title: Interactions between Helicobacter pylori and other risk factors for peptic ulcer bleeding.
abstract: OBJECTIVE
  To investigate the role of Helicobacter pylori, expressing the virulence marker CAGA (cytotoxin associated gene product A) in ulcer complications and its interaction with nonsteroidal anti-inflammatory drugs (NSAIDs) and other risk factors.
  
  
  METHODS
  Case control study using conditional logistic regression analysis.
  
  
  METHODS
  University and City Hospitals, Nottingham.
  
  
  METHODS
  203 consecutive patients with ulcer bleeding and 203 age- and sex-matched controls.
  
  
  RESULTS
  Ulcer bleeding was more likely with positive H. pylori serology (odds ratio = 3.3, 95% CI: 1.7--6.6 for CagA positive, but only OR = 1.6, 95% CI: 0.7-3.7 for CagA negative serology), current smoking (OR 2.2, 95% CI: 1.04-4.7), aspirin < or = 300 mg daily (OR 7.7, 95% CI: 2.8-20.6), all other nonsteroidal anti-inflammatory drugs (NSAIDs: OR 10.6, 95% CI: 3.1-35.7 for < or = 1 defined daily dose lower and OR 22.6, 95% CI: 6.2-82.0 for higher doses) and past ulcer history (OR 5.6, 95% CI: 2.3-14.1). Aspirin < or = 300 mg daily was used by 25.1% of patients vs. 7.4% of controls. Smoking only enhanced risk in the presence of H. pylori, with a synergistic interaction (interaction odds ratio = 4.9, 2.4-9.9, P=0.002). Conversely, risks with non-aspirin NSAIDs were reduced in the presence of H. pylori, particularly if CagA-positive (interaction odds ratio=0.21, 0.05-0.9, P=0.03).
  
  
  CONCLUSIONS
  CagA positive H. pylori infection is associated with an increased risk of ulcer bleeding. The risk from non-aspirin NSAIDs is even higher, but is less in H. pylori infected people. Low-dose aspirin is now commonly associated with ulcer bleeding.
authors.affiliation: Division of Gastroenterology, University Hospital, Nottingham, UK.
authors.forename: W A
authors.initials: WA
authors.lastname: Stack
authors.forename: J C
authors.initials: JC
authors.lastname: Atherton
authors.forename: G M
authors.initials: GM
authors.lastname: Hawkey
authors.forename: R F A
authors.initials: RF
authors.lastname: Logan
authors.forename: C J
authors.initials: CJ
authors.lastname: Hawkey
mesh_terms: D000328:Adult; D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects; D000942:Antigens, Bacterial; D001241:Aspirin / Q000009:adverse effects; D001426:Bacterial Proteins / Q000235:genetics; D016022:Case-Control Studies; D004381:Duodenal Ulcer / Q000139:chemically induced / Q000150:complications / Q000209:etiology / Q000382:microbiology; D005260:Female; D016481:Helicobacter Infections / Q000150:complications* / Q000188:drug therapy / Q000382:microbiology; D016480:Helicobacter pylori / Q000235:genetics / Q000472:pathogenicity*; D006801:Humans; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D010438:Peptic Ulcer Hemorrhage / Q000139:chemically induced / Q000150:complications / Q000209:etiology* / Q000382:microbiology*; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori; D001241:Aspirin