Abstract
Background: Recent studies have investigated the role of Helicobacter pylori infection in the development of gastric mucosa-associated lymphoid tissue (MALT) lymphoma. It is estimated that approximately 0.1% of people infected with H. pylori develop gastric MALT. However, the role of the CagA antigen, the highest causative agent of H. pylori, in increasing the risk of gastric MALT remains unclear and controversial. A systematic review and meta-analysis were conducted to evaluate the effect of cagA status on the development of gastric MALT.Methods: All articles evaluating the status of the cagA gene in the development of gastric MALT were collected using systematic searches in online databases, including PubMed, Scopus, Embase, and Google Scholar, regardless of publication date. The association between cagA and gastric MALT was assessed using the odds ratio (OR) summary. In addition, a random-effects model was used in cases with significant heterogeneity.Results: A total of 10 studies met our inclusion criteria, among which 1,860 patients participated. We observed a meaningful association between cagA status and gastric MALT, especially in Western countries (OR: 1.30; 0.90–1.87 with 95% CIs). However, the heterogeneity was significant; therefore, the results should be interpreted with caution. Surprisingly, a strong positive association was observed between cagA status and high-grade lymphomas (OR: 6.43; 2.45–16.84 with 95% CIs). In addition, no study has evaluated the correlation between cagA and vacA, but we observed an inverse association between vacA and gastric MALT risk (OR: 0.92; 0.57–1.50 with 95% CIs). Conclusion: CagA may not play a significant role in the early stages of gastric MALT, but it can be translocated to B cells and affect the development of high-grade lymphomas.
Helicobacter pylori Infection and Gastric Dysbiosis: Can Probiotics Administration Be Useful to Treat This Condition?
