Gastric fundic gland polyps in south-east Scotland: absence of adenomatous polyposis coli gene mutations and a strikingly low prevalence of Helicobacter pylori infection.

BACKGROUND AND AIM: 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. Copyright 2002 Blackwell Publishing Asia Pty Ltd