Abstract
We present a case of a 71-year-old woman with a history of high-grade serous ovarian adenocarcinoma, treated with neoadjuvant chemotherapy, surgery, and adjuvant chemotherapy. A maintenance treatment combining bevacizumab and olaparib was introduced consecutively. Bevacizumab was stopped 7 months later due to neurological complications. The patient developed severe, progressive anemia, leading to significant clinical management challenges, with hemoglobin levels as low as 54 g/L. Despite initially adapting and finally discontinuing olaparib, the patient remained transfusion dependent, without notable improvement. Common causes of anemia, such as iron deficiency, vitamin deficiency, autoimmune and infectious causes, were ruled out. Bone marrow biopsies revealed a clonal cytotoxic T-LGL population and a DNMT3A mutation without evidence of myelodysplasia or metastatic infiltration. A further decline in reticulocytes and the appearance of warm autoantibodies (IgG) indicated an increasingly mixed anemia profile. High-dose corticosteroids resulted in rapid hematological improvement. This case highlights a severe anemia of mixed origin with central hypo-regenerative components due to prolonged PARP inhibitor toxicity and a hemolytic mechanism associated with warm autoantibodies. The prolonged toxic effect of olaparib, in conjunction with confounding factors (DNMT3A mutation, warm autoantibodies, T-LGL clone), underscores the need for a comprehensive hematological assessment. The patient's response emphasizes the complexity of managing drug-induced hematologic toxicity and the potential for overlapping hematologic conditions.