Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Multicenter Study
, 10 (1), 69-75

Does Helicobacter Pylori Exacerbate Gastric Mucosal Injury in Users of Nonsteroidal Anti-Inflammatory Drugs? A Multicenter, Retrospective, Case-Control Study

Affiliations
Multicenter Study

Does Helicobacter Pylori Exacerbate Gastric Mucosal Injury in Users of Nonsteroidal Anti-Inflammatory Drugs? A Multicenter, Retrospective, Case-Control Study

Yoshiyasu Kono et al. Gut Liver.

Abstract

Background/aims: The interaction between nonsteroidal anti-inflammatory drugs (NSAIDs) and Helicobacter pylori remains controversial. We retrospectively investigated whether H. pylori infection exacerbates severe gastric mucosal injury among chronic NSAID users.

Methods: From January 2010 to December 2013, a total of 245 long-term NSAID (including low-dose aspirin) users who had undergone an esophagogastroduodenoscopy and had been evaluated for H. pylori infection were enrolled at Okayama University Hospital and Tsuyama Chuo Hospital. The degree of gastric mucosal injury was assessed according to the modified Lanza score (MLS). Severe gastric mucosal injury was defined as an MLS ≥4. Univariate and multivariate logistic regression analyses were performed.

Results: In the univariate analysis, age ≥75 years (odds ratio [OR], 2.4; 95% confidence interval [CI], 1.3 to 4.2), H. pylori-positivity (OR, 2.0; 95% CI, 1.2 to 3.5), and the concomitant use of proton pump inhibitors (PPIs) (OR, 0.48; 95% CI, 0.26 to 0.86) were significantly associated with severe gastric mucosal injury. The multivariate analysis was adjusted by age and sex and demonstrated that H. pylori-positivity (OR, 1.8; 95% CI, 1.0 to 3.3) and the concomitant use of PPIs (OR, 0.53; 95% CI, 0.28 to 0.99) significantly contributed to severe gastric mucosal injury.

Conclusions: H. pylori infection exacerbates severe gastric mucosal injury among chronic NSAID users.

Keywords: Anti-inflammatory agents, non-steroidal; Gastric mucosal injury; Helicobacter pylori; Proton pump inhibitors.

Figures

Fig. 1
Fig. 1
Comparison of the modified Lanza score (MLS) between Helicobacter pylori-negative subjects and H. pylori-positive subjects in all cases. The mean MLS was significantly higher in H. pylori-positive subjects than in H. pylori-negative subjects (each column indicates the mean±SD; 2.3±2.3 vs 1.7±2.1, p=0.037).
Fig. 2
Fig. 2
Comparison of the incidence of severe gastric mucosal injury (modified Lanza score [MLS] ≥4) between Helicobacter pylori-negative subjects and H. pylori-positive subjects in all cases. The percentage of patients with MLS ≥4 was significantly higher among H. pylori-positive patients than in H. pylori-negative patients (41% vs 26%, p=0.013).
Fig. 3
Fig. 3
Comparison of the modified Lanza score (MLS) between Helicobacter pylori-negative subjects and H. pylori-positive subjects, according to the degree of gastric atrophy. The difference in the mean MLS between H. pylori-negative and H. pylori-positive subjects was larger among the subjects with no or closed-type gastric atrophy than among those with open-type gastric atrophy (each column indicates the mean±SD; 1.6±2.1 vs 2.3±2.4, p=0.093 in the subjects with no or closed-type gastric atrophy, and 1.7±2.2 vs 2.2±2.3, p=0.28 in the subjects with open-type gastric atrophy, respectively).
Fig. 4
Fig. 4
Comparison of the incidence of severe gastric mucosal injury (modified Lanza score [MLS] ≥4) between Helicobacter pylori-negative and H. pylori-positive subjects, according to the degree of gastric atrophy. Among the subjects with no or closed-type gastric atrophy, the percentage of patients with MLS ≥4 was significantly higher in H. pylori-positive than in H. pylori-negative subjects; however, it was not significantly higher among the subjects with open-type gastric atrophy (43% vs 24%, p=0.043 in the subjects with no or closed-type gastric atrophy, and 39% vs 28%, p=0.29 in the subjects with open-type gastric atrophy, respectively).

Similar articles

See all similar articles

Cited by 2 PubMed Central articles

References

    1. Huang JQ, Sridhar S, Hunt RH. Role of Helicobacter pylori infection and non-steroidal anti-inflammatory drugs in peptic-ulcer disease: a meta-analysis. Lancet. 2002;359:14–22. doi: 10.1016/S0140-6736(02)07273-2. - DOI - PubMed
    1. Nishikawa K, Sugiyama T, Kato M, et al. Non-Helicobacter pylori and non-NSAID peptic ulcer disease in the Japanese population. Eur J Gastroenterol Hepatol. 2000;12:635–640. doi: 10.1097/00042737-200012060-00010. - DOI - PubMed
    1. Lanza FL, Chan FK, Quigley EM Practice Parameters Committee of the American College of Gastroenterology. Guidelines for prevention of NSAID-related ulcer complications. Am J Gastroenterol. 2009;104:728–738. doi: 10.1038/ajg.2009.115. - DOI - PubMed
    1. Malfertheiner P, Chan FK, McColl KE. Peptic ulcer disease. Lancet. 2009;374:1449–1461. doi: 10.1016/S0140-6736(09)60938-7. - DOI - PubMed
    1. Elliott SL, Ferris RJ, Giraud AS, Cook GA, Skeljo MV, Yeomans ND. Indomethacin damage to rat gastric mucosa is markedly dependent on luminal pH. Clin Exp Pharmacol Physiol. 1996;23:432–434. doi: 10.1111/j.1440-1681.1996.tb02754.x. - DOI - PubMed

Publication types

MeSH terms

Substances

Feedback