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Mechanisms of hypertension associated with BAY 43-9006

Maria Luisa Veronese1, Ari Mosenkis, Keith T Flaherty

  • 1Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA 19104, USA.

Journal of Clinical Oncology : Official Journal of the American Society of Clinical Oncology
|February 1, 2006
PubMed
Abstract

Insights

Sorafenib (BAY 43-9006) treatment significantly increases blood pressure (BP) in patients. This hypertension is sustained, and vascular stiffness increases, with no clear role for measured circulating factors.

Area of Science:

  • Oncology
  • Pharmacology
  • Cardiovascular Medicine

Background:

  • BAY 43-9006 (sorafenib) is a targeted therapy inhibiting Raf kinase and VEGF receptor-2.
  • Sorafenib is known to affect angiogenesis in tumor xenografts.
  • Understanding its impact on patient physiology, particularly blood pressure, is crucial.

Purpose of the Study:

  • To investigate the incidence, severity, and mechanism of blood pressure elevation in patients treated with BAY 43-9006.
  • To assess the relationship between sorafenib therapy and changes in blood pressure.
  • To explore potential contributing factors to sorafenib-induced hypertension.

Main Methods:

  • Twenty patients received BAY 43-9006 (400 mg orally twice daily).
  • Blood pressure and heart rate were monitored every 3 weeks for 18 weeks.
  • Vascular stiffness, VEGF, catecholamines, and other humoral factors were assessed at various time points.

Main Results:

  • 75% of patients experienced a systolic blood pressure increase of >= 10 mmHg, and 60% saw an increase of >= 20 mmHg after 3 weeks.
  • Significant increases in vascular stiffness were observed during the study period.
  • No significant changes in measured humoral factors were found, though a potential inverse relationship between catecholamines and SBP was noted.

Conclusions:

  • BAY 43-9006 treatment is associated with significant and sustained blood pressure elevation.
  • The observed hypertension appears independent of major circulating humoral factors.
  • Increased vascular stiffness may contribute to sorafenib-induced hypertension.

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