Article
Atrophic gastritis and Helicobacter
pylori infection in outpatients referred for
gastroscopy
A Oksanena, P Sipponenb, R Karttunenc, A Miettinend, L Veijolaa, S Sarnae, H Rautelind
a Herttoniemi
Municipal Hospital, FIN-00800 Helsinki, Finland, b Department of Pathology, Jorvi
Hospital, FIN-02740 Espoo, Finland, c Department of Medical Microbiology, University
of Oulu, FIN-90220 Oulu, Finland, d Department
of Bacteriology and Immunology, Haartman Institute, University of
Helsinki and Helsinki University Central Hospital Diagnostics,
FIN-00014 Helsinki, Finland, e Department of Public Health, University of
Helsinki, FIN-00300 Helsinki, Finland
Correspondence to: Dr Hilpi Rautelin, Department of Bacteriology and Immunology, PO Box 21, FIN-00014 University of Helsinki, Finland
Accepted for publication 20 October 1999
BACKGROUND
Atrophic
gastritis has been shown to be one of the long term sequelae of
Helicobacter pylori infection.
AIMS
To determine the
prevalence of atrophic gastritis in outpatients, to study the accuracy
of serological methods for revealing atrophy, and to define the
association of H pylori infection with atrophic gastritis in these patients.
PATIENTS/METHODS
A
total of 207 consecutive outpatients referred for gastroscopy were
included. Biopsy specimens from the antrum and corpus were assessed
histologically according to the Sydney system. Serum samples were
studied for H pylori IgG and IgA antibodies
by enzyme immunoassay, CagA antibodies by immunoblot, pepsinogen I by
an immunoenzymometric assay, gastrin by radioimmunoassay, and parietal cell antibodies by indirect immunofluorescence.
RESULTS
Histological
examination revealed atrophic gastritis in 52 (25%) of 207 patients.
H pylori and CagA antibodies were strongly associated with atrophic antral gastritis but poorly associated with
atrophic corpus gastritis. Low serum pepsinogen I was the most
sensitive and specific indicator of moderate and severe atrophic corpus
gastritis. All six patients with moderate atrophic corpus gastritis had
H pylori infection but eight of 10 patients
with severe atrophic corpus had increased parietal cell antibodies and
nine had no signs of H pylori infection.
CONCLUSIONS
Atrophic
antral gastritis was strongly associated with CagA positive
H pylori infection. Severe atrophic corpus
gastritis was not determined by H pylori
tests but low serum pepsinogen I, high gastrin, and parietal
cell antibodies may be valuable in detecting these changes.
Keywords: Helicobacter pylori; atrophic gastritis; CagA antibodies; Helicobacter pylori antibodies; pepsinogen; parietal cell antibodies
© 2000 by Gut
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