Amiodarone Induced Thyrotoxicosis: A Case of Refractory Disease Treated With Thyroidectomy

Abstract

Abstract Amiodarone induced thyrotoxicosis (AIT) is a challenging diagnosis that affects 3-5% of patients taking amiodarone in the United States. Type I AIT is seen in patients with preexisting thyroid disease and is generally treated with thionamides while type II AIT represents a destructive thyroiditis that responds to glucocorticoids. A mixed type exists and is associated with higher mortality, especially in older adults with cardiovascular disease. Thyroidectomy is considered a last resort option for patients intolerant or refractory to medical treatment. A 70 year-old male with a history of coronary artery disease, ventricular tachycardia (VT), and heart failure was referred to the endocrine clinic for abnormal thyroid function tests that showed TSH <0.0023 uIU/mL (0.4-4.7), Free T4 2.51 ng/dL (0.7-1.48) and Free T3 5.37 pg/mL (1.71-3.71). He endorsed palpitations, excessive sweating, tremors, and reported taking amiodarone for 3 years prior to presentation. Vitals showed normal pulse and blood pressure. Thyroid autoantibodies including TSI and TBII were within normal limits. Thyroid ultrasound showed mild thyromegaly with normal vascularity and no nodules. AIT was suspected and he was started on methimazole 20 mg daily, prednisone 30 mg daily and continued on his home metoprolol 100 mg daily. Methimazole and prednisone were both up titrated in a week because his labs did not improve. One month later, he presented to the hospital with acute exacerbation of heart failure. His TFTs showed (TSH <0.0021 uIU/mL, FT4 >5.0 ng/dL, FT3 4.61 pg/mL). Thyroid RAIU showed severely decreased uptake secondary to the high iodine content of amiodarone. He remained thyrotoxic despite using higher doses of prednisone (60 mg daily) and methimazole (90 mg daily). He was changed to PTU (900 mg daily) and started on cholestyramine, with no improvement in overall status. Several weeks after admission, a total thyroidectomy was performed. His postoperative course was unremarkable except for hypoparathyroidism. He was clinically and biochemically euthyroid one week after his procedure. At 6 months follow up, he remained stable on levothyroxine 100 mcg/day but continued to require calcitriol and calcium supplementation. We present an interesting case of mixed type AIT refractory to medical therapy associated with cardiovascular compromise. This case highlights the challenges in the diagnosis and management of such patients. Thyroid autoantibodies, thyroid ultrasound and RAIU were more indicative of Type II AIT, however, lack of response to high dose steroids was inconsistent with the diagnosis. While receiving the treatment for both Type I and II AIT, our patient had persistent clinical and biochemical thyrotoxicosis and required thyroidectomy. Although most AIT patients are treated medically, thyroidectomy is reserved for those most severe and refractory cases and is considered a viable option in such patients.