Prevalence of Helicobacter Pylori in Patients with Barrett’s Esophagus:_Chinese Journal of Evidence-Based Medicine

Authors：

LIU Fangxun , WANG Weihong , SHUAI Xiaowei

Department of Gastroenterology, Peking University First Hospital, Beijing 100034, China;

Corresponding author：

Keywords：

Barrett’s esophagus; Gastroesophageal reflux disease; Helicobacter pylori; Meta-analysis

DOI：

10.7507/1672-2531.20080238

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Objective 　We aimed to evaluate the prevalence of H.pylori infection and the prevalence of cagA+ strains in patients with and without Barrett’s esophagus.
Methods 　A full literature search to February 2008 was conducted in PubMed, MEDLINE and EMbase databases to identify case-control studies or cohort studies evaluating the prevalence of H.pylori in patients with or without Barrett’s esophagus. Summary odds ratios (OR) and 95% confidence interval (CI) were calculated by RevMan 4.2.8.
Results 　Nineteen studies were identified (16 case-controlled studies and 3 cohort studies). In case controlled studies, the prevalence of H.pylori infection significantly decreased in patients with Barrett’s esophagus as compared subjects with normal endoscopic appearance, with a overall OR of 0.56 (95%CI 0.40 to 0.79). The prevalence of H.pylori infection was no statistically significant difference in patients with Barrett’s esophagus as compared to those with gastroesophageal reflux disease, with a overall OR of 0.86 (95% CI 0.74 to 1.00). In cohort studies, the prevalence of H. pylori was no statistically significant difference in patients with Barrett’s esophagus as compared to patients with normal endoscopic appearance or patients with gastroesophageal reflux disease, with a overall OR of 1.12 (95%CI 0.77 to 1.61) and 1.10 (95%CI 0.32 to 3.83). When the analysis was stratified by the status of cagA, the prevalence of cagA positive strains significantly decreased in patients with Barrett’s esophagus as compared both to subjects with normal endoscopic appearance with OR 0.30 and 95% CI 0.12 to 0.74, and to those with gastroesophageal reflux disease (OR 0.55; 95%CI 0.33 to 0.94). Irrespective of the presence of intestinal metaplasia, similar magnitude for the reduction of H.pylori infection was observed for patients with Barrett’s esophagus and those with normal endoscopic appearance. While accompared with the presence of intestinal metaplasia, Barrett’s esophagus was associated with a significantly reduction as compared to the patients with gastroesophageal reflux disease (OR 0.81, 95%CI 0.68 to 0.98). When stratified analyses were performed, a significant reduction of H.pylori infection was observed only in patients with long-segment Barrett’s esophagus (OR 0.54; 95%CI 0.35 to 0.82), but not in those with short-segment Barrett’s esophagus (OR 0.72; 95%CI 0.43 to 1.20).
Conclusion 　 This meta-analysis indicated that the prevalence of H.pylori infection, especially the prevalence of cagA positive strains was significantly lower in patients with Barrett’s esophagus than in subjects with normal endoscopic appearance. However, the prevalence of H. pylori infection was no statistical difference in patients with Barrett’s esophagus as compared to those with gastroesophageal reflux disease. Colonization with cagA positive strains may be protective against the formation of Barrett’s esophagus.

Citation： LIU Fangxun,WANG Weihong,SHUAI Xiaowei. Prevalence of Helicobacter Pylori in Patients with Barrett’s Esophagus:. Chinese Journal of Evidence-Based Medicine, 2008, 08(12): 1086-1093. doi: 10.7507/1672-2531.20080238 Copy

1.	Sharma P, Falk GW, Weston AP, et al. Dysplasia and cancer in a large multicenter cohort of patients with Barrett’s esophagus. Clin Gastroenterol Hepatol, 2006, 4(5): 566-572.
2.	Freys SM, Fuchs KH, Heimbucher J, et al. [Epidemiology and pathophysiology of Barrett esophagus]. Zentralbl Chir, 2000, 125(5): 406-413.
3.	Cremonini F, Di Caro S, Delgado-Aros S, et al. Meta-analysis: the relationship between Helicobacter pylori infection and gastrooesophageal reflux disease. Aliment Pharmacol Ther, 2003, 18(3): 279-289.
4.	Raghunath A, Hungin AP, Wooff D, et al. Prevalence of Helicobacter pylori in patients with gastro-oesophageal reflux disease: systematic review. BMJ, 2003, 326(7392): 737.
5.	Sozzi M, Valentini M, Figura N, et al. Atrophic gastritis and intestinal metaplasia in Helicobacter pylori infection: the role of CagA status. Am J Gastroenterol, 1998, 93(3): 375-379.
6.	Vaezi MF, Falk GW, Peek RM, et al. CagA-positive strains of Helicobacter pylori may protect against Barrett’s esophagus. Am J Gastroenterol, 2000, 95(9): 2206-2211.
7.	Loffeld RJ, Werdmuller BF, Kuster JG, et al. Colonization with cagApositive Helicobacter pylori strains inversely associated with reflux esophagitis and Barrett’s esophagus. Digestion, 2000, 62(2-3): 95-99.
8.	Henihan RD, Stuart RC, Nolan N, et al. Barrett’s esophagus and the presence of Helicobacter pylori. Am J Gastroenterol, 1998, 93(4): 542-546.
9.	Vicari JJ, Peek RM, Falk GW, et al. The seroprevalence of cagA-positive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease. Gastroenterology, 1998, 115(1): 50-57.
10.	Ferrandez A, Benito R, Arenas J, et al. CagA-positive Helicobacter pylori infection is not associated with decreased risk of Barrett’s esophagus in a population with high H. pylori infection rate. BMC Gastroenterol, 2006, 6: 7.
11.	Helicobacter pylori in Barrett’s oesophagus. Gruppo Operativo per lo Studio Delle Precancerosi Esofagee (GOSPE)--Precancerous Lesions of the Oesophagus Task Force, Italy. Histopathology, 1991, 18(6): 568-570.
12.	Lichtenstein MJ, Mulrow CD, Elwood PC. Guidelines for reading case-control studies. J Chronic Dis, 1987, 40(9): 893-903.
13.	刘关键, 吴泰相, 康德英. Meta-分析中的统计学过程. 中国临床康复, 2003, 7(4): 538-539.
14.	吴泰相, 刘关键, 赵娜,等. 观察性研究系统评价/Meta-分析的方法. 中国循证医学杂志, 2004, 4(5): 337-341.
15.	Kudo M, Gutierrez O, El-Zimaity HM, et al. CagA in Barrett’s oesophagus in Colombia, a country with a high prevalence of gastric cancer. J Clin Pathol, 2005, 58(3): 259-262.
16.	Gisbert JP, de Pedro A, Losa C, et al. Helicobacter pylori and gastroesophageal reflux disease: lack of influence of infection on twenty-four-hour esophageal pH monitoring and endoscopic findings. J Clin Gastroenterol, 2001, 32(3): 210-214.
17.	Schenk BE, Kuipers EJ, Klinkenberg-Knol EC, et al. Helicobacter pylori and the efficacy of omeprazole therapy for gastroesophageal reflux disease. Am J Gastroenterol, 1999, 94(4): 884-887.
18.	Rajendra S, Ackroyd R, Robertson IK, et al. Helicobacter pylori, ethnicity, and the gastroesophageal reflux disease spectrum: a study from the East. Helicobacter, 2007, 12(2): 177-183.
19.	Abe Y, Ohara S, Koike T, et al. The prevalence of Helicobacter pylori infection and the status of gastric acid secretion in patients with Barrett’s esophagus in Japan. Am J Gastroenterol, 2004, 99(7): 1213-1221.
20.	Newton M, Bryan R, Burnham WR, et al. Evaluation of Helicobacter pylori in reflux oesophagitis and Barrett’s oesophagus. Gut, 1997, 40(1): 9-13.
21.	Vieth M, Masoud B, Meining A, et al. Helicobacter pylori infection: protection against Barrett’s mucosa and neoplasia? Digestion, 2000, 62(4): 225-231.
22.	Loffeld RJ, van der Putten AB. Helicobacter pylori and gastrooesophageal reflux disease: a cross-sectional epidemiological study. Neth J Med, 2004, 62(6): 188-191.
23.	Weston AP, Badr AS, Topalovski M, et al. Prospective evaluation of the prevalence of gastric Helicobacter pylori infection in patients with GERD, Barrett’s esophagus, Barrett’s dysplasia, and Barrett’s adenocarcinoma. Am J Gastroenterol, 2000, 95(2): 387-394.
24.	Rugge M, Russo V, Busatto G, et al. The phenotype of gastric mucosa coexisting with Barrett’s oesophagus. J Clin Pathol, 2001, 54(6): 456-460.
25.	Ackermark P, Kuipers EJ, Wolf C, et al. Colonization with cagApositive Helicobacter pylori strains in intestinal metaplasia of the esophagus and the esophagogastric junction. Am J Gastroenterol, 2003, 98(8): 1719-1724.
26.	Werdmuller BF, Loffeld RJ. Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis. Dig Dis Sci, 1997, 42(1): 103-105.
27.	Lord RV, Frommer DJ, Inder S, et al. Prevalence of Helicobacter pylori infection in 160 patients with Barrett’s oesophagus or Barrett’s adenocarcinoma. Aust N Z J Surg, 2000, 70(1): 26-33.
28.	Johansson J, Hakansson HO, Mellblom L, et al. Risk factors for Barrett’s oesophagus: a population-based approach. Scand J Gastroenterol, 2007, 42(2): 148-156.
29.	Zhang J, Chen XL, Wang KM, et al. Relationship of gastric Helicobacter pylori infection to Barrett’s esophagus and gastroesophageal reflux disease in Chinese. World J Gastroenterol, 2004, 10(5): 672-675.
30.	Kiltz U, Baier J, Schmidt WE, et al. Barrett’s metaplasia and Helicobacter pylori infection. Am J Gastroenterol, 1999, 94(7): 1985-1986.
31.	Inomata Y, Koike T, Ohara S, et al. Preservation of gastric acid secretion may be important for the development of gastroesophageal junction adenocarcinoma in Japanese people, irrespective of the H. pylori infection status. Am J Gastroenterol, 2006, 101(5): 926-933.
32.	Yamashita Y, Inoue H, Ohta K, et al. Manometric and hormonal changes after distal partial gastrectomy. Aliment Pharmacol Ther, 2000, 14(Suppl 1): 166-169.
33.	I to S, Yoshihi ro K, Kato T, et al . [Cor relat ion between Campylobacter pylori and chronic atrophic gastritis]. Nippon Shokakibyo Gakkai Zasshi, 1990, 87(9): 1815-1821.
34.	el-Omar EM, Penman ID, Ardill JE, et al. Helicobacter pylori infection and abnormalities of acid secretion in patients with duodenal ulcer disease. Gastroenterology, 1995, 109(3): 681-691.
35.	Klauser AG, Schindlbeck NE, Muller-Lissner SA. Symptoms in gastro-oesophageal reflux disease. Lancet, 1990, 335(8683): 205-208.
36.	Crabtree JE, Taylor JD, Wyatt JI, et al. Mucosal IgA recognition of Helicobacter pylori 120 kDa protein, peptic ulceration, and gastric pathology. Lancet, 1991, 338(8763): 332-335.
37.	Kuipers EJ, Perez-Perez GI, Meuwissen SG, et al. Helicobacter pylori and atrophic gastritis: importance of the cagA status. J Natl Cancer Inst, 1995, 87(23): 1777-1780.
38.	Peek RM Jr, Vaezi MF, Falk GW, et al. Role of Helicobacter pylori cagA(+) strains and specific host immune responses on the development of premalignant and malignant lesions in the gastric cardia. Int J Cancer, 1999, 82(4): 520-524.
39.	Sampliner RE. Updated guidelines for the diagnosis, surveillance, and therapy of Barrett’s esophagus. Am J Gastroenterol, 2002, 97(8): 1888-1895.
40.	Takubo K, Honma N, Sawabe M, et al. [Biopsy methods and pathology of Barrett’s esophagus]. Nippon Rinsho, 2005, 63(8): 1429-1433.
41.	Pereira AD, Suspiro A, Chaves P, et al. Short segments of Barrett’s epithelium and intestinal metaplasia in normal appearing oesophagogastric junctions: the same or two different entities? Gut, 1998, 42(5): 659-662.
42.	Morales TG, Sampliner RE, Bhattacharyya A. Intestinal metaplasia of the gastric cardia. Am J Gastroenterol, 1997, 92(3): 414-418.
43.	Goldblum JR, Vicari JJ, Falk GW, et al. Inflammation and intestinal metaplasia of the gastric cardia: the role of gastroesophageal reflux and H. pylori infection. Gastroenterology, 1998, 114(4): 633-639.
44.	Berlin JA. Invited commentary: benefits of heterogeneity in metaanalysis of data from epidemiologic studies. Am J Epidemiol, 1995, 142(4): 383-387.
45.	Colditz GA, Burdick E, Mosteller F. Heterogeneity in meta-analysis of data from epidemiologic studies: a commentary. Am J Epidemiol, 1995, 142(4): 371-382.
46.	Juni P, Holenstein F, Sterne J, et al. Direction and impact of language bias in meta-analyses of controlled trials: empirical study. Int J Epidemiol, 2002, 31(1): 115-123.

1. Sharma P, Falk GW, Weston AP, et al. Dysplasia and cancer in a large multicenter cohort of patients with Barrett’s esophagus. Clin Gastroenterol Hepatol, 2006, 4(5): 566-572.
2. Freys SM, Fuchs KH, Heimbucher J, et al. [Epidemiology and pathophysiology of Barrett esophagus]. Zentralbl Chir, 2000, 125(5): 406-413.
3. Cremonini F, Di Caro S, Delgado-Aros S, et al. Meta-analysis: the relationship between Helicobacter pylori infection and gastrooesophageal reflux disease. Aliment Pharmacol Ther, 2003, 18(3): 279-289.
4. Raghunath A, Hungin AP, Wooff D, et al. Prevalence of Helicobacter pylori in patients with gastro-oesophageal reflux disease: systematic review. BMJ, 2003, 326(7392): 737.
5. Sozzi M, Valentini M, Figura N, et al. Atrophic gastritis and intestinal metaplasia in Helicobacter pylori infection: the role of CagA status. Am J Gastroenterol, 1998, 93(3): 375-379.
6. Vaezi MF, Falk GW, Peek RM, et al. CagA-positive strains of Helicobacter pylori may protect against Barrett’s esophagus. Am J Gastroenterol, 2000, 95(9): 2206-2211.
7. Loffeld RJ, Werdmuller BF, Kuster JG, et al. Colonization with cagApositive Helicobacter pylori strains inversely associated with reflux esophagitis and Barrett’s esophagus. Digestion, 2000, 62(2-3): 95-99.
8. Henihan RD, Stuart RC, Nolan N, et al. Barrett’s esophagus and the presence of Helicobacter pylori. Am J Gastroenterol, 1998, 93(4): 542-546.
9. Vicari JJ, Peek RM, Falk GW, et al. The seroprevalence of cagA-positive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease. Gastroenterology, 1998, 115(1): 50-57.
10. Ferrandez A, Benito R, Arenas J, et al. CagA-positive Helicobacter pylori infection is not associated with decreased risk of Barrett’s esophagus in a population with high H. pylori infection rate. BMC Gastroenterol, 2006, 6: 7.
11. Helicobacter pylori in Barrett’s oesophagus. Gruppo Operativo per lo Studio Delle Precancerosi Esofagee (GOSPE)--Precancerous Lesions of the Oesophagus Task Force, Italy. Histopathology, 1991, 18(6): 568-570.
12. Lichtenstein MJ, Mulrow CD, Elwood PC. Guidelines for reading case-control studies. J Chronic Dis, 1987, 40(9): 893-903.
13. 刘关键, 吴泰相, 康德英. Meta-分析中的统计学过程. 中国临床康复, 2003, 7(4): 538-539.
14. 吴泰相, 刘关键, 赵娜,等. 观察性研究系统评价/Meta-分析的方法. 中国循证医学杂志, 2004, 4(5): 337-341.
15. Kudo M, Gutierrez O, El-Zimaity HM, et al. CagA in Barrett’s oesophagus in Colombia, a country with a high prevalence of gastric cancer. J Clin Pathol, 2005, 58(3): 259-262.
16. Gisbert JP, de Pedro A, Losa C, et al. Helicobacter pylori and gastroesophageal reflux disease: lack of influence of infection on twenty-four-hour esophageal pH monitoring and endoscopic findings. J Clin Gastroenterol, 2001, 32(3): 210-214.
17. Schenk BE, Kuipers EJ, Klinkenberg-Knol EC, et al. Helicobacter pylori and the efficacy of omeprazole therapy for gastroesophageal reflux disease. Am J Gastroenterol, 1999, 94(4): 884-887.
18. Rajendra S, Ackroyd R, Robertson IK, et al. Helicobacter pylori, ethnicity, and the gastroesophageal reflux disease spectrum: a study from the East. Helicobacter, 2007, 12(2): 177-183.
19. Abe Y, Ohara S, Koike T, et al. The prevalence of Helicobacter pylori infection and the status of gastric acid secretion in patients with Barrett’s esophagus in Japan. Am J Gastroenterol, 2004, 99(7): 1213-1221.
20. Newton M, Bryan R, Burnham WR, et al. Evaluation of Helicobacter pylori in reflux oesophagitis and Barrett’s oesophagus. Gut, 1997, 40(1): 9-13.
21. Vieth M, Masoud B, Meining A, et al. Helicobacter pylori infection: protection against Barrett’s mucosa and neoplasia? Digestion, 2000, 62(4): 225-231.
22. Loffeld RJ, van der Putten AB. Helicobacter pylori and gastrooesophageal reflux disease: a cross-sectional epidemiological study. Neth J Med, 2004, 62(6): 188-191.
23. Weston AP, Badr AS, Topalovski M, et al. Prospective evaluation of the prevalence of gastric Helicobacter pylori infection in patients with GERD, Barrett’s esophagus, Barrett’s dysplasia, and Barrett’s adenocarcinoma. Am J Gastroenterol, 2000, 95(2): 387-394.
24. Rugge M, Russo V, Busatto G, et al. The phenotype of gastric mucosa coexisting with Barrett’s oesophagus. J Clin Pathol, 2001, 54(6): 456-460.
25. Ackermark P, Kuipers EJ, Wolf C, et al. Colonization with cagApositive Helicobacter pylori strains in intestinal metaplasia of the esophagus and the esophagogastric junction. Am J Gastroenterol, 2003, 98(8): 1719-1724.
26. Werdmuller BF, Loffeld RJ. Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis. Dig Dis Sci, 1997, 42(1): 103-105.
27. Lord RV, Frommer DJ, Inder S, et al. Prevalence of Helicobacter pylori infection in 160 patients with Barrett’s oesophagus or Barrett’s adenocarcinoma. Aust N Z J Surg, 2000, 70(1): 26-33.
28. Johansson J, Hakansson HO, Mellblom L, et al. Risk factors for Barrett’s oesophagus: a population-based approach. Scand J Gastroenterol, 2007, 42(2): 148-156.
29. Zhang J, Chen XL, Wang KM, et al. Relationship of gastric Helicobacter pylori infection to Barrett’s esophagus and gastroesophageal reflux disease in Chinese. World J Gastroenterol, 2004, 10(5): 672-675.
30. Kiltz U, Baier J, Schmidt WE, et al. Barrett’s metaplasia and Helicobacter pylori infection. Am J Gastroenterol, 1999, 94(7): 1985-1986.
31. Inomata Y, Koike T, Ohara S, et al. Preservation of gastric acid secretion may be important for the development of gastroesophageal junction adenocarcinoma in Japanese people, irrespective of the H. pylori infection status. Am J Gastroenterol, 2006, 101(5): 926-933.
32. Yamashita Y, Inoue H, Ohta K, et al. Manometric and hormonal changes after distal partial gastrectomy. Aliment Pharmacol Ther, 2000, 14(Suppl 1): 166-169.
33. I to S, Yoshihi ro K, Kato T, et al . [Cor relat ion between Campylobacter pylori and chronic atrophic gastritis]. Nippon Shokakibyo Gakkai Zasshi, 1990, 87(9): 1815-1821.
34. el-Omar EM, Penman ID, Ardill JE, et al. Helicobacter pylori infection and abnormalities of acid secretion in patients with duodenal ulcer disease. Gastroenterology, 1995, 109(3): 681-691.
35. Klauser AG, Schindlbeck NE, Muller-Lissner SA. Symptoms in gastro-oesophageal reflux disease. Lancet, 1990, 335(8683): 205-208.
36. Crabtree JE, Taylor JD, Wyatt JI, et al. Mucosal IgA recognition of Helicobacter pylori 120 kDa protein, peptic ulceration, and gastric pathology. Lancet, 1991, 338(8763): 332-335.
37. Kuipers EJ, Perez-Perez GI, Meuwissen SG, et al. Helicobacter pylori and atrophic gastritis: importance of the cagA status. J Natl Cancer Inst, 1995, 87(23): 1777-1780.
38. Peek RM Jr, Vaezi MF, Falk GW, et al. Role of Helicobacter pylori cagA(+) strains and specific host immune responses on the development of premalignant and malignant lesions in the gastric cardia. Int J Cancer, 1999, 82(4): 520-524.
39. Sampliner RE. Updated guidelines for the diagnosis, surveillance, and therapy of Barrett’s esophagus. Am J Gastroenterol, 2002, 97(8): 1888-1895.
40. Takubo K, Honma N, Sawabe M, et al. [Biopsy methods and pathology of Barrett’s esophagus]. Nippon Rinsho, 2005, 63(8): 1429-1433.
41. Pereira AD, Suspiro A, Chaves P, et al. Short segments of Barrett’s epithelium and intestinal metaplasia in normal appearing oesophagogastric junctions: the same or two different entities? Gut, 1998, 42(5): 659-662.
42. Morales TG, Sampliner RE, Bhattacharyya A. Intestinal metaplasia of the gastric cardia. Am J Gastroenterol, 1997, 92(3): 414-418.
43. Goldblum JR, Vicari JJ, Falk GW, et al. Inflammation and intestinal metaplasia of the gastric cardia: the role of gastroesophageal reflux and H. pylori infection. Gastroenterology, 1998, 114(4): 633-639.
44. Berlin JA. Invited commentary: benefits of heterogeneity in metaanalysis of data from epidemiologic studies. Am J Epidemiol, 1995, 142(4): 383-387.
45. Colditz GA, Burdick E, Mosteller F. Heterogeneity in meta-analysis of data from epidemiologic studies: a commentary. Am J Epidemiol, 1995, 142(4): 371-382.
46. Juni P, Holenstein F, Sterne J, et al. Direction and impact of language bias in meta-analyses of controlled trials: empirical study. Int J Epidemiol, 2002, 31(1): 115-123.

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