S5509 A 2-System Toxicity: Drug-Induced Liver Injury Leading to Bone Marrow Failure

Introduction: Drug-induced liver injury (DILI) is an unpredictable adverse reaction to medications or supplements and remains a leading cause of acute liver failure. While most cases resolve with withdrawal of the offending agent, rare complications can occur, including hepatitis-associated aplastic anemia (HAAA)—a condition characterized by bone marrow failure and pancytopenia following acute hepatic injury. Though its pathogenesis is not fully understood, immune-mediated destruction of hematopoietic precursors is thought to play a central role. We describe a rare case of supplement-induced DILI that progressed to aplastic anemia in an otherwise healthy adult. Case Description/Methods: A 43-year-old man with a history of heavy alcohol use presented with scleral icterus and diffuse pruritus. He had been taking an over-the-counter metabolism supplement containing dehydroepiandrosterone, saw palmetto, and ginseng daily for one month. Labs showed hepatocellular injury (alanine aminotransferase 3285 U/L, aspartate aminotransferase 2913 U/L) and hyperbilirubinemia (total bilirubin 17.5 mg/dL). Viral hepatitis and autoimmune serologies were negative. MRI revealed no biliary obstruction or hepatic mass. He was treated with N-acetylcysteine, resulting in gradual improvement of liver function. Liver biopsy confirmed acute and chronic inflammation consistent with DILI. Follow-up labs revealed thrombocytopenia (<10 K/µL) and severe neutropenia (ANC 0.35 K/µL). Platelet transfusions were ineffective. Initial bone marrow biopsy showed hypocellularity (30%) with decreased megakaryocytes and no evidence of malignancy. One month later, bilateral iliac crest biopsies showed worsening cellularity (10%–20%) with atypical lymphocytes, consistent with aplastic anemia. The patient was started on eltrombopag (150 mg daily) and continued receiving platelet transfusions. He declined bone marrow transplantation. Over 4 years, his blood counts gradually improved, with platelets rising to 73 K/µL and ANC to 0.90 K/µL. Discussion: HAAA is a rare and life-threatening complication of DILI. While its mechanism remains unclear, it is presumed to involve immune-mediated suppression of hematopoiesis. Treatment typically includes transfusions, immunosuppressive therapy, hematopoietic growth factors, and bone marrow transplantation. This case underscores the importance of recognizing supplements as potential triggers of systemic toxicity and highlights the need for further research to guide clinical management of HAAA.