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Helicobacter pylori with stronger intensity of CagA phosphorylation lead to an increased risk of gastric intestinal metaplasia and cancer.

Chuang CH, Yang HB, Sheu SM, Hung KH, Wu JJ, Cheng HC, Chang WL, Sheu BS - BMC Microbiol. (2011)

Bottom Line: Nearly all Taiwanese H. pylori stains are cagA-genopositive and encode CagA protein.In this study, we evaluated whether different intensity of tyrosine phosphorylated-CagA (p-CagA) had an impact on the clinical diseases and histological outcomes in this area.The p-CagA was sparse in 30 (20.5%), weak in 59 (40.5%), and strong in 57 (39%) isolates.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Internal Medicine, National Cheng Kung University, Tainan, Taiwan.

ABSTRACT

Background: Nearly all Taiwanese H. pylori stains are cagA-genopositive and encode CagA protein. In this study, we evaluated whether different intensity of tyrosine phosphorylated-CagA (p-CagA) had an impact on the clinical diseases and histological outcomes in this area.

Results: We enrolled 469 dyspeptic patients and prospectively obtained the gastric biopsy specimens and the H. pylori isolates. These patients were categorized according to the clinical diseases, such as duodenal ulcer, gastric ulcer, gastric cancer, and gastritis with or without intestinal metaplasia. Their gastric specimens were reviewed by the updated Sydney's system. Furthermore, a total of 146 patients were randomly selected from each clinical category for evaluation of their isolates' p-CagA intensity by in vitro AGS cells co-culture. The p-CagA was sparse in 30 (20.5%), weak in 59 (40.5%), and strong in 57 (39%) isolates. The isolates from the patients of gastric cancer or gastritis with intestinal metaplasia had stronger p-CagA intensity than those of gastritis without intestinal metaplasia (p ≤ 0.002). Moreover, the patients infected with isolates with strong or weak p-CagA intensity had a higher risk of gastric intestinal metaplasia (p < 0.05, odds ratio 3.09~15.26) than those infected with sparse p-CagA isolates.

Conclusions: Infection with H. pylori stains with stronger p-CagA intensity may lead to an increased risk of gastric intestinal metaplasia and cancer.

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The patients infected with strains with strong or weak p-CagA intensity had more corpus-predominant gastritis than those infected with strains with sparse p-CagA intensity (p = 0.001, Pearson chi-square test).
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Figure 5: The patients infected with strains with strong or weak p-CagA intensity had more corpus-predominant gastritis than those infected with strains with sparse p-CagA intensity (p = 0.001, Pearson chi-square test).

Mentions: In Figure 5, a higher proportion of patients infected with a strain with strong p-CagA intensity had corpus-predominant gastritis (59.6%), as compared to those infected with strains with weak (40%) or sparse (25.9%) p-CagA intensity (p = 0.001). The adjusted odds ratio for age, gender, and clinical diagnoses by logistic regression was 3.15 (1.07~9.31) for patients infected with H. pylori with strong p-CagA intensity and 1.49 (0.51~4.35) for those infected with strains with weak p-CagA intensity, as compared with those with sparse p-CagA intensity.


Helicobacter pylori with stronger intensity of CagA phosphorylation lead to an increased risk of gastric intestinal metaplasia and cancer.

Chuang CH, Yang HB, Sheu SM, Hung KH, Wu JJ, Cheng HC, Chang WL, Sheu BS - BMC Microbiol. (2011)

The patients infected with strains with strong or weak p-CagA intensity had more corpus-predominant gastritis than those infected with strains with sparse p-CagA intensity (p = 0.001, Pearson chi-square test).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3117684&req=5

Figure 5: The patients infected with strains with strong or weak p-CagA intensity had more corpus-predominant gastritis than those infected with strains with sparse p-CagA intensity (p = 0.001, Pearson chi-square test).
Mentions: In Figure 5, a higher proportion of patients infected with a strain with strong p-CagA intensity had corpus-predominant gastritis (59.6%), as compared to those infected with strains with weak (40%) or sparse (25.9%) p-CagA intensity (p = 0.001). The adjusted odds ratio for age, gender, and clinical diagnoses by logistic regression was 3.15 (1.07~9.31) for patients infected with H. pylori with strong p-CagA intensity and 1.49 (0.51~4.35) for those infected with strains with weak p-CagA intensity, as compared with those with sparse p-CagA intensity.

Bottom Line: Nearly all Taiwanese H. pylori stains are cagA-genopositive and encode CagA protein.In this study, we evaluated whether different intensity of tyrosine phosphorylated-CagA (p-CagA) had an impact on the clinical diseases and histological outcomes in this area.The p-CagA was sparse in 30 (20.5%), weak in 59 (40.5%), and strong in 57 (39%) isolates.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Internal Medicine, National Cheng Kung University, Tainan, Taiwan.

ABSTRACT

Background: Nearly all Taiwanese H. pylori stains are cagA-genopositive and encode CagA protein. In this study, we evaluated whether different intensity of tyrosine phosphorylated-CagA (p-CagA) had an impact on the clinical diseases and histological outcomes in this area.

Results: We enrolled 469 dyspeptic patients and prospectively obtained the gastric biopsy specimens and the H. pylori isolates. These patients were categorized according to the clinical diseases, such as duodenal ulcer, gastric ulcer, gastric cancer, and gastritis with or without intestinal metaplasia. Their gastric specimens were reviewed by the updated Sydney's system. Furthermore, a total of 146 patients were randomly selected from each clinical category for evaluation of their isolates' p-CagA intensity by in vitro AGS cells co-culture. The p-CagA was sparse in 30 (20.5%), weak in 59 (40.5%), and strong in 57 (39%) isolates. The isolates from the patients of gastric cancer or gastritis with intestinal metaplasia had stronger p-CagA intensity than those of gastritis without intestinal metaplasia (p ≤ 0.002). Moreover, the patients infected with isolates with strong or weak p-CagA intensity had a higher risk of gastric intestinal metaplasia (p < 0.05, odds ratio 3.09~15.26) than those infected with sparse p-CagA isolates.

Conclusions: Infection with H. pylori stains with stronger p-CagA intensity may lead to an increased risk of gastric intestinal metaplasia and cancer.

Show MeSH
Related in: MedlinePlus