Tags

Type your tag names separated by a space and hit enter

Role of Helicobacter pylori infection in gastroduodenal injury and gastric prostaglandin synthesis during long term/low dose aspirin therapy: a prospective placebo-controlled, double-blind randomized trial.
Am J Gastroenterol. 2001 Jun; 96(6):1751-7.AJ

Abstract

OBJECTIVES

Whether gastric infection with Helicobacter pylori increases the risk of gastric mucosal injury during long term/low dose aspirin therapy is unknown. We examined whether H. pylori infection enhances upper GI mucosal damage, assessed endoscopically, in volunteers given low dose aspirin. We studied 61 healthy men and women, 29 with and 32 without active H. pylori infection.

METHODS

We treated volunteers for 45 days with a placebo or aspirin (either 81 mg every day or 325 mg every 3 days). Gastroduodenal mucosal damage was then assessed by endoscopy, as was gastric histology and ex vivo gastric mucosal prostaglandin E2 and F2alpha synthesis rates.

RESULTS

Erosive disease from low dose aspirin (erosions and/or ulcers) occurred in 50% of H. pylori-infected volunteers and in 16% of their noninfected counterparts (p = 0.02). Aspirin caused a significantly higher average mucosal injury score in the gastric antrum in H. pylori-infected participants than in noninfected subjects (p = 0.03), and two H. pylori-infected subjects developed antral gastric ulcers. Subjects with H. pylori gastritis treated with the placebo had nearly 50% higher gastric mucosal prostaglandin (E2 plus F2alpha) synthesis rates than their noninfected counterparts (108 +/- 6 ng/g/min versus 75 +/- 6 ng/g/min, p < 0.001). Aspirin reduced mucosal prostaglandin synthesis to similar levels in infected and noninfected participants.

CONCLUSIONS

Long term/low dose aspirin therapy led to more gastric mucosal damage when H. pylori gastritis was present than when it was absent, despite similar degrees of gastric mucosal prostaglandin depletion.

Authors+Show Affiliations

Department of Veterans Affairs Medical Center, Dallas, Texas 75216, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

11419825

Citation

Feldman, M, et al. "Role of Helicobacter Pylori Infection in Gastroduodenal Injury and Gastric Prostaglandin Synthesis During Long Term/low Dose Aspirin Therapy: a Prospective Placebo-controlled, Double-blind Randomized Trial." The American Journal of Gastroenterology, vol. 96, no. 6, 2001, pp. 1751-7.
Feldman M, Cryer B, Mallat D, et al. Role of Helicobacter pylori infection in gastroduodenal injury and gastric prostaglandin synthesis during long term/low dose aspirin therapy: a prospective placebo-controlled, double-blind randomized trial. Am J Gastroenterol. 2001;96(6):1751-7.
Feldman, M., Cryer, B., Mallat, D., & Go, M. F. (2001). Role of Helicobacter pylori infection in gastroduodenal injury and gastric prostaglandin synthesis during long term/low dose aspirin therapy: a prospective placebo-controlled, double-blind randomized trial. The American Journal of Gastroenterology, 96(6), 1751-7.
Feldman M, et al. Role of Helicobacter Pylori Infection in Gastroduodenal Injury and Gastric Prostaglandin Synthesis During Long Term/low Dose Aspirin Therapy: a Prospective Placebo-controlled, Double-blind Randomized Trial. Am J Gastroenterol. 2001;96(6):1751-7. PubMed PMID: 11419825.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of Helicobacter pylori infection in gastroduodenal injury and gastric prostaglandin synthesis during long term/low dose aspirin therapy: a prospective placebo-controlled, double-blind randomized trial. AU - Feldman,M, AU - Cryer,B, AU - Mallat,D, AU - Go,M F, PY - 2001/6/23/pubmed PY - 2001/8/31/medline PY - 2001/6/23/entrez SP - 1751 EP - 7 JF - The American journal of gastroenterology JO - Am J Gastroenterol VL - 96 IS - 6 N2 - OBJECTIVES: Whether gastric infection with Helicobacter pylori increases the risk of gastric mucosal injury during long term/low dose aspirin therapy is unknown. We examined whether H. pylori infection enhances upper GI mucosal damage, assessed endoscopically, in volunteers given low dose aspirin. We studied 61 healthy men and women, 29 with and 32 without active H. pylori infection. METHODS: We treated volunteers for 45 days with a placebo or aspirin (either 81 mg every day or 325 mg every 3 days). Gastroduodenal mucosal damage was then assessed by endoscopy, as was gastric histology and ex vivo gastric mucosal prostaglandin E2 and F2alpha synthesis rates. RESULTS: Erosive disease from low dose aspirin (erosions and/or ulcers) occurred in 50% of H. pylori-infected volunteers and in 16% of their noninfected counterparts (p = 0.02). Aspirin caused a significantly higher average mucosal injury score in the gastric antrum in H. pylori-infected participants than in noninfected subjects (p = 0.03), and two H. pylori-infected subjects developed antral gastric ulcers. Subjects with H. pylori gastritis treated with the placebo had nearly 50% higher gastric mucosal prostaglandin (E2 plus F2alpha) synthesis rates than their noninfected counterparts (108 +/- 6 ng/g/min versus 75 +/- 6 ng/g/min, p < 0.001). Aspirin reduced mucosal prostaglandin synthesis to similar levels in infected and noninfected participants. CONCLUSIONS: Long term/low dose aspirin therapy led to more gastric mucosal damage when H. pylori gastritis was present than when it was absent, despite similar degrees of gastric mucosal prostaglandin depletion. SN - 0002-9270 UR - https://www.unboundmedicine.com/medline/citation/11419825/Role_of_Helicobacter_pylori_infection_in_gastroduodenal_injury_and_gastric_prostaglandin_synthesis_during_long_term/low_dose_aspirin_therapy:_a_prospective_placebo_controlled_double_blind_randomized_trial_ L2 - https://doi.org/10.1111/j.1572-0241.2001.03928.x DB - PRIME DP - Unbound Medicine ER -