+ and vacuolizing cytotoxin (VacA
)-specific strains of Helicobacter pylori
have been associated with different risks for developing gastric lesions. We aim to summarize a possible association between these genotypes and the risk for developing different gastric phenotypes.
Materials and methods
A MEDLINE database (PubMed) search was performed and a meta-analysis conducted.
Forty-four studies were retrieved, all with either a case–control (n
=13) or cross-sectional (n
=31) design, including 17 374 patients. CagA
positivity was associated with an increased risk for gastric cancer [odds ratio (OR) 2.09 (95% confidence interval (CI), 1.48–2.94)] compared with that in individuals without gastric lesions [OR 2.44 (95% CI 1.27–4.70)] and in those with previously identified gastritis. In addition, there was an increased risk for peptic ulcer disease
[OR 1.69 (95% CI 1.12–2.55)]. Individuals harboring the H. pylori
s1 (vs. s2), m1 (vs. m2), s1m1 (vs. s1m2), and s1m1 (vs. s2m2) had an increased risk for development of cancer [OR of 5.32 (95% CI 2.76–10.26), 2.50 (95% CI 1.67–3.750), 2.58 (95% CI 1.24–5.38), and 4.36 (95% CI 2.08–9.10), respectively]. s1m1 strains (vs. s2m2) were also associated with peptic ulcer disease
[OR 2.04 (1.01–4.13)].
Our results indicate that individuals infected with CagA
+ H. pylori
strains and those infected with VacA
s1 and m1 strains have an increased risk for gastric cancer. Cohort studies are welcome to integrate this information in the management of at-risk individuals such as those with precancerous cancer conditions and/or a family history of gastric cancer.