VEGFR-TKIs 在癌症治疗中的高血压毒性:发生率、机制和管理策略。
Hypertension toxicity of VEGFR-TKIs in cancer treatment: incidence, mechanisms, and management strategies.
发表日期:2024 Sep 30
作者:
Yan-Xi Du, Xu Li, Si-Wen Ji, Na Niu
来源:
ARCHIVES OF TOXICOLOGY
摘要:
血管内皮生长因子受体酪氨酸激酶抑制剂(VEGFR-TKI)是一类靶向抗癌药物,包括帕唑帕尼、舒尼替尼、阿西替尼等。目前,VEGFR-TKIs广泛应用于多种肿瘤的临床治疗,可以延长患者的生存期,甚至治愈肿瘤。然而,VEGFR-TKIs 的使用经常与心血管不良事件的发生相关,其中高血压是最常见的。高血压及其并发症可显着影响患者的预后,可能危及患者的生命,严重时会导致治疗减少甚至停止。本综述讨论了 VEGFR-TKIs 引起的高血压发病率、毒性机制、管理策略和未来研究方向。此外,VEGFR-TKIs引起的高血压可能与盐敏感性有关,高血压副作用的可能机制是血管舒张剂失衡、毛细血管密度降低、肾损伤、氧化应激导致的内皮功能受损、淋巴管密度降低和“关闭”。 ——目标效应”。全面了解 VEGFR-TKI 癌症治疗引起的高血压毒性,可以增强临床实践,从而改善肿瘤患者 VEGFR-TKI 的预后结果。© 2024。作者获得 Springer-Verlag GmbH 独家许可德国,施普林格自然的一部分。
Vascular endothelial growth factor receptor tyrosine kinase inhibitors (VEGFR-TKIs) are a class of targeted anticancer agents that include pazopanib, sunitinib, axitinib, and others. Currently, VEGFR-TKIs are widely used in the clinical treatment of various tumors, which can prolong patients' survival and even cure tumors. However, the use of VEGFR-TKIs is frequently associated with the occurrence of cardiovascular adverse events, with hypertension being the most prevalent. Hypertension and its complications can significantly impact the prognosis of patients, potentially jeopardizing their lives and resulting in the reduction or even cessation of treatment in severe cases. This review addresses the incidence of hypertension due to VEGFR-TKIs, mechanisms of toxicity, management strategies, and future research directions. In addition, hypertension due to VEGFR-TKIs may be associated with salt sensitivity, and possible mechanisms of hypertensive side effects are vasodilator imbalance, decreased capillary density, renal injury, impaired endothelial function due to oxidative stress, decreased lymphatic vascular density, and "off-target effect". A comprehensive understanding of hypertension toxicity due to cancer treatment with VEGFR-TKIs, can enhance clinical practice, thereby improving the prognostic outcomes of VEGFR-TKIs in oncology patients.© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.