Lesson of the Week: Myxoedema revealed by simvastatin induced myopathy

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Abstract
Case report A 42 year old man had a blood test for lipid analysis organised by his general practitioner; the results showed a cholesterol concentration of 10.9 mmol/l (desirable 5000 IU/l(38-220 IU/l)). A diagnosis of simvastatin induced myopathy was postulated, and the general practitioner was advised to stop the drug and monitor plasma enzyme activities every two weeks. Although simvastatin was discontinued, the raised plasma creatine kinase and aspartate aminotransferase activities failed to return to normal and eight weeks later were 2372 IU/l and 157 IU/l respectively. It seemed at this stage that, although simvastatin may have contributed to the increased plasma enzyme activities, it could not have been the sole cause. An alternative explanation was that the patient's hypercholesterolaemia and raised skeletal muscle enzyme activities were primarily due to myxoedema, with simvastatin acting as an exacerbating factor for the development of muscle toxicity. Thyroid function tests were therefore performed; the results showed primary hypothyroidism (total thyroxine concentration <20 nmol/l (70-140 nmo/l) and thyroid stimulating hormone concentration 106 mU/l (0.3-3.8 mU/l)). All the ancillary tests leading to the final diagnosis in this case were initiated by the chemical pathology department. The patient had no signs or symptoms to suggest hypothyroidism, and he did not complain of any muscle symptoms during this episode. His general practitioner began treatment with thyroxine - 100 μg/day, which was increased to 150 and 200 μg/day, with biochemical checks every four to six weeks after each dose increment (table). View this table: In this window In a new window Biochemical variables (with normal ranges) during thyroxine treatment