Published online Feb 8, 2016. doi: 10.4254/wjh.v8.i4.231
Peer-review started: October 4, 2015
First decision: November 4, 2015
Revised: November 30, 2015
Accepted: January 16, 2016
Article in press: January 19, 2016
Published online: February 8, 2016
Core tip: Portal hypertensive gastropathy (PHG) is diagnosed by characteristic endoscopic findings of variably erythematous, small, polygonal areas surrounded by a whitish, reticular border in a mosaic pattern in the gastric fundus/body in a patient with portal hypertension of any etiology. The pathophysiology of PHG is inadequately understood. Portal hypertension is a prerequisite to develop PHG. PHG increases in frequency with increasing portal hypertension, liver disease progression, duration of liver disease, presence of esophageal varices, and endoscopic variceal obliteration. Pathogenesis is related to a hyperdynamic circulation induced by portal hypertension. Gastric mucosa in PHG exhibits greater susceptibility to gastrotoxic chemicals and poor wound healing. Acute or chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate and rarely fatal. Endoscopic therapy is rarely useful. Pharmacotherapy for acute bleeding includes octreotide with concomitant proton-pump-inhibitor therapy, or alternatively vasopressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent re-bleeding after acute bleeding or for chronic bleeding. Transjugular-intrahepatic-portosystemic-shunt and liver transplantation is ultimate therapies because they treat the underlying portal hypertension.