title: Eradication of Helicobacter pylori normalizes elevated mucosal levels of epidermal growth factor and its receptor.
abstract: OBJECTIVE
  Helicobacter pylori (H. pylori) infection has been linked to gastric cancer. The factors that promote carcinogenesis remain unknown. Epidermal growth factor (EGF) has been shown to be a potent epithelial mitogen and oncoprotein when sustained over expression occurs. Our aim was to compare gastric mucosal levels of EGF and its receptor (EGFR) among controls, H. pylori infected subjects, and subjects following H. pylori eradication using quantitative flow cytometric analysis.
  
  
  METHODS
  Patients referred for evaluation of dyspepsia underwent EGD and six antral biopsies were performed (two each for rapid urease testing (RUT), histopathology, and flow cytometry). Controls were those found to be H. pylori negative while subjects had confirmed infection. The study patients were treated, then had repeat EGD with biopsies.
  
  
  RESULTS
  There were 17 controls and 28 cases. Mean EGF and EGFR values were 2.69 and 2.46 for controls and 4.67 and 4.64 for subjects. Subjects' mean EGF was 73% higher (p = .035) and EGFR was 88% higher (p = 0.029) than controls. After treatment, the subjects' mean values declined 55% (p = 0.0001) for EGF and 40% (p = 0.002) for EGFR. Three subjects had persistent infection and showed no change in their EGF/EGFR levels. No difference was found among factor levels with respect to endoscopic findings.
  
  
  CONCLUSIONS
  Both EGF and EGFR from gastric antral biopsies are increased nearly 2-fold in infection with H. pylori. Infection eradication reduces levels of both factors to those of controls. One major pathogenic mechanism for gastric mucosal hyperproliferation and possibly carcinogenesis related to H. pylori may be the over expression of EGF and increased receptor density of EGFR on gastric mucosal cells.
authors.affiliation: Department of Gastroenterology, Naval Medical Center, Portsmouth, Virginia 23708, USA.
authors.forename: W J
authors.initials: WJ
authors.lastname: Coyle
authors.forename: R E
authors.initials: RE
authors.lastname: Sedlack
authors.forename: R
authors.initials: R
authors.lastname: Nemec
authors.forename: R
authors.initials: R
authors.lastname: Peterson
authors.forename: T
authors.initials: T
authors.lastname: Duntemann
authors.forename: M
authors.initials: M
authors.lastname: Murphy
authors.forename: J M
authors.initials: JM
authors.lastname: Lawson
mesh_terms: D000328:Adult; D000863:Antacids / Q000627:therapeutic use; D000900:Anti-Bacterial Agents; D000897:Anti-Ulcer Agents / Q000627:therapeutic use; D001706:Biopsy; D001729:Bismuth / Q000627:therapeutic use; D002908:Chronic Disease; D004359:Drug Therapy, Combination / Q000627:therapeutic use; D004815:Epidermal Growth Factor / Q000378:metabolism*; D066246:ErbB Receptors / Q000378:metabolism*; D005260:Female; D005434:Flow Cytometry; D005753:Gastric Mucosa / Q000378:metabolism* / Q000473:pathology; D005756:Gastritis / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000188:drug therapy* / Q000378:metabolism / Q000382:microbiology; D016480:Helicobacter pylori / Q000302:isolation & purification; D006801:Humans; D008297:Male; D008875:Middle Aged; D009853:Omeprazole / Q000627:therapeutic use; D009942:Organometallic Compounds / Q000627:therapeutic use; D011446:Prospective Studies; D012459:Salicylates / Q000627:therapeutic use
chemical_list: D000863:Antacids; D000900:Anti-Bacterial Agents; D000897:Anti-Ulcer Agents; D009942:Organometallic Compounds; D012459:Salicylates; D004815:Epidermal Growth Factor; C015715:bismuth subsalicylate; D066246:ErbB Receptors; D009853:Omeprazole; D001729:Bismuth