Primary Motility  Disorders of the  Esophagus
 The Esophageal
 Mucosa
 The
 Esophagogastric  Junction
 Barrett's
 Esophagus

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OESO©2015
 
Volume: Barrett's Esophagus
Chapter: Pathophysiology
 

In patients with Barrett's esophagus, what is the prevalence of Helicobacter pylori infection in the antrum? In the cardia?

D.J. Bowrey, G.W.B. Clark (Cardiff, Leeds)

Seroepidemiology indicates that 30%-40% of Western populations have evidence of infection with the Helicobacter pylori bacterium [1]. While the population prevalence of Barrett's esophagus is unclear, hospital studies have estimated that 10% of patients undergoing endoscopy for reflux symptoms have evidence of endoscopically visible Barrett's esophagus [2]. Given these observations, it would not be surprising if the two conditions coexisted in some individuals. Whether the frequency of this dual pathology is more or less than would be anticipated by chance alone has recently been questioned.

It is noteworthy that when Barrett's mucosa comprises a combination of intestinal and gastric type epithelia, H. pylori can infect only the gastric type mucosa. When H. pylori organisms are observed on Barrett's mucosa, their presence in the stomach is invariable. The Table I summarizes the findings of the best studies reported in the literature. The consensus is that there is no difference in the prevalence of H. pylori infection between patients with Barrett's esophagus and control subjects. In the only study that did identify a difference in H. pylori colonization rate, Loffeld et al. [9] detected H. pylori in 44 of 71 patients (62%) with Barrett's esophagus. Comparison was made with two sets of agematched controls, patients with non-ulcer dyspepsia and healthy blood donors. Patients with Barrett's esophagus aged 21-40 years had a higher frequency of H. pylori colonization

Table I. Prevalence of H. pylori in esophageal and gastric biopsies of patients with Barrett's esophagus (BE) compared to gastric biopsies from control subjects.

(80%) than both control groups (non-ulcer dyspeptics 38%, blood donors 24%). Patients with Barrett's esophagus aged 41-60 years had a higher frequency of H. pylori colonization (67%) than the blood donor controls (43%), but not patients with non-ulcer dyspepsia (68%).

In the best of the studies, Vicari et al. [7] compared the frequency of H. pylori between 153 patients with gastroesophageal reflux disease (GERD) to 57 patient controls. Reflux patients were subdivided into three groups according to disease severity: GERD, uncomplicated Barrett's esophagus and Barrett's esophagus complicated by dysplasia or carcinoma. There was no significant difference in the H. pylori colonization rate between either the three reflux groups, nor between controls and patients. However, the prevalence of cagA+ strains of H. pylori diminished progressively with the severity of the reflux disease (controls 42%, gastroesophageal reflux 37%, uncomplicated Barrett's esophagus 13%, complicated Barrett's esophagus 0%). In effect, patients infected with cagA+ strains of H. pylori were protected against the more severe forms of GERD. Overall, patients colonized with cagA+ strains of H. pylori were three times less likely to have a severe form of reflux disease than patients colonized with cagA- strains. This implies that rather than H. pylori infection per se, it is the strain of the organism that may dictate the clinical consequences.

In summary, the frequency of gastric H. pylori infection in patients with Barrett's esophagus will depend upon the prevalence of H. pylori infection in their indigenous population, but it should be no different from that of age and sex matched controls from the same locality.

In a detailed study of 24 patients with H. pylori gastritis, Genta et al. [10] obtained endoscopic biopsies from five antral sites, six corpus sites and two sites within 5 mm of the squamocolumnar junction. The numbers of H. pylori organisms and the density of the inflammatory infiltrate were graded. A less rigorous protocol was used to biopsy the cardia and antrum of a further 18 patients with H. pylori infection. Overall H. pylori was identified in cardiac mucosa in 95% of patients, in the corpus in 98% and in the antrum in 97%. There was no difference in the density of bacterial colonization between the three mucosal types and only minor differences in the intensity of the inflammatory response between the three mucosal types. The authors concluded that cardiac mucosa was as vulnerable to H. pylori infection as antral mucosa. Similar findings have been reported by Hackelsberger et al. [11].

There is good evidence then to indicate that H. pylori causes a pangastritis rather than a localized gastritis. The rates of H. pylori infection in cardiac mucosa will be no different from those seen in fundic and antral mucosae.

One potential pitfall is the influence of acid suppression therapy. Proton pump inhibitors (PPI) result in a decrease in bacterial numbers and as a result, if gastric biopsies are obtained whilst patients are receiving treatment, false negative results may occur. Graham et al. [12] have shown that after four weeks of PPI, the numbers of bacteria decreased in both antrum and corpus, with a more marked effect on the antrum. Biopsies and culture indicated that in 54% of patients, organisms could be detected in both the antrum and corpus, in 24% of patients, organisms could only be detected in the corpus, in 21% of patients organisms were absent from both antrum and corpus, while in 1% of patients, organisms could be detected in the antrum alone. Given the morphological similarities between cardiac and antral mucosae, it is likely that cardiac mucosa will behave in an analogous fashion. For this reason, PPI should be discontinued prior to endoscopy and biopsy.

References

1. Megraud F. Epidemiology of Helicobacter pylori infection. Gastroenterol Clin North Am 1993;22:73-88.

2. Bremner CG, Bremner RM. Barrett's esophagus. Surg Clin North Am 1997;77:1115-1137.

3. Paull G, Yeardley JH. Gastric and esophageal Campylobacter pylori in patients with Barrett's esophagus. Gastroenterology 1988;95:216-218.

4. Werdmuller BFM, Loffeld RJLF. Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis. Dig Dis Sci 1997;42:103-105.

5. Csendes A, Smok G, Cerda G, Burdiles P, Mazza D, Csendes P. Prevalence of Helicobacter pylori infection in 190 control subjects and in 23

6. patients with gastroesophageal reflux, erosive esophagitis or Barrett's esophagus. Dis Esophagus 1997;10:38-42. 6. Newton M, Bryan R, Burnham WR, Kamm MA. Evaluation of Helicobacter pylori in reflux oesophagitis and Barrett's oesophagus. Gut 1997;40:9-13.

7. Vicari JJ, Peek RM, Falk GW, Goldblum JR, Easley KA, Schnell J, Perez-Perez GI, Halter SA, Rice TW, Blaser MJ, Richter JE. The seroprevalence of cagA-positive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease. Gastroenterology 1998;115:50-57.

8. Oberg S, Peters JH, Nigro JJ, Theisen J, Hagen JA, DeMeester SR, Bremner CG, DeMeester TR. Helicobacter pylori is not associated with the manifestations of gastroesophageal reflux disease. Arch Surg 1999;134:722-726.

9. Loffeld RJLF, Tije BJT, Arends JW. Prevalence and significance of Helicobacter pylori in patients with Barrett's esophagus. Am J Gastroenterol 1992;87:1598-1600.

10. Genta RM, Huberman RM, Graham DY. The gastric cardia in Helicobacter pylori infection. Hum Pathol 1994;25:915919.

11. Hackelsberger A, Gunther T, Schultze V, Labenz J, Roessner A, Malfertheiner P. Prevalence and pattern of Helicobacter pylori gastritis in the gastric cardia. Am J Gastroenterol 1997;92:2220-2224.

12. Graham DY, Genta R, Evans DG, Reddy R, Clarridge JE, Olson CA, Edmonds AL, Siepman N. Helicobacter pylori does not migrate from the antrum to the corpus in response to omeprazole. Am J Gastroenterol 1996;91:2120-2124.


Publication date: August 2003 OESO©2015