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OESO©2015
 
Volume: The Esophagogastric Junction
Chapter: Particular problems in medical therapy
 

Can healing of esophagitis without acid suppression be envisaged by eradication of Helicobacter pylori?

F.K.L. Chan, J.J.Y. Sung (Hong-Kong)

Although Helicobacter pylori infection is well documented in the pathogenesis of peptic ulcer disease, the role of H. pylori in gastroesophageal reflux disease (GERD) remains controversial.

Does H. pylori infection predispose to the development of GERD?

Early reports revealed a variable prevalence of H. pylori in the Barrett's epithelium, ranging from 0 to 62% [1-4]. The conflicting results were partly related to the relatively small number of patients studied. Recently, two larger series found a significantly lower prevalence of H. pylori in GERD patients than in sex and age matched control subjects [5, 6]. In the study reported by Werdmuller et al., 240 GERD patients and 399 controls were assessed for the H. pylori status. H. pylori was present in only 30% of GERD patients compared with 51% in the control group [5]. Similar results were also obtained in a Japanese study, that GERD patients had a lower prevalence of H. pylori and less severe gastritis [6]. These results indicate that H. pylori infection does not increase the risk of developing GERD.

While most patients respond to acid suppression therapy regardless of the H. pylori status, there were anecdotal reports suggesting that H. pylori might play a role in refractory esophagitis. In a small double-blind controlled trial involving 20 patients suffering from ulcerative reflux esophagitis, combination of cimetidine with colloidal bismuth resulted in better healing than treatment with cimetidine alone [7]. In the study by Rosioru et al., 4 out of 15 children with refractory esophagitis who were H. pylori positive responded to amoxicillin plus bismuth subsalicylate [8]. In another case report, the addition of antibiotics to antireflux therapy caused healing of a H. pylori positive Barrett's ulcer [9]. These results suggest that H. pylori might act as a secondary invader in a subgroup of GERD patients. More data is required to substantiate this claim.

Does H. pylori infection protect patients from developing GERD?

If H. pylori does not play any pathogenetic role in the development of GERD, would it actually be protecting patients from this condition? It is well known that reflux esophagitis is uncommon in Asian population. In a recent study which recruited over 2,000 Chinese patients, the incidence of endoscopic reflux esophagitis is only 5% [10]. Although this study did not indicate the prevalence of H. pylori in their patient group, prevalence of the infection is, in general, high in this area. Furthermore, in another study, the severity of GERD appears to be inversely related to the H. pylori status. Schenk et al. followed
137 GERD patients for a mean period of 6 months. Patients who were H. pylori negative had more severe esophagitis and more frequently had Barrett's esophagus than that of H. pylori positive patients [11].

The protective role of H. pylori is further supported by the results of recent studies that the risk of developing GERD is increased after H. pylori eradication. Hischl et al. reported the development of reflux esophagitis in 10 out of 16 duodenal ulcer patients after successful eradication of H. pylori during a mean follow-up of 43 months [12]. Sacca et al. observed that 24 out of 169 patients (14%) had mild esophagitis 6 months after anti-Helicobacter treatment for duodenal ulcer [13]. In a recent large-scale study, reflux esophagitis developed in 63 (25.8%) of 244 duodenal ulcer patients within 3 years after H. pylori eradication, whereas only 28 (12.9%) of 216 duodenal ulcer patients who remained H. pylori positive developed GERD [14]. These observations might be explained by the fact that gastric acid output is reduced in the presence of H. pylori-associated corpus gastritis, eradication of H. pylori allows recovery of acid secretion and therefore predisposes to the development of GERD [15].

 

Should H. pylori be eradicated in GERD patients?

Acid suppression is the main stay of treatment in the management of reflux esophagitis. However, recent studies suggested that eradication of H. pylori increased gastric acid output. Verdu et al. found that omeprazole caused a smaller reduction in gastric acidity in patients infected with H. pylori than those who were H. pylori negative [16]. In a subsequent study, eradication of H. pylori caused a marked decrease in the acid suppressing effect of omeprazole, raising the 24-hour median gastric pH from 3.0 to 5.5 [17]. Therefore, H. pylori eradication may theoretically have an adverse effect on the treatment of esophagitis. Nevertheless, the clinical relevance of this observation remains disputable. Schenk et al. found that in GERD patients requiring maintenance omeprazole therapy, the efficacy of treatment was not affected by the H. pylori status [11]. Eradication of H. pylori therefore should not be regarded as a contraindication in the treatment of reflux esophagitis.

On the other hand, there is increasing concern that patients with reflux esophagitis and coexisting H. pylori infection who are treated with maintenance omeprazole may have an increased risk of atrophic gastritis. Kuipers et al. followed up two separate cohorts who were treated for reflux esophagitis for 3-8 years; 105 patients received maintenance omeprazole and 72 patients underwent fundoplication alone. In the omeprazole group, atrophic gastritis developed in 18 out of 59 patients infected with H. pylori, whereas none of the 31 infected patients in the fundoplication group developed atrophic gastritis [18]. Nevertheless, this study was non-randomized, the two cohorts were derived from different countries, and the effect of H. pylori eradication on the subsequent incidence of atrophic gastritis was not examined. Until more data is available, it would be unnecessary to recommend eradication of H. pylori before starting maintenance acid suppression therapy for GERD.

 

In summary, there is no evidence to indicate that H. pylori contributes to the development of GERD. Although there were anecdotal reports of clinical improvement after eradication of H. pylori in patients with refractory esophagitis, the number of patients studied was too small for any conclusion to be drawn at this moment, On the other hand, there is increasing evidence that the presence of H. pylori may actually protect against the development of GERD. This observation however cannot be regarded as a reason for not treating the infection. Further studies are required to determine whether eradication of H. pylori is necessary to reduce the risk of atrophic gastritis before using maintenance potent acid suppression therapy. At present, eradication of H. pylori cannot be regarded as an adjuvant or alternative treatment for GERD.

References

1. Talley NJ, Cameron AJ, Shorter RG, et al. Campylobacter pylori and Barrett's esophagus. Mayo Clin Proc 1988;63:1176-1180.

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

3. Honck JA, Lucas JG. Absence of Campylobacter-like organisms in Barrett's esophagus. Arch Pathol Lab Med 1989;113:470-472.

4. Loffeld RJ, Ten Tije BJ, et al. Prevalence and significance of Helicobacter pylori in patients with Barrett's esophagus. Am J Gastroenterol 1992;87:1598-1600.

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

6. Mihara M, Haruma K, Kamada T, et al. Low prevalence of Helicobacter pylori infection in patients with reflux esophagitis. Gut 1996;39(suppl 2):A94.

7. Borkent MV, Beker JA. Treatment of ulcerative reflux esophagitis with colloidal bismuth subcitrate in combination with cimetidine. Gut 1988;29:385-389.

8. Rosioru C, Glassman MS, Halata MS, et al. Esophagitis and Helicobacter pylori in children: incidence and therapeutic implications. Am J Gastroenterol 1993;88(4):51O-513.

9. De Giacomo C, Fiocca R, Villani L, et al. Barrett's ulcer and Campylobacter-like organisms infection in a child. J Pediatr Gastroenterol Nutr 1988;7(5):766-768.

10. Chang CS, Poon SK, Lien HC, et al. The incidence of reflux esophagitis among the Chinese. Am J Gastroenterol 1997;92:668-671.

11. Schenk BE, Kuipers EJ, Klinkenberg-Knol EC, et al. H. pylori, GERD, and efficacy of omeprazole therapy. Gastroenterology 1997;112:A282.

12. Hischl AM, Schutze K, Hentschel E, et al. Serological, microbiological and clinical results of a 43 month follow-up after successful eradication of H. pylori in duodenal ulcer patients, Am J Gastroenterol 1994;89:1374.

13. Sacca N, De Medici A, Rodino S, et al. Reflux esophagitis: a complication of Helicobacter pylori eradication therapy? Gut 1996;139(suppl):A91.

14. Labenz J, Blum AL, Bayerdorffer E, et al. Curing of Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis. Gastroenterology 1997;112:1442-1447.

15. Ruiz B, Correa P, Fontham ETH, et al. Antral atrophy, Helicobacter pylori colonization, and gastric pH. Am J Clin Pathol 1996;105:96-101.

16. Verdu EF, Armstrong D, Fraser R, et al. Effect of Helicobacter pylori status on intragastric pH during treatment with omeprazole. Gut 1995;36:539-543.

17. Labenz J, Tillenburg B, Peitz U, et al. Helicobacter pylori augments the pH-increasing effect of omeprazole in patients with duodenal ulcer. Gastroenterology 1996;110:725-732.

18. Kuipers EJ, Lundell L, Klinkenberg-Knol EC, et al. Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication. N Engl J Med 1996;334:1018-1022.


Publication date: May 1998 OESO©2015