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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 <i>Helicobacter pylori</i> (<i>H. pylori</i>) infection are reportedly related. However, the mechanism is not fully understood. This study aimed to elucidate the relationship between <i>H. pylori</i> 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-<i>H. pylori</i>-Ab positivity, and atrophic gastritis status were significantly different between the normal and incompetent pylori (<i>p</i> = 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-<i>H. pylori</i>-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, <i>p</i> = 0.001). In conclusion, pyloric incompetence was associated with <i>H. pylori</i> infection and moderately correlated to the severity of atrophic gastritis in non-operated stomachs.