Literature DB >> 3335295

Campylobacter pyloridis-associated chronic active antral gastritis. A prospective study of its prevalence and the effects of antibacterial and antiulcer treatment.

E A Rauws1, W Langenberg, H J Houthoff, H C Zanen, G N Tytgat.   

Abstract

To determine the clinical importance of Campylobacter pyloridis infection, its association with gastric inflammation, and the response to drug therapy, patients with a duodenal or gastric ulcer (n = 63), patients with nonulcer dyspepsia (n = 240), and asymptomatic volunteers (n = 34) were studied. In a prospective longitudinal study, the type, intensity, and distribution of inflammation in antral biopsy specimens were correlated with the presence of C. pyloridis. Campylobacter pyloridis was cultured from antral biopsy specimens in 98% of the ulcer patients, 70% of the nonulcer dyspepsia patients, and 20% of the asymptomatic volunteers. The dependency of chronic active gastritis on the presence of C. pyloridis was shown by an association of gastritis with positive culture and healing of gastritis with negative culture after various therapeutic regimens. Spontaneous disappearance of C. pyloridis never occurred. Colloidal bismuth subcitrate, amoxicillin, and the combination of colloidal bismuth subcitrate and amoxicillin were effective therapies in eradicating C. pyloridis. Recolonization with the same bacterial subtype and recurrence of gastritis frequently occurred within 1 mo after initial eradication. In this study we demonstrate ultimate normalization of gastric mucosa after successful eradication of C. pyloridis. Especially complete normalization of gastric mucosa after amoxicillin monotherapy provides additional strong evidence for a true cause-effect relationship between C. pyloridis colonization and gastritis.

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Year:  1988        PMID: 3335295

Source DB:  PubMed          Journal:  Gastroenterology        ISSN: 0016-5085            Impact factor:   22.682


  213 in total

1.  Correlation between epithelial cell proliferation and histological grading in gastric mucosa.

Authors:  D A Lynch; N P Mapstone; A M Clarke; P Jackson; P Moayyedi; M F Dixon; P Quirke; A T Axon
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2.  CXC chemokines Gro(alpha)/IL-8 and IP-10/MIG in Helicobacter pylori gastritis.

Authors:  M Eck; B Schmausser; K Scheller; A Toksoy; M Kraus; T Menzel; H K Müller-Hermelink; R Gillitzer
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Review 3.  Role of Helicobacter pylori in duodenal ulcer.

Authors:  E A Rauws
Journal:  Drugs       Date:  1992-12       Impact factor: 9.546

Review 4.  Helicobacter pylori.

Authors:  B Drumm
Journal:  Arch Dis Child       Date:  1990-11       Impact factor: 3.791

Review 5.  Gastritis.

Authors:  R G Strickland
Journal:  Springer Semin Immunopathol       Date:  1990

6.  Lansoprazole, a novel benzimidazole proton pump inhibitor, and its related compounds have selective activity against Helicobacter pylori.

Authors:  T Iwahi; H Satoh; M Nakao; T Iwasaki; T Yamazaki; K Kubo; T Tamura; A Imada
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7.  Anti-Helicobacter pylori therapy significantly reduces Helicobacter pylori -induced gastric mucosal damage in Mongolian gerbils.

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Journal:  World J Gastroenterol       Date:  2005-02-21       Impact factor: 5.742

8.  Histological study of chronic gastritis from the United Arab Emirates using the Sydney system of classification.

Authors:  A M Zaitoun
Journal:  J Clin Pathol       Date:  1994-09       Impact factor: 3.411

9.  Aetiology of peptic ulcer: a prospective population study in Norway.

Authors:  R Johnsen; O H Førde; B Straume; P G Burhol
Journal:  J Epidemiol Community Health       Date:  1994-04       Impact factor: 3.710

10.  Alpha1,4GlcNAc-capped mucin-type O-glycan inhibits cholesterol alpha-glucosyltransferase from Helicobacter pylori and suppresses H. pylori growth.

Authors:  Heeseob Lee; Ping Wang; Hitomi Hoshino; Yuki Ito; Motohiro Kobayashi; Jun Nakayama; Peter H Seeberger; Minoru Fukuda
Journal:  Glycobiology       Date:  2008-05-05       Impact factor: 4.313

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