THU659 Plasmapheresis As A Therapy For Amiodarone-induced Thyrotoxicosis: A Case Report And Literature Review

Abstract

Abstract Disclosure: C.L. Loughner: None. P.L. Bononi: None. Introduction: Amiodarone-induced thyrotoxicosis (AIT) is a common cause of hyperthyroidism. Treatment consists of stabilizing the thyroid followed by thyroidectomy1. Plasmapheresis has been suggested as a temporary measure when illness severity precludes standard therapy. Here, we review current literature and provide a case of AIT treated with plasmapheresis. Clinical Case: A 71-year-old male was seen for progressive subclinical hyperthyroidism, diagnosed several years prior. Three years ago, he started taking amiodarone for paroxysmal ventricular tachycardia. One month prior to admission, he was admitted for decompensated heart failure and had TSH 0.02 mcU/mL (n 0.4-4.4 mcU/mL), free T4 4.48 ng/dL (n 0.7-1.9 ng/dL), and free T3 2.58 pg/mL (n 2.0-4.4 pg/mL). Amiodarone was halved after being diagnosed with AIT. Methimazole and prednisone were started. He was readmitted one month later. TSH was undetectable at admission and free T4 was 4.04 ng/dL. Amiodarone was discontinued. His hepatic enzymes were elevated, necessitating the discontinuation of methimazole. His heart failure precluded thyroidectomy. Due to the limitation of treatment options, the patient was given three rounds of plasmapheresis to reduce thyroid hormone levels. His free T4 dropped to 2.81 ng/dL. The patient underwent total thyroidectomy once stable. His free T4 was 1.73 after and was started on levothyroxine. Clinical Lesson: When patients are unable to have standard treatment of AIT, other options must be considered. While there are some case reports3,4, there are currently no RCTs for plasmapheresis for AIT. In the case of this patient with cardiac complications from AIT and concurrent hepatic impairment, plasmapheresis provided stability of thyroid hormones until surgical correction could be achieved.