Association between Helicobacter pylori and Gastric Cancers

Correspondence to: Kadir Ozturk Department of Gastroenterology, Gulhane School of Medicine, Etlik, Kecioren, Ankara 06010, Turkey Tel: +90-3123044045, Fax: +90-3123044047, E-mail: [email protected] Received on July 10, 2015. Accepted on August 1, 2015. Published online January 19, 2016 pISSN 1976-2283 eISSN 2005-1212 https://doi.org/10.5009/gnl15316 To the Editor, Gastric cancer is the third most common cause of cancerrelated deaths in both sexes worldwide. Helicobacter pylori infection is the greatest known risk factor for the development of gastric cancer. H. pylori can cause chronic active gastritis and atrophic gastritis by producing persistent acute-on-chronic inflammation. Therefore, screening and treatment of H. pylori is an important strategy for preventing gastric cancer in high-risk populations, particularly among Japanese and Korean populations. We recently read the paper by Kim et al., who evaluated the clinicopathologic features of H. pylori infection-negative gastric cancer (HPIN-GC) compared with H. pylori infectionpositive gastric cancer (HPIP-GC). Based on their results, the authors concluded that the prevalence of HPIN-GC was extremely low, and its clinicopathologic characteristics were similar to that of HPIP-GC. However, we believe that certain additional points should be discussed. First, patients with gastric cancer were divided into two groups according to the H. pylori status in the study. One hundred sixty-four patients with past infection (by anti-H. pylori IgG positivity) or an eradication history of H. pylori were included as the HPIP-GC group. However, patients with current H. pylori infection have a higher risk of developing gastric cancer compared with patients with past infection or an eradication history of H. pylori because the eradication of H. pylori reduces the risk of gastric cancer. Several clinical studies have reported that the successful treatment of H. pylori decreases the risk of developing gastric cancer by approximately 3 fold. Therefore, we suggest that patients with gastric cancer should be categorized into three groups: patients with current, past, and negative H. pylori infection. Therefore, Kim et al. could also evaluate the effect of H. pylori eradication on gastric cancer in their study. Second, Kim et al. have defined current H. pylori infections according to the results from at least one of the following tests: histological, rapid urease, and culture. However, the American College of Gastroenterology guidelines for the management of H. pylori infection recommends using at least two different tests to diagnose of H. pylori except culture. Therefore, this issue might be a reason for the small number of patients with HPINGC compared with previous studies. Third, the concentrations of serum pepsinogen (PG) I and II were measured in fasting serum samples, and patients with PG I/II ratio ≤3 were considered to have atrophic gastritis. Importantly, the serum levels of PG cannot provide accurately identifications if proton pump inhibitors are used. However, information on the use of these drugs is not available in this study. Finally, infection with CagA-positive H. pylori strain has been associated with a higher risk of developing gastric cancer because it is a more virulent strain. However, Kim et al. did not assess genetic analyses for H. pylori. Therefore, we conclude that the study by Kim et al. should be rearranged to account for the above-mentioned suggestions before interpretations are provided. This could provide the readers of the journal with clearer information regarding the relationship between H. pylori infection and gastric cancer.