Continuation of Amiodarone Delays Restoration of Euthyroidism in Patients with Type 2 Amiodarone-Induced Thyrotoxicosis Treated with Prednisone: A Pilot Study

Publisher Website
Google Scholar
Abstract
Type 2 amiodarone-induced thyrotoxicosis (AIT) is a destructive thyroiditis usually responsive to glucocorticoids. Whether continuation of amiodarone affects treatment outcome is unsettled. The objective of the study was to compare the outcome of glucocorticoid treatment in type 2 AIT patients who continued or withdrew amiodarone. This was a matched retrospective cohort study. The study was conducted at a university center. 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). All patients were treated with oral prednisone. Patients whose thyrotoxicosis recurred after glucocorticoid withdrawal were treated with a second course of prednisone. Time and rate of cure were measured. 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. 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.

This publication has 0 references indexed in Scilit: