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Updated: Apr 15, 2026
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Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats
Published on: August 1, 2018
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[Portal hypertensive gastropathy]
T S Semenova1, E M Pal'tseva2, S B Zhigalova1
1Otdelenie ékstrennoĭ khirurgii i portal'noĭ gipertenzii.
Arkhiv Patologii
|April 7, 2015
Summary
Portal hypertensive gastropathy (PHG) lacks definitive diagnostic features. This review explores its pathogenesis, including endothelial dysfunction, apoptosis, damaging factors, and H. pylori infection, aiding differential diagnosis with GAVE syndrome.
Area of Science:
- Gastroenterology
- Pathology
- Hepatology
Background:
- Portal hypertensive gastropathy (PHG) presents diverse morphological changes, with no consensus on pathognomonic features.
- The pathogenesis of PHG involves multiple contributing mechanisms.
- Distinguishing PHG from Gastric Antral Vascular Ectasia (GAVE) syndrome is clinically important.
Purpose of the Study:
- To review and synthesize current literature on the pathogenesis of PHG.
- To elucidate the roles of endothelial dysfunction, apoptosis, damaging factors, and H. pylori infection in PHG development.
- To compare histological features of PHG and GAVE syndrome for differential diagnosis.
Main Methods:
- Comprehensive literature review on PHG pathogenesis.
- Analysis of data on endothelial dysfunction, apoptosis, damaging factors, and H. pylori.
- Comparative histological analysis between PHG and GAVE syndrome.
Main Results:
- Multiple factors contribute to PHG, including endothelial dysfunction and H. pylori.
- Apoptosis and damaging factors also play roles in PHG development.
- Distinct histological features aid in differentiating PHG from GAVE syndrome.
Conclusions:
- Understanding the multifactorial pathogenesis of PHG is crucial for accurate diagnosis.
- Histological examination is valuable for differential diagnosis between PHG and GAVE syndrome.
- Further research is needed to establish pathognomonic features for PHG.
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