title: Correlation between Helicobacter pylori infection and low-dose aspirin use on damage of the upper gastrointestinal tract.
abstract: OBJECTIVE
  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.
authors.affiliation: Endoscopy Center, Tokyo Medical University Hospital, Tokyo, Japan.
authors.forename: Mari
authors.initials: M
authors.lastname: Fukuzawa
authors.forename: Takashi
authors.initials: T
authors.lastname: Kawai
authors.forename: Masataka
authors.initials: M
authors.lastname: Watanabe
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Tomiyama
authors.forename: Akira
authors.initials: A
authors.lastname: Yamashina
authors.forename: Fuminori
authors.initials: F
authors.lastname: Moriyasu
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000009:adverse effects*; D001241:Aspirin / Q000008:administration & dosage / Q000009:adverse effects*; D016009:Chi-Square Distribution; D016099:Endoscopy, Gastrointestinal; D005260:Female; D005748:Gastric Fundus / Q000187:drug effects / Q000382:microbiology; D005753:Gastric Mucosa / Q000187:drug effects / Q000382:microbiology; D005757:Gastritis, Atrophic / Q000139:chemically induced / Q000209:etiology* / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications / Q000382:microbiology*; D016480:Helicobacter pylori / Q000472:pathogenicity*; D006785:Hospitals, University; D006801:Humans; D007564:Japan; D008297:Male; D008875:Middle Aged; D011706:Pyloric Antrum / Q000187:drug effects / Q000382:microbiology; D018570:Risk Assessment; D012307:Risk Factors; D013270:Stomach / Q000187:drug effects* / Q000382:microbiology* / Q000473:pathology; D013276:Stomach Ulcer / Q000139:chemically induced / Q000209:etiology* / Q000382:microbiology / Q000473:pathology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D001241:Aspirin