MON-447 Amiodarone induced thyroiditis

Abstract Disclosure: H. Marasandra Ramesh: None. A. Sharma: None. V.A. Kothari: None. F.J. Lee: None. Introduction: Amiodarone, an iodine-rich antiarrhythmic drug, is known to cause thyroid dysfunction in 15-20% of patients, with amiodarone-induced thyroiditis (AIT) presenting a complex diagnostic and therapeutic challenge. AIT manifests in two forms: type 1, iodine-induced hyperthyroidism, typically occurring in pre-existing thyroid abnormalities like Grave’s, and type 2, a drug-induced destructive thyroiditis in an otherwise normal thyroid. Amiodarone-induced hypothyroidism occurs if there is a failure to escape from Wolff Chaikoff effect, more commonly in patients with Hashimoto’s. Case presentation: A 74-year-old male with a past medial history of atrial fibrillation, ischemic cardiomyopathy, hypertension, hyperlipidemia, chronic kidney disease stage 3, was seen at the endocrinology clinic for abnormal thyroid labs. He presented with symptoms of fatigue, drowsiness, weight loss of 18 lbs in 2 months, dry skin, diarrhea and cold intolerance. Labs were pertinent for elevated thyroid stimulating hormone of 7.11 uIu/ml (normal: 0.27-4.2 uIu/ml), free T4 of 2.1 ng/dl (normal:0.9-1.7 ng/dl ), total T3 of 78 ng/dl (normal: 80-200 ng/dl). He was initiated on amiodarone about 4 months prior to presentation. His previous thyroid function tests were normal. He was initially diagnosed with suspected type 2 amiodarone induced thyroiditis and treated with a course of prednisone for 10 days. The following month, he was hospitalized for the treatment of rhabdomyolysis and myopathy when he presented with symptoms of extreme fatigue and myalgia. Labs during hospitalization showed elevated creatine kinase of 5200 U/L and deranged liver function tests of aspartate transaminase of 65 U/L, alanine transaminase of 274 U/L and alkaline phosphatase of 172 U/L. Atorvastatin and amiodarone were stopped at this time. The rhabdomyolysis could be precipitated by the prolonged usage of amiodarone and atorvastatin which could have been worsened by prolonged amiodarone induced thyroiditis. Thyroid ultrasound revealed no hypervascularity or no thyroid gland enlargement. He closely followed up in the clinic after 6 months. The patient was doing well and repeat labs showed normalization of thyroid function tests: TSH of 2.67 uIu/ml, fT4 of 1.3 ng/dl, total T 3 of 103 thereby confirming the diagnosis of type 2 amiodarone induced thyroiditis. Conclusion: Type 1 AIT is usually treated with thioamides, enhanced by potassium perchlorate to block iodine uptake, while type 2 AIT is best treated with oral glucocorticoids. Mixed forms may require a combination of these therapies. In refractory cases, thyroidectomy can be considered. Effective management depends on precise diagnosis and a tailored treatment approach. Amiodarone, even if stopped, remains in the body for about 142 days due to its lipophilic nature which may cause persistent symptoms. Presentation: Monday, July 14, 2025