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.