ArticleFrontiers in oncology2026
Romiplostim for refractory chemotherapy-induced thrombocytopenia in a long-term survivor of limited-stage small cell lung cancer: a case report.
Article in Frontiers in oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Aggressive chemoradiotherapy for limited-stage small cell lung cancer (SCLC) frequently causes severe hematologic toxicities, particularly chemotherapy-induced thrombocytopenia (CIT), which can compromise treatment efficacy. While thrombopoietin receptor agonists (TPO-RAs) are preferred for CIT management, refractory cases pose significant challenges. Case presentation: A patient with stage IIIC (cT3N3M0) limited-stage SCLC achieved a durable partial response exceeding five years following etoposide/cisplatin chemotherapy and concurrent thoracic radiotherapy (60 Gy). However, severe, persistent, and refractory CIT developed, unresponsive to multiple interventions including recombinant human thrombopoietin (rhTPO), avatrombopag, eltrombopag, corticosteroids, thalidomide, tretinoin, and intermittent platelet transfusions. Bone marrow aspiration confirmed profound hypocellularity and megakaryocytic hypoplasia. Intervention & outcome: Initiation of subcutaneous romiplostim successfully elevated and maintained platelet counts, enabling sustained disease control. Platelet counts declined rapidly below 100×10&xxx2079;/L upon extending the dosing interval beyond 3-4 weeks, indicating that platelet maintenance remained dependent on continued romiplostim administration. Conclusion: This case demonstrates romiplostim's efficacy in managing severe, refractory CIT following intensive SCLC therapy, facilitating long-term disease control in a sustained responder. It highlights the critical role of TPO-RAs in this setting but underscores challenges including ongoing dependence on continued romiplostim for platelet maintenance and the need for strategies to coordinate romiplostim with future systemic therapies should disease progression occur. The potential for loss of romiplostim response necessitates exploration of alternative approaches.
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