Case Presentation: A 21 year old male college student with a history of depression presented to the Emergency Department with cola colored urine. He exercises 3-4 times per week and hydrates well while exercising. He denied illicit drug, tobacco, alcohol or energy drink use. Recently, he had seen a psychiatrist for increased depressive symptoms and was started on bupropion and trazodone. Upon presentation, his physical exam was unremarkable. His labs revealed normal electrolytes and renal function, an elevated alanine aminotransferase (ALT) at 363 IU/L and aspartate aminotransferase (AST) at 1437 IU/L, and a urinalysis with 100 protein, 250 blood, and 3 RBCs. His creatinine phosphokinase (CK) level was 95,597 IU/L. Urine drug screen and ethanol level were unremarkable. The patient was admitted and maintained on aggressive IV fluids. He did not develop any renal injury during the admission. The etiology of the patient’s rhabdomyolysis was initially unclear as the elevation of his CK was out of proportion to what would be expected from routine exercise. His inflammatory markers were normal making inflammatory myositis less likely. Other labs including TSH, PTH, Monospot, and EBV serologies were negative making endocrine and viral causes less likely. McArdle’s disease and autoimmune myositis were considered, however ANA and extractable nuclear antibody panel were negative, making these diagnoses less likely. Ultimately, the etiology was determined to be due to an adverse effect of either one, or the combination, of the patient’s recently started anti-depressants. Psychiatry was consulted and both trazodone and bupropion were discontinued. On discharge, CK had decreased to 4268 IU/L, AST decreased to 223 IU/L, and ALT decreased to 195 IU/L. These labs all normalized within 2 weeks of discharge.
Discussion: Rhabdomyolysis is defined as an injury of skeletal muscle, which causes a release of intracellular contents into the circulation. Rhabdomyolysis starts with injury to the myocyte membrane and altered energy production. This then leads to increased calcium concentrations and initiation of cellular destructive processes, which then cause lysis of the cells and release of cellular contents including electrolytes, enzymes, proteins and purine metabolites. The etiology of rhabdomyolysis can be grouped into 4 main categories: 1. Hypoxic (i.e CO or cyanide exposure, compartment syndrome, prolonged surgery); 2. Physical (i.e. trauma, burns, prolonged/extreme exertion, seizures); 3. Chemical (i.e. alcohol, medications, illicit substances); and 4. Biologic (i.e. infectious myositis, hypothyroidism, hyperaldosteronism). The incidence of drug-induced rhabdomyolysis is largely unknown as it is seldom reported. There is one reported case of rhabdomyolysis felt to be caused by bupropion, however, exposure to other medications could not be excluded as possible contributors. Overall mortality for rhabdomyolysis ranges from 2% to 46%, with higher mortality in patients with acute renal failure. Therefore, it is important to elucidate the etiology of rhabdomyolysis, especially if found to be drug-induced, so that the offending agent(s) can be discontinued as soon as possible.
Conclusions: We report this case of drug-induced rhabdomyolysis to remind hospital medicine physicians that excessive exercise is not always the etiology of rhabdomyolysis in younger patients and alternative etiologies need to be considered in this patient population.