These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: The interaction of H. pylori infection and NSAIDs in cyclooxygenase-2 mRNA expression in gastric antral, corpus mucosa, and gastric ulcer.
    Author: Wu CY, Wu MS, Chen CJ, Li MC, Lin JT, Chen GH.
    Journal: J Clin Gastroenterol; 2005 Jan; 39(1):50-5. PubMed ID: 15599211.
    Abstract:
    BACKGROUND: Although Helicobacter pylori infection and use of nonsteroidal anti-inflammatory drugs (NSAIDs) are the two major causes of gastric ulcer, their interaction remains controversial. We constructed a prospective cohort study to evaluate how these two factors influence the expression of COX-2 mRNA in gastric antral, corpus mucosa, and gastric ulcer. METHODS: Tissues were obtained by endoscopic biopsy of gastric antral, corpus mucosa, and gastric ulcer. The presence of H. pylori was determined by culture or histology using Giemsa stain. NSAID use was assessed by structured questionnaire and medical record review. The expression of COX-2 mRNA was detected by the TaqMan quantitative RT-PCR system. RESULTS: H. pylori infection was associated with increased COX-2 expression only in antral mucosa (0.77 +/- 0.13 vs. 0.31 +/- 0.07, P < 0.01). NSAID use was significantly associated with decreased COX-2 expression in ulcer (4.49 +/- 1.50 vs. 9.82 +/- 2.48, P < 0.05) but not in antral or corpus mucosa. Regarding the interaction between H. pylori and NSAID, we found that H. pylori infection was associated with increased COX-2 expression in antral mucosa for both NSAID users and nonusers. In NSAID users, H. pylori infection was not associated with increased COX-2 expression in ulcer edge. CONCLUSION: H. pylori infection was associated with increased COX-2 expression in gastric antral mucosa for both NSAID users and nonusers, but not in gastric ulcer, where the effect of NSAID inhibition plays a major role. With these observations, we can interpret indirectly that H. pylori eradication does not interfere with gastric ulcer healing in NSAID users.
    [Abstract] [Full Text] [Related] [New Search]