High blood pressure induced by antiangiogenic therapy in the oncologic patient

Abstract

Introduction: high blood pressure is a multifactorial disease; there is a wide range of stimuli that can trigger it, including drugs. Objective: to describe the pathophysiological mechanisms involved in the development of hypertension induced by treatment with antiangiogenic drugs in oncological patients. Methods: a search for information was carried out in the PubMed/MEDLINE, SciELO and Scopus databases. Twenty-four bibliographic references were chosen. Development: the mechanisms of blood pressure elevation in patients treated with antiangiogenic agents are multifactorial. The mechanisms involved are not seen in isolation, but some are cause and/or effect of others. This interrelationship is shown during inhibition of vascular endothelial growth factor A, which is associated with a decrease in serum levels of nitric oxide metabolites, which triggers sodium retention and increased local and systemic blood pressure, showing changes in renal dynamics. Monitoring is necessary to allow early diagnosis and adequate treatment. This suggests that the use of appropriate antihypertensive drugs may be necessary for maintenance therapy to avoid dose interruption/discontinuation. Conclusions: there are several pathophysiological mechanisms related to the development of hypertension during treatment with antiangiogenic drugs such as induction of vascular endothelial growth factor A, variations in nitric oxide production, increased expression of pre-hypertensive agents such as endothelin-1, microvascular rare- fraction, activation of the renin-angiotensin system and oxidative stress.

Keywords

• hipertensión
• inhibidores de la angiogénesis
• endotelina-1
• factor a de crecimiento endotelial vascular
• neoplasias.