Underlying Mechanism of Portal Hypertensive Gastropathy in Cirrhosis: A Hemodynamic and Morphological Approach

A Hemodynamic and Morphological Approach

Lílian Amorim Curvêlo; Walnei Brabosa; Rachel Rhor; Valéria Lanzoni; Edison Roberto Parise; Angelo Paulo Ferrari; Mario Kondo

Disclosures

J Gastroenterol Hepatol. 2009;24(9):1541-1546. 

In This Article

Abstract and Introduction

Abstract

Background and Aim: Portal hypertensive gastropathy (PHG) is an important cause of bleeding in patients with cirrhosis associated with portal hypertension. Histologically, the condition is characterized by dilation of the mucosal and submucosal vessels of the stomach; however, its mechanisms remain unclear. The aim of the present cross-sectional study was to evaluate the role of portal and systemic hemodynamic features, humoral factors and hepatocellular function in the development and severity of PHG in patients with cirrhosis.
Methods: Forty-six patients with cirrhosis of different etiologies underwent endoscopy. Portal hypertension was evaluated by hepatic venous pressure gradient (HVPG). The gastric mucosa was analyzed using two diagnostic methods: endoscopy according to the McCormack criteria and histological by histomorphometric analysis.
Results: The prevalence of PHG according to the endoscopic and histomorphometric methods was 93.4% and 76.1%, respectively. There were no statistically significant differences in HVPG measurements between the patients with mild (16.0 ± 5.9 mmHg) and severe PHG (16.9 ± 6.5 mmHg; P = 0.80) or between patients who did not have (15.2 ± 8.0 mmHg) and those who had PHG (16.3 ± 5.7 mmHg). No correlation was found between the presence or severity of PHG and systemic vascular resistance index (P = 0.53 and 0.34, respectively), Child-Pugh classification (P = 0.73 and 0.78, respectively) or glucagon levels (P = 0.59 and 0.62, respectively).
Conclusions: The present data show no correlation between the presence or the severity of PHG and portal pressure, Child-Pugh classification or systemic hemodynamics, suggesting that other factors may be involved in the physiopathology of PHG, such as local gastric mucosal factors or other underlying factors.

Introduction

Portal hypertensive gastropathy (PHG) is a poorly understood complication resulting from portal hypertension syndrome. It is defined as a condition in which macroscopic alterations occur in the gastric mucosa, which are associated with mucosal and submucosal vascular ectasia in the absence of any histological evidence of an inflammatory process.

The clinical significance of this condition lies in its potential to lead to acute and chronic bleeding in patients with cirrhosis and portal hypertension, further aggravating hepatocellular function in these patients. The physiopathology of portal hypertensive gastropathy has yet to be fully clarified. Various studies have been carried out resulting in a wide diversity of hypotheses, the majority of them suggesting that increased pressure of the portal venous system, increased splanchnic blood flow and changes in the regulatory mechanism of the local vascular tonus are involved.

The increase in gastric blood flow is part of the generalized hemodynamic alterations that develop in these patients and some investigators have suggested a correlation between the severity of portal hypertensive gastropathy and increased gastric mucosa perfusion.[1] It is therefore probable that alterations occur in the regulatory mechanism of the vascular tonus of the stomach, triggered by the action of nitric oxide (NO), tumor necrosis factor alpha (TNF-α), endothelins, glucagon and prostaglandins, leading to the alterations in the gastric mucosa that are associated with portal hypertension.[1,2,3]

The aim of the present study was to evaluate the role of portal and systemic hemodynamic features, humoral factors and hepatocellular function in the development and severity of PHG in patients with cirrhosis.

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