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2005, Number 1

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Bioquimia 2005; 30 (1)

Metaplasia development in patients with chronic gastritis is associated with ureC+, cagA+ and vacA+ Helicobacter pylori infection

Ocádiz-Delgado R, Sobrino-Cossío S, García-García L, Marroquín-Chavira A, Hernández-Mote R, Gariglio P

Language: Spanish
References: 50
Page: 13-22
PDF size: 92.74 Kb.


ABSTRACT

Gastric metaplasia progression is a consequence of chronic gastritis (CG). Patients with this condition are frequently infected by Helicobacter pylori (Hp) and show several symptoms including gastric ulcer formation. In addition, they present an increased risk for the development of gastric adenocarcinoma. Various pathogenicity markers for Hp such as ureC, vacA and cagA genes have been described. Evidence indicates that direct injury to the epithelial mucosa is caused by cytotoxins and enzymes codified by these genes. The aim of this study was to establish a relationship between the presence of pathogenic Hp strains and metaplasia progression in patients with CG. For better understanding the progression of gastroesophagic metaplasia, we detected the presence of Hp ureC, cagA and vacA positive strains in patients with CG. Using the polymerase chain reaction (PCR), we have analyzed 130 samples obtained from 65 patients with CG (mean age: 43.3 years), including samples from two anatomical areas: cardia and gastric antral. We have detected that 92% of CG patients are Hp positive compared to approximately 50% in normal persons older than 40 years (reported previously by other groups); 6% of the CG patients were diagnosed as Barrett´s Esophagous positive, 50% of these patients were positive for either ureC(+), cagA(+) and/or vacA(+) Hp strains. A strong tendency to develop metaplasia was observed in those patients diagnosed with CG that were infected with high-pathogenicity-strains in both anatomical areas. These results suggest that infection with high-pathogenicity Hp strains, combined with CG can be considered a major risk factor to develop a precancerous condition.


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