Literature DB >> 9163441

Equally high prevalences of infection with cagA-positive Helicobacter pylori in Chinese patients with peptic ulcer disease and those with chronic gastritis-associated dyspepsia.

Z J Pan1, R W van der Hulst, M Feller, S D Xiao, G N Tytgat, J Dankert, A van der Ende.   

Abstract

Approximately 60% of Helicobacter pylori isolates in the Western world possess the cytotoxin-associated gene A (cagA). cagA-positive H. pylori is found to be associated with peptic ulcer disease (PUD) and gastric adenocarcinoma. To investigate the cagA status of H. pylori isolates from Chinese patients with PUD and chronic gastritis (CG), H. pylori populations from 83 patients, 48 with PUD and 35 with CG, were assessed by two different cagA-specific PCRs, Southern blotting, and colony hybridization. The combined results from PCR, Southern blotting, and colony hybridization indicate a prevalence of cagA-positive H. pylori isolates of 98% (47 of 48) among Chinese PUD patients and 100% (35 of 35) among Chinese CG patients. Amplification with primer sets 1 and 2 yielded 52 and 95% of the 82 cagA-positive Chinese H. pylori, respectively. In contrast, the sensitivity of cagA-specific PCR for cagA-positive H. pylori isolates from Dutch patients with primer set 1 was 92% (112 of 122) and that with primer set 2 was 91% (50 of 55). The prevalence of cagA-positive H. pylori populations in Chinese patients with PUD and CG is almost universally high. Therefore, cagA cannot be used as a marker for the presence of PUD in Chinese patients. Our data further suggest that allelic variation in cagA may exist and that distinct H. pylori genotypes may circulate in China and Western Europe.

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Year:  1997        PMID: 9163441      PMCID: PMC229746          DOI: 10.1128/jcm.35.6.1344-1347.1997

Source DB:  PubMed          Journal:  J Clin Microbiol        ISSN: 0095-1137            Impact factor:   5.948


  24 in total

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Authors:  M F Dixon
Journal:  J Gastroenterol Hepatol       Date:  1991 Mar-Apr       Impact factor: 4.029

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

Authors:  E A Rauws; W Langenberg; H J Houthoff; H C Zanen; G N Tytgat
Journal:  Gastroenterology       Date:  1988-01       Impact factor: 22.682

3.  Unidentified curved bacilli on gastric epithelium in active chronic gastritis.

Authors:  J R Warren; B Marshall
Journal:  Lancet       Date:  1983-06-04       Impact factor: 79.321

Review 4.  Helicobacter pylori and peptic ulcer disease.

Authors:  R W Van der Hulst; G N Tytgat
Journal:  Scand J Gastroenterol Suppl       Date:  1996

5.  Mucosal IgA recognition of Helicobacter pylori 120 kDa protein, peptic ulceration, and gastric pathology.

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Journal:  Lancet       Date:  1991-08-10       Impact factor: 79.321

6.  Identification of Campylobacter pyloridis isolates by restriction endonuclease DNA analysis.

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Journal:  J Clin Microbiol       Date:  1986-09       Impact factor: 5.948

7.  Prevalence of Helicobacter pylori infection and histologic gastritis in asymptomatic persons.

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Journal:  N Engl J Med       Date:  1989-12-07       Impact factor: 91.245

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Authors:  J H Oudbier; W Langenberg; E A Rauws; C Bruin-Mosch
Journal:  J Clin Microbiol       Date:  1990-03       Impact factor: 5.948

9.  Characterization of and human serologic response to proteins in Helicobacter pylori broth culture supernatants with vacuolizing cytotoxin activity.

Authors:  T L Cover; C P Dooley; M J Blaser
Journal:  Infect Immun       Date:  1990-03       Impact factor: 3.441

10.  Antibody response of patients against a 120 kDa surface protein of Campylobacter pylori.

Authors:  I Apel; E Jacobs; M Kist; W Bredt
Journal:  Zentralbl Bakteriol Mikrobiol Hyg A       Date:  1988-04
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  63 in total

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2.  Helicobacter pylori: the primary cause of duodenal ulceration or a secondary infection?

Authors:  M Hobsley; F I Tovey
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3.  Increased expression of IL-10 and IL-12 (p40) mRNA in Helicobacter pylori infected gastric mucosa: relation to bacterial cag status and peptic ulceration.

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Journal:  J Clin Pathol       Date:  1999-09       Impact factor: 3.411

4.  Co-expression in Helicobacter pylori of cagA and non-opsonic neutrophil activation enhances the association with peptic ulcer disease.

Authors:  D Danielsson; S M Farmery; B Blomberg; S Perry; H Rautelin; J E Crabtree
Journal:  J Clin Pathol       Date:  2000-04       Impact factor: 3.411

5.  Consensus and variable region PCR analysis of Helicobacter pylori 3' region of cagA gene in isolates from individuals with or without peptic ulcer.

Authors:  C A Rota; J C Pereira-Lima; C Blaya; N B Nardi
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6.  Responses of endoscopy patients in Ladakh, India, to Helicobacter pylori whole-cell and Cag A antigens.

Authors:  Judith Romero-Gallo; Guillermo I Pérez-Pérez; Richard P Novick; Patrick Kamath; Tsering Norbu; Martin J Blaser
Journal:  Clin Diagn Lab Immunol       Date:  2002-11

7.  Interleukin-10 (-819 C/T) and tumor necrosis factor-alpha (-308 G/A) gene variants influence gastritis and lymphoid follicle development.

Authors:  B R Achyut; Priya Tripathi; Uday Chand Ghoshal; Nikhil Moorchung; Balraj Mittal
Journal:  Dig Dis Sci       Date:  2007-08-24       Impact factor: 3.199

8.  A new subtype of 3' region of cagA gene in Helicobacter pylori strains isolated from Zhejiang Province in China.

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Journal:  World J Gastroenterol       Date:  2004-11-15       Impact factor: 5.742

9.  Prevalence of virulence-associated genotypes of Helicobacter pylori and correlation with severity of gastric pathology in patients from western Sicily, Italy.

Authors:  A Chiarini; C Calà; C Bonura; A Gullo; G Giuliana; S Peralta; F D'Arpa; A Giammanco
Journal:  Eur J Clin Microbiol Infect Dis       Date:  2008-10-29       Impact factor: 3.267

10.  Helicobacter pylori induces apoptosis of macrophages in association with alterations in the mitochondrial pathway.

Authors:  Rena J Menaker; Peter J M Ceponis; Nicola L Jones
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