Goiter and hypothyroidism during re-treatment with amiodarone in a patient who previously experienced amiodarone-induced thyrotoxicosis.
A 55-year-old woman who had been receiving treatment with amiodarone for recurrent supraventricular tachyarrhythmias became thyrotoxic after 30 months of treatment. The thyroid gland was not enlarged or tender. Amiodarone was discontinued, and thyrotoxicosis gradually abated. A thyroid scan performed at that time revealed a gland of normal size and texture. Six months later, amiodarone treatment was reinstated due to life-threatening tachyarrhythmia; however, the patient remained euthyroid. Three years later, multinodular goiter began to develop, and 5 years after that, the patient became hypothyroid. Tests for thyroid autoantibodies, as well as inhibitory and stimulatory antibodies, were negative, and fine needle aspiration biopsy revealed an adenomatous goiter. Treatment with amiodarone was continued; however, therapy with L-thyroxin was initiated, followed by a complete regression of the goiter. The patient has since required a maintenance dose of L-thyroxin. The possible mechanisms by which iodine-containing drugs induce thyroid disfunction are reviewed, suggesting this case was caused by an alteration in the sensitivity of the intrinsic autoregulation of the thyroid gland to iodine.
Kaplan
J
J
Internal Department, Rambam Medical Center, Haifa, Israel.
Ish-Shalom
S
S
D000638:Amiodarone / Q000009:adverse effects*; D005260:Female; D006042:Goiter / Q000139:chemically induced* / Q000473:pathology; D006801:Humans; D007037:Hypothyroidism / Q000139:chemically induced*; D008875:Middle Aged; D013617:Tachycardia, Supraventricular / Q000188:drug therapy; D013971:Thyrotoxicosis / Q000139:chemically induced
D000638:Amiodarone