Akademik Veri Yönetim Sistemi
Journal of oncological sciences, cilt.11, sa.2, ss.1-6, 2025 (Scopus, TRDizin)
Thrombotic microangiopathy (TMA) is a rare hematologic complication characterized by microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and variable involvement of organ systems. Drug-induced TMA (DI-TMA) is most commonly associated with agents such as mitomycin C and gemcitabine. Etoposide, a chemotherapeutic agent frequently used in lung cancer treatment, is rarely implicated. Recognition of DI-TMA is particularly challenging in oncology patients, in whom cytopenias often have multifactorial etiologies. We present a 60-year-old woman with a history of stage IIIC2 endometrial cancer in remission who subsequently developed metastatic large-cell lung carcinoma. She was treated with carboplatin and etoposide. Following the initial two cycles of chemotherapy, the patient developed severe anemia and thrombocytopenia, along with elevated lactate dehydrogenase, indirect hyperbilirubinemia, decreased haptoglobin, and peripheral blood schistocytosis-consistent with MAHA. ADAMTS13 activity was normal, and no renal or neurologic dysfunction was present. A diagnosis of etoposide-induced TMA was established. Etoposide was discontinued, corticosteroid therapy was initiated, and the patient subsequently demonstrated hematological recovery. Chemotherapy was resumed with irinotecan as an alternative agent. This case highlights etoposide as a potential etiologic agent of TMA in patients with lung cancer. Given the non-specific clinical presentation and overlap with chemotherapy-induced cytopenias, early recognition and prompt drug withdrawal are essential for achieving hematologic recovery. Clinicians should consider DI-TMA in oncology patients with new-onset hemolysis and thrombocytopenia-even in the absence of classic TMA organ involvement