S5611 IVIG-Induced Severe Transaminitis: A Case Report

Introduction: Intravenous immunoglobulin (IVIG) treats diverse conditions including neuromuscular and hematologic emergencies, and immunodeficiency disorders, often with favorable outcomes and life-saving potential. While generally well-tolerated, some common reactions include fever, anaphylaxis, hemolysis, and acute kidney injury (AKI). This case presents an unusual occurrence of IVIG-induced transaminitis and thrombocytopenia, which are not well-documented complications. Case Description/Methods: A 59-year-old man presented to the Emergency Department with a 10-day history of shortness of breath, sub-waist numbness and tingling, and bowel incontinence. Further work-up, including lumbar puncture, helped diagnose Guillain Barre syndrome (GBS) and neurology consultation prompted IVIG initiation. Within 12 to 18 hours of IVIG initiation, the laboratory tests showed marked transaminitis (ALT/AST 1309/871 U/L). Subsequently in the next 12 hours, the patient developed a fever of 40.4°C, with hypotension and acute respiratory decline, requiring intubation and mechanical ventilation. Further tests revealed new onset thrombocytopenia (88,000/µL) with rapid progression, necessitating platelet transfusion. Peripheral smear excluded DIC and TTP. Significantly elevated ferritin and low complement levels were noted. A bone marrow biopsy ruled out hemophagocytic lymphohistiocytosis and bone marrow suppression. IVIG was paused for 2 days and subsequently restarted. The patient was treated with pulse dose steroids and plasmapheresis. He developed AKI requiring hemodialysis; a kidney biopsy showed severe tubular injury without immune complex deposition or dysproteinemia. The patient remained intubated with multiple failed extubation attempts, continued hemodialysis, and ultimately transitioned to comfort care, expiring after 39 days. Discussion: This case emphasizes the importance of considering IVIG-induced liver dysfunction and thrombocytopenia. The rapid onset of transaminitis following the IVIG infusion and prior to the onset of hypotension strongly suggests IVIG as the causative agent. While the proposed mechanisms for the transaminitis are not fully understood, the stabilizing agent maltose in IVIG is hypothesized to contribute to liver injury. In debilitating conditions like GBS, if IVIG is deemed necessary despite adverse effects, clinicians should consider using a preparation lacking the implicated stabilizer or with a lower IgG concentration, or slowing the infusion rate to potentially mitigate these reactions.