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Objectives High-dose intravenous immunoglobulin (IVIG) is frequently used to manage hematologic manifestations of SLE, such as cytopenias and macrophage activation syndrome (MAS). IVIG-induced hemolysis, though uncommon, is a recognized complication, particularly after high-dose infusions. We report a case of severe IVIG-induced hemolytic anemia in a patient with SLE and APS, refractory to glucocorticoids, successfully treated with ravulizumab, a terminal complement inhibitor.Methods A 30-year-old woman with triple-positive APS and new-onset SLE (malar rash, high anti-dsDNA, hypocomplementemia) was admitted for respiratory distress. Following a comprehensive diagnostic work-up, including chest CT, bronchoscopy with bronchoalveolar lavage, and exclusion of infection and malignancy, lupus pneumonitis was diagnosed. She received high-dose methylprednisolone pulses and two infusions of low-dose cyclophosphamide (Euro-Lupus protocol). Four days after the second cyclophosphamide pulse, she developed fever, pancytopenia (Hb 9.4 g/dL), and hyperferritinemia with Direct Coombs negative. Suspecting MAS, she was treated with IVIG (2 g/kg) and methylprednisolone. Fever, leukopenia, and thrombocytopenia resolved, but severe hemolysis ensued (Hb nadir 4.9 g/dL, LDH >2000 IU/L, undetectable haptoglobin, hemoglobinuria, DAT 2+ for IgG) (fig 1). Complement levels dropped sharply. Peripheral smear showed red cell agglutination without schistocytes. Normal renal function and ADAMTS13 activity excluded TMA and TTP, and PNH was ruled out by flow cytometry. Despite high-dose steroids, transfusions, hemolysis persisted. Her profile — female sex, blood type A+, high-dose IVIG, active SLE/APS — matched known risk factors for IVIG-induced hemolysis, thought to result from passive isoagglutinin transfer and secondary complement activation.Results Although IVIG- induced hemolysis is typically self-limited or responsive to glucocorticoids our patient represents a treatment-resistant case. Given life-threatening, complement-mediated hemolysis ravulizumab was administered (2700mg IV) off-label. Within 72 hours, LDH declined, haptoglobin normalized, and hemoglobin stabilized. ( figure 1) Hemoglobinuria resolved, complement levels normalized, and DAT became negative. The patient was discharged on a steroid taper and remains relapse-free at nine-month follow-up.Abstract PO:04:097 Figure 1Course of Hemolytic Anaemia following IVIG infusion and therapeutic interventions. Laboratory normal values: Hb (12.5-16.5 g/dl), LDH (<244 U/L), C3 (81-157 mg/dl), C4 (12.9-39.2 mg/dl), Haptoglobin (0.4-2.5 g/dl) and Direct Coombs (-). After pulses of MP (Methylprednisolone), the patient was on MP 100 mg/24 h, with gradual tapering down to MP 32 mg/24 h on day 18Conclusions This is the first report of ravulizumab use for IVIG-induced hemolytic anemia. It highlights that IVIG can trigger severe complement-mediated hemolysis in high-risk SLE/APS patients. Complement inhibition may represent a novel therapeutic approach in select, life-threatening cases of drug-induced hemolysis unresponsive to standard immunosuppression, especially in patients with autoimmune diseases.