title: Gastric mucosal hydrophobicity in duodenal ulceration: role of Helicobacter pylori infection density and mucus lipids.
abstract: OBJECTIVE
  Gastric mucosal hydrophobicity is reduced in Helicobacter pylori infection. Infection density is increased in duodenal ulcer (DU) compared with H. pylori gastritis alone, but it is unknown whether there is a corresponding difference in hydrophobicity or whether hydrophobicity is related to infection density or to mucus lipids. The aim of this study was to determine the relationship between H. pylori infection density and mucosal hydrophobicity, and between mucus lipids and hydrophobicity, and to compare results in patients with H. pylori-induced gastritis with and without DU.
  
  
  METHODS
  Fifty-four patients, including 29 H. pylori-positive (15 with DU and 14 with gastritis alone) and 25 H. pylori-negative controls, were studied. Hydrophobicity was determined by goniometry and infection density by histology. Mucus lipids were determined by colorimetry and phospholipase A2 activity by radioenzymatic assay.
  
  
  RESULTS
  Hydrophobicity was reduced in DU compared with gastritis alone (39 degrees vs. 48 degrees; P < 0.05) and with healthy controls (39 degrees vs. 60 degrees; P < 0.0001). Hydrophobicity correlated with infection density (Rs = -0.55; P < 0.01). Mucus triglyceride level was modestly increased with infection, but mucus phospholipids or lipolysis were unrelated to H. pylori and hydrophobicity.
  
  
  CONCLUSIONS
  Mucosal hydrophobicity is reduced in H. pylori-positive patients with DU compared with those having gastritic only. Hydrophobicity correlates with infection density but not with mucus lipid levels.
authors.affiliation: Department of Medicine, St. George's Hospital Medical School, London, England.
authors.forename: M
authors.initials: M
authors.lastname: Asante
authors.forename: H
authors.initials: H
authors.lastname: Ahmed
authors.forename: P
authors.initials: P
authors.lastname: Patel
authors.forename: T
authors.initials: T
authors.lastname: Davis
authors.forename: C
authors.initials: C
authors.lastname: Finlayson
authors.forename: M
authors.initials: M
authors.lastname: Mendall
authors.forename: T
authors.initials: T
authors.lastname: Northfield
mesh_terms: D000328:Adult; D000368:Aged; D003124:Colorimetry; D004381:Duodenal Ulcer / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D005750:Gastric Juice / Q000201:enzymology; D005753:Gastric Mucosa / Q000737:chemistry / Q000382:microbiology / Q000503:physiopathology*; D005756:Gastritis / Q000150:complications / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology; D016481:Helicobacter Infections / Q000382:microbiology / Q000503:physiopathology*; D016480:Helicobacter pylori / Q000502:physiology*; D006801:Humans; D008055:Lipids / Q000032:analysis / Q000502:physiology*; D008297:Male; D008875:Middle Aged; D009093:Mucus / Q000737:chemistry / Q000502:physiology*; D010741:Phospholipases A / Q000032:analysis; D054467:Phospholipases A2; D010743:Phospholipids / Q000032:analysis / Q000502:physiology; D015203:Reproducibility of Results; D014280:Triglycerides / Q000032:analysis / Q000502:physiology
chemical_list: D008055:Lipids; D010743:Phospholipids; D014280:Triglycerides; D010741:Phospholipases A; D054467:Phospholipases A2