Thrombotic microangiopathy (TMA) is a rare, life-threatening syndrome characterized by microvascular thrombosis, hemolytic anemia, thrombocytopenia, and organ dysfunction. While it can be induced by infections, drugs, malignancies, autoimmune disorders, or genetic defects, TMA is particularly uncommon in second breast cancer (SBC) patients with a history of Hodgkin lymphoma (HL). We describe a 45-year-old female who developed metastatic SBC 18 years after curative HL treatment. The diagnosis of TMA was established on the basis of thrombocytopenia, hemolytic anemia (elevated lactate dehydrogenase, low haptoglobin, and a reticulocyte count of 5.72%), and multi-organ dysfunction, following the exclusion of thrombotic thrombocytopenic purpura and Shiga toxin-producing Escherichia coli (STEC)-hemolytic uremic syndrome. In this case, the multifactorial etiology-stemming from both paraneoplastic endothelial injury and chemotherapy-induced toxicity-complicated the clinical picture. Despite aggressive supportive measures, including plasma exchange and antibiotics, the patient's condition rapidly deteriorated, culminating in fatal cerebral hemorrhage. This case highlights the diagnostic and therapeutic challenges of TMA in patients with complex oncologic histories, as exemplified by its rare occurrence in a patient with SBC post-HL. Although supportive care remains paramount, our findings suggest that complement inhibition with eculizumab may offer benefits in select cases, such as chemotherapy-induced and paraneoplastic TMA. Early detection and targeted intervention are crucial, warranting further research into eculizumab's potential role in high-risk settings.
Wang et al. (Tue,) studied this question.
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