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

Richard W. Goodgame, Hoda M. Malaty, Hala M T El-Zimaity, David Y. Graham

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Background. Gastric sucrose permeability is a noninvasive marker that reliably increases in association with gastrointestinal injury due to use of nonsteroidal antiinflammatory drugs. Despite the effect of Helicobacter pylori infection on the gastric mucosa, in a previous study we were unable to demonstrate that H. pylori infection was associated with abnormal gastric sucrose permeability. Our goal in this study was to explore further whether H. pylori infection changed gastric permeability; therefore, we evaluated the effect of treatment of H. pylori infection on gastric permeability to sucrose and the relation of sucrose permeability to density of polymorphonuclear leukocytes. Materials and Methods. Five hundred milliliters of a solution containing 100 gm of sucrose was ingested by the subject at bedtime. Overnight urine was collected and assayed for sucrose by high-performance liquid chromatography. Sucrose permeability was assessed both before and approximately 4 weeks after anti-H. pylon therapy. Results. Seventeen asymptomatic H. pylori-infected volunteers participated; 8 were cured. Sucrose permeability was in the range commonly found in normal controls both before and after anti-H. pylori therapy (mean excretion, 76.3 mg; range, 13-171 mg). Gastric sucrose permeability correlated with the density of polymorphonulcear cell infiltration of the mucosa. Cure of the H. pylori infection was associated with a small but significant decrease in sucrose permeability (98.8 ± 18 mg to 51.7 ± 9.8 mg (p = .01). Sucrose permeability was greater in those with a high density of mucosal polymorphonuclear cells compared to those with lower scores (119.5 ± 4 vs 71.4 ± 13 for those with scores ≥ 5 compared to scores ≤ 4; p = .023). Failed therapy resulted in an increase in the mucosal density of polymorphonuclear infiltration and sucrose permeability (56.4 ± 13 mg-99.7 ± 19 mg pretreatment vs posttreatment, respectively; p = .031). Conclusion. H. pylori gastritis causes a small but measurable increase in gastric permeability to sucrose that may reflect epithelial transmigration of neutrophils.

Original languageEnglish (US)
Pages (from-to)44-47
Number of pages4
JournalHelicobacter
Volume2
Issue number1
StatePublished - 1997
Externally publishedYes

Fingerprint

Helicobacter Infections
Helicobacter pylori
Sucrose
Permeability
Stomach
Neutrophils
Gastritis
Therapeutics
Gastric Mucosa
Volunteers
Mucous Membrane
Anti-Inflammatory Agents
Cell Count
High Pressure Liquid Chromatography
Urine

Keywords

  • Therapy
  • Transmigration

ASJC Scopus subject areas

  • Microbiology
  • Gastroenterology

Cite this

Goodgame, R. W., Malaty, H. M., El-Zimaity, H. M. T., & Graham, D. Y. (1997). Decrease in gastric permeability to sucrose following cure of Helicobacter pylori infection. Helicobacter, 2(1), 44-47.

Decrease in gastric permeability to sucrose following cure of Helicobacter pylori infection. / Goodgame, Richard W.; Malaty, Hoda M.; El-Zimaity, Hala M T; Graham, David Y.

In: Helicobacter, Vol. 2, No. 1, 1997, p. 44-47.

Research output: Contribution to journalArticle

Goodgame, RW, Malaty, HM, El-Zimaity, HMT & Graham, DY 1997, 'Decrease in gastric permeability to sucrose following cure of Helicobacter pylori infection', Helicobacter, vol. 2, no. 1, pp. 44-47.
Goodgame RW, Malaty HM, El-Zimaity HMT, Graham DY. Decrease in gastric permeability to sucrose following cure of Helicobacter pylori infection. Helicobacter. 1997;2(1):44-47.
Goodgame, Richard W. ; Malaty, Hoda M. ; El-Zimaity, Hala M T ; Graham, David Y. / Decrease in gastric permeability to sucrose following cure of Helicobacter pylori infection. In: Helicobacter. 1997 ; Vol. 2, No. 1. pp. 44-47.
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AB - Background. Gastric sucrose permeability is a noninvasive marker that reliably increases in association with gastrointestinal injury due to use of nonsteroidal antiinflammatory drugs. Despite the effect of Helicobacter pylori infection on the gastric mucosa, in a previous study we were unable to demonstrate that H. pylori infection was associated with abnormal gastric sucrose permeability. Our goal in this study was to explore further whether H. pylori infection changed gastric permeability; therefore, we evaluated the effect of treatment of H. pylori infection on gastric permeability to sucrose and the relation of sucrose permeability to density of polymorphonuclear leukocytes. Materials and Methods. Five hundred milliliters of a solution containing 100 gm of sucrose was ingested by the subject at bedtime. Overnight urine was collected and assayed for sucrose by high-performance liquid chromatography. Sucrose permeability was assessed both before and approximately 4 weeks after anti-H. pylon therapy. Results. Seventeen asymptomatic H. pylori-infected volunteers participated; 8 were cured. Sucrose permeability was in the range commonly found in normal controls both before and after anti-H. pylori therapy (mean excretion, 76.3 mg; range, 13-171 mg). Gastric sucrose permeability correlated with the density of polymorphonulcear cell infiltration of the mucosa. Cure of the H. pylori infection was associated with a small but significant decrease in sucrose permeability (98.8 ± 18 mg to 51.7 ± 9.8 mg (p = .01). Sucrose permeability was greater in those with a high density of mucosal polymorphonuclear cells compared to those with lower scores (119.5 ± 4 vs 71.4 ± 13 for those with scores ≥ 5 compared to scores ≤ 4; p = .023). Failed therapy resulted in an increase in the mucosal density of polymorphonuclear infiltration and sucrose permeability (56.4 ± 13 mg-99.7 ± 19 mg pretreatment vs posttreatment, respectively; p = .031). Conclusion. H. pylori gastritis causes a small but measurable increase in gastric permeability to sucrose that may reflect epithelial transmigration of neutrophils.

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