SAT-388 The Storm That Wouldn’t Subside: A Complex Case of Amiodarone-Induced Hyperthyroidism

Abstract Disclosure: A. Malipeddi: None. J. Rivera-Mora: None. R. Abdelmasih: None. N. Shah: None. L. Belalcazar: None. Introduction: Amiodarone, an antiarrhythmic agent is known to alter thyroid function. While most patients with amiodarone-induced thyrotoxicosis (AIT) respond to standard therapies, we describe a case with persistent AIT that illustrates the challenges clinicians may encounter with its diagnosis and management. Case: A 53-year-old man with a history of atrial fibrillation (AFIB), heart failure with reduced ejection fraction (EF) 15-20% and diabetes, presented to the emergency room in rapid ventricular response (RVR). Labs showed TSH <0.02 mIU/L and FT4 >6.99 ng/dL. Exam did not show goiter or eye involvement but revealed a foot ulcer. Burch-Wartofsky score was 45. Despite starting standard therapy for thyroid storm with betablockers, maximal thionamide and cholestyramine, there was no clinical improvement. Thyroid antibodies were negative, ESR was 120 mm/hr. Neck ultrasound showed no nodules or increased vascularity, suggesting AIT2. Prednisone 30 mg daily was added, but episodes of RVR persisted and FT4 levels remained elevated. Steroid dose was increased to 40 mg; potassium iodide was introduced, yet FT4 levels did not decrease. On day 20, plasmapheresis (PLEX) was started, providing some improvement. Thyroidectomy was planned as soon as FT4 reached < 3 despite the increased surgical risk. Records identified prior long-term oral amiodarone use and 2 recent admissions for AFIB with RVR, during which amiodarone infusions were given. A technetium-99 scan revealed no tracer uptake. After 5 PLEX sessions and increasing prednisone to 60 mg (0.6 mg/kg/day), his FT4 normalized with clinical improvement, averting the need for thyroidectomy. Thionamide and resin doses were tapered but not stopped and patient successfully underwent cardiac catheterization and toe amputation. Steroid hyperglycemia was difficult to control requiring > 200 units of insulin/day. Discussion: This case demonstrates the diagnostic complexity and therapeutic challenges of AIT. Standard high-dose prednisone and thionamides did not achieve adequate control. PLEX provided only temporary relief. It is important to not delay increases in prednisone dose if patients with suspected AIT2 do not improve on conventional doses, even if severe steroid-induced hyperglycemia may be a concern. Multimodal therapy is warranted when the patient is at high risk, their clinical course is complicated by a protracted treatment response, and/or when both AIT1 and AIT2 are suspected. Presentation: Saturday, July 12, 2025

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Journal
Journal of the Endocrine Society
Published
2025-10-01
DOI
https://doi.org/10.1210/jendso/bvaf149.2303
Primary Topic
Ion channel regulation and function
Type
article
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article

SAT-388 The Storm That Wouldn’t Subside: A Complex Case of Amiodarone-Induced Hyperthyroidism

L. Maria Belalcazar, Apoorva Malipeddi, Randa Abdelmasih, Nisarg A. Shah et al.
Journal of the Endocrine Society
Ion channel regulation and function
article

SAT-388 The Storm That Wouldn’t Subside: A Complex Case of Amiodarone-Induced Hyperthyroidism

L. Maria Belalcazar, Apoorva Malipeddi, Randa Abdelmasih, Nisarg A. Shah, Jhonatan Daniel Rivera-Mora
article en

Abstract

Abstract Disclosure: A. Malipeddi: None. J. Rivera-Mora: None. R. Abdelmasih: None. N. Shah: None. L. Belalcazar: None. Introduction: Amiodarone, an antiarrhythmic agent is known to alter thyroid function. While most patients with amiodarone-induced thyrotoxicosis (AIT) respond to standard therapies, we describe a case with persistent AIT that illustrates the challenges clinicians may encounter with its diagnosis and management. Case: A 53-year-old man with a history of atrial fibrillation (AFIB), heart failure with reduced ejection fraction (EF) 15-20% and diabetes, presented to the emergency room in rapid ventricular response (RVR). Labs showed TSH <0.02 mIU/L and FT4 >6.99 ng/dL. Exam did not show goiter or eye involvement but revealed a foot ulcer. Burch-Wartofsky score was 45. Despite starting standard therapy for thyroid storm with betablockers, maximal thionamide and cholestyramine, there was no clinical improvement. Thyroid antibodies were negative, ESR was 120 mm/hr. Neck ultrasound showed no nodules or increased vascularity, suggesting AIT2. Prednisone 30 mg daily was added, but episodes of RVR persisted and FT4 levels remained elevated. Steroid dose was increased to 40 mg; potassium iodide was introduced, yet FT4 levels did not decrease. On day 20, plasmapheresis (PLEX) was started, providing some improvement. Thyroidectomy was planned as soon as FT4 reached < 3 despite the increased surgical risk. Records identified prior long-term oral amiodarone use and 2 recent admissions for AFIB with RVR, during which amiodarone infusions were given. A technetium-99 scan revealed no tracer uptake. After 5 PLEX sessions and increasing prednisone to 60 mg (0.6 mg/kg/day), his FT4 normalized with clinical improvement, averting the need for thyroidectomy. Thionamide and resin doses were tapered but not stopped and patient successfully underwent cardiac catheterization and toe amputation. Steroid hyperglycemia was difficult to control requiring > 200 units of insulin/day. Discussion: This case demonstrates the diagnostic complexity and therapeutic challenges of AIT. Standard high-dose prednisone and thionamides did not achieve adequate control. PLEX provided only temporary relief. It is important to not delay increases in prednisone dose if patients with suspected AIT2 do not improve on conventional doses, even if severe steroid-induced hyperglycemia may be a concern. Multimodal therapy is warranted when the patient is at high risk, their clinical course is complicated by a protracted treatment response, and/or when both AIT1 and AIT2 are suspected. Presentation: Saturday, July 12, 2025

Journal of the Endocrine SocietyVol. 9(Supplement_1)
The University of Texas Medical Branch at Galveston (US)
Openalex Percentile: Top 73%
Ion channel regulation and function
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