Gastric mucosal atrophy, intestinal metaplasia, and Helicobacter pylori status in patients with gastritis with or without bile reflux: Is the presence of bile reflux good or bad?

Yıl 2020, Cilt: 19 Sayı: 2, 49 - 56, 04.10.2020

Muhammet Aydın Şule Namlı Mehmet Aydın Hüseyin Akyol

https://doi.org/10.17941/agd.800877

Öz

Background and Aims: To investigate the relation between bile reflux and gastric mucosal atrophy, intestinal metaplasia, and Helicobacter pylori status in patients with gastritis. Materials and Methods: A total of 217 patients (mean ± SD; age: 33.2±7.9 years; 51.2% males) with gastritis were divided into two groups: patients with intragastric bile reflux (n = 134; confirmed by pathology in 20 patients) and without bile reflux (control group; n = 83). The status of Helicobacter pylori and presence of intestinal metaplasia and gastric atrophy were evaluated with respect to the presence of bile reflux. Results: A positive Helicobacter pylori status, intestinal metaplasia, and gastric atrophy were observed in 85 (39.2%), 72 (33.2%), and 66 (30.4%) patients, respectively. No significant difference was noted between patients with gastritis with or without bile reflux in terms of a positive Helicobacter pylori status (38.8% vs. 45.8%), intestinal metaplasia (32.8% vs. 33.7%), and gastric atrophy (30.6% vs. 30.1%). However, the pathological confirmation of bile reflux gastritis was associated with a significantly lower rate of Helicobacter pylori positivity (0.0% vs. 45.6%; p = 0.001), intestinal metaplasia (5.0% vs. 37.7%; p = 0.009), and gastric atrophy (0.0% vs. 36.0%; p = 0.003). In patients with bile reflux (n = 134), the intestinal metaplasia and gastric mucosal atrophy rates were similar with respect to the H. pylori status. Conclusion: The rates of Helicobacter pylori positivity, intestinal metaplasia, and gastric atrophy were similar in patients with gastritis with or without bile reflux. However, the frequency of Helicobacter pylori, intestinal metaplasia, and gastric mucosal atrophy was lower in patients with pathologically confirmed biliary gastritis.

Anahtar Kelimeler

Bile reflux gastritis, gastric mucosal atrophy, intestinal metaplasia, Helicobacter pylori status

Safra reflüsü bulunan ve bulunmayan gastrit hastalarında gastrik mukozal atrofi, intestinal metaplazi ve Helicobacter pylori durumu: Safra iyi mi kötü mü?

Öz

Giriş ve Amaç: Mideye safra asidi reflüsü ve atrofi ile intestinal metaplazi riski çeşitli çalışmalarda ele alınmış ve farklı sonuçlar elde edilmiştir. Bu çalışmanın amacı gastrit hastalarında safra reflüsünün gastrik mukozal atrofi, intestinal metaplazi ve Helicobacter pylori arasındaki ilişkiyi araştırmaktır. Gereç ve Yöntem: Çalışmaya gastrit bulunan toplam 217 hasta dahil edilmiş olup hastalar, intragastrik safra reflüsü bulunan (134 hasta) (n=20 patoloji ile doğrulanmış) ve safra reflüsü bulunmayan 83 hasta kontrol grubu olmak üzere iki gruba ayrılmıştır. Helicobacter pylori durumu ve intestinal metaplazi ile gastrit atrofi varlığı, safra reflüsü ve safra reflüsü gastriti varlığı açısından değerlendirilmiştir. Bulgular: Safra reflüsü bulunan ve bulunmayan gastrit hastaları arasında Helicobacter pylori pozitifliği (%38.8 vs %45.8), intestinal metaplazi (%32.8 vs %33.7) ve gastrik atrofi (%30.6 vs %30.1) açısından anlamlı fark saptanmamıştır. Bununla birlikte safra reflüsü gastritinin patolojik doğrulama eksikliği anlamlı derecede daha düşük Helicobacter pylori pozitifliği (%0.00 vs %45.6, p=0.001), intestinal metaplazi (%5.0 vs %37.7, p=0.009) ve gastrik atrofi (%0.0 vs %36.0, p=0.003) ile ilişkili bulunmuştur. Sonuç: Bulgularımız safra reflüsü bulunan ve bulunmayan gastrit hastaları arasında Helicobacter pylori poizitifliği, intestinal metaplazi ve gastrik atrofi oranlarının benzer olduğunu ortaya çıkarmıştır. Ancak patolojik olarak doğrulanan safra gastriti bulunan hastalarda Helicobacter pylori, metaplazi ve atrofi sıklığının daha az olduğu saptanmıştır.

Anahtar Kelimeler

Safra reflüsü gastriti, gastrik mukozal atrofi, intestinal metaplazi, Helicobacter pylori durumu

Kaynakça

• 1. Testoni PA, Fanti L, Passaretti S, et al. Interdigestive motility pattern in subjects with duodenogastric bile reflux. Scand J Gastroenterol 1987;22:757-62.
• 2. McCabe ME, Dilly CK. New causes for the old problem of bile reflux gastritis. Clin Gastroenterol Hepatol 2018;16:1389-92.
• 3. Tang SJ, Wu R, Bhaijee F. Intestinal Metaplasia of the Stomach. VJGIEN 2013;1:187-9.
• 4. Kekki M, Siurala M, Varis K, et al. Classification principles and genetic of chronic gastritis. Scand J Gastroenterol Suppl 1987;141:1-28.
• 5. Misiewicz JJ, Price AB, Tytgat GNJ, et al. The Sydney System. A new classification of gastritis. J Gastroenterol Hepatol 1991;6:207-52.
• 6. Watari J, Chen N, Amenta PS, et al. Helicobacter pylori associated chronic gastritis, clinical syndromes, precancerous lesions, and pathogenesis of gastric cancer development. World J Gastroenterol 2014;20:5461-73.
• 7. Park YH, Kim N. Review of atrophic gastritis and intestinal metaplasia as a premalignant lesion of gastric cancer. J Cancer Prev 2015;20:25-40.
• 8. Liu KS, Wong IO, Leung WK. Helicobacter pylori associated gastric intestinal metaplasia: Treatment and surveillance. World J Gastroenterol 2016;22:1311-20.
• 9. Sobala GM, O’Connor HJ, Dewar EP, et al. Bile reflux and intestinal metaplasia in gastric mucosa. J Clin Pathol 1993;46:235-40.
• 10. Nakamura M, Haruma K, Kamada T, et al. Duodenogastric reflux is associated with antral metaplasic gasiritis. Gastrointest Endosc 2001; 53:53-9.
• 11. Matsuhisa T, Tsukui T. Relation between reflux of bile acids into the stomach and gastric mucosal atrophy, intestinal metaplasia in biopsy specimens. Takeshi J Clin Biochem Nutr 2012;50:217-21.
• 12. Matsuhisa T, Arakawa T, Watanabe T, et al. Relation between bile acid reflux into the stomach and the risk of atrophic gastritis and intestinal metaplasia: a multicenter study of 2283 cases. Dig Endosc 2013;25:519-25.
• 13. Lee Y, Tokunaga A, Tajiri T, et al. Inflammation of the gastric remnant after gastrectomy: mucosal erythema is associated with bile reflux and inflammatory cellularinfiltration is associated with Helicobacter pylori infection. J Gastroenterol 2004;39:520-6.
• 14. Kondo K, Suzuki H, Nagayo T. The influence of gastro-jejunal anastomoisis on gastrocarcinogenesis in rats. Jpn J Cancer Res 1984;75:362-9.
• 15. Kaminishi M, Sadatsuki H, Joshima Y, Oohara T, Kondo Y. A new method for production of chronic gastric ulcer by duodenogastric reflux in rats. Gastroenterology 1987;92:1913-8.
• 16. Mason RC, Taylor PR, Filipe MI, McColl I. Pancreatoduodenal secretions and genesis of gastric stump carcinoma in rat. Gut 1988;29:830-4.
• 17. Seto Y, Kobori O, Shimizu E, Morioka Y. The role of alkaline reflux in esophageal carcinogenesis in rats. Int J Cancer 1991;49:758-63.
• 18. Miwa K, Fujimura T, Hasegawa H, et al. Is bile or are pancreaticoduodenal secretions related to gastric carcinogenesis in rats with reflux through pylorus? J Cancer Res Clin Oncol 1992;118:570-4.
• 19. Bayram G, Ödemiş B, Çiçek B, et al. Effect on alkalen reflux gastritis, histology on the antral mucosa and Helicobacter pylori colonization of cholecystectomy. Akademik Gastroenterology Dergisi 2005;4:13-7.
• 20. Atak I, Ozdil K, Yücel M, et al. The effect of laparoscopic cholecystectomy on the development of alkaline reflux gastritis and intestinal metaplasia. Hepatogastroenterology 2012;59:59-61.
• 21. Chen SL, Mo JZ, Cao ZJ, Chen XY, Xiao SD.Effectt of bile reflux on gastric mucosal lesions in patient with dyspepsia or chronic gastritis. World J Gastroenterol 2005;11:2834-7.
• 22. Morris A, Nicholson G. Ingestion of Campylobacter pyloridis causes gastritis and raised fasting gastric PH. Am J Gastroenterol 1987;82:192-9.
• 23. Stolte M, Eidt S, Ohnsmann A. Differences in Helicobacter pylori associated gastritis in the antrum and body of the stomach. Z Gastroenterol 1990;28:229-33.
• 24. Sobala GM, O'Connor HJ, Dewar EP, et al. Bile reflux and intestinal metaplasia in gastric mucosa. J Clin Pathol 1993;46:235-40.
• 25. Kubo M, Sasako M, Gotoda T, et al. Endoscopic evaluation of the remnant stomach after gastrectomy: proposal for a new classification. Gastric Cancer 2002;5:83-9.
• 26. Safe AF, Nwose OM, Sheehan L, Mountford RA. Spontaneous bile reflux in the elderly. Gerontology. 1993;39(6):338-345.
• 27. Tomtitchong P, Onda M, Matsukura N, et al. Helicobacter pylori infection in the remnant stomach after gastrectomy: with special reference to the difference between Billroth I and II anastomoses. J Clin Gastroenterol 1998;27(Suppl 1):S154-8.
• 28. Kuipers EJ, Thijs JC, Festen HP. The prevalence of Helicobacter pylori in peptic ulcer disease. Aliment Pharmacol Ther 1995;9(Suppl 2):59-69.
• 29. Gad Elhak N, Abd Elwahab M, Nasif WA, et al. Prevalence of Helicobacter pylori, gastric myoelectrical activity, gastric mucosal changes and dyspeptic symptoms before and after laparoscopic cholecystectomy. Hepatogastroenterology 2004;51:485-90.
• 30. Jiang JX, Liu Q, Zhao B, et al. Risk factors for intestinal metaplasia in a southeastern Chinese population: an analysis of 28,745 cases. J Cancer Res Clin Oncol 2017;143:409-18.
• 31. Muller-Lissner SA. Bile reflux is increased in cigarette smokers. Gastroenterology 1986;90:1205-9.
• 32. Giacosa A, Cheli R. Smoke and chronic gastritis. Mt Sinai J Med 1982;49:475-8.