Poster Presentation ESA-SRB-ANZOS 2025 in conjunction with ENSA

Thyrotoxic periodic paralysis complicated by carbimazole-associated myositis (124669)

Harsan Kanagaretnam 1 , Kajanan Parameshwaran 1 , Kirtan Ganda 1 , Markus Seibel 1
  1. Concord Hopsital, Sydney, NSW, Australia

Thyrotoxic periodic paralysis (TPP) is a rare complication of hyperthyroidism characterised by transient hypokalaemia-induced muscle weakness (1). It predominantly affects Asian men and may be triggered by physical exertion or high-carbohydrate meals (2). Carbimazole, a commonly used anti-thyroid medication, is rarely associated with myositis, an inflammatory skeletal muscle condition (3, 4).

A man in his 30s of East Asian descent presented with acute generalised weakness following intense exercise and a carbohydrate-rich meal. Investigations revealed profound hypokalaemia, elevated creatine kinase (CK), and thyrotoxicosis due to Graves’ disease. He was diagnosed with TPP and recovered fully after potassium replacement and starting carbimazole. Three months later, he developed myalgia without weakness and persistently elevated CK. Autoimmune and genetic testing were negative, and muscle biopsy showed non-specific myopathic changes. Symptoms resolved after switching from carbimazole to propylthiouracil. At follow-up, thyroid function remained stable and CK levels normalised.

This case highlights two rare complications: TPP and presumed carbimazole-induced myositis. To our knowledge, this is the first published case report describing both conditions in the same individual. TPP results from a thyroid hormone-mediated intracellular potassium shift, causing hypokalaemia and muscle weakness (5). Management includes potassium replacement, beta-blockers in select cases, and restoring euthyroid status to prevent recurrence (6, 7). Carbimazole-induced myositis, though uncommon, is a recognised adverse effect and may present with myalgia, elevated CK, and non-specific biopsy findings (8, 9, 10). Management options include dose reduction, drug cessation, switching to propylthiouracil, or definitive therapy like thyroidectomy or radioactive iodine (8, 9, 11). Early recognition is key, with resolution often seen after drug withdrawal or substitution.

Clinicians should consider TPP in young Asian males with hypokalaemic paralysis and monitor for myositis in patients on carbimazole. Prompt recognition and switching to an alternative anti-thyroid agent can improve outcomes and support safer long-term management (1, 8).

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  11. Tsang CC, Hui WS, Lo KM, Yeung JHM, Cheung YL., Anti-Thyroid Drugs-Related Myopathy: Is Carbimazole the Real Culprit? Int J Endocrinol Metab 2015; 13(1): e17570