Introduction
The mechanism of aspirin-induced gastric mucosal injury is thought to be mediated by multiple processes involving either topical or systemic effects. Recently, it has been reported that topical effects play a pivotal role in causing gastric mucosal injury. (1, 2). It is known that almost all aspirin-induced gastric mucosal injuries were observed in low intragastic pH condition (pH<4) (3). Though it depends on the severity and distribution of gastritis caused by Helicobacter pylori (H. pylori), gastric acid secretion is recovered after the eradication of H. pylori (4). Therefore, because intragastric pH may decrease dramatically, the prevalence and severity of gastric mucosal injuries in patients taking aspirin may also change after the eradication.
Aims & Methods
The aim of this study is to reveal the relationship between H. pylori infection and gastric mucosal injuries in patients taking aspirin. This study was a retrospective cross-sectional study. Data were extracted from the records of subjects who underwent upper gastrointestinal endoscopy at our department between April 2015 and March 2020. We focused on the subjects taking only aspirin as an anti-thrombotic agent, and selected the subjects whose H. pylori infection status was known. After that we divided into three groups (non-infection, current infection, and past infection of H. pylori) and compared the severity of gastric mucosal injury, individually. Severity of gastric mucosal injury was evaluated endoscopically based on the modified LANZA score (m-LANZA score). Statistical analyses were performed by using Fisher’s exact test. We evaluated separately for subjects with concomitant use of potassium-competitive acid blocker (P-CAB) or PPI (user) and subjects without concomitant use of P-CAB, PPI nor histamine H2 receptor antagonist (H2RA) (nonuser).
Results
311 subjects out of 6,031 were taking only aspirin as an anti-thrombotic agent. In group of non-infection (43 men, 32 women; mean age 69.0±15.6 years), average MLS was 0.51±1.16 (user: n=45, score0=33, score1=8, score2=1, score3=1, score4=0, score5=2) and 1.21±1.70 (nonuser: n=29, score0=18, score1=0, score2=3, score3=5, score4=1, score5=2). In group of current infection (12 men, 5 women; mean age 67.7±11.4 years), average MLS was 0.86±1.86 (user: n=7, score0=5, score1=1, score2=0, score3=0, score4=0, score5=1) and 1.29±1.89 (nonuser: n=7, score0=4, score1=0, score2=2, score3=0, score4=0, score5=1). In group of past infection (107 men, 51 women; mean age 74.7±7.5 years), average MLS was 0.39±1.07 (user: n=104, score0=86, score1=8, score2=4, score3=2, score4=1, score5=3) and 0.90±1.62 (nonuser: n=49, score0=34, score1=4, score2=3, score3=4, score4=2, score5=4). There was a statistically significantly difference between user and nonuser in group of non-infection (p=0.040) and in group of past infection (p=0.023). Mean MLS in group of current infection was high more than expected because intragastric pH might be high in H. pylori-positive patients. We considered because many subjects which were H. pylori-positive but whose gastric acid secretion was not so impaired might be included in this study.
Conclusion
There was no significant difference between H. pylori infection and gastric mucosal injuries in patients taking low dose aspirin. However, concomitant use of P-CAB or PPI can prevent gastric mucosal injuries in pylori-negative patients taking low dose aspirin.
References
(1) Musumba C, et al. Review article: cellular molecular mechanisms of NSAID-induced peptic ulcers. Aliment Pharmacol Ther. 30:517-531 2009
(2) Mashita Y, et al. Oral but parenteral aspirin upregulates COX-2 expression in rat stomachs. a relationship between COX-2 expression and PG deficiency. Digestion. 73:124-132 2006
(3) Nishino M, et al. Relationship between low-dose aspirin-induced gastric mucosal injury and intragastric pH in healthy volunteers. Dig Dis Sci. 55:1627-1636, 2010
(4) El-Omar EM, et al. Helicobacter pylori infection and chronic gastric hyposecretion. Gastroenterology. 113:15-24 1997
