24 hour esophageal pH changes in patients with peptic ulcer disease before and after Helicobacter pylori eradication.
- Author:
Cheol Hee PARK
1
;
Jong Hyeok KIM
;
Hak Yang KIM
;
Gwang Ho BAIK
;
Joon Ho MOON
;
Chul Sung PARK
;
Kil Chan OH
;
Do Kyun JIN
;
Jin Cheol PARK
;
Kyoung Oh KIM
;
Kyo Sang YOO
;
Tai Ho HAN
;
Sang Hoon PARK
;
Choong Kee PARK
;
Hyeong Su KIM
Author Information
1. Department of Internal Medicine, College of Medicine, Hallym University, Anyang, Korea. kjh825@hallym.or.kr
- Publication Type:Original Article
- Keywords:
Helicobacter pylori;
GERD;
Peptic ulcer
- MeSH:
Azure Stains;
Breath Tests;
Esophageal pH Monitoring;
Esophagitis, Peptic;
Gastroesophageal Reflux;
Helicobacter pylori*;
Helicobacter*;
Humans;
Hydrogen-Ion Concentration*;
Incidence;
Peptic Ulcer*;
Prevalence;
Risk Factors;
Urea;
Urease
- From:Korean Journal of Medicine
2004;67(2):146-152
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: There are many arguments that Helicobacter pylori is a protective factor or a risk factor for GERD. Some authors reported a high incidence of reflux esophagitis in patients who had received Helicobacter pylori eradication therapy. We studied the prevalence of pathologic gastroesophageal reflux in Helicobacter pylori positive peptic ulcer patients and the effects of Helicobacter pylori eradication therapy on development of pathologic gastroesophageal reflux. METHODS: A total of 44 patients with endoscopically documented peptic ulcer disease and Helicobacter pylori infection underwent 24-hour esophageal pH monitoring and received a week of triple therapy. After three months of cessation of triple therapy, patients underwent 24-hour esophageal pH monitoring again. 24-hour esophageal pH monitoring of 44 patients were compared before and after the triple therapy. Helicobacter pylori status was evaluated by Giemsa stain, rapid urease test and urea breath test at each examination. RESULTS: The patients were classified into cured and ongoing Helicobacter pylori infection group. In cured patients group, there was no significant difference in the prevalence of pathologic gastroesophageal reflux before and after Helicobacter pylori eradication (p=0.8). In 44 patients, 30 patients had pathologic gastroesophageal reflux before eradication. In these patients, 27 patients cured Helicobacter pylori infection and 3 patients were ongoing Helicobacter pylori infection. Among 27 patients who cured Helicobacter pylori infection, 5 patients recovered from pathologic gastroesophageal reflux after eradication. In patients without pathologic gastroesophageal reflux before eradication, the prevalence of pathologic gastroesophageal reflux was not associated with Helicobacter pylori eradication (p=1). CONCLUSION: We find that the prevalence of pathologic gastroesophageal reflux in patients with peptic ulcer is high before Helicobacter pylori eradication. We suggest that Helicobacter pylori eradication in patients with peptic ulcer disease is not associated with development of pathologic gastroesophageal reflux.
