title: Relationship between the mucosal production of reactive oxygen radicals and density of Helicobacter pylori in patients with duodenal ulcer.
abstract: OBJECTIVE
  To investigate the associations between the mucosal production of reactive oxygen radicals (RORs) in the gastric antrum and duodenum, Helicobacter pylori density and duodenal ulcer (DU).
  
  
  METHODS
  Forty-seven endoscoped patients, comprising 22 with DU and 25 non-ulcer subjects, were included in the study.
  
  
  METHODS
  Antral and duodenal biopsies were taken for histology, Helicobacter pylori culture and measurement of chemiluminescence. Biopsies were homogenized and cultured on Columbia blood agar plate. Colonies of H. pylori were counted and bacterial density expressed as colony-forming units (cfu)/mg of biopsy. Chemiluminescence was measured by luminometry and the results expressed as millivolt (mV)/min/mg of biopsy, after subtraction of background count.
  
  
  RESULTS
  Thirty-one of 47 (66%) patients had antral H. pylori and 6/47 (12.8%) had proven duodenal colonization. Increased chemiluminescence (median (interquartile)) was found in H. pylori-infected patients compared to those without H. pylori in antral (90.0 (26.0, 249.0) vs. 7.0 (0.0, 10.0), P<0.001) and duodenal mucosa (22.0 (10.0, 100.0) vs. -2.5 (-10.0, 0.0) P<0.001). A positive correlation was found between antral H. pylori density and chemiluminescence response in both the antrum (r=0.77) and duodenum (r=0.52). DU patients showed an increased chemiluminescence compared to those non-ulcer subjects with or without H. pylori infection in antrum (163.5 (44.5, 297.8) vs. 33.0 (8.7, 168.0) (P=0.046) vs. 2.7 (0.1, 10.0), P<0.01) and duodenum (45.0 (17.5, 100.0) vs. 15.0 (-1.25, 22.5) vs. -2.5 (-10, 0.0), P<0.01).
  
  
  CONCLUSIONS
  Increased production of RORs in the antrum and duodenum was found to be related to antral H. pylori density and associated with duodenal ulceration. The association between antral H. pylori and ROR release in the duodenum may be important in the pathogenesis of duodenal ulceration.
authors.affiliation: Department of Gastroenterology, Royal Infirmary, Glasgow, UK.
authors.forename: Q
authors.initials: Q
authors.lastname: Zhang
authors.forename: J B
authors.initials: JB
authors.lastname: Dawodu
authors.forename: G
authors.initials: G
authors.lastname: Etolhi
authors.forename: A
authors.initials: A
authors.lastname: Husain
authors.forename: C G
authors.initials: CG
authors.lastname: Gemmell
authors.forename: R I
authors.initials: RI
authors.lastname: Russell
mesh_terms: D001706:Biopsy; D003603:Cytotoxins / Q000032:analysis; D004381:Duodenal Ulcer / Q000378:metabolism* / Q000382:microbiology*; D004386:Duodenum / Q000378:metabolism / Q000382:microbiology; D005753:Gastric Mucosa / Q000378:metabolism / Q000382:microbiology; D016480:Helicobacter pylori / Q000737:chemistry / Q000302:isolation & purification*; D006801:Humans; D007413:Intestinal Mucosa / Q000378:metabolism / Q000382:microbiology; D009504:Neutrophils / Q000166:cytology; D011706:Pyloric Antrum / Q000378:metabolism / Q000382:microbiology; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D003603:Cytotoxins; D017382:Reactive Oxygen Species