Case reports in hepatology · 2026
Oxymetholone-Associated Cholestatic Drug-Induced Liver Injury With Profound Hyperbilirubinaemia: A Longitudinal Case Report.
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Taha Hatem Mousa, Khalifa Baha' Husam, Hassan Majd Y, Taha Khaled Hatem
Аннотация
BACKGROUND: Cholestatic liver injury from 17α-alkylated anabolic-androgenic steroids is established. We report a longitudinally documented case that emphasises phenotype definition and the limits of agent-specific attribution.
CASE PRESENTATION: A 26-year-old man presented on Day 29 after self-administering oral oxymetholone 50 mg/day with intramuscular testosterone enanthate 250 mg/week. Peak total bilirubin was 24.6 mg/dL (direct bilirubin 21.3 mg/dL), alanine aminotransferase 5.6 × the upper limit of normal (ULN) and alkaline phosphatase 2.9 × ULN; the R-ratio was 1.91, indicating cholestatic injury. International normalised ratio (≤ 1.04), albumin (≥ 4.1 g/dL) and creatinine (0.8-0.9 mg/dL) remained preserved. Ultrasonography with hepatic Doppler showed a nondilated biliary tree (common bile duct 1-2 mm), patent visualised vessels and no sonographic evidence of obstruction. The available viral, autoimmune, metabolic and haemolytic evaluation identified no alternative cause. Updated RUCAM assessment was limited by ursodeoxycholic acid use during dechallenge and incomplete molecular virology; concomitant testosterone and absent chemical verification of the products precluded definitive single-agent attribution. Both agents were withdrawn on Day 30; ursodeoxycholic acid and antipruritic therapies were used as supportive care.
OUTCOME: Total bilirubin decreased by 69.1% by Day 57 and by 91.5% by Day 85. Pruritus resolved, daily function returned and renal and hepatic synthetic function remained preserved.
CONCLUSION: This report provides granular 8-week follow-up of an established phenotype. The course supports oxymetholone as the principal suspect, but recovery cannot be attributed to supportive pharmacotherapy in this uncontrolled case.
CASE PRESENTATION: A 26-year-old man presented on Day 29 after self-administering oral oxymetholone 50 mg/day with intramuscular testosterone enanthate 250 mg/week. Peak total bilirubin was 24.6 mg/dL (direct bilirubin 21.3 mg/dL), alanine aminotransferase 5.6 × the upper limit of normal (ULN) and alkaline phosphatase 2.9 × ULN; the R-ratio was 1.91, indicating cholestatic injury. International normalised ratio (≤ 1.04), albumin (≥ 4.1 g/dL) and creatinine (0.8-0.9 mg/dL) remained preserved. Ultrasonography with hepatic Doppler showed a nondilated biliary tree (common bile duct 1-2 mm), patent visualised vessels and no sonographic evidence of obstruction. The available viral, autoimmune, metabolic and haemolytic evaluation identified no alternative cause. Updated RUCAM assessment was limited by ursodeoxycholic acid use during dechallenge and incomplete molecular virology; concomitant testosterone and absent chemical verification of the products precluded definitive single-agent attribution. Both agents were withdrawn on Day 30; ursodeoxycholic acid and antipruritic therapies were used as supportive care.
OUTCOME: Total bilirubin decreased by 69.1% by Day 57 and by 91.5% by Day 85. Pruritus resolved, daily function returned and renal and hepatic synthetic function remained preserved.
CONCLUSION: This report provides granular 8-week follow-up of an established phenotype. The course supports oxymetholone as the principal suspect, but recovery cannot be attributed to supportive pharmacotherapy in this uncontrolled case.