Virginia Research Day 2025

Medical Resident Research Case Reports

08 Thyrotoxic Twist: A Case of Amiodarone Induced Thyrotoxicosis

Dr. Anthony Conforti, DO.; Dr. William Arvan, MD.; Dr. Kimberly Bird, MD.; Dr. Michael Caplan, MD Corresponding author: anthony.conforti@LPNT.net

Department of Medicine, Sovah Health, Danville, VA

Following his diagnosis of AIT, the patient was prescribed a high dose of methimazole, 30mg per day, with steroids, and amiodarone was subsequently discontinued. Ultimately, he underwent catheter ablation with successful conversion to normal sinus rhythm and has since been doing well. Discussion: Amiodarone is a popular anti arrhythmic with well-established adverse effects of thyroid dysfunction. Whereas amiodarone-induced hypothyroidism is a straightforward disease process, AIT has an elaborate pathophysiology requiring complex management. This case is noteworthy as it perfectly illustrates a chronological depiction of AIT, supported by serial thyroid function tests, and further highlights the complexities of this disease state. Furthermore, it encourages clinicians to consider hyperthyroidism as a complication of amiodarone, considering that AIT can result in endocrine emergencies with poor resultant outcomes.

Introduction: Amiodarone-induced thyrotoxicosis (AIT) is an exceedingly rare condition affecting only 3% of patients prescribed amiodarone in North America. Due to the intrinsic and iodine related effects of this medication, patients may develop hyperthyroidism, presenting with symptoms including heat intolerance, nervousness, weight loss, and palpitations. Diagnostic confirmation and further disease classification are achieved through laboratory testing, radioiodine uptake, and imaging. Type 1 AIT results from increased thyroid hormone biosynthesis and is treated with high doses of methimazole or propylthiouracil. In contrast, Type 2 AIT results from thyroid gland destruction and is treated with high-intensity steroids. Mixed forms of AIT are classified in cases where differentiation is impossible. In such instances, the recommended treatment is a combination of thioamides and steroids. The discontinuation of amiodarone must be combined with concomitant thyroid suppression due to the prolonged terminal half-life of amiodarone, which is estimated between 58-142 days.

Case Presentation: We present an 85-year old white man with a past medical history significant for longstanding atrial fibrillation, using apixaban for chronic anticoagulation and a combination of metoprolol and amiodarone for rate and rhythm control, respectively. He initially presented to his primary care physician complaining of severe fatigue and generalized weakness. Further history revealed that he was started on amiodarone by his cardiologist one year prior after an unsuccessful cardioversion. Upon arrival at the clinic, he was tachypneic and tachycardic, with a heart rate in the 120s. The hematologic evaluation was negative for thyroid-stimulating immunoglobulin (TSI), antithyroglobulin antibodies, and thyroid peroxidase (TPO) antibodies. Thyroid ultrasound demonstrated a homogeneous thyroid with normal vascularity and no discrete nodules. By trending his thyroid function tests, it became evident that his Thyroid Stimulating Hormone (TSH) levels had insidiously dropped with a corresponding rise in free Thyroxine (fT4), beginning just weeks after the initiation of amiodarone.

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