Effects of aspirin and Helicobacter pylori on the gastroduodenal mucosal permeability to sucrose

A. A. Rabassa, R. Goodgame, F. M. Sutton, C. N. Ou, C. Rognerud, D. Y. Graham

Research output: Contribution to journalArticle

45 Citations (Scopus)

Abstract

Background - A non-invasive marker is needed to identify patients with significant gastrointestinal injury due to non-steroidal anti-inflammatory drugs. Gastrointestinal permeability to sucrose has been suggested as such a test. Aims - To assess the utility of sucrose permeability as a marker of gastroduodenal mucosal injury after single and multiple doses of aspirin, to identify the site of increased sucrose permeability, to explore the relation between sucrose permeability and endoscopic findings, and to evaluate whether Helicobacter pylori infection influenced gastroduodenal sucrose permeability. Methods - After a fasting urine was obtained, 500 ml of a solution containing 100 g of sucrose was ingested. Urine was collected for five hours and assayed for sucrose by high performance liquid chromatography. Sucrose permeability was also assessed 20 minutes after ingestion of 650 mg of aspirin and eight to 12 hours after a 72 hour course of 650 mg aspirin four times a day. The site of increased permeability was identified after pyloric occlusion with a double balloon tube. Results - Thirty seven healthy volunteers participated. Sucrose permeability (mean (SEM)) increased after both single (195.2 (27) mg and multiple (196.4 (31) mg) doses of aspirin compared with baseline (53.7 (10) mg; p<0.0005). Balloon pyloric occlusion confirmed that the site of increased sucrose permeability was the stomach. The effect of aspirin on sucrose permeability was similar in those with and without H pylori infection. Conclusion - These results confirm the use of sucrose permeability as a marker of aspirin induced gastroduodenal mucosal injury and identify the stomach as the major site of increased permeability. H pylori infection does not seem to change gastric mucosal sucrose permeability either at baseline or after ingestion of aspirin.

Original languageEnglish (US)
Pages (from-to)159-163
Number of pages5
JournalGut
Volume39
Issue number2
StatePublished - 1996
Externally publishedYes

Fingerprint

Helicobacter pylori
Aspirin
Sucrose
Permeability
Stomach
Pylorus
Wounds and Injuries
Eating
Urine
Balloon Occlusion
Helicobacter Infections
Infection
Fasting
Healthy Volunteers
Anti-Inflammatory Agents
High Pressure Liquid Chromatography

Keywords

  • Aspirin
  • Gastric permeability
  • Helicobacter pylori
  • Intestinal permeability
  • Non-steroidal inflammatory drugs
  • Sucrose permeability

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Rabassa, A. A., Goodgame, R., Sutton, F. M., Ou, C. N., Rognerud, C., & Graham, D. Y. (1996). Effects of aspirin and Helicobacter pylori on the gastroduodenal mucosal permeability to sucrose. Gut, 39(2), 159-163.

Effects of aspirin and Helicobacter pylori on the gastroduodenal mucosal permeability to sucrose. / Rabassa, A. A.; Goodgame, R.; Sutton, F. M.; Ou, C. N.; Rognerud, C.; Graham, D. Y.

In: Gut, Vol. 39, No. 2, 1996, p. 159-163.

Research output: Contribution to journalArticle

Rabassa, AA, Goodgame, R, Sutton, FM, Ou, CN, Rognerud, C & Graham, DY 1996, 'Effects of aspirin and Helicobacter pylori on the gastroduodenal mucosal permeability to sucrose', Gut, vol. 39, no. 2, pp. 159-163.
Rabassa AA, Goodgame R, Sutton FM, Ou CN, Rognerud C, Graham DY. Effects of aspirin and Helicobacter pylori on the gastroduodenal mucosal permeability to sucrose. Gut. 1996;39(2):159-163.
Rabassa, A. A. ; Goodgame, R. ; Sutton, F. M. ; Ou, C. N. ; Rognerud, C. ; Graham, D. Y. / Effects of aspirin and Helicobacter pylori on the gastroduodenal mucosal permeability to sucrose. In: Gut. 1996 ; Vol. 39, No. 2. pp. 159-163.
@article{16b30bb9f4f44a02a3820e8768a29853,
title = "Effects of aspirin and Helicobacter pylori on the gastroduodenal mucosal permeability to sucrose",
abstract = "Background - A non-invasive marker is needed to identify patients with significant gastrointestinal injury due to non-steroidal anti-inflammatory drugs. Gastrointestinal permeability to sucrose has been suggested as such a test. Aims - To assess the utility of sucrose permeability as a marker of gastroduodenal mucosal injury after single and multiple doses of aspirin, to identify the site of increased sucrose permeability, to explore the relation between sucrose permeability and endoscopic findings, and to evaluate whether Helicobacter pylori infection influenced gastroduodenal sucrose permeability. Methods - After a fasting urine was obtained, 500 ml of a solution containing 100 g of sucrose was ingested. Urine was collected for five hours and assayed for sucrose by high performance liquid chromatography. Sucrose permeability was also assessed 20 minutes after ingestion of 650 mg of aspirin and eight to 12 hours after a 72 hour course of 650 mg aspirin four times a day. The site of increased permeability was identified after pyloric occlusion with a double balloon tube. Results - Thirty seven healthy volunteers participated. Sucrose permeability (mean (SEM)) increased after both single (195.2 (27) mg and multiple (196.4 (31) mg) doses of aspirin compared with baseline (53.7 (10) mg; p<0.0005). Balloon pyloric occlusion confirmed that the site of increased sucrose permeability was the stomach. The effect of aspirin on sucrose permeability was similar in those with and without H pylori infection. Conclusion - These results confirm the use of sucrose permeability as a marker of aspirin induced gastroduodenal mucosal injury and identify the stomach as the major site of increased permeability. H pylori infection does not seem to change gastric mucosal sucrose permeability either at baseline or after ingestion of aspirin.",
keywords = "Aspirin, Gastric permeability, Helicobacter pylori, Intestinal permeability, Non-steroidal inflammatory drugs, Sucrose permeability",
author = "Rabassa, {A. A.} and R. Goodgame and Sutton, {F. M.} and Ou, {C. N.} and C. Rognerud and Graham, {D. Y.}",
year = "1996",
language = "English (US)",
volume = "39",
pages = "159--163",
journal = "Gut",
issn = "0017-5749",
publisher = "BMJ Publishing Group",
number = "2",

}

TY - JOUR

T1 - Effects of aspirin and Helicobacter pylori on the gastroduodenal mucosal permeability to sucrose

AU - Rabassa, A. A.

AU - Goodgame, R.

AU - Sutton, F. M.

AU - Ou, C. N.

AU - Rognerud, C.

AU - Graham, D. Y.

PY - 1996

Y1 - 1996

N2 - Background - A non-invasive marker is needed to identify patients with significant gastrointestinal injury due to non-steroidal anti-inflammatory drugs. Gastrointestinal permeability to sucrose has been suggested as such a test. Aims - To assess the utility of sucrose permeability as a marker of gastroduodenal mucosal injury after single and multiple doses of aspirin, to identify the site of increased sucrose permeability, to explore the relation between sucrose permeability and endoscopic findings, and to evaluate whether Helicobacter pylori infection influenced gastroduodenal sucrose permeability. Methods - After a fasting urine was obtained, 500 ml of a solution containing 100 g of sucrose was ingested. Urine was collected for five hours and assayed for sucrose by high performance liquid chromatography. Sucrose permeability was also assessed 20 minutes after ingestion of 650 mg of aspirin and eight to 12 hours after a 72 hour course of 650 mg aspirin four times a day. The site of increased permeability was identified after pyloric occlusion with a double balloon tube. Results - Thirty seven healthy volunteers participated. Sucrose permeability (mean (SEM)) increased after both single (195.2 (27) mg and multiple (196.4 (31) mg) doses of aspirin compared with baseline (53.7 (10) mg; p<0.0005). Balloon pyloric occlusion confirmed that the site of increased sucrose permeability was the stomach. The effect of aspirin on sucrose permeability was similar in those with and without H pylori infection. Conclusion - These results confirm the use of sucrose permeability as a marker of aspirin induced gastroduodenal mucosal injury and identify the stomach as the major site of increased permeability. H pylori infection does not seem to change gastric mucosal sucrose permeability either at baseline or after ingestion of aspirin.

AB - Background - A non-invasive marker is needed to identify patients with significant gastrointestinal injury due to non-steroidal anti-inflammatory drugs. Gastrointestinal permeability to sucrose has been suggested as such a test. Aims - To assess the utility of sucrose permeability as a marker of gastroduodenal mucosal injury after single and multiple doses of aspirin, to identify the site of increased sucrose permeability, to explore the relation between sucrose permeability and endoscopic findings, and to evaluate whether Helicobacter pylori infection influenced gastroduodenal sucrose permeability. Methods - After a fasting urine was obtained, 500 ml of a solution containing 100 g of sucrose was ingested. Urine was collected for five hours and assayed for sucrose by high performance liquid chromatography. Sucrose permeability was also assessed 20 minutes after ingestion of 650 mg of aspirin and eight to 12 hours after a 72 hour course of 650 mg aspirin four times a day. The site of increased permeability was identified after pyloric occlusion with a double balloon tube. Results - Thirty seven healthy volunteers participated. Sucrose permeability (mean (SEM)) increased after both single (195.2 (27) mg and multiple (196.4 (31) mg) doses of aspirin compared with baseline (53.7 (10) mg; p<0.0005). Balloon pyloric occlusion confirmed that the site of increased sucrose permeability was the stomach. The effect of aspirin on sucrose permeability was similar in those with and without H pylori infection. Conclusion - These results confirm the use of sucrose permeability as a marker of aspirin induced gastroduodenal mucosal injury and identify the stomach as the major site of increased permeability. H pylori infection does not seem to change gastric mucosal sucrose permeability either at baseline or after ingestion of aspirin.

KW - Aspirin

KW - Gastric permeability

KW - Helicobacter pylori

KW - Intestinal permeability

KW - Non-steroidal inflammatory drugs

KW - Sucrose permeability

UR - http://www.scopus.com/inward/record.url?scp=0029815921&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029815921&partnerID=8YFLogxK

M3 - Article

C2 - 8977334

AN - SCOPUS:0029815921

VL - 39

SP - 159

EP - 163

JO - Gut

JF - Gut

SN - 0017-5749

IS - 2

ER -