SAT-592 Amiodarone-Induced Cure Of Graves' Disease

Abstract

INTRODUCTION While amiodarone-induced thyrotoxicosis is known to potentially exacerbate latent subclinical hyperthyroidism, we describe a rare case of amiodarone-induced hypothyroidism in a patient with longstanding subclinical hyperthyroidism secondary to Graves disease. CASE The patient is a 66-year-old woman with longstanding subclinical hyperthyroidism due to Graves’ disease and non-toxic multi-nodular goiter. Her mild Graves’ disease was diagnosed nine years back when she presented with hyperthyroidism, negative thyrotropin receptor antibodies (TRAb), and homogenously increased radioactive iodine uptake. The thyroid sonogram and RAI scan had shown bilateral nontoxic nodules, with benign fine needle aspiration cytology. She was intermittently and successfully treated with methimazole 2.5 mg daily, and had no interest in receiving Radioactive Iodine therapy. Her course over the subsequent years was significant for diagnosis of breast cancer treated with lumpectomy and paclitaxel-adriamycin, complicated by the onset of severe congestive heart failure and permanent atrial fibrillation, for which she was started on oral Amiodarone 200mg twice a day. Her serum TSH subsequently increased from baseline 4.53 mcIU/mL (normal 0.73-4.60 mcIU/mL) to 6.04 mIU/L at 6 weeks. Amiodarone dose was tapered to a daily dose and later discontinued because of a prolonged QT on electrocardiogram. Repeat thyroid testing at six months showed a markedly elevated TSH at 66.32 mcIU/mL (normal 0.73-4.60 mcIU/mL) with a serum T4 of less than 0.25 ng/dl (normal 0.58-1.64 ng/dl). TRAb and thyroid peroxidase antibodies remained negative. So with a provisional diagnosis of amiodarone-induced hypothyroidism, methimazole was discontinued and levothyroxine 25 mcg daily started. A follow-up testing one month later showed a TSH of 11.5 mcIU/mL and serum T4 of 0.72 ng/dl. DISCUSSION Amiodarone, through its high iodine content, has been associated with hypothyroidism as well as hyperthyroidism in both normal and dysfunctional thyroid glands. It typically induces thyrotoxicosis in autonomously functioning thyroid glands by stimulating excessive thyroid hormone biosynthesis in response to iodine load, whereas it typically induces hypothyroidism in patients with underlying autoimmune thyroiditis likely because of failure to escape Wolf-Chaikoff effect. Our patient illustrates a very rare and interesting permanent cure of Graves’ disease followed by hypothyroidism after amiodarone exposure.