SUN-558 Methimazole Treatment of Thyrotoxicosis in the Setting of Ischemic Hepatitis

Introduction: Thyroid storm is a rare, life threatening condition with a reported mortality rate of up to 30 percent. Immediate treatment is critical and should begin with a beta-blocker, iodine, thionamides, and glucocorticoids. Thionamides are avoided in hepatic dysfunction. We report a case of treatment of thyrotoxicosis using methimazole in a patient with ischemic hepatitis. Clinical case: A 54 year old woman with history of untreated Graves’ disease was admitted to the ICU in atrial fibrillation with rapid ventricular response and multi-organ failure. Just prior to admission, she had undergone CT imaging with IV contrast. Laboratory testing revealed an undetectable TSH (0.3-4 uIU/mL), free T4 4.0 ng/dL (0.8-1.4 ng/dL) with a TSI level of 514 (<140% baseline). Liver function testing showed an alkaline phosphatase level of 258 units/L (39-119), AST 74 units/L (12-67), and ALT 75 units/L (14-37), total bilirubin 2.3 mg/dL (0.1-1.0). She became pulseless requiring cardiopulmonary resuscitation, endotracheal intubation, and vasopressors. Treatment with esmolol was started due to hemodynamic instability with a left ventricular ejection fraction of 10% post-arrest. Hydrocortisone, SSKI, cholestyramine, and one dose of methimazole were administered. She developed ischemic hepatitis with an AST 1092 units/L and ALT 2003 units/L the day following her arrest. With marked elevation in her liver enzymes, methimazole was held and lithium therapy initiated. Given ongoing instability, inability to undergo thyroidectomy, and rising thyroid hormone level, on day 3 of hospitalization, methimazole was resumed once her liver enzymes were down trending. Her hemodynamics, liver dysfunction and thyrotoxicosis improved and on day 21, she was able to successfully undergo total thyroidectomy. Discussion: A thionamide is the cornerstone in thyrotoxicosis treatment by blocking de novo thyroid hormone synthesis. PTU is the preferred thionamide the treatment of life-threatening thyroid storm in an ICU setting as it also inhibits T4 to T3 conversion. However, it carries significant risk for cholestatic hepatotoxicity. Methimazole has been shown to be less hepatotoxic and is the preferred agent in the non-ICU setting. Neither agent is generally utilized with significant hepatic derangement. Plasmapheresis has been used as a bridge to total thyroidectomy in patients who are intolerant to traditional therapy. In this case, the patient remained too unstable for urgent thyroidectomy. Given she had received iodine via IV contrast, RAI was not a therapeutic option. With limited treatment options, methimazole was resumed with plans to discontinue if there was further derangement in her liver enzymes. Conclusion: This case highlights consideration of methimazole for the management of severe thyrotoxicosis in individuals with hepatitis, unrelated to thionamide therapy, when other options are limited.