title: Plugs clog the glandular outlets in fundic gland polyps.
abstract: A systematic histologic analysis of 62 gastric fundic gland polyps (FGP) was carried out. All FGP (100%) showed foveolar cells with hypertrophic cytoplasm. In 95% of the FGP, parietal cells ballooned into the lumen and in 93%, exfoliated anucleated structures with eosinophilic granules were found. Plugs of anucleated structures with eosinophilic granules, most likely derived from exfoliated parietal cells, were found to clog the outlets of the glands in 86% of the FGP. None of the 30 control gastric biopsies without FGP had similar cellular aberrations. FGP seems to evolve by cellular aberrations affecting parietal cells. This is not surprising considering that genetic mutations are recorded in FGP with a common APC/b-catenin pathway in both FAP and sporadic cases. The genetic mutations in FGP might alter the biological behavior of the parietal cells, leading to increased exfoliation with clogging of the outlets of the glands. Thus, the blocking of the glandular outflow by plugs of anucleated structures with eosinophilic granules is the most likely cause for the cystic accumulation of "normal" glandular secretions.
authors.affiliation: Gastrointestinal and Liver Pathology Research Laboratory, Department of Pathology, Karolinska Institute and University Hospital, Stockholm, Sweden. Carlos.Rubio@ki.se
authors.forename: Carlos A
authors.initials: CA
authors.lastname: Rubio
mesh_terms: D011125:Adenomatous Polyposis Coli / Q000453:epidemiology / Q000235:genetics / Q000473:pathology; D003594:Cytoplasmic Granules / Q000473:pathology; D005748:Gastric Fundus / Q000473:pathology* / Q000601:surgery; D005753:Gastric Mucosa / Q000473:pathology*; D005756:Gastritis / Q000235:genetics / Q000473:pathology; D006801:Humans; D009154:Mutation; D011127:Polyps / Q000453:epidemiology / Q000235:genetics / Q000473:pathology*; D013548:Sweden / Q000453:epidemiology