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

Department of Endocrinology and Metabolism (F.B., L.T., E.D., F.A.-L., E.M.), University of Pisa, 56124 Pisa, Italy; Department of Clinical Medicine (L.B., M.L.T.), University of Insubria, 21100 Varese, Italy; and the Unit of Epidemiology and Biostatistics (G.R.), Institute of Clinical Physiology, National Research Council (CNR), 56100 Pisa, Italy

Address all correspondence and requests for reprints to: Dr. Fausto Bogazzi, Department of Endocrinology, University of Pisa, Ospedale Cisanello, Via Paradisa, 2, 56124 Pisa, Italy. E-mail: f.bogazzi{at}endoc.med.unipi.it or fbogazzi{at}hotmail.com.

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/kg·d) 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.

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