Role of vascular endothelial growth factor in portal hypertensive gastropathy

Citation
K. Tsugawa et al., Role of vascular endothelial growth factor in portal hypertensive gastropathy, DIGESTION, 61(2), 2000, pp. 98-106
Citations number
50
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
DIGESTION
ISSN journal
00122823 → ACNP
Volume
61
Issue
2
Year of publication
2000
Pages
98 - 106
Database
ISI
SICI code
0012-2823(2000)61:2<98:ROVEGF>2.0.ZU;2-S
Abstract
Background and Aims: Portal hypertensive gastropathy (PHG) is now recognize d as a distinct entity; however, the angiogenesis in the portal hypertensiv e gastric mucosa has yet to be elucidated. Vascular endothelial growth fact or (VEGF) is a potent angiogenic factor involved in both physiological and pathological angiogenesis. The aim of this study was thus to examine the fu nction of VEGF in the portal hypertensive and non-portal hypertensive gastr ic mucosa. Method: Forty-five cirrhotic patients were divided into 3 groups as follows. Group I included 15 patients without PHG who were treated with 1.5 g teprenone/day for 8 weeks: PHG(-)-t. Group II included 15 patients w ith PHG who were not treated with teprenone: PHG(+)-n. Group III included 1 5 patients with PHG who were treated with teprenone for 8 weeks: PGH(+)t. T he gastric mucosal blood flow (GMBF), the concentration of gastric mucosal VEGF and hexosamine and the endoscopic findings were studied both before an d after medication. Results: Before teprenone treatment, the GMBF in the an trum, fundus, fornix were significantly higher in PHG(+)-n than PHG(-)-t. A fter treatment, the GMBF in the fundus and fornix significantly decreased m ore than before treatment in the PHG(+)-t After treatment, the GMBF in the antrum increased significantly more than before treatment in PHG(-)-t. The gastric VEGF and hexoxamine concentration in the antrum were significantly higher in PHG(+)-n than in PHG(-)-t. After treatment, the gastric VEGF and hexosamine concentration in the antrum significantly decreased in PHG(+)-t while no change in concentration was recognized in PHG(+)-n. In the endosco pic findings, a decrease in the PHG score was recognized in 2 patients in P HG(+)-t. Conclusion: Portal hypertensive gastric mucosal change was thus fo und to trigger a high concentration of VEGF and hexosamine. Such increased activity of VEGF and hexosamine may thus account for the presence of active congestion in PHG. Copyright (C) 2000 S. Karger AG, Basel.