A 26-year-old Caucasian male with no significant past medical history presented with fatigue, pruritus, jaundice, dark urine and clay colored stools for 1 month. The patient had been taking methyl-1-etiochoenolol-epietiocholanolone, an androgenic anabolic steroid (AAS).
Initially, at an outpatient clinic he was found to have a total bilirubin (Tbili) of 6 mg/dl. He was advised to discontinue the AAS. He discontinued the AAS but the patients' symptoms worsened. Repeat blood work 2 weeks later showed a Tbili of 32.5 mg/d, which prompted inpatient management.
The patient denied use of other hepatotoxic drugs, herbal supplements, tobacco, illicit drugs or alcohol. He had a similar episode 5 years ago; he had been taking a similar AAS and developed mild jaundice, which resolved spontaneously once he discontinued the AAS.
On exam, his vital signs were normal. He was extensively jaundiced, had a normal mental status without asterixis, and normal cardio-respiratory and abdominal exam without ascites or hepatomegaly. Liver biochemistries revealed aspartate aminotransferase (AST) 67 U/l, alanine transaminase (ALT) 106 U/L, alkaline phosphatase 166 U/l, Tbili 36 mg/dl, and international normalized ratio (INR) 0.95. Complete blood cell count (CBC) and Renal Function Panel (RFP) were normal. An extensive infectious, autoimmune, and metabolic work was negative. His abdominal ultrasound was normal.
At this stage, he was initiated on a 4-day trial of MARS therapy due to refractory hyperbilirubinemia after standard medical therapy (SMT). By day 3 of MARS therapy his pruritus, fatigue, hemoglobinuria and jaundice improved. Liver biochemistries at that time revealed AST 95 U/l, ALT 147 U/l, alkaline phosphatase 166 U/l, Tbili 24.3 mg/dl and INR 1.01. CBC and RFP remained normal.
Over the course of his therapy, he remained hemodynamically stable, clinically improved and his Tbili decreased to 20.7 mg/dl. A percutaneous liver biopsy was performed showing severe cholestasis with bile duct injury/inflammation and hepatocyte injury without steatosis (Fig. 1), consistent with DILI. Patient was discharge with outpatient follow-up. 
At 2 months follow-up he ceased taking AAS and noted a resolution of his fatigue, jaundice, pruritus, and abnormal stool and urine color. Labs showed AST 56, ALT 104 and Tbili 3.3 mg/dl.