“Amiodarone-Induced Grave's Disease: development of the full Grave's spectrum following amiodarone therapy”

: Background Amiodarone, a medication commonly used for management of cardiac arrythmias, is known for its multitude of side effects notoriously affecting the thyroid gland. Amiodarone creating thyroid gland dysfunction such as hypothyroidism and amiodarone induced thyrotoxicosis (AIT) types I and II has been well described; however, the development of the full Grave’s spectrum including primary gland autoimmune stimulation with ophthalmopathy and pretibial myxedema has not been previously reported. Case Presentation In this report, we describe a 77-year-old male with no personal or family history of thyroid or autoimmune disease with atrial fibrillation managed with amiodarone for several years that presented to his primary care office with ptosis and lower extremity swelling and erythema. A diagnosis of Grave’s Disease was confirmed with elevated levels of thyroid stimulating immunoglobulins 87.5 Iu/L (reference: 0.00-0.55 Iu/L), TSH <0.001 IU/mL (reference: 0.5-5.0 Iu/L), and free T4 level 1.73 ng/dL (reference: 0.58-1.64 ng/dL). Further evaluation revealed bilateral proptosis, periorbital edema, 20 pound weight loss, and bilateral lower extremity swelling and erythema attributed to pretibial myxedema all of which improved with methimazole, selenium, prednisone, and teprotumumab. Discussion While AIT Types I and II are characterized by the development of thyrotoxicosis, the ocular manifestations and pretibial myxedema seen with Grave’s Disease are not present. Amiodarone has been shown to increase the number of la-positive T cells which have also been found to be increased in patients with thyrotoxicosis secondary to Grave Disease. Conclusion This case highlights a potential relationship between amiodarone and development of fulminant Grave’s Disease which has not been previously described.