ArticleCureus2026
Refractory Amiodarone-Induced Thyrotoxicosis Requiring the Consideration of Thyroidectomy: A Case Report and Review of Management Challenges.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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4 authors.
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Abstract
Amiodarone-induced thyrotoxicosis (AIT) is an uncommon but clinically significant complication of amiodarone therapy that may be associated with substantial morbidity, particularly in patients with underlying cardiovascular disease. We report the case of a 61-year-old gentleman with a history of atrial fibrillation, ischaemic heart disease, heart failure, and obesity, who developed severe thyrotoxicosis after approximately 3.5 years of amiodarone treatment. Routine thyroid function monitoring showed stable thyroid levels for three years; however, despite an abnormality identified at a later stage, the patient remained asymptomatic. Shortly after, he was admitted with vomiting, abdominal discomfort, poor mobility, weight loss, and a free thyroxine (fT4) level exceeding 100 pmol/L. Carbimazole therapy was initiated, but persistent thyrotoxicosis necessitated dose escalation, discontinuation of amiodarone, and commencement of prednisolone for suspected AIT. During a subsequent admission, the patient developed euglycaemic diabetic ketoacidosis and later steroid-induced diabetes, requiring treatment and both diabetic and endocrine team involvement. Thyroid ultrasound demonstrated normal-low vascularity without focal abnormalities, and thyroid autoantibodies were negative. Although thyroid function tests initially improved with combined medical therapy, biochemical response later plateaued with a fT4 level of 52 pmol/L at the end of month 8, prompting referral for thyroidectomy. This case describes a challenging presentation of AIT with an incomplete response to conventional medical management and progression to consideration of definitive surgical treatment.
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