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Correlation between Helicobacter pylori infection and low‐dose aspirin use on damage of the upper gastrointestinal tract
Author(s) -
Fukuzawa Mari,
Kawai Takashi,
Watanabe Masataka,
Tomiyama Hirofumi,
Yamashina Akira,
Moriyasu Fuminori
Publication year - 2012
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.2012.07077.x
Subject(s) - medicine , gastroenterology , aspirin , helicobacter pylori , antrum , stomach , helicobacter pylori infection , analysis of variance
Background and Aim: Low‐dose aspirin (LDA), and Helicobacter pylori (HP) infection are considered the two primary causes of peptic ulceration. The interaction between HP infection and non‐steroidal anti‐inflammatory drugs is, however, a matter of considerable discussion and controversy. In this study, we investigated possible synergistic or negative interactions between HP infection and LDA in gastric mucosal lesions, according to lesion site. Methods: The subjects were 120 patients attending the Cardiology Outpatients Department (average age, 67.1 ± 8.9 years; male : female ratio 2.9:1). Endoscopic findings were graded using the Modified Lanza score. Lesions were scored for the antral, body and fundal regions. Ulcers were defined as mucosal defects ≥ 5 mm in size. Results: There were 55 HP‐positive and 65 HP‐negative subjects, and 91 subjects on LDA therapy. The gastric antral Lanza scores were HP(−) LDA(−): 0.2 ± 1.6, HP(−) LDA(+): 1.8 ± 1.5, HP(+) LDA(−): 0.3 ± 0.7, and HP(+) LDA(+): 0.5 ± 1.0. The gastric body and fundal Lanza scores were 0.0 ± 0.0, 0.8 ± 0.9, 0.4 ± 1.1, and 1.0 ± 1.5, respectively, and 0.1 ± 0.3, 0.5 ± 0.9, 0.1 ± 0.3, and 0.1 ± 0.3, respectively. Variance analysis of the correlation between HP infection and LDA by regional Lanza scores identified both HP infection and LDA use as factors that significantly influence the antral Lanza score. However, LDA was an aggressive factor, and HP infection a protective factor. In the gastric body, LDA was a non‐significant, and HP infection a significant, aggressive factor. In the gastric fundus, neither HP infection nor LDA was a significant factor (LDA was an aggressive factor, and HP infection a protective factor). Conclusions: LDA had aggressive effects in all gastric lesions; on the other hand, HP infection had protective effects in the antrum and fundus in the stomach, and aggressive effects in the body in the stomach.