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Increased risk of developing atrophic gastritis in patients infected with CagA+ Helicobacter pylori

Sande, N; Nikulin, M; Nilsson, I; Wadström, Torkel LU ; Laxen, F; Harkonen, M; Suovaniemi, O and Sipponen, P (2001) In Scandinavian Journal of Gastroenterology 36(9). p.928-933
Abstract
BACKGROUND: To clarify the possible role of CagA positive (CagA+) Helicobacter pylori strains in the development of atrophic gastritis, the prevalence of antibodies to H. pylori and CagA (120 kD protein) was studied among subjects with atrophic and non-atrophic gastritis. METHODS: The study population was randomly selected among 12,252 Finnish men who were screened for atrophic corpus gastritis with serum pepsinogen I-assay (S-PGI). S-PGI level was used as a selection criterion. Group A consisted of 295 subjects with S-PGI <25 microg/l (low), group B of 320 subjects with S-PGI 25-100 microg/l (normal) and group C of 338 subjects with S-PGI >100 microg/l (high). Antibodies to H. pylori were measured with EIA and immunoblot analysis... (More)
BACKGROUND: To clarify the possible role of CagA positive (CagA+) Helicobacter pylori strains in the development of atrophic gastritis, the prevalence of antibodies to H. pylori and CagA (120 kD protein) was studied among subjects with atrophic and non-atrophic gastritis. METHODS: The study population was randomly selected among 12,252 Finnish men who were screened for atrophic corpus gastritis with serum pepsinogen I-assay (S-PGI). S-PGI level was used as a selection criterion. Group A consisted of 295 subjects with S-PGI <25 microg/l (low), group B of 320 subjects with S-PGI 25-100 microg/l (normal) and group C of 338 subjects with S-PGI >100 microg/l (high). Antibodies to H. pylori were measured with EIA and immunoblot analysis and antibodies to CagA with immunoblot analysis. Endoscopical and histological examinations were performed for 203 patients from group A. RESULTS: The prevalence of antibodies to H. pylori was significantly lower in group B than in groups A or C (P < 0.0001, chi-squared test). There was a significant association between the prevalence of antibodies to CagA and the lowered level of S-PGI (P < 0.0001, Jonckheere-Terpstra trend test). There was also a linear decrease in the prevalence of antibodies to CagA as the atrophic corpus gastritis became more severe (P < 0.0001, linear-by-linear trend test). CONCLUSION: The presence of antibodies to CagA seems to be associated with development of atrophic corpus gastritis. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Atrophic, Gastritis, Caga, Protein, Gastric, Cancer, Helicobacter, Pylori, Pepsinogen
in
Scandinavian Journal of Gastroenterology
volume
36
issue
9
pages
928 - 933
publisher
Taylor & Francis
external identifiers
  • pmid:11521982
  • scopus:0034913090
ISSN
1502-7708
DOI
language
English
LU publication?
yes
id
cba5dcaa-21b7-43be-821e-a2332ea4ebbc (old id 1120963)
date added to LUP
2008-07-14 09:50:34
date last changed
2018-05-29 10:50:58
@article{cba5dcaa-21b7-43be-821e-a2332ea4ebbc,
  abstract     = {BACKGROUND: To clarify the possible role of CagA positive (CagA+) Helicobacter pylori strains in the development of atrophic gastritis, the prevalence of antibodies to H. pylori and CagA (120 kD protein) was studied among subjects with atrophic and non-atrophic gastritis. METHODS: The study population was randomly selected among 12,252 Finnish men who were screened for atrophic corpus gastritis with serum pepsinogen I-assay (S-PGI). S-PGI level was used as a selection criterion. Group A consisted of 295 subjects with S-PGI &lt;25 microg/l (low), group B of 320 subjects with S-PGI 25-100 microg/l (normal) and group C of 338 subjects with S-PGI &gt;100 microg/l (high). Antibodies to H. pylori were measured with EIA and immunoblot analysis and antibodies to CagA with immunoblot analysis. Endoscopical and histological examinations were performed for 203 patients from group A. RESULTS: The prevalence of antibodies to H. pylori was significantly lower in group B than in groups A or C (P &lt; 0.0001, chi-squared test). There was a significant association between the prevalence of antibodies to CagA and the lowered level of S-PGI (P &lt; 0.0001, Jonckheere-Terpstra trend test). There was also a linear decrease in the prevalence of antibodies to CagA as the atrophic corpus gastritis became more severe (P &lt; 0.0001, linear-by-linear trend test). CONCLUSION: The presence of antibodies to CagA seems to be associated with development of atrophic corpus gastritis.},
  author       = {Sande, N and Nikulin, M and Nilsson, I and Wadström, Torkel and Laxen, F and Harkonen, M and Suovaniemi, O and Sipponen, P},
  issn         = {1502-7708},
  keyword      = {Atrophic,Gastritis,Caga,Protein,Gastric,Cancer,Helicobacter,Pylori,Pepsinogen},
  language     = {eng},
  number       = {9},
  pages        = {928--933},
  publisher    = {Taylor & Francis},
  series       = {Scandinavian Journal of Gastroenterology},
  title        = {Increased risk of developing atrophic gastritis in patients infected with CagA+ Helicobacter pylori},
  url          = {http://dx.doi.org/},
  volume       = {36},
  year         = {2001},
}