Peshin Supriya, Dharia Adit, Takrori Ehab, Kaur Jasmeet, Thanikachalam Kannan, Iyer Renuka
Norton Community Hospital, Norton, VA 24273, USA.
HCA Florida Healthcare, USF Morsani College of Medicine GME Oak Hill Program, Orlando, FL 32801, USA.
Curr Oncol. 2025 Aug 14;32(8):455. doi: 10.3390/curroncol32080455.
Chemotherapy-induced thrombocytopenia (CIT) is a common yet underrecognized complication of systemic chemotherapy, particularly in gastrointestinal (GI) cancers. Despite progress in targeted and immune-based therapies, platinum-based and fluoropyrimidine regimens, especially oxaliplatin-containing protocols, remain standard in GI cancer treatment and are linked to high rates of CIT. This complication often leads to treatment delays, dose reductions, and elevated bleeding risk. This review provides a comprehensive overview of the pathophysiology, clinical implications, and management strategies of CIT in GI malignancies. CIT arises from several mechanisms: direct cytotoxicity to megakaryocyte progenitors, disruption of the marrow microenvironment, thrombopoietin dysregulation, and immune-mediated platelet destruction. Platinum agents, antimetabolites, and immune checkpoint inhibitors can contribute to these effects. Oxaliplatin-induced CIT may occur acutely via immune mechanisms or chronically through marrow suppression. CIT affects 20-25% of solid tumor patients, with highest rates in those receiving gemcitabine (64%), carboplatin (58%), and oxaliplatin (50%). Within GI cancer regimens, FOLFOXIRI and S-1 plus oxaliplatin show higher CIT incidence compared to FOLFIRI and CAPIRI. Thrombocytopenia is graded by severity, from mild (Grade 1-2) to severe (Grade 3-4), and often necessitates treatment adjustments, transfusions, or supportive therapies. Current strategies include chemotherapy dose modification, platelet transfusion, and thrombopoietin receptor agonists (TPO-RAs) like romiplostim and eltrombopag. While platelet transfusions help in acute settings, TPO-RAs may preserve dose intensity and reduce bleeding. Emerging agents targeting megakaryopoiesis and marrow protection offer promising avenues for long-term management.
化疗诱导的血小板减少症（CIT）是全身化疗常见但未得到充分认识的并发症，在胃肠道（GI）癌症中尤为如此。尽管靶向治疗和免疫治疗取得了进展，但铂类和氟嘧啶方案，尤其是含奥沙利铂的方案，仍是胃肠道癌症治疗的标准方案，且与高CIT发生率相关。这种并发症常导致治疗延迟、剂量减少和出血风险增加。本综述全面概述了胃肠道恶性肿瘤中CIT的病理生理学、临床意义和管理策略。CIT由多种机制引起：对巨核细胞祖细胞的直接细胞毒性、骨髓微环境的破坏、血小板生成素失调以及免疫介导的血小板破坏。铂类药物、抗代谢物和免疫检查点抑制剂均可导致这些效应。奥沙利铂诱导的CIT可能通过免疫机制急性发生，或通过骨髓抑制慢性发生。CIT影响20%-25%的实体瘤患者，接受吉西他滨（64%）、卡铂（58%）和奥沙利铂（50%）治疗的患者发生率最高。在胃肠道癌症治疗方案中，与FOLFIRI和CAPIRI相比，FOLFOXIRI和S-1加奥沙利铂的CIT发生率更高。血小板减少症按严重程度分级，从轻度（1-2级）到重度（3-4级），通常需要调整治疗、输血或支持治疗。目前的策略包括化疗剂量调整、血小板输注以及罗米司亭和艾曲泊帕等血小板生成素受体激动剂（TPO-RAs）。虽然血小板输注在急性情况下有帮助，但TPO-RAs可能维持剂量强度并减少出血。针对巨核细胞生成和骨髓保护的新型药物为长期管理提供了有前景的途径。
