Effect of gastric helicobacter pylori colonization in the development of erosive esophagitis in patients with hiatal hernia.

Abstract

There may be various factors that determine gastroesophageal reflux disease (GERD) as a result of hiatal hernia (HH) (such as the size of the hernia, age, other host and environmental factors) and the presence of protective factors to explain the absence of reflux disease should not be ignored. Helicobacter pylori (Hp) infection can prevent the development of GERD or cause it. This study aimed to determine whether Hp colonized in the stomach and hernia affects the development of erosive esophagitis (EE) in patients with HH. In this case-controlled study, 111 patients with HH were eligible for the study. Study group with EE (n = 61, 55%) and control group without EE (n = 50, 45%) were formed. Groups were compared for gastric Hp and Hp in the hernia. While the frequency of Hp in the antrum was 55.7% in the group with EE, it was 30% in the control group (p = 0.01, OR: 2.94 in 95% CI 1.34-6.46). The rates in terms of HP frequency in the corpus were 43.6% and 32.1%, respectively, (p = 0.45). Hp colonization in HH was detected in 18 cases (29.50%) and 14 cases (28%), respectively, (p = 0.86). In regression analysis, antral Hp was found to be effective in the development of EE (p = 0.01). As a result of this study, we think that antral Hp may have a causative role in the development of reflux esophagitis, but the presence of Hp in HH does not have an effective role in reflux esophagitis formation.