Related Experiment Video
Updated: Oct 23, 2025

Invasive Hemodynamic Characterization of the Portal-hypertensive Syndrome in Cirrhotic Rats
Published on: August 1, 2018
Differences between sporadic hyperplastic gastric polyps and portal hypertensive gastric polyps: a review
Lucile Héroin1, Antonio Saviano1,2,3, Tanguy Fenouil4
1Gastroenterology and Hepatology Unit, Hôpitaux Universitaires de Strasbourg.
Abstract:
Portal hypertension (PH) is one of the most severe complications of chronic liver diseases. It is defined as an increase in pressure in the portal venous system which results in a portosystemic gradient >5 mmHg. In the western world, cirrhosis is the most frequent cause of PH, mainly due to nonalcoholic fatty liver disease and alcoholic liver disease. Patients with PH have esophageal varices in 68-73% of cases, portal hypertensive gastropathy in 51-73% and hyperplastic polyps (HPs) in 0.9-2%. Recent studies have shown that HPs found in PH patients are different from classical HPs. They constitute a new entity called portal hypertensive polyps (PHPs). The main difference between sporadic HPs and PHP is the presence of larger and more numerous vascular capillaries in the lamina propria. The clinical course of PHPs is unknown. Their physiopathology seems different from HPs: the increased congestion caused by higher portal pressure in the stomach may induce capillaries proliferation and neoangiogenesis. PHPs may be responsible for symptoms, such as pyloric obstruction, iron deficiency and anemia. Their prevalence in portal hypertensive and cirrhotic patients is from 1% to 8%. PHPs can be single or numerous, in the antrum or the gastric corpus. Their size ranges from 2 to 3 cm. PHPs seem to disappear or shrink with the treatment of PH. They should be resected in case of symptom and if >10 mm, after Helicobacter pylori eradication if present. However, their recurrence is frequent (40-79%), thus surveillance endoscopy is mandatory, at the same time as esophageal varices.
More Related Videos
Related Concept Videos
Esophageal Varices-I: Introduction
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Gastritis-I: Introduction and Types
Acute gastritis presents as a sudden inflammation triggered by various stressors to the stomach lining, such as exposure to corrosive agents, local irritants like aspirin and other NSAIDs, alcohol consumption, radiation therapy, physical trauma, severe burns, sepsis,...
Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
Esophageal Varices-II: Clinical Features and Management
In the initial assessment, a thorough review of the patient's medical history is vital to identify risk factors such as liver disease, alcohol...

