title: Gastric fundic gland polyps in south-east Scotland: absence of adenomatous polyposis coli gene mutations and a strikingly low prevalence of Helicobacter pylori infection.
abstract: OBJECTIVE
  Fundic gland polyps (FGP) were originally described in association with familial polyposis syndromes, but it is now accepted that the majority of FGP are picked up incidentally in up to 1.9% of routine endoscopies in dyspeptic patients. The familial adenomatous polyposis phenotype arises from germline mutations of the adenomatous polyposis coli (APC) gene. We aimed to see if there was any association between the presence of FGP, Helicobacter pylori, and two common APC gene mutations.
  
  
  METHODS
  From a search of histopathology records in our unit, 85 consecutive patients were identified with a definite histological diagnosis of FGP between 1989 and 1997. Case notes could be retrieved in 48 cases to show the indication for endoscopy and endoscopic findings. Twenty-six patients (mean age 61 years, range 40-83 years) were tested for H. pylori status, and for the 1306 and 1061 bp deletions of the APC gene by the use of an enzyme-linked immunoassay and polymerase chain reaction techniques, respectively.
  
  
  RESULTS
  Eighty-nine percent of patients underwent an endoscopy because of dyspepsia; 4.2% were anaemic, 4.2% had hematemesis and 1.2% had dysphagia. Only one patient was seropositive for H. pylori and no patient carried either APC gene deletion.
  
  
  CONCLUSIONS
  This genetic information on those with FGP confirms previous phenotypic studies in that the majority of FGP are not associated with familial polyposis syndromes. The significance of such a strikingly low incidence of H. pylori infection in a dyspeptic population remains unclear.
authors.affiliation: Gastrointestinal Unit, Department of Pathology, Western General Hospital, Edinburgh, UK. agshand@hotmail.com
authors.forename: Alan G
authors.initials: AG
authors.lastname: Shand
authors.forename: Andrew C
authors.initials: AC
authors.lastname: Taylor
authors.forename: Mala
authors.initials: M
authors.lastname: Banerjee
authors.forename: Alastair
authors.initials: A
authors.lastname: Lessels
authors.forename: John
authors.initials: J
authors.lastname: Coia
authors.forename: Caroline
authors.initials: C
authors.lastname: Clark
authors.forename: Naiva
authors.initials: N
authors.lastname: Haites
authors.forename: Subrata
authors.initials: S
authors.lastname: Ghosh
mesh_terms: D011125:Adenomatous Polyposis Coli / Q000453:epidemiology* / Q000235:genetics; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D004252:DNA Mutational Analysis; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005748:Gastric Fundus / Q000473:pathology*; D005753:Gastric Mucosa / Q000473:pathology*; D017491:Genes, APC; D018095:Germ-Line Mutation; D016481:Helicobacter Infections / Q000453:epidemiology*; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011127:Polyps / Q000453:epidemiology* / Q000235:genetics / Q000473:pathology; D015995:Prevalence; D012189:Retrospective Studies; D012606:Scotland / Q000453:epidemiology; D013274:Stomach Neoplasms / Q000453:epidemiology* / Q000235:genetics / Q000473:pathology