The relation between Helicobacter pylori gastritis, and reflux esophagitis

Year 2007, Volume: 6 Issue: 3, 115 - 119, 01.12.2007

Hilmi Ataseven Bülent Ödemiş Mehmet Arhan İbrahim Ertuğrul Mehmet İbiş Gülden Aydoğ Erkan Parlak Nurgül Şaşmaz Erkan Parlak

Abstract

Background and aim: The relation between gastroesophageal reflux disease and Helicobacter pylori infection is controversial. The aim of this study was to investigate the relation between the presence of Helicobacter pylori and the histological and topografical features of Helicobacter pylori gastritis, and the severity of esophagitis. Material and methods: 129 patients (84 male and 45 female) with esophagitis diagnosed during upper gastrointestinal endoscopy were enrolled into the study. Ages of patients, gender, alcohol abuse and symptoms of reflux disease, medical history of surgery were also recorded. Los Angles classification was used for reflux esophagitis. Biopsies from antrum and the body of stomach were obtained. Sydney classification was used for gastritis. Results: Grade A esophagitis was found in 44,2% of all patients, grade B esophagitis in 46,5%, grade C esophagitis in 8.5% and grade D esophagitis in 0.8%. Total Helicobacter pylori rate was 73%, 68,2% in antrum and 68,2% in the body of stomach. There was no significant association between the presence, severity and distribution of Helicobacter pylori in antrum and the body of stomach and the severity of esophagitis. There was no significant association the presence of activation, inflamation, atrophy and intestinal metaplasia in both location and the severity of esophagitis. The rates of inflamation was similar in antrum and the body of stomach (%95.3 and %92.2). The rate of activation was significantly higher in antrum (66.7%) than in the body of stomach (47.3%). The rate of atrophy was significantly higher in antrum (58.1%) than in the body of stomach (24%). Conclusion: The frequency of Helicobacter pylori in patients with esophagitis was similar to the frequency reported in our country. Chronic active gastritis and chronic atrophic gastritis was more frequent in the antrun than in the body of stomach. These findings indicate that the types of histological gastritis caused by Helicobacter pylori rather than the presence of Helicobacter pylori is associated with esophagitis.

Keywords

Key Words: Esophagitis, Helicobacter pylori, gastritis

Reflü özofajit ile Helikobakter pilori ve gastrit ilişkisi

Abstract

Giriş ve Amaç: Helikobakter pilori enfeksiyonu ile gastroözofageal reflü hastalığı arasındaki ilişki tartışmalıdır. Bu çalışmanın amacı Helikobakter pilori'nin varlığı ve Helikobakter pilori gastritinin histolojik ve topografik özellikleri ile özofajit şiddeti arasındaki ilişkiyi araştırmaktı. Gereç ve Yöntem: Çalışmaya endoskopide reflü özofajit saptanan toplam 129 (84 erkek ve 45 kadın) hasta alındı. Tüm hastaların yaş, cinsiyet, alkol kullanma öyküsü ve reflü semptomları, cerrahi öyküsü sorgulandı. Reflü özofajit şiddeti Los Angeles klasifikasyonuna göre yapıldı. Bütün hastalardan antrum ve korpustan biyopsiler alındı. Gastrit için histopatolojik inceleme Sydney sınıflama sistemine göre yapıldı. Bulgular: Hastaların %44.2'sinde evre A, % 46.5'inde evre B, %8.5'inde evre C ve %0.8'inde evre D özofajit izlendi. Toplam Helikobakter pilori pozitiflik oranı %73, antrumda %68.2, korpusta %68.2 idi. Antrum ve korpusta Helikobakter pilori varlığı, şiddeti ve dağılımı ile özofajit evresi arasında anlamlı bir ilişki yoktu. Sydney sistemine göre Helikobakter pilori dışındaki gastrit için tanımlanan diğer parametrelerle özofajit evresi arasında da anlamlı bir ilişki yoktu. İnflamasyon oranları antrum ve korpusta benzerdi (sırayla %95.3 ve %92.2). Antrumdaki atrofi sıklığı (%58.1) korpustaki atrofi sıklığına (%24) göre anlamlı olarak daha yüksekti. Aktivasyon sıklığı antrumda (%66.7) korpusa göre (%47.3) anlamlı olarak daha yüksekti. Sonuç: Özofajitli hastalardaki Helikobakter pilori sıklığı ülkemiz için bildirilen Helikobakter pilori sıklığına benzer bulunmuştur. Kronik aktif gastrit ve kronik atrofik gastrit antrumda korpusa göre anlamlı şekilde daha yüksekti. Bu bulgular Helikobakter pilori'nin varlığından ziyade oluşturduğu histolojik gastrit tipinin özofajit ile ilişkili olabileceğini düşündürmektedir.

Keywords

Özofajit, Helikobakter pilori, gastrit

References

• DeVault KR, Castell DO. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. Am J Gastroenterol 2005; 100:190.
• 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: 681-91.
• Hopkins RJ, Girardi LS, Turney EA. Relationship between Helicobacter pylori eradication and reduced duodenal and gastric ulcer recurrence: A review. Gastroenterology 1996; 110: 1244-52.
• Uemura N, Okamato S, Yamamoto S, et al. Helicobacter pylori infection and the development of gastric cancer. N Engl J Med 2001; 345: 784-9.
• Vicari JJ, Peek RM, Falk GW, et al. The seroprevalence of CagApositive Helicobacter pylori strains in the spectrum of gastroesophageal reflux disease. Gastroenterology 1998; 115: 50-7.
• Loffeld RJ, van der Putten AB. Helicobacter pylori and gastrooesophageal reflux disease: a cross-sectional epidemiological study. Neth J Med 2004; 62: 188-91.
• Wu JC, Sung JJ, Ng EK, et al. Prevalence and distribution of Helicobacter pylori in gastroesophageal reflux disease: a study from the East. Am J Gastroenterol 1999; 94:1790-4.
• Labenz J, Malfertheiner P. Helicobacter pylori in gastrooesophageal reflux disease: causal agent, independent or protective factor? Gut 1997; 41: 277-80.
• Zentilin P, Iiritano E, Vignale C, et al. Helicobacter pylori infection is not involved in the pathogenesis of either erosive or non-erosive gastro-oesophageal reflux disease. Aliment Pharmacol Ther 2003; 17: 1057-64.
• Moayyedi P, Bardhan C, Young L, et al. Helicobacter pylori eradication does not exacerbate reflux symptoms in gastroesophageal reflux disease. Gastroenterolgy 2001; 121: 1120-6.
• Kusano M, Ino K, Yamada T, et al. Interobserver and intraobserver variation in endoscopic assessment of GERD using the "Los Angeles" classification. Gastrointest Endosc 1999; 49: 700
• Misiewicz JJ, Tytgat GNJ, Goodwin CS, et al. The Sydney system: a new classification of gastritis. J Gastroenterol Hepatol 1991; 6:209.
• Dixon MF, Genta RM, Harley JH, et al. Classification and grading of gastritis The updated Sydney system. Am J Surg Pathol 1996; 20 (10): 1161-81.
• Werdmuller BF, Loffeld RJ. Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis. Dig Dis Sci 1997;42:103–5.
• O'Connor HJ. Review article. Helicobacter pylori and gastrooesophageal reflux disease-clinical implications and management. Aliment Pharmacol Ther 1999; 13: 117-27.
• Wu JC, Sung JJ, Chan FK, et al. Helicobacter pylori infection is associated with milder gastro-oesophageal reflux disease. Aliment Pharmacol Ther 2000; 14: 427–32.
• Labenz J, Blum AL, Bayerdorffer E, et al. Curing Helicobacter pylori infection in patients with duodenal ulcer may provoke reflux esophagitis. Gastroenterology 1997; 112: 1442-7.
• Sacca N, De Medici A, Rodino S, et al. Reflux esophagitis: a complication of Helicobacter pylori eradication therapy? Endoscopy 1997; 29: 224.
• O’Connor HJ, McGee C, Ghabash NM, et al. Prevalence of esophagitis in H. pylori-positive peptic ulcer disease and the impact of eradication therapy. Hepatogastroenterology 2001; 48: 1064–8.
• Us D, Hascelik G. Seroprevalence of Helicobacter pylori infection in an asymptomatic Turkish population. J Infect 1998; 37: 148-50.
• Newton M, Kamm MA, Talbot IC, et al. Fundal gastritis as a potential cause of reflux oesophagitis. Dis Esophagus 2000; 13: 56-60.
• Mihara T, Adachi K, Komazawa Y. Characteristics of gastritis in patients with Helicobacter pylori positive reflux esophagitis. J Gastroenterol Hepatol 2005; 20: 682–7.
• Malfertheiner P, Dent J, Zeijlon L, et al. Impact of Helicobacter pylori eradication on heartburn in patients with gastric or duodenal ulcer disease – results from a randomized trial programme. Aliment Pharmacol Ther 2002; 16: 1431–42.
• Ishiki K, Mizuno M, Take S, et al. Helicobacter pylori eradication improves pre-existing reflux esophagitis in patients with duodenal ulcer disease. Clin Gastroenterol Hepatol 2004; 2: 474–9.
• Vakil N, Talley NJ, Stolte M, et al. Patterns of gastritis and the effect of eradicating Helicobacter pylori on gastro-oesophageal reflux disease in Western patients with non-ulcer dyspepsia. Aliment Pharmacol Ther 2006; 24: 55-63.
• Hamada H, Haruma K, Mihara M, et al. High incidence of reflux esophagitis after eradication therapy for Helicobacter pylori: impacts of hiatal hernia and corpus gastritis. Aliment Pharmacol Ther 2000; 14: 729–35.