Continuation of amiodarone delays restoration of euthyroidism in patients with type 2 amiodarone-induced thyrotoxicosis treated with prednisone: a pilot study.

CONTEXT: 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.

DESIGN

This was a matched retrospective cohort study.

SETTING

The study was conducted at a university center.

PATIENTS: 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).

INTERVENTION: All patients were treated with oral prednisone. Patients whose thyrotoxicosis recurred after glucocorticoid withdrawal were treated with a second course of prednisone.

MAIN OUTCOME MEASURE: 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.