Endocrine Abstracts

Thyrotoxicosis causing hypokalaemic paralysis is a known complication among Asians, Myopathy as a result of thyrotoxicosis or caused by antithyroid drugs (ATD) is rare. Myositis, resulting in a rise in creatinine kinase levels (CK) is commonly seen in overt hypothyroidism, however, rapid lowering in circulating thyroid hormone levels during the treatment of Graves’ disease could result in myalgia and elevated CK levels. This complication needs to be actively diagnosed when patients are symptomatic for muscle pain after initiation of ATD therapy in Graves’ disease. The following case of Graves’ who started on carbimazole (CMZ) developed myositis secondary to relative hypothyroidism illustrates this phenomenon. A 23-year-old lady presented to the Emergency Department with myalgia and muscle cramps without weakness. She had been diagnosed by primary care to have Graves’ disease 2 months earlier, having presented with clinical and biochemical hyperthyroidism. Labs: (FT4 [Free Thyroxine] >100 pmol/l [Reference Interval (RI): 12 – 22], TSH [Thyroid Stimulating Hormone] <0.005 mIU/l [RI: 0.27 – 4.2]) and high titres of TSH receptor antibody (6.2 IU/l [RI: <1.8]). She had been treated with CMZ 20 mg twice a day, which improved her thyrotoxicosis but resulted in a rapid lowering of FT4 within a month. Her symptoms had developed a month after starting CMZ, which had already been adjusted to 15 mg daily with FT4 8.1 pmol/l and TSH 0.020 mIU/l at the point of review. CK was elevated at 2300 U/l (RI: 24 – 200). Systems review was unremarkable and renal function was normal, with no other cause of myositis identified. CK and myalgia improved with hydration and reduction of CMZ dose to 5 mg daily. Thyroid hormone has multiple effects on skeletal muscle, and there have been increasing reports of myositis after treatment of Graves’ disease. While the mechanism remains unknown, associations with ATD and relative hypothyroidism have been suggested. Given that patients on treatment are generally on ATD and have reductions in levels of thyroid hormone, etiology is difficult to determine. As musculoskeletal complaints are common in patients with hyperthyroidism, relative hypothyroidism-induced myositis may be more common than reported. Anticipating this condition will allow clinicians to intervene with early dose reduction to alleviate myositis. Reduction of ATD doses with close monitoring instead of discontinuing treatment or extensive investigation may be a prudent course of action.