Prospective evaluation of the prevalence of gastric Helicobacter pylori infection in patients with GERD, Barrett's esophagus, Barrett's dysplasia, and Barrett's adenocarcinoma.
OBJECTIVE
This study was undertaken to prospectively determine the prevalence of gastric H. pylori infection in Barrett's esophagus and Barrett's complicated by dysplasia or adenocarcinoma.


METHODS
The prevalence of H. pylori was determined in Barrett's esophagus patients compared to a control population of patients with gastroesophageal reflux disease (GERD) only. All patients had a minimum of 10 gastric surveillance biopsies obtained. H. pylori colonization was determined upon the basis of hematoxylin and eosin and use of a modified Giemsa and or Steiner's silver stain of all gastric biopsy specimens.


RESULTS
Two hundred and eighty-nine Barrett's patients and 217 GERD control patients were included in the study. H. pylori was found in 95/289 (32.9%) of the Barrett's patients, compared with 96/217 (44.2%) of the GERD controls (NS). Forty-seven of the Barrett's patients had low-grade dysplasia/indefinite dysplasia, 14 high-grade dysplasia, and 20 Barrett's adenocarcinoma. When Barrett's was subgrouped according to absence of dysplasia, and presence of low-grade dysplasia, high-grade dysplasia, or adenocarcinoma, H. pylori prevalence was found to be significantly less for patients with Barrett's high-grade dysplasia (14.3%) and adenocarcinoma (15.0%) versus patients with GERD alone (44.2%), Barrett's alone (35.1%), or Barrett's with low-grade dysplasia (36.2%) (p = 0.016). This difference could not be explained by differences between Barrett's esophagus patients infected with H. pylori and those who were not with respect to gender, smoking history, alcohol consumption, use of proton pump inhibitor, or length of Barrett's mucosa.


CONCLUSIONS
Barrett's high-grade dysplasia and adenocarcinoma are significantly more prevalent in patients who are not infected with H. pylori. H. pylori appears to have a protective effect against the development of Barrett's adenocarcinoma.
Weston
A P
AP
Veterans Administration Medical Center, Kansas City, Missouri, 64128, USA.
Badr
A S
AS
Topalovski
M
M
Cherian
R
R
Dixon
A
A
Hassanein
R S
RS
D000230:Adenocarcinoma / Q000453:epidemiology / Q000382:microbiology*; D000428:Alcohol Drinking / Q000453:epidemiology; D000704:Analysis of Variance; D001471:Barrett Esophagus / Q000453:epidemiology / Q000382:microbiology* / Q000473:pathology; D001706:Biopsy; D016009:Chi-Square Distribution; D004396:Coloring Agents; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D004938:Esophageal Neoplasms / Q000453:epidemiology / Q000382:microbiology*; D004945:Esophagoscopy; D005260:Female; D005500:Follow-Up Studies; D005764:Gastroesophageal Reflux / Q000188:drug therapy / Q000453:epidemiology / Q000382:microbiology*; D016481:Helicobacter Infections / Q000453:epidemiology*; D016480:Helicobacter pylori / Q000254:growth & development; D006801:Humans; D007615:Kansas / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D011446:Prospective Studies; D054328:Proton Pump Inhibitors; D012907:Smoking / Q000453:epidemiology; D013272:Stomach Diseases / Q000453:epidemiology / Q000382:microbiology*
D004396:Coloring Agents; D004791:Enzyme Inhibitors; D054328:Proton Pump Inhibitors