Helicobacter pylori infection correlates with severity of reflux esophagitis: with manometry findings

J Gastroenterol. 1999 Oct;34(5):553-9. doi: 10.1007/s005350050372.

Abstract

The role of Helicobacter pylori infection in the development and exacerbation of reflux esophagitis was investigated. The prevalence of Helicobacter pylori infection, the severity of atrophic gastritis, and esophageal motility (determined by esophageal manometry by an infusion catheter method) were assessed in patients with mild (n = 46) and severe (n = 27) reflux esophagitis and subjects without reflux (n = 28). Compared with the prevalence of Helicobacter pylori infection in the non-reflux group, the prevalence in the mild and severe reflux groups (60.7%, 47.8%, and 14.8%, respectively) was significantly (P < 0.05) lower. Atrophic gastritis was milder in both reflux groups than in the non-reflux group. The degree of gastritis was also milder in the severe reflux group than in the mild reflux group. The esophageal sphincter pressure was significantly (P < 0.05) lower in the reflux groups than in the non-reflux group, and the amplitude of primary peristalsis was significantly (P < 0.05) lower in the severe reflux group than in the non-reflux group. There were no significant differences between reflux patients with and without Helicobacter pylori infection in the parameters of esophageal manometry. These data imply that a low prevalence of Helicobacter pylori infection may result in a milder grade of atrophic gastritis, and consequently, exacerbate reflux esophagitis.

MeSH terms

  • Analysis of Variance
  • Esophagitis, Peptic / microbiology*
  • Esophagitis, Peptic / physiopathology*
  • Female
  • Gastritis, Atrophic / microbiology*
  • Gastritis, Atrophic / physiopathology*
  • Helicobacter Infections / diagnosis
  • Helicobacter Infections / physiopathology*
  • Helicobacter pylori* / isolation & purification
  • Humans
  • Male
  • Manometry
  • Middle Aged
  • Pepsinogen A / blood
  • Severity of Illness Index

Substances

  • Pepsinogen A