title: Clinical significance of cytotoxin-associated gene A status of Helicobacter pylori among non-steroidal anti-inflammatory drug users with peptic ulcer bleeding: a multicenter case-control study.
abstract: BACKGROUND
  The role of Helicobacter pylori infection and especially of the cytotoxin-associated gene A (CagA) product strain in peptic ulcer bleeding among non-steroidal anti-inflammatory drugs (NSAIDs) users remains controversial.
  
  
  METHODS
  A case-control study was carried out including 191 consecutive chronic NSAIDs users admitted to hospital because of peptic ulcer bleeding. Peptic ulcer was verified by endoscopy. Controls comprised 196 chronic NSAIDs users without signs of bleeding of similar age and gender to cases. Multivariate regression analysis was performed for further evaluation of the relationship between H. pylori, CagA status and other risk factors.
  
  
  RESULTS
  H. pylori infection was present in 121 (63.4%) cases compared with 119 (60.7%) controls (odds ratio (OR) = 1.14, 95% CI, 0.76-1.72). CagA-positive strains were found to be significantly more frequent in cases than in controls (65/106 versus 41/99 P = 0.008). Current smoking (OR = 2.65; 95% CI, 1.14-6.15; P= 0.02), CagA status (OR = 2.28; 95% CI, 1.24-4.19; P = 0.008), dyspepsia (OR = 6.89; 95% CI, 1.84-25.76; P = 0.004) and past history of peptic ulcer disease (OR=3.15; 95% CI, 1.43-6.92; P=0.004) were associated significantly with increased risk of bleeding peptic ulcer.
  
  
  CONCLUSIONS
  The results suggest that CagA-positive H. pylori infection is associated with a more than 2-fold increased risk of bleeding peptic ulcer among chronic NSAIDs users.
authors.affiliation: Dept of Gastroenterology, Polyclinic General Hospital, Vrilissia, Athens, Greece. abc0403@otenet.gr
authors.forename: D
authors.initials: D
authors.lastname: Tzourmakliotis
authors.forename: M
authors.initials: M
authors.lastname: Economou
authors.forename: S
authors.initials: S
authors.lastname: Manolakopoulos
authors.forename: S
authors.initials: S
authors.lastname: Bethanis
authors.forename: C
authors.initials: C
authors.lastname: Bergele
authors.forename: J
authors.initials: J
authors.lastname: Lakoumentas
authors.forename: P
authors.initials: P
authors.lastname: Sclavos
authors.forename: H
authors.initials: H
authors.lastname: Milionis
authors.forename: A
authors.initials: A
authors.lastname: Margeli
authors.forename: E
authors.initials: E
authors.lastname: Vogiatzakis
authors.forename: A
authors.initials: A
authors.lastname: Avgerinos
mesh_terms: D000328:Adult; D000368:Aged; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage*; D000907:Antibodies, Bacterial / Q000097:blood; D000942:Antigens, Bacterial / Q000502:physiology*; D001426:Bacterial Proteins / Q000502:physiology*; D016022:Case-Control Studies; D004381:Duodenal Ulcer / Q000150:complications / Q000382:microbiology; D005260:Female; D016481:Helicobacter Infections / Q000150:complications / Q000503:physiopathology*; D016480:Helicobacter pylori / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010438:Peptic Ulcer Hemorrhage / Q000097:blood / Q000382:microbiology*; D012307:Risk Factors; D013276:Stomach Ulcer / Q000150:complications / Q000382:microbiology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori