A Clinical Study on the Pathogenesis of Portal Hypertensive Gastropathy

Abstract

We investigated the mechanisms for the development of portal hypertensive gastropathy (PHG) in patients with portal hypertension and liver cirrhosis on the basis of pathologic findings, tissue blood flow and amount of hexosamine in the gastric mucosa. We found histologic changes including congestion, vasodilatation in both arterioles and venules and interstitial edema, decreased tissue blood flow and decreased concentration of hexosamine in mucosal layer of upper part of the stomach. These changes were closely related to microcirculatory disturbance, and were correlated with the existence and the degree of PHG. Therefore, we speculate that not only secondary congestion (passive congestion) of gastric wall caused by portal hypertension and mucosal ischemia but primary congestion (active congestion) due to a hyperdynamic circulatory state in the submucosal layer may play important roles in the development of PHG. Furthermore, the decreased production of mucopolysaccharides which may disrupt the protective mechanisms of gastric mucosa may also be involved in the pathogenesis of PHG.