Testosterone
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Various toxicities: case report A 53-year-old man developed myositis, rhabdomyolysis, hypercalcaemia, focal segmental glomerulosclerosis and left ventricular hypertrophy during treatment with unspecified growth hormones and testosterone for body building. The man presented with severe constipation for many weeks. He had been receiving tamsulosin and lansoprazole as over-thecounter medications; of note, he had also been receiving testosterone 350 mg/day [route not stated] and unspecified growth hormones 2 IU/day on a ’6 weeks on and 4 weeks off’ regimen for more than 20 years. Examination revealed mild ankle oedema. He was found to have hard globular masses under both axillae. Laboratory investigations on admission showed a high level for corrected calcium, serum urea, serum creatinine, protein/creatinine ratio, serum creatine kinase, TSH, vitamin A (hypervitaminosis A), whereas low values noted for estimated glomerular filtration rate, free thyroxine and calcitriol [1,25 vitamin D3]. His urine protein value was 4+ (proteinuria). Whole body MRI scans revealed muscle oedema and appearances of myositis with areas of ossification and calcification within the muscle bellies of his upper and lower limbs. Echocardiography demonstrated concentric left ventricular (LV) hypertrophy, a moderate bicuspid aortic stenosis (AS) along with a peak gradient of 39mm Hg and an ejection fraction of 44–53%. Cardiac MRI scan confirmed AS with severely impaired LV function. A slightly worse function inferiorly was indicative of the right coronary artery disease. The clinical picture suggested that myositis and his medications were responsible for LVH. Autoimmune antibodies, including anti-Ro and anti-Jo-1 antibodies were found to be positive. Thigh muscle biopsy (vastus medialis and lateralis) revealed an active inflammatory myositis along with chronic myopathic changes and mineral deposition. Sections showed positive results for markers of inflammation (CD3) and fibre formation (CD45), which confirmed an acute on chronic inflammatory process. Special stains and paraffin sections ruled out amyloid and vasculitis within the muscle. There were no visible granulomata. In the kidney, most glomeruli were globally sclerosed and some glomeruli showed segmental sclerosis; there was moderate to severe tubular atrophy along with interstitial fibrosis and a moderate chronic inflammatory infiltrate. The surviving proximal tubules showed a mild dilatation consistent with hyperplasia and a mild acute tubular injury along with occasional foci of calcification, suggestive of acute kidney injury (AKI). Focal segmental glomerulosclerosis secondary to hypercalcaemia was diagnosed. The myositis, rhabdomyolysis, hypercalcaemia, focal segmental glomerulosclerosis and left ventricular hypertrophy were attributed to unspecified growth hormones and testosterone [times to reactions onsets not stated]. The man was rapidly rehydrated with provision of sodium chloride [normal saline]. He also received pamidronic acid [pamidronate] for hypercalcaemia and AKI, alo
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