Anabolic-androgenic Steroid-induced Cholestasis, Acute Kidney Injury, and Pancreatitis

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Purpose: Anabolic-androgenic steroids (AAS) are a popular class of drugs used to enhance performance and muscle mass. Its appeal lies in the ability to increase muscle strength through anabolic effects. Cholestasis associated with AAS is well documented. The alkylated compound increases oral bioavailability and causes impaired biliary secretion, typically leading to pure cholestasis. Pancreatitis is not a known sequelae of AAS. Renal side effects, although rare, have been reported in the literature. We report a case of a patient with a history of non-cirrhotic hepatitis C who presented with jaundice, pancreatitis, and acute kidney injury from AAS. After 3 months of use, he began to experience abdominal pain, nausea, vomiting, progressive jaundice, and pale stool for three weeks. Physical exam was notable for scleral icterus, epigastric tenderness, and lethargy. Laboratory values demonstrated a BUN of 144 mg/dL, serum Cr 8 mg/dL, total bilirubin 65.7 mg/dL, AST 50 U/L, ALT 46 U/L, alkaline phosphatase 352 U/L, INR 1.1, and lipase 2273 U/L. CT abdomen showed prominence of the pancreatic parenchyma with mild stranding, and hepatomegaly without ascites, masses, or ductal dilatation. The patient was medically managed with bicarbonate, Protonix, N-acetylcysteine infusions and Ursodiol. Liver biopsy was considered, but not done, given multiple active medical issues and patient's bilirubin started to improve with abovementioned care. His pancreatitis was mild, and improved with conservative management. Hemodialysis was done emergently for acidosis and hyperkalemia. At follow-up 1 year after hospitalization, his liver tests returned to his baseline with improvement in renal function as well. Though cholestatic liver injury has been described in the literature, there is sparse information regarding acute kidney injury and pancreatitis owing to anabolic-androgenic steroids. Hepatotoxicity with AAS can cause cholestasis and peliosis hepatis, which is reversible upon discontinuation. Hepatomas have also been reported. What makes this case unique is its multiorgan involvement. With pancreatitis, no known mechanism of injury has been described, but ruling out gallstones and eliciting medication and toxin history is important. Focal segmental glomerulosclerosis and acute tubular necrosis have been described secondary to AAS use. Public awareness and education is needed to prevent this from occurring. Once exposed to AAS, patients should be followed closely to assess improvement in clinical parameters and ensure ongoing counseling for abstinence. This rare case demonstrates the atypical and multiorgan effects of AAS. Early recognition and aggressive supportive care can lead to improved survival.