Barrett食管患者幽門螺桿菌感染率的Meta分析_《中國循證醫學雜志》

作者：

劉芳勛 , 王蔚虹 , 帥曉瑋

北京大學第一醫院（北京 100034）;

關鍵詞：

Barrett 食管胃食管反流病螺桿菌，幽門 Meta 分析

DOI：

10.7507/1672-2531.20080238

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目的　分析Barrett食管患者幽門螺桿菌感染率及cagA陽性的幽門螺桿菌感染率，并與內鏡檢查正常者和胃食管反流病患者比較，探討幽門螺桿菌（Helicobacter pylori，Hp）感染與Barrett 食管的關系。
方法　計算機檢索MEDLINE和EMbase數據庫至2008 年2 月，納入比較Barrett食管患者和內鏡檢查正常者及胃食管反流病（gastroesophageal reflux disease，GERD）患者Hp 感染率的病例對照研究或隊列研究。統計分析采用RevMan4.2.8，計算比值比OR（95%CI）。
結果　共納入19篇文獻，包括16篇病例對照研究和3篇隊列研究。病例對照研究分析結果顯示，Barrett食管患者比內鏡檢查正常者Hp感染率低［OR 0.56， 95%CI（0.40，0.79）］，與GERD 患者相比差異無統計學意義［OR 0.86， 95%CI（ 0.74，1.00）］。隊列研究的分析結果顯示，Barrett食管患者與內鏡檢查正常者及GERD患者相比Hp 感染率差異無統計學意義［OR 1.12，95%CI（0.77，1.61）；OR1.10，95%CI（0.32，3.83）］。cagA陽性Hp感染率較內鏡正常者及GERD患者低［OR 0.30，95%CI（0.12，0. 74）；OR 0.55，95%CI（0.33，0.94）］。病例對照研究長節段較短節段Barrett 食管Hp感染率低［OR 0.32，95%CI（0.16，0.66）］。而隊列研究結果顯示，長節段較短節段Barrett食管患者Hp感染率差異無統計學意義［OR 0.66， 95%CI（0.29，1.48）］。
結論　 Barrett 食管患者和GERD患者Hp感染率無差別，Barrett食管患者Hp感染率，特別是cagA陽性Hp菌株感染率較內鏡檢查正常者明顯減少。

引用本文： 劉芳勛,王蔚虹,帥曉瑋. Barrett食管患者幽門螺桿菌感染率的Meta分析. 中國循證醫學雜志, 2008, 08(12): 1086-1093. doi: 10.7507/1672-2531.20080238 復制

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.	劉關鍵, 吳泰相, 康德英. Meta-分析中的統計學過程. 中國臨床康復, 2003, 7(4): 538-539.
14.	吳泰相, 劉關鍵, 趙娜,等. 觀察性研究系統評價/Meta-分析的方法. 中國循證醫學雜志, 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. 劉關鍵, 吳泰相, 康德英. Meta-分析中的統計學過程. 中國臨床康復, 2003, 7(4): 538-539.
14. 吳泰相, 劉關鍵, 趙娜,等. 觀察性研究系統評價/Meta-分析的方法. 中國循證醫學雜志, 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.

《中國循證醫學雜志》

Barrett食管患者幽門螺桿菌感染率的Meta分析

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《中國循證醫學雜志》

Barrett食管患者幽門螺桿菌感染率的Meta分析

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