Anabolic steroid-induced rhabdomyolysis

Abstract

A 25-year-old male with no prior medical history presented with bilateral thigh and calf pain. He was a professional dancer, who had not been dancing for a year following an appendicectomy and was now getting back into training. Two days before presentation he had increased the intensity and duration of his workout to maximum 45 minutes on a cross-trainer. The next day he noticed pain in his legs which intensified with muscle cramps and 24 hours later he presented to accident and emergency. He was sent home on diclofenac tablets,with a diagnosis of musculo-skeletal pain. He re-presented 2 days later with difficulty walking. He admitted taking two preparations of anabolic steroids recently. On examination, his legs were diffusely tender in the region of the quadriceps and the inferior portion of gastrocnemius, but they were soft, with no warmth or swelling. He had reduced power at the hip flexors and occasional muscle spasms but no focal neurology. Creatinine kinase (CK) was 17 171 iu/litre (normal range for men <250 iu/litre), with normal renal function and no myoglobinuria. Orthopaedic review found no evidence of compartment syndrome and he was treated with intravenous fluids, diazepam and paracetamol. His CK initially decreased but then increased to peak at 22 226 iu/litre on day three, with evidence of myoglobinuria. Management continued with hydration and urinary alkalinization. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) levels were normal and human immunodeficiency virus (HIV) test was negative. Magnetic resonance imaging (MRI) of his legs showed areas of high signal in several muscle groups with no focal areas of necrosis (Figure 1). Following a muscle biopsy, he was started on oral prednisolone and then a course of methylprednisolone, during which CK levels decreased rapidly. His muscle biopsy and electromyography (EMG), were reported as normal and an autoantibody screen was negative, hence the steroids were rapidly tapered off. At discharge, his CK had continued to decrease (1100 iu/litre) and his mobility slowly improved. A diagnosis of anabolic steroid-induced rhabdomyolysis was made. He had been taking two steroid preparations; WinstrolTM (stanazolol) and PrimabolanTM (metenolon). He had used WinstrolTM several times in the past and on this occasion he had used four ampoules each a week apart. However, he used only one ampoule of PrimabolanTM a few days before presentation. He usually injected into his thighs.