A male of East Asian background in his 30s presented to the emergency department with acute onset global muscle weakness, elevated creatine kinase, profound hypokalaemia and hyperthyroidism. A diagnosis of thyrotoxic periodic paralysis was made and the myopathy resolved promptly with potassium replacement. However, 3 months after being commenced on carbimazole for hyperthyroidism, the patient developed myalgias without weakness associated with an elevated creatine kinase. The myositis panel was negative, while a muscle biopsy showed nonspecific, mild myopathic changes with minimal lymphocytic inflammation. As a change in therapy from carbimazole to propylthiouracil resulted in prompt symptom improvement and normalisation of serum creatine kinase levels, a presumptive diagnosis of carbimazole-induced myositis was made. Genetic testing for hereditary skeletal muscle channelopathies did not identify any gene of interest.
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Kanagaretnam et al. (2024) studied this question.
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