Literature DB >> 16944298

Helicobacter pylori infection is associated with a high incidence of intestinal metaplasia in the gastric mucosa of patients at inner-city hospitals in New York.

J Schneller1, R Gupta, J Mustafa, R Villanueva, E W Straus, R D Raffaniello.   

Abstract

Gastric carcinogenesis is a multistep process progressing from chronic gastritis, through glandular atrophy (GA), intestinal metaplasia (IM) and dysplasia. Infection of the stomach with H. pylori increases the risk of developing gastric cancer. Few studies have examined the degree to which Hp-induced changes occur in specific populations. In the present study, we examined the association between Hp infection and histological changes in the gastric mucosa of patients at two inner-city hospitals in New York. Patients enrolled in this study were undergoing endoscopy for gastrointestinal complaints. One antral biopsy was taken for detecting and genotyping Hp by PCR. Additional biopsies were taken from the antrum and fundic region for histological analysis and were scored with respect to acute and chronic inflammation, GA, IM and Hp infestation according to the Sydney classification. Hp strains infecting these patients were genotyped with respect to the expression of Hp virulence factors including VacA, CagA, and BabA2. Samples were collected from 126 patients at Kings County Hospital in Brooklyn and St. John's Episcopal Hospital in Queens. Hp infection rates were highest in Blacks (41.6%) and Hispanics (29.4%) and lowest in Caucasians (18.8%). Scores for acute and chronic inflammation and IM were higher in Hp-infected individuals in both the antrum and fundic regions, whereas Hp infection did not affect the incidence or intensity of GA. In Hp-infected individuals, the incidence of IM was greater in the antrum (Hp-infected 37.8% vs. non-infected 9.2%, p < 0.05) and fundic region (Hp-infected 15.1% vs. noninfected 1.8%, p < 0.05). Genotyping of the Hp strains infecting these patients revealed that the predominant VacA allele was s1 bm 1 and that the CagA gene was present in 69.8% of Hp-infected samples. Interestingly, the BabA2 gene was detected in only four samples (9.3%). The incidence of IM in the antrum was higher in CagA + samples when compared with CagA- samples (52.2% vs. 15.4%, respectively). Our findings indicate that the virulent Hp strain infecting minority patients treated at inner-city hospitals in New York City is associated with a high incidence of IM and that these patients may be at greater risk for developing gastric cancer than the general population.

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Year:  2006        PMID: 16944298     DOI: 10.1007/s10620-006-9167-4

Source DB:  PubMed          Journal:  Dig Dis Sci        ISSN: 0163-2116            Impact factor:   3.199


  34 in total

Review 1.  Helicobacter pylori infection and gastric cancer.

Authors:  A R Goldstone; P Quirke; M F Dixon
Journal:  J Pathol       Date:  1996-06       Impact factor: 7.996

2.  Helicobacter pylori and gastric cancer: state of the art.

Authors:  P Correa
Journal:  Cancer Epidemiol Biomarkers Prev       Date:  1996-06       Impact factor: 4.254

3.  Helicobacter pylori genotypes may determine gastric histopathology.

Authors:  C Nogueira; C Figueiredo; F Carneiro; A T Gomes; R Barreira; P Figueira; C Salgado; L Belo; A Peixoto; J C Bravo; L E Bravo; J L Realpe; A P Plaisier; W G Quint; B Ruiz; P Correa; L J van Doorn
Journal:  Am J Pathol       Date:  2001-02       Impact factor: 4.307

Review 4.  Helicobacter pylori and gastric cancer.

Authors:  J M Scheiman; A F Cutler
Journal:  Am J Med       Date:  1999-02       Impact factor: 4.965

5.  Helicobacter pylori babA2, cagA, and s1 vacA genes work synergistically in causing intestinal metaplasia.

Authors:  C-F Zambon; F Navaglia; D Basso; M Rugge; M Plebani
Journal:  J Clin Pathol       Date:  2003-04       Impact factor: 3.411

6.  Patients younger than 40 years with gastric carcinoma: Helicobacter pylori genotype and associated gastritis phenotype.

Authors:  M Rugge; G Busatto; M Cassaro; Y H Shiao; V Russo; G Leandro; C Avellini; A Fabiano; A Sidoni; A Covacci
Journal:  Cancer       Date:  1999-06-15       Impact factor: 6.860

7.  Key importance of the Helicobacter pylori adherence factor blood group antigen binding adhesin during chronic gastric inflammation.

Authors:  C Prinz; M Schöniger; R Rad; I Becker; E Keiditsch; S Wagenpfeil; M Classen; T Rösch; W Schepp; M Gerhard
Journal:  Cancer Res       Date:  2001-03-01       Impact factor: 12.701

8.  Helicobacter pylori cagA status and s and m alleles of vacA in isolates from individuals with a variety of H. pylori-associated gastric diseases.

Authors:  D G Evans; D M Queiroz; E N Mendes; D J Evans
Journal:  J Clin Microbiol       Date:  1998-11       Impact factor: 5.948

Review 9.  Oncogenic mechanisms of the Helicobacter pylori CagA protein.

Authors:  Masanori Hatakeyama
Journal:  Nat Rev Cancer       Date:  2004-09       Impact factor: 60.716

10.  Genomic-sequence comparison of two unrelated isolates of the human gastric pathogen Helicobacter pylori.

Authors:  R A Alm; L S Ling; D T Moir; B L King; E D Brown; P C Doig; D R Smith; B Noonan; B C Guild; B L deJonge; G Carmel; P J Tummino; A Caruso; M Uria-Nickelsen; D M Mills; C Ives; R Gibson; D Merberg; S D Mills; Q Jiang; D E Taylor; G F Vovis; T J Trust
Journal:  Nature       Date:  1999-01-14       Impact factor: 49.962

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  3 in total

1.  Variations in the multimerization region of the Helicobacter pylori cytotoxin CagA affect virulence.

Authors:  Daiva Ahire; Tricia Alston; Robert Raffaniello
Journal:  Oncol Lett       Date:  2017-01-02       Impact factor: 2.967

Review 2.  Autoimmune atrophic gastritis: current perspectives.

Authors:  Artem Minalyan; Jihane N Benhammou; Aida Artashesyan; Michael S Lewis; Joseph R Pisegna
Journal:  Clin Exp Gastroenterol       Date:  2017-02-07

Review 3.  Autoimmunity and Gastric Cancer.

Authors:  Nicola Bizzaro; Antonio Antico; Danilo Villalta
Journal:  Int J Mol Sci       Date:  2018-01-26       Impact factor: 5.923

  3 in total

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