← 返回

重新发现多发性骨髓瘤中的止血异常:新时代

英文原题:Rediscovering hemostasis abnormalities in multiple myeloma: The new era.

查看英文原题

Rediscovering hemostasis abnormalities in multiple myeloma: The new era.

PubMed 2024/07/04(内容时间) Heliyon

分数与星级只用于站内排序 —— 不代表疗效、安全性或个人适用性。

中文摘要

多发性骨髓瘤(MM)是一种由克隆性浆细胞异常增殖引起的恶性肿瘤。其发生出血和血栓并发症的风险较高,这与不良预后和生存期缩短相关。多种因素参与止血平衡的破坏,包括疾病特异性因素、患者特异性因素以及改变促凝、抗凝和纤溶的药物因素。近年来,随着单克隆抗体、嵌合抗原受体修饰T细胞疗法、针对BCMA的抗体药物偶联物、programmed death-1抑制剂、export protein 1抑制剂、组蛋白去乙酰化酶抑制剂、免疫调节药物、蛋白酶体抑制剂和Bcl-2抑制剂等新疗法的引入,MM患者的治疗进入了新时代。此外,这引发了一个问题,即这些新疗法是否会改变MM患者的止血平衡,这凸显了MM止血异常潜在病理生理机制及预防策略的重要性。在这篇综述中,我们更新了MM止血异常的机制、新药对止血平衡的影响以及可靠的治疗策略。

展开英文摘要原文

Multiple myeloma (MM) is a malignancy arisen from the abnormal proliferation of clonal plasma cells. It has a high risk of developing bleeding and thrombotic complications, which are related to poor prognosis and decreased survival. Multiple factors are involved in the breaking of the hemostasis balance, including disease specific factors, patient-specific factors, and drug factors that change pro-and anticoagulant and fibrinolysis.

Recently, with the introduction of new treatments such as monoclonal antibodies, chimeric antigen receptor modified T-cell therapy, antibody-drug conjugates directed against BCMA, programmed death-1 inhibitor, export protein 1 inhibitors, histone deacetylase inhibitors, immunomodulatory drugs, proteasome inhibitors and Bcl-2 inhibitors, the therapy of MM patients has entered into a new era.

Furthermore, it arouses a question whether these new treatments would alter the hemostasis balance in MM patients, which highlights the importance of the underlying pathophysiology of hemostasis abnormalities in MM, and on prophylaxis approaches. In this review, we updated the mechanisms of hemostasis abnormalities in MM, the impact of the new drugs on hemostasis balance and reliable therapeutic strategies.

论文信息

作者
Huang Y、Wang C、Wang H、Liu H、Zhou L
单位
Department of Hematology, Affiliated Hospital of Nantong University, Jiangsu, 226001, China.China
文献类型
综述
期刊
Heliyon2024 Jul 15
原文标识
PubMed 39055831 · DOI 10.1016/j.heliyon.2024.e34111