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Updated: Aug 20, 2026

Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats
Published on: August 1, 2018
Portal hypertensive gastropathy (PHG)
Rusmir Mesihovic1, Dzanela Prohic, Mehmed Gribajcevic
1Gastroenterohepatology Clinical, Clinical Centre University of Sarajevo, Bosnia and Herzegovina. SMIR@HOTMAIL.COM
Abstract:
Portal hypertenisive gastropathy (PHG) and GAVE syndrome are recently discovered entities who can be associated with bloodloss from gastrointestinal tract at patients with or without liver cirrhosis. PHG will be developed at 65% of patients with portal hypertension caused by liver cirrhosis but it could be developed at portal hypertension which is not caused by the liver cirrhosis. PHG is often assosiated with portal hypertension patients and presence of esofageal and /or gastric varices. Mechanism of pathogenesis PHG is still not completely cleared up, but regulation of gastric nitric oxide level, postaglandins, tumor necrosis factor (TNF) and epidermal growth factor production could be important factors in development of portal hypertensive gastropathy. Mechanisms who participate in originating of Gastric Antral Vascular Ectasia (GAVE) are also not completly clear. Classic characteristics of this syndrome are red, often haemorrhagic lesions most often located in stomach antrum, and who could result in blood loss. More than 70% of patients with GAVE syndrome have no cirrhosis or portal hypertension. But when liver cirrhosis is present, it is very difficult to make difference between GAVE and PHG. This review will be focused on incidence, clinical importance, etiology, pathofisiology and treatment of PHG, and how to differentiate between GAVE syndrom and PHG in a case that there exists.
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