دورية أكاديمية

血管内皮生长因子及其受体抑制剂相关性高血压病理生理机制 及临床诊疗的研究进展.

التفاصيل البيبلوغرافية
العنوان: 血管内皮生长因子及其受体抑制剂相关性高血压病理生理机制 及临床诊疗的研究进展. (Chinese)
Alternate Title: Research progress in pathophysiological mechanism and clinical diagnosis and treatment of hypertension associated with vascular endothelial growth factor and its receptor inhibitors. (English)
المؤلفون: 张 莉, 夏彬凤, 黄慧慧, 王 茹, 孔 敏, 尹 霞
المصدر: Journal of Jilin University (Medicine Edition); May2024, Vol. 50 Issue 3, p854-863, 10p
Abstract (English): Cancer therapy-related cardiovascular toxicity (CTR-CVT) is gradually becoming a critical factor affecting the prognosis of cancer survivors. Vascular endothelial growth factor (VEGF) and its receptor inhibitors (VEGFIs), developed as novel anti-cancer drugs targeting VEGF, are now widely used in clinical practice. They can extend the survival period of the cancer patients and improve the prognosis of the patients. However, the hypertension induced by VEGFIs, as the most common CTR-CVT, may limit and impact their use and leads to severe cardiovascular diseases (CVD). It is essential to closely monitor blood pressure in the cancer patients treated with VEGFIs, conduct early assessments, and optimize the management to achieve the best anti-cancer efficacy and minimize the risk of CTR-CVT. This review discusses the clinical manifestations, pathogenesis, diagnosis, and treatment strategies of VEGFIs-related hypertension, in order to provide better guidances for managing and addressing VEGFIs-related hypertension for the clinicians. [ABSTRACT FROM AUTHOR]
Abstract (Chinese): 肿瘤治疗相关心血管毒性 (CTR-CVT) 逐渐成为影响肿瘤幸存者预后的关键因素。以血 管内皮生长因子 (VEGF) 为靶点研发的 VEGF 及其受体抑制剂 (VEGFIs) 作为新型抗肿瘤药物现 已广泛应用于临床, 可延长肿瘤患者的生存周期, 改善患者预后, 但 VEGFIs 诱导的高血压作为其最 常见的 CTR-CVT, 可能会限制和影响其应用并引起严重心血管疾病 (CVD)。对应用 VEGFIs 治疗 的 肿 瘤 患 者 应 密 切 监 测 血 压, 早 期 评 估, 优 化 管 理, 使 患 者 获 得 最 佳 的 抗 肿 瘤 疗 效 和 最 低 的 CTRCVT 风险。现就 VEGFIs 相关性高血压的临床表现、发病机制、诊断和治疗策略进行综述, 旨在为临 床医生更好地管理和应对 VEGFIs 相关性高血压提供参考。 [ABSTRACT FROM AUTHOR]
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قاعدة البيانات: Complementary Index
الوصف
تدمد:1671587X
DOI:10.13481/j.1671-587X.20240333