosis (AIT) can threaten the hemodynamic stability of adult patients with congenital heart disease (CHD). Here, we describe the natural history and treatment response of AIT in this at-risk population.
  
  
  METHODS
  We studied retrospectively all cases of AIT that occurred in CHD patients at our institution after a minimum of 3 months on amiodarone. Subjects were identified from the cohort of adults with CHD who were treated at the Mayo Clinic Adult CHD clinic between 1987 and 2009.
  
  
  RESULTS
  We identified 23 cases of AIT: 7 were type 1, 13 were type 2, and 3 were undefined due to insufficient data. Most patients were symptomatic (17 of 23, 74%), with arrhythmia and weight loss as the most common symptoms. The majority (12 of 23, 52%) were initially observed; 10 patients (43%) were treated medically and 1 patient (5%) underwent thyroidectomy. Four patients from the observation group eventually required active treatment and 3 patients from the medical group required surgery. Asymptomatic patients tended to resolve under observation (5 of 7, 71.4%) rather than progress to active treatment (0 of 4) (P = .06). Discontinuation of amiodarone, AIT type, or use of perchlorate did not impact AIT duration.
  
  
  CONCLUSIONS
  AIT in CHD patients exhibits a wide range of severity and sensitivity to medical therapy. Asymptomatic patients display a trend toward AIT resolution with observation alone. Amiodarone continuation does not appear to impact management outcome or disease duration. Additional studies in this high-risk population could identify elements of pathophysiology that would point toward better disease prevention and treatment.
authors.affiliation: Department of Internal Medicine, Division of Endocrinology, Diabetes, Metabolism and Nutrition, Mayo Clinic, Rochester, Minnesota.
authors.forename: Marius N
authors.initials: MN
authors.lastname: Stan
authors.affiliation: Department of Endocrinology, Central DuPage Hospital, Winfield, Illinois.
authors.forename: Matheni
authors.initials: M
authors.lastname: Sathananthan
authors.affiliation: Department of Internal Medicine, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota.
authors.forename: Carole A
authors.initials: CA
authors.lastname: Warnes
authors.affiliation: Department of Internal Medicine, Division of Endocrinology, Diabetes, Metabolism and Nutrition, Mayo Clinic, Rochester, Minnesota.
authors.forename: Michael D
authors.initials: MD
authors.lastname: Brennan
authors.affiliation: Department of Health Sciences Research, Division of Biostatistics, Mayo Clinic, Rochester, Minnesota.
authors.forename: Prabin
authors.initials: P
authors.lastname: Thapa
authors.affiliation: Department of Internal Medicine, Division of Endocrinology, Diabetes, Metabolism and Nutrition, Mayo Clinic, Rochester, Minnesota.
authors.forename: Rebecca S
authors.initials: RS
authors.lastname: Bahn
mesh_terms: D000328:Adult; D000638:Amiodarone / Q000009:adverse effects*; D005260:Female; D006330:Heart Defects, Congenital / Q000150:complications* / Q000503:physiopathology; D006801:Humans; D008297:Male; D012189:Retrospective Studies; D013971:Thyrotoxicosis / Q000139:chemically induced* / Q000188:drug therapy
chemical_list: D000638:Amiodarone