Gastroduodenal Lesions Associated with Portal Hypertension: An Extensive Review

Abstract

The block of the portal flow by obstacles in prehepatic, hepatic or posthepatic site and alterations of the splanchnic blood flow are the pathological conditions that lead to portal hypertension. The portal hypertension can cause also others gastroduodenal lesions, potentially hemorrhagic, in addition to esophageal varices commonly developed and habitual source of bleeding in these patients. The gastroduodenal lesions associated with portal hypertension, usually encountered in the clinical practice, are portal hypertensive gastropaty, gastric antral vascular ectasia, gastric and duodenal ulcer, isolated gastric varices. The pathophysiology and clinical, diagnostic and therapeutic features of these lesions are examined.

Spectrum of gastric Lesions in Portal Hypertension and Its Association with H. Pylori

“…Eventually, the gastric mucosa becomes more prone to injury by noxious agents such as non-steroidal anti-inflammatory drugs and H. pylori, ending up with erosions, ulcers, and bleeding. 5,9 In our study, we reported the spectrum of lesions of gastric mucosa by endoscopy and histopathology in patients with portal hypertension and correlate these findings to upper gastrointestinal (GI) bleeding. WLE is the diagnostic modality for gastric mucosal lesions.…”

“…Mucosal barrier weakening produced by portal hypertension-related mucosal hemodynamic alterations and exposure to noxious substances can be described as two key contributors. 5 Helicobacter pylori (H. pylori), a spiral gramnegative bacteria that is resistant to gastric juice, infects roughly 50 -70 % of the world population, with the highest frequency in low-income areas. It was found to exacerbate local gastric inflammatory response through release of inflammatory cytokines resulting in a wide range of gastric pathologies.…”

Gastric Microvasculature in Portal Hypertension

“…There are studies that reported decreased mucosal blood flow [21][22][23][24], similarly there are others who reported the reverse [25][26][27][28][29]. Severity of histological and gross morphological changes are related to degree and duration of portal hypertension [30][31][32]. Altered gastric haemodynamics possibly induce activation of various cytokines and growth factors.…”

“…Altered gastric haemodynamics possibly induce activation of various cytokines and growth factors. Gastric mucosa in PHG is reported to contain increased vascular endothelial growth factor [32,33]. Tumour necrosis factor is implicated to play a major role in the pathogenesis of PHG for increase blood to gastric mucosa by stimulating nitric oxide (NO) production by inducing NO synthase.…”

“…Tumour necrosis factor is implicated to play a major role in the pathogenesis of PHG for increase blood to gastric mucosa by stimulating nitric oxide (NO) production by inducing NO synthase. Administration of antitumour necrosis factor-alpha normalizes gastric blood flow [32]. Compromised gastric mucosa is more susceptible to any form of mucosal injury to any noxious substance including bile acids and NSAIDs [34,35].…”