Portal Hypertensive Gastropathy and Gastric Antral Vascular Ectasia.
10.4166/kjg.2010.56.3.186
- Author:
Won Hyeok CHOE
1
Author Information
1. Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea. 20050101@kuh.ac.kr
- Publication Type:Review ; English Abstract
- Keywords:
Gastric antral vascular ectasia;
Liver cirrhosis;
Hypertension, Portal;
Portal hypertensive gastropathy
- MeSH:
Esophageal and Gastric Varices/*diagnosis/etiology/therapy;
Gastric Antral Vascular Ectasia/*diagnosis/etiology/therapy;
Gastric Mucosa/metabolism/pathology;
Humans;
Hypertension, Portal/*complications;
Portasystemic Shunt, Transjugular Intrahepatic;
Vasodilator Agents/therapeutic use
- From:The Korean Journal of Gastroenterology
2010;56(3):186-191
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Portal hypertensive gastropathy (PHG) is a term used to define the endoscopic findings of gastric mucosa with a characteristic mosaic-like pattern with or without red spots, and a common finding in patients with portal hypertension. These endoscopic findings correspond to dilated mucosal capillaries without inflammation. The pathogenesis of PHG in not well known, but portal hypertension and some humoral factors seem to be crucial factors for its development. Pharmacological (e.g. propranolol), or interventional radiological (such as transjugular intrahepatic portosystemic shunt) procedures may be useful in preventing re-bleeding from PHG. The classic features of gastric antral vascular ectasia (GAVE) syndrome include red, often haemorrhagic lesions predominantly located in the gastric antrum which can result in significant blood loss. Although the pathogenesis of GAVE is not clearly defined, it seems to be a separate disease entity from PHG, because GAVE generally does not respond to a reduction of portal pressures. Endoscopic ablation (such as argon plasma coagulation) is the first-line treatment of choice. This review will focus on the incidence, clinical importance, etiology, pathophysiology, and treatment of PHG and GAVE syndrome in the setting of portal hypertension.
