Effect of H. pylori eradication on gastric preneoplastic lesions and gastritis progression

Background: It is assumed that the sequence of events in gastric cancer is as follows: chronic gastritis, atrophy, intestinal metaplasia (IM), dysplasia and carcinoma. It is also known that Helicobacter  pylori (H.pylori) can be involved in the chain of these chronic phenomena.
 
Objectives: This study investigated to compare the changes in the grades of gastric preneoplastic lesions over time in cases with H. pylori eradication and in cases where H. pylori could not be eradicated. In addition, it was aimed to retrospectively examine whether there was a significant change in the severity of gastritis and the degree of gastric preneoplastic lesion in cases in which H. pylori could be eradicated.
 
Methods: Patients who had dyspeptic complaints and were diagnosed with H. pylori gastritis, atrophy and intestinal metaplasia or dysplasia were enrolled in the study between January 2009- January 2016. Patients who underwent H. pylori eradication therapy were included in the study in terms of surveillance programs for gastric carcinoma. The medical records of the patients were reviewed retrospectively. Atrophy, intestinal metaplasia and dysplasia grades were determined during the first endoscopy. The Operative Link for Gastritis Assessment (OLGA) and The Operative Link on Gastritis Intestinal Metaplasia Assessment (OLGIM) scores were recorded. Severe gastritis define as OLGA stage III-IV and/or OLGIM stage III-IV.
 
Results: In total, 5736 patients were enrolled. 97 patients who were diagnosed with intestinal metaplasia and/or atrophy as a result of endoscopic biopsy and were followed up regularly by surveillance were included in our study. According to the initial endoscopy, gastric atrophy was detected in 75.3% (73) of the cases and intestinal metaplasia was detected in 75.3% (73). Severe gastritis  was detected in 17.5% (17) and low-grade dysplasia was detected in 3.1% (3). According to the latest endoscopic biopsy results H. pylori was eradicated in 27.8% (27) of the cases. In the group with successful eradication of H.pylori, a statistically significant decrease was observed in the frequency of atrophy and intestinal metaplasia at the last visit. A nearly significant decrease was observed in the frequency of severe gastritis (p=0.06). Significant decreases were detected in OLGA (1.2 ± 1.0 vs. 0.4 ± 0.5) and OLGIM (1.3 ± 1.2 vs. 0.7 ± 0.9) scores. (p ˂ .001 and p=.03. respectively). In the group with successful eradication of H.pylori in a mean follow-up of 23.6 months, dysplasia disappeared in 2 patients who were found at the first visit.
 In the group with unsuccessful eradication of H.pylori, there was no significant change in the frequency of severe gastritis or dysplasia. Nearly significant (0.8 ± 0.6 vs. 0.5 ± 0.8. p=.052) change was detected in the OLGA score, while in the OLGIM score (1.4 ± 1.1 vs. 1.0 ± 1.1. p=.002) a significant decrease was detected.
Conclusions: A statistically significant decrease in the frequency of atrophy and intestinal metaplasia, a significant decrease was also detected in OLGA and OLGIM scores were observed with the success of eradication of H. pylori in gastric cancer. A nearly significant decrease was observed in the frequency of severe gastritis. We believe that H. pylori eradication treatment should be performed in H. pylori-positive precancerous gastric lesions
 