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THU662 Poor Response To Medical Treatment In A Patient With Amiodarone-induced Hyperthyroidism: A Therapeutic Dilemma
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Abstract
Disclosure: A.A. Asiri: None. R. Sulimani: None. W. Alkhidady: None.
Introduction: Hyperthyroidism is a well-known complication of amiodarone therapy. An incidence of 3% is reported in North America1, and even higher percentages in amiodarone deplete areas of about 10%.2 Treatment of amiodarone-induced hyperthyroidism (AIH) is challenging, it depends on various factors including the type of AIH, dependence of the patient’s cardiac condition on amiodarone therapy, other complications or comorbidities of the patient such as hepatic injury or dysfunction and the response of the patient to antithyroid therapy. Clinical Case: We present a case of a 32-year-old lady with a therapeutic dilemma in treating type I AIH, resistant to medical therapy. Our patient first had acquired COVID-19-induced myocarditis in 2020 and subsequently developed sustained ventricular tachycardia and was treated with amiodarone and placed on an implantable cardioverter-defibrillators (ICD) device. Two years later in 2022, the patient developed type I amiodarone-induced hyperthyroidism, with a free T4 reaching 100 pmol/L (Reference range 15-22 pmol/L) and complicated with transaminitis. She was unresponsive to medical therapy including: anti-thyroid medications, IV high-dose hydrocortisone, potassium iodide drops, and cholestyramine. She also developed adverse events with two of the antithyroid medications, Carbimazole and PTU; where she had elevated liver enzymes more than five time upper limit of normal and a generalized skin rash with PTU. Plasmapheresis was not an option as some of her cardiac medications drug levels could be affected. She underwent an emergent total thyroidectomy with dual beta blockade (Propranolol and Sotalol) successfully without any post op events. Her T4 level normalized within 8 days of her operation and her liver enzymes normalized within 2 weeks. Conclusion: We report the success and safety of surgical management in a patient with a cardiac arrhythmia and uncontrolled severe amiodarone-induced hyperthyroidism in the setting of adequate beta blockade. References: 1. Goldschlager N, Epstein AE, Naccarelli G, et al. Practical guidelines for clinicians who treat patients with amiodarone. Practice Guidelines Subcommittee, North American Society of Pacing and Electrophysiology. Arch Intern Med. 2000;160:1741–8. 2. Martino E, Aghini-Lombardi F, Mariotti S, et al. Environmental iodine intake and thyroid dysfunction during chronic amiodarone therapy. Ann Intern Med. 1984;101:28–34.
Presentation: Thursday, June 15, 2023
The Endocrine Society
Title: THU662 Poor Response To Medical Treatment In A Patient With Amiodarone-induced Hyperthyroidism: A Therapeutic Dilemma
Description:
Abstract
Disclosure: A.
A.
Asiri: None.
R.
Sulimani: None.
W.
Alkhidady: None.
Introduction: Hyperthyroidism is a well-known complication of amiodarone therapy.
An incidence of 3% is reported in North America1, and even higher percentages in amiodarone deplete areas of about 10%.
2 Treatment of amiodarone-induced hyperthyroidism (AIH) is challenging, it depends on various factors including the type of AIH, dependence of the patient’s cardiac condition on amiodarone therapy, other complications or comorbidities of the patient such as hepatic injury or dysfunction and the response of the patient to antithyroid therapy.
Clinical Case: We present a case of a 32-year-old lady with a therapeutic dilemma in treating type I AIH, resistant to medical therapy.
Our patient first had acquired COVID-19-induced myocarditis in 2020 and subsequently developed sustained ventricular tachycardia and was treated with amiodarone and placed on an implantable cardioverter-defibrillators (ICD) device.
Two years later in 2022, the patient developed type I amiodarone-induced hyperthyroidism, with a free T4 reaching 100 pmol/L (Reference range 15-22 pmol/L) and complicated with transaminitis.
She was unresponsive to medical therapy including: anti-thyroid medications, IV high-dose hydrocortisone, potassium iodide drops, and cholestyramine.
She also developed adverse events with two of the antithyroid medications, Carbimazole and PTU; where she had elevated liver enzymes more than five time upper limit of normal and a generalized skin rash with PTU.
Plasmapheresis was not an option as some of her cardiac medications drug levels could be affected.
She underwent an emergent total thyroidectomy with dual beta blockade (Propranolol and Sotalol) successfully without any post op events.
Her T4 level normalized within 8 days of her operation and her liver enzymes normalized within 2 weeks.
Conclusion: We report the success and safety of surgical management in a patient with a cardiac arrhythmia and uncontrolled severe amiodarone-induced hyperthyroidism in the setting of adequate beta blockade.
References: 1.
Goldschlager N, Epstein AE, Naccarelli G, et al.
Practical guidelines for clinicians who treat patients with amiodarone.
Practice Guidelines Subcommittee, North American Society of Pacing and Electrophysiology.
Arch Intern Med.
2000;160:1741–8.
2.
Martino E, Aghini-Lombardi F, Mariotti S, et al.
Environmental iodine intake and thyroid dysfunction during chronic amiodarone therapy.
Ann Intern Med.
1984;101:28–34.
Presentation: Thursday, June 15, 2023.
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