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首页> 外文期刊>Clinical and applied thrombosis/hemostasis : >Investigation of Proposed Mechanisms of Chemotherapy-Induced Venous Thromboembolism
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Investigation of Proposed Mechanisms of Chemotherapy-Induced Venous Thromboembolism

机译：化疗诱导的静脉血栓栓塞的拟议机制研究

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Venous thromboembolism (VTE) during chemotherapy is common, with 7% mortality in metastatic breast cancer (MBC). In a prospective cohort study of patients with breast cancer, we investigated whether vascular endothelial cell activation (VECA), and whether apoptosis, is the cause of chemotherapy-induced VTE. Methods: Serum markers of VECA, E-selectin (E-sel), vascular cell adhesion molecule 1 (VCAM-1) and d -dimer (fibrin degradation and hypercoagulability marker) were measured prechemotherapy and at 1, 4, and 8 days following chemotherapy. Clinical deep vein thrombosis (DVT) or pulmonary embolism and occult DVT detected by duplex ultrasound imaging were recorded as VTE-positive (VTE+). In patients with MBC, hypercoagulable response to chemotherapy was compared between patients with and without cancer progression. Development of VTE and cancer progression was assessed 3 months following starting chemotherapy. Results: Of the 134 patients, 10 (7.5%) developed VTE (6 [17%] of 36 MBC receiving palliation, 0 of 11 receiving neoadjuvant to downsize tumor, and 4 [5%] of 87 early breast cancer receiving adjuvant chemotherapy, P = .06). Levels of E-sel and VCAM-1 decreased in response to chemotherapy (P d -dimer (geometric mean) increased by 36% in the 21 patients with MBC responding to chemotherapy but steadily decreased by 11% in the 15 who progressed (day 4, P Conclusions: During chemotherapy for breast cancer, VECA is induced; however, this is not the primary mechanism for VTE. Chemotherapy-induced apoptosis may enhance hypercoagulability and initiate VTE.
机译：化疗期间静脉血栓栓塞（VTE）很常见，转移性乳腺癌（MBC）的死亡率为7％。在一项针对乳腺癌患者的前瞻性队列研究中，我们调查了血管内皮细胞活化（VECA）和细胞凋亡是否是化疗诱导的VTE的原因。方法：在化疗前，化疗后第1、4和8天测量VECA，E-选择素（E-sel），血管细胞粘附分子1（VCAM-1）和d-二聚体的血清标志物（纤维蛋白降解和高凝标志物）。化学疗法。通过双重超声成像检测到的临床深静脉血栓形成（DVT）或肺栓塞和隐匿性DVT被记录为VTE阳性（VTE +）。在MBC患者中，比较有无癌症进展的患者对化疗的高凝反应。开始化疗后3个月评估了VTE的发生和癌症的进展。结果：在134例患者中，有10例（7.5％）发生了VTE（36例接受MBC缓解的MBC中有6例[17％]，接受缩小肿瘤的新辅助治疗的11例中有0例，接受辅助化疗的87例早期乳腺癌中的4例[5％] P = .06）。对化疗有反应的E-sel和VCAM-1水平降低（21例对化疗有反应的MBC患者的P d-二聚体（几何平均数）增加了36％，而在进展的15例中稳定下降了11％（第4天）结论：在乳腺癌化疗过程中，VECA被诱导，但这不是VTE的主要机制，化学诱导的细胞凋亡可能增强高凝性并引发VTE。

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