Abstract
Disclosure: K. Akella: None. W. Beauti: None. P. Pasqualicchio: None. T. Batarseh: None. A. Pareddy: None. A. Yaqub: None. Introduction: Thyroid gland dysfunction is associated with significant morbidity and mortality. The antiarrhythmic drug, amiodarone can cause significant thyroid dysfunction. Patients on amiodarone therapy should have thyroid levels checked before and during treatment. Our case highlights the diagnostic and therapeutic challenges associated with managing amiodarone-induced thyrotoxicosis (AIT) in a patient awaiting heart transplant. Case Description: A 53-year-old male with a history of paroxysmal atrial fibrillation, heart failure secondary to familial Lamin A/C (LMNA) cardiomyopathy listed for cardiac transplant, and cardiac sarcoidosis s/p ICD presented for evaluation after sustaining recurrent ICD shocks. On the exam, his thyroid gland was not enlarged, nor did he have exophthalmos, lid lag or thyroid bruit. The 12-lead EKG and ICD device interrogation showed polymorphic ventricular tachycardia. He was on amiodarone therapy for 22 months. Laboratory testing revealed undetectable thyroid stimulating hormone (TSH) levels and receptor antibody, markedly elevated free T4 to 5.45 ng/dL(0.61-1.76 ng/dL) and T3 of 146.4 ng/dL (60.0-220.0 ng/dL). Ultrasound of the thyroid showed normal echotexture without any nodules, and normal thyroid vascularity. The patient reported a personal and familial history of thyroid disease that could not be verified. His thyroid function was normal prior to amiodarone initiation with TSH of 2.98 uIU/mL(0.45-4.12 uIU/mL). There was no history of neck radiation, biotin or lithium use. His personal history of thyroid disease and T4:T3 ratio suggested Type 1 AIT, whereas his normal thyroid ultrasound, normal T3, and onset 22 months after starting therapy suggested Type 2 AIT. Therefore, he was simultaneously treated with both prednisone and methimazole, each at 120mg daily. The patient’s thyroid levels improved and he was able to receive a transplant. Methimazole and prednisone were successfully weaned. Discussion: Amiodarone causes thyrotoxicosis through high iodine content that induces thyroid hormone synthesis (type 1 AIT) or by directly destroying thyroid follicular cells to release pre-formed thyroid hormone into circulation (type 2 AIT). Type 1 AIT is seen in patients with underlying thyroid gland disease and treated with methimazole or propylthiouracil. Type 2 AIT is treated with glucocorticoids. This case challenged the current understanding of AIT treatment. The combination of methimazole and prednisone at exceedingly high doses was successful yet slow in improving his state. He was not a candidate for thyroidectomy due to his end-stage heart failure. This case highlights the challenges associated with treating AIT in a critically ill patient. It illustrates the importance of early initiation of combined therapy. The case also emphasizes the importance of monitoring thyroid function prior to and during amiodarone treatment. Presentation: Sunday, July 13, 2025