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Updated: Dec 28, 2025

An Intravital Microscopy-Based Approach to Assess Intestinal Permeability and Epithelial Cell Shedding Performance
Published on: December 3, 2020
Functional study of the gastric mucosal barrier in hepatic cirrhosis
Insights
Patients with hepatic cirrhosis show increased back-diffusion of chloride (Cl-) and hydrogen (H+) ions across the gastric wall. This suggests an impaired gastric mucosal barrier in cirrhosis, potentially linked to observed histological changes.
Area of Science:
- Gastroenterology
- Hepatic Cirrhosis Research
- Gastric Physiology
Background:
- Hepatic cirrhosis can lead to systemic complications affecting various organs.
- The integrity of the gastric mucosal barrier is crucial for maintaining gastric health.
- Alterations in gastric ionic flux may indicate mucosal damage.
Purpose of the Study:
- To investigate the net ionic flux across the gastric wall in patients with hepatic cirrhosis.
- To compare ionic flux in cirrhotic patients with healthy controls.
- To correlate ionic flux findings with histological examination of the gastric mucosa.
Main Methods:
- Measurement of net ionic flux (Cl-, H+, Na+) through the gastric wall.
- Comparison between eleven patients with hepatic cirrhosis and five normal controls.
- Gastric biopsy for histological assessment of mucosal integrity.
Main Results:
- Significantly increased back-diffusion of chloride (Cl-) and hydrogen (H+) ions in the cirrhotic group.
- Nine out of eleven cirrhotic patients exhibited H+ loss exceeding normal limits.
- Histological findings included vasodilatation, edema, mucosal hemorrhage, and epithelial desquamation in cirrhotic patients.
Conclusions:
- Patients with hepatic cirrhosis demonstrate an elevated loss of H+ and Cl- across the gastric wall.
- The observed ionic flux abnormalities, coupled with histological evidence of mucosal damage, suggest a compromised gastric mucosal barrier in hepatic cirrhosis.
Abstract:
The net ionic flux through the gastric wall was determined in eleven patients with hepatic cirrhosis and five normal controls. The back-diffusion of C1- and H+ was significantly increased in the cirrhotic group. In nine patients of this group the H+ loss was above the upper limits of normal. The Na+ flux was positive in both the control and the cirrhotic group. The Na+ flux towards the gastric cavity in the cirrhotic patients was not proportional to the loss of H+. Vasodilatation and edema of the lamina propria was always present as judged by gastric biopsy; in five cases mucosal hemorrhage was observed, in three superficial epithelial desquamation and in one melaena due to hemorrhagic gastritis. One the basis of the increase in H+ loss and the histological findings, we suspect an alteration in the gastric mucosal barrier in the patients with hepatic cirrhosis.
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