Carbimazole 1.25mg/5ml oral solution

Amiodarone-induced thyrotoxicosis (AIT) is a complex endocrine disorder associated with significant morbidity, particularly in patients with underlying cardiac disease. Type 2 AIT, a destructive thyroiditis, is typically managed with corticosteroids. However, treatment becomes challenging when glucocorticoids are contraindicated. We present the case of a 37-year-old male with atrial fibrillation, dilated cardiomyopathy, and McCune-Albright syndrome who developed persistent biochemical thyrotoxicosis while on amiodarone therapy. Despite suppressed thyroid-stimulating hormone and elevated free thyroxine levels, he remained clinically asymptomatic. A thyroid uptake scan demonstrated low uptake consistent with type 2 AIT, although thyroid receptor antibodies were positive, suggesting possible mixed pathology. Management was complicated by coexisting liver lesions, precluding corticosteroid therapy. The patient was managed with low-dose carbimazole, resulting in gradual normalization of thyroid function. This case highlights the complexity of diagnosing and managing AIT and demonstrates that thionamides may be a viable alternative in selected patients in whom corticosteroids are contraindicated, particularly in cases with overlapping features of type 1 and type 2 AIT.

Abstract licence: CC BY

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.

Abstract licence: CC BY