Abstract #1382972: Between a Rock and a Hard Place: A Case of Amiodarone Induced Thyrotoxicosis Presenting with Methimazole Induced Agranulocytosis

Abstract

Amiodarone is a frequently used anti-arrhythmic drug which may often cause thyroid dysfunction. Management of amiodarone induced thyrotoxicosis (AIT) often hinges on distinguishing between type I and II AIT which is not often possible. When antithyroid drugs (ATD) are used, higher than average doses are often needed, increasing risk for complications. We report a case of a 67-year-old man who presented with palpitations, tremors, hyperdefecation and weight loss, consistent with thyrotoxicosis. He had been treated with amiodarone for paroxysmal atrial fibrillation (a-fib) for several years. Admission labs showed TSH < 0.01 uIU/ml (0.36-3.74 uIU/ml), free T4 3.32 ng/dL (0.76-1.46), total T3 237 ng/dL (86-192), negative thyrotropin receptor blocking antibodies < 1.10 IU/L (0.0-1.75), thyroglobulin antibodies < 20 IU/mL (0.0-40.0) and thyroid peroxidase antibodies < 10.0 IU/mL (0.0-35.0). Thyroid ultrasound showed a mildly enlarged, heterogeneous thyroid without discrete nodules and normal vascularity. He was treated empirically for both type I and type II AIT with methimazole 40 mg and prednisone 40 mg. Despite treatment, he returned with similar complaints one month later. EKG showed a-fib with a heart rate of 120 bpm. Repeat labs showed TSH < 0.01 uIU/ml, free T4 4.01 ng/dL and total T3 146 ng/dL. His overall evaluation was consistent with impending thyroid storm. CBC was notable for a WBC and ANC of 4.0 10ˆ3 cells/μL and 520 cells/μL respectively, which decreased further to a nadir of 2.6 10ˆ3 cells/μL and 62 cells/μL the following day. The inability to use ATDs in the setting of severe agranulocytosis made thyroidectomy an attractive option. His WBC improved with discontinuation of methimazole and resolved completely a day after administration of G-CSF. He was treated with potassium Iodide, prednisone, cholestyramine and metoprolol in preparation for surgery. He did well after surgery and was discharged home in stable condition on postoperative day two. AIT types I and II are distinct clinical entities. First line treatment consists of ATDs for AIT type I, and steroids for AIT type II. In the acute setting it may be difficult to distinguish between both types and some patients may have features of both. Importantly, a 10-fold increased risk for ATD associated agranulocytosis has been reported in patients with AIT compared to thyrotoxicosis due to other etiologies. Higher doses of ATDs are often required in AIT and the risk for agranulocytosis from ATDs is likely dose dependent. Although neutropenia resolves in most patient in 1-3 weeks after cessation of ATDs, use of G-CSF may shorten recovery times, decrease risk for infections and shorten hospital stays.