Infection of Helicobacter pylori in gastric adaptation to continued administration of aspirin in humans

Konturek, J. W.; Dembiński, Artur; Konturek, Stanisław J.; Stachura, Jerzy; Domschke, Wolfram

doi:10.1016/s0016-5085(98)70474-3

Cited by 102 publications

(64 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Two studies found a reduced risk of GU complications among H. pylori -infected patients taking ASA or NSAIDs [23,26]. This could be because H. pylori induces an increase in gastric mucosal prostaglandin E 2 levels that may partially reverse the mucosal toxicity of ASA or NSAIDs [74,75,76]. H. pylori infection may suppress gastric acid secretion in some individuals [77].…”

Section: Discussionmentioning

confidence: 99%

Systematic Review of the Epidemiology of Complicated Peptic Ulcer Disease: Incidence, Recurrence, Risk Factors and Mortality

Lau

Sung²,

Hill³

et al. 2011

Digestion

452

334

View full text Add to dashboard Cite

Background/Aims: The incidence of uncomplicated peptic ulcer has decreased in recent years. It is unclear what the impact of this has been on the epidemiology of peptic ulcer complications. This systematic review aimed to determine the incidence, recurrence and mortality of complicated peptic ulcer and the risk factors associated with these events. Methods: Systematic PubMed searches. Results: Overall, 93 studies were identified. Annual incidence estimates of peptic ulcer hemorrhage and perforation were 19.4–57.0 and 3.8–14 per 100,000 individuals, respectively. The average 7-day recurrence of hemorrhage was 13.9% (95% CI: 8.4–19.4), and the average long-term recurrence of perforation was 12.2% (95% CI: 2.5–21.9). Risk factors for peptic ulcer complications and their recurrence included nonsteroidal anti-inflammatory drug and/or acetylsalicylic acid use, Helicobacter pylori infection and ulcer size ≧1 cm. Proton pump inhibitor use reduced the risk of peptic ulcer hemorrhage. Average 30-day mortality was 8.6% (95% CI: 5.8–11.4) after hemorrhage and 23.5% (95% CI: 15.5–31.0) after perforation. Older age, comorbidity, shock and delayed treatment were associated with increased mortality. Conclusions: Complicated peptic ulcer remains a substantial healthcare problem which places patients at a high risk of recurrent complications and death.

show abstract

Section: Discussionmentioning

confidence: 99%

Systematic Review of the Epidemiology of Complicated Peptic Ulcer Disease: Incidence, Recurrence, Risk Factors and Mortality

Lau

Sung²,

Hill³

et al. 2011

Digestion

452

334

View full text Add to dashboard Cite

show abstract

“…Some clinical studies have reported no interaction between H. pylori and NSAIDs or of a protective role of H. pylori in patients given NSAIDs (19,24,27). Other studies have shown harmful effects of H. pylori in patients given NSAIDs (1,4,25). There are many reasons for these controversies, including differences in the characteristics of subjects, differences in methods of approach, relatively small sample sizes, etc.…”

mentioning

confidence: 99%

Effects of Nonsteroidal Anti-Inflammatory Drugs on Helicobacter pylori -Infected Gastric Mucosae of Mice: Apoptosis, Cell Proliferation, and Inflammatory Activity

Kim¹,

Lee²,

Lee³

et al. 2001

Infect Immun

View full text Add to dashboard Cite

Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) are two well-known important causative factors of gastric damage. While H. pylori increases apoptosis and the proliferation of gastric epithelial cells and is an important factor in peptic ulcer and gastric cancer, NSAIDs induce cell apoptosis and have antineoplastic effects. We investigated the effects of NSAIDs (a nonselective cyclooxygenase [COX] inhibitor [indomethacin] and a selective COX-2 inhibitor [NS-398]) on the apoptosis and proliferation of gastric epithelial cells and gastric inflammation in H. pylori-infected mice. C57BL/6 mice were sacrificed 8 weeks after H. pylori SS1 inoculation. Indomethacin (2 mg/kg) or NS-398 (10 mg/kg) was administered subcutaneously once daily for 10 days before sacrifice. The following were assessed: gastric inflammatory activity, gastric COX protein expression by Western blotting; gastric prostaglandin E 2 levels by enzyme immunoassay, apoptosis by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling, and cell proliferation by Ki67 immunostaining. Compared to the controls, H. pylori infection and/or NSAID treatment increased COX-1 and COX-2 protein expression. Gastric prostaglandin E 2 levels, apoptotic index, cell proliferation index, neutrophil activity, and the degree of chronic inflammation were all increased by H. pylori infection, and these effects were significantly decreased by indomethacin treatment. However, NS-398 treatment after H. pylori infection did not induce a significant reduction, although it did result in a tendency to decrease. These results show that NSAIDs can reverse the increased apoptosis and proliferation of epithelial cells and inflammatory activity in the stomachs of H. pylori-infected mice and that, like COX-2 activation, COX-1 induction contributes to the change of gastric mucosal cell turnover and inflammation induced by H. pylori infection.

show abstract

“…In previous studies, a short-term course of aspirin did not cause diffuse histological injury, and the eradication of H. pylori restored gastric adaptation to aspirin (42,43). It is generally recognized that H. pylori infection does not worsen mucosal injury with aspirin or NSAIDs because H. pylori infection is associated with increased mucosal levels of prostaglandins (44,45).…”

Section: Discussionmentioning

confidence: 91%

Low-dose Aspirin Delays Gastric Healing after Helicobacter pylori Eradication

et al. 2011

View full text Add to dashboard Cite

Background and Aim Helicobacter pylori (H. pylori) and aspirin are the major causes of gastric injury, and eradication of H. pylori can restore mucosal injury such as gastric ulcer. The aim of the present study was to investigate the effects of low-dose aspirin on the healing process, determined by endoscopic features, after H. pylori eradication. Methods From 2001 to 2008, 12,887 patients underwent endoscopic examination at our hospital. From these, 100 patients with and 100 patients without H. pylori infection were analyzed to identify the endoscopic features characteristic of H. pylori-infected stomach. Based on these characteristic features, we observed the healing process of 89 patients not taking low-dose aspirin and 12 patients taking low-dose aspirin for 6 months, 1 year, and 5 years, which was successful in eradicating H. pylori. Results Diffuse redness (DR) of the fundic mucosa was the characteristic feature of H. pylori-infected stomach, whereas reddish streaks (RS) on the greater curvature of the antrum was the characteristic finding in non-infected stomach. In the no aspirin group, DR faded by 6 months and new expression of RS was observed 1 year after H. pylori eradication. In contrast, in the aspirin group, both fading of DR and the expression of RS were observed 5 years after eradication. Conclusion Low-dose aspirin delayed the early phase of the healing process in the gastric mucosa after H. pylori eradication.

show abstract

Infection of Helicobacter pylori in gastric adaptation to continued administration of aspirin in humans

Cited by 102 publications

References 36 publications

Systematic Review of the Epidemiology of Complicated Peptic Ulcer Disease: Incidence, Recurrence, Risk Factors and Mortality

Systematic Review of the Epidemiology of Complicated Peptic Ulcer Disease: Incidence, Recurrence, Risk Factors and Mortality

Effects of Nonsteroidal Anti-Inflammatory Drugs on Helicobacter pylori -Infected Gastric Mucosae of Mice: Apoptosis, Cell Proliferation, and Inflammatory Activity

Low-dose Aspirin Delays Gastric Healing after Helicobacter pylori Eradication

Contact Info

Product

Resources

About