Terbinafine
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Rhabdomyolysis, acute kidney injury and hepatotoxicity: case report A 22-year-old man developed rhabdomyolysis, acute kidney injury (AKI) and hepatotoxicity during treatment with terbinafine for tinea infection. The man presented to an emergency department with a two day history of dark urine, nausea and vomiting. Nine days before this presentation, he started receiving terbinafine [terbinafine hydrochloride] 250 mg/day [route not stated] for a cutaneous ringworm infection (tinea infection). Two days before the current presentation, he experienced bilateral thigh swelling and pain, which he ascribed it to a 15-minute work-out of low-to-moderate intensity. He received one dose of diclofenac, which led to resolution of the pain within 24 hours. He continued receiving terbinafine therapy. The next day, he started experiencing nausea and repeated emesis. He also observed that he was producing less urine and the colour of the urine appeared dark, which eventually brought him to the emergency department. He did not have any medical issue before his ringworm infection. At the time, his estimated glomerular filtration rate (eGFR) was greater than 120 mL/min. Initial investigations revealed a creatinine of 514 µmol/L and creatine kinase (CK) of >100000 U/L, and a concern of severe rhabdomyolysis and AKI was made. Electrolytes revealed a high phosphate level (hyperphosphataemia) and a low ionised calcium level (hypocalcaemia). AST and ALT were elevated, concerning for hepatotoxicity. Urine qualitative testing for myoglobin was found to be positive. He was admitted under the internal medicine service. Therapy with terbinafine was discontinued. The man was treated conservatively for rhabdomyolysis with IV fluids (sodium chloride [normal saline]) and bicarbonate drip. He was placed on telemetry. His electrolytes were monitored closely. Following 12 hours of fluid resuscitation, he remained anuric, and the serum creatinine continued to increase. To avert further complications of rhabdomyolysis and AKI, he was initiated on intermittent haemodialysis. IV fluids were discontinued following 24 hours of resuscitation, as he developed volume overload; instead, volume status was adjusted through haemodialysis. During the following week, he continued to improve. His creatinine kinase decreased. ALT and AST continued to normalise. Although his urine output remained less than 100 mL/24 hours, he was medically well otherwise. After one week, he was discharged and was continued on 3 dialysis treatments every week as an outpatient. After discharge, his urine output gradually improved. Over approximately one month, he was successfully weaned off dialysis. His creatinine level improved consistently over the ensuing several weeks. Zhou S, et al. Rhabdomyolysis and Acute Kidney Injury Associated With Terbinafine Use: A Case Report. Canadian Journal of Kidney Health and Disease 7: no pagination, 803515690 Jan 2020. Available from: URL: http://doi.org/10.1177/2054358120951371
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