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Related Experiment Videos

Decrease in gastric permeability to sucrose following cure of Helicobacter pylori infection

R W Goodgame1, H M Malaty, H M el-Zimaity

  • 1Department of Medicine, Veterans Affairs Medical Center, Houston, TX 77030, USA.

Helicobacter
|March 1, 1997
PubMed
Summary

Helicobacter pylori infection slightly increases gastric sucrose permeability, which decreases after successful treatment. This change correlates with neutrophil infiltration in the gastric mucosa.

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Area of Science:

  • Gastroenterology
  • Infectious Diseases
  • Pathophysiology

Background:

  • Gastric sucrose permeability is a validated marker for gastrointestinal injury, particularly from NSAIDs.
  • Previous studies did not link Helicobacter pylori (H. pylori) infection to abnormal gastric sucrose permeability.
  • H. pylori infection impacts the gastric mucosa, necessitating further investigation into its effect on gastric permeability.

Purpose of the Study:

  • To investigate if H. pylori infection alters gastric permeability to sucrose.
  • To evaluate the impact of H. pylori eradication therapy on gastric sucrose permeability.
  • To determine the relationship between gastric sucrose permeability and the density of polymorphonuclear leukocytes in the gastric mucosa.

Main Methods:

  • Subjects ingested a sucrose solution, and overnight urine was collected.

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  • Gastric sucrose permeability was measured using high-performance liquid chromatography before and after H. pylori treatment.
  • Polymorphonuclear leukocyte density in gastric biopsies was assessed.

    • Main Results:

    • Successful H. pylori eradication led to a significant decrease in gastric sucrose permeability.
    • Gastric sucrose permeability positively correlated with the density of mucosal polymorphonuclear cell infiltration.
    • Failed H. pylori therapy was associated with increased polymorphonuclear infiltration and sucrose permeability.

    Conclusions:

    • H. pylori gastritis induces a measurable increase in gastric sucrose permeability.
    • This increase in permeability may be attributed to neutrophil transmigration across the gastric epithelium.
    • H. pylori eradication therapy can reverse the observed changes in gastric permeability.