Abstract
Duodenogastric reflux (DGR) causes bile reflux gastritis (BRG) and may develop into gastric cancer. DGR is classified as primary in non-operated stomachs or secondary to surgical intervention. Primary DGR and Helicobacter pylori (H. pylori) infection are reportedly related. However, the mechanism is not fully understood. This study aimed to elucidate the relationship between H. pylori infection and pyloric incompetence in a non-operated stomach. A total of 502 non-operated participants who underwent an upper intestinal endoscopy were prospectively enrolled. Endoscopic findings (EAC, endoscopic atrophy classification; nodular gastritis; xanthoma; fundic gland polyp; and incompetence of pylorus), sex, age, gastrin, pepsinogen (PG) I and PG II levels were evaluated. PG I/PG II ratio, anti-H. pylori-Ab positivity, and atrophic gastritis status were significantly different between the normal and incompetent pylori (p = 0.043, <0.001, and 0.001, respectively). Open-type atrophic gastritis was significantly higher in the incompetent pylori. Incompetence of the pylorus and EAC were moderately correlated (Cramer’s V = 0.25). Multivariate analysis revealed that the presence of anti-H. pylori-Ab was the only independent factor associated with the incompetence of the pylorus, with an adjusted odds ratio of 2.70 (95% CI: 1.47–4.94, p = 0.001). In conclusion, pyloric incompetence was associated with H. pylori infection and moderately correlated to the severity of atrophic gastritis in non-operated stomachs.
Highlights
Among reflux diseases in the gastrointestinal (GI) tract, the competence of the junctions is critical
The presence of anti-H. pylori antibodies was the only independent factor associated with pyloric incompetence, with an adjusted odds ratio of 2.70
We demonstrated that H. pylori infection was an independent factor for pyloric incompetence in non-operated stomachs
Summary
Among reflux diseases in the gastrointestinal (GI) tract, the competence of the junctions is critical. Long-term DGR has already been known to cause pathological conditions, such as chronic gastritis, foveolar hyperplasia, intestinal metaplasia, gastric dysplasia, and gastric cancer [9,10,11,12,13,14]. In primary DGR/BRG, gastroduodenal ulcers were proposed as one of the factors for pyloric incompetence [16]. Read et al demonstrated that the reflux occurred within 30 s from the time that an individual would start to smoke, as viewed in most cases of 13 normal volunteers [22]. It seemed that a consensus had been reached regarding the cause of DGR
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