SAT483 Role of Cholestyramine in Refractory Amiodarone-induced Thyrotoxicosis

Disclosure: H. Zhao: None. J. Leung: None. Role of Cholestyramine in Refractory Amiodarone-Induced Thyrotoxicosis. Background: Amiodarone-induced thyrotoxicosis (AIT) is divided into type 1 (AIT1; treated with thioamides) and type 2 (AIT2; treated with glucocorticoids). Combined therapy is utilized in mixed or indefinite forms. When medical treatment is unsuccessful, radioiodine ablation or thyroidectomy are considered. Clinical Case: A 76-year-old gentleman, with a history of atrial fibrillation treated with amiodarone, presented with recurrent atrial fibrillation refractory to cardioversion. Investigations revealed TSH <0.01, FT4 58.1 (ref 10.0-20.0 pmol/L), FT3 16.0 (ref 3.5-6.5 pmol/L), TPO negative and TRAB negative. As thyroid ultrasound revealed absence of focal nodules or hypervascularity and technetium pertechnetate scan demonstrated no thyroid activity, AIT2 was suspected. Prednisone was initiated and amiodarone discontinued. Due to minimal response after a month, a mixed type was suggested and methimazole added. Despite intensification of the antithyroid regimen, FT4 increased to 59.5. Methimazole was discontinued for radioiodine ablation assessment. Given low thyroid uptake (<3%), ablation was deemed unlikely beneficial. After patient refused thyroidectomy, cholestyramine was initiated, resulting in significant improvement, with FT4 declining from 46.0 to 29.0 in 2 weeks. Euthyroidism was achieved after 2 months of cholestyramine treatment and medications were stopped. At 6 months post presentation, he developed amiodarone-related hypothyroidism and began levothyroxine. Conclusion: Previous reports propose that cholestyramine, an ion exchange resin, interrupts enterohepatic circulation of thyroid hormone and demonstrated the use of cholestyramine in refractory Grave’s hyperthyroidism. This is one of the first few reports demonstrating the possible role of cholestyramine in AIT refractory to first line medical therapy. Presentation Date: Saturday, June 17, 2023