Glucocorticoid Response in Amiodarone-Induced Thyrotoxicosis Resulting from Destructive Thyroiditis Is Predicted by Thyroid Volume and Serum Free Thyroid Hormone Concentrations

Context: Amiodarone-induced thyrotoxicosis (AIT) resulting from destructive thyroiditis (type 2) is commonly treated with glucocorticoids, but time needed to restore euthyroidism may be unacceptable for patients with underlying cardiac disorders. Objective: The objective of this prospective study was to identify factors affecting the response to glucocorticoids in a large cohort of patients with type 2 AIT followed prospectively. Setting: This study was conducted at university centers. Patients: Sixty-six untreated patients with type 2 AIT were enrolled in the study. Intervention: All patients were treated with prednisone (initial dose, 0.5 mg/kgd) as long as needed to restore euthyroidism, defined as cure of AIT. Main Outcome Measure: The main outcome measure was cure time. Results: The median cure time was 30 d (95% confidence interval, 23-37 d). Serum free T4 concentration (picograms per milliliter) and thyroid volume (milliliters per square meter) (and, to a lesser extent, serum free T3 concentration) at diagnosis were the main determinants of response to glucocorticoids, with a cure hazard ratio of 0.97 (95% confidence interval, 0.95-0.99; P 0.005) and 0.84 (95% confidence interval, 0.77-0.91; P 0.000) for unit of increment, respectively. AIT was cured in all patients with a complete follow-up; euthyroidism was reached in 30 d or less in 60% of patients but in more than 90 d in 16%. A prompt control of thyrotoxicosis (30 d of treatment) was more frequent (77%) in patients with serum basal free T4 concentration no greater than 50 pg/ml and thyroid volume (normalized for body surface area) no greater than 12 ml/m2. The cure probability and the mean cure time in an individual patient can be obtained using a formula generated by multiple regression models. Conclusions: Baseline serum thyroid hormone concentrations and thyroid volume help identify patients with type 2 AIT at risk of a delayed response to glucocorticoids.