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Acute blood pressure elevation associated with biological therapies for cancer: a focus on VEGF signaling pathway inhibitors.

Authors :
Pucci G
Milan A
Paini A
Salvetti M
Cerasari A
Vaudo G
Source :
Expert opinion on biological therapy [Expert Opin Biol Ther] 2019 May; Vol. 19 (5), pp. 433-442. Date of Electronic Publication: 2019 Apr 08.
Publication Year :
2019

Abstract

Introduction: Treatment with biological agents interfering with mechanisms of angiogenesis, such as vascular endothelial growth factor (VEGF) signaling pathway (VSP) inhibitors, was associated with an enhanced risk of acute and severe blood pressure (BP) increase and development of hypertensive emergencies. Areas covered: The present article will review the scientific literature reporting hypertensive emergencies as a complication of biological treatment with VSP inhibitors. Hypertensive emergency is a life-threatening condition characterized by very high BP values (>180/110 mmHg) associated with acute organ damage. The exact mechanism of action is still incompletely clarified. Endothelial dysfunction following reduced bioavailability of nitric oxide has been hypothesized to play an important role in promoting hypertension and the occurrence of acute organ damage. Expert opinion: Prevention, prompt recognition and treatment of hypertensive emergencies associated with treatment with VSP-inhibitors are essential to reduce the risk of adverse events. Not infrequently, the occurrence of hypertensive emergency led to VSP treatment discontinuation, with potential negative consequences on patient overall survival. The present review aims at providing detailed knowledge for the clinician regarding this specific issue, which could be of high impact in usual clinical practice, given the increasing burden of indications to treatment with biological agents targeted to the VEGF pathway.

Details

Language :
English
ISSN :
1744-7682
Volume :
19
Issue :
5
Database :
MEDLINE
Journal :
Expert opinion on biological therapy
Publication Type :
Academic Journal
Accession number :
30888868
Full Text :
https://doi.org/10.1080/14712598.2019.1594770