Araştırma Makalesi
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The effect of alkaline reflux gasritis on intragastric pH and helicobacter pylori colonization

Yıl 2020, Cilt: 4 Sayı: 1, 24 - 28, 30.04.2020

Öz

Aim: The relationship between alkaline reflux gastritis and Helicobacter pylori remains unclear. It
is thought that bile and pancreatic fluids escaping into the stomach as a result of duodenogastric
reflux cause chemical irritation and pH changes in the gastric mucosa. However, the effect of
intragastric pH changes on Helicobacter pylori and duodenal contents on intragastric pH are not
known. The aim of this study was to investigate the relationship between intragastric pH and the
presence of Helicobacter pylori in patients with alkaline reflux gastritis.

Material and Methods: The patients who detected alkaline reflux gastritis (n = 30) and antral gastritis for the control group (n=35)
by gastroscopy were included in the study. During gastroscopy of all patients pH was measured from the liquid sample taken from
the stomach and rapid urease test was performed from the sample taken from the antrum.


Results: The mean intragastric pH in cases with alkaline reflux gastritis was similar to the control group (3.43±1.94, 3.2±2.02,
p=0.504, respectively). The rates of rapid urease test positivity were similar in both alkaline reflux gastritis and control groups
(p=0.461). Intragastric pH was found to be alkaline or acidic was not associated with rapid urease test positivity in both groups.


Conclusion: We believe that intragastric pH is acidic in patients with alkaline reflux gastritis too and both duodenogastric bile reflux
and intragastric pH changes have no effect on Helicobacter pylori colonization

Kaynakça

  • Referans1: 1. Fein M, et al. Fiberoptic technique for 24-hour bile reflux monitoring. Standards and normal values for gastric monitoring. Dig Dis Sci 1996; 41: 216- 225.
  • Referans2: Hyun JJ, et al. Correlation Between Bile Reflux Gastritis and Biliary Excreted Contrast Media in the Stomach. J Comput Assist Tomogr 2017; 41: 696–701.
  • Referans3: O’Connor HJ, et al. Campylobacter like organisms and reflux gastritis. J Clin Pathol 1986; 39: 531-534
  • Referans4: Gad Elhak N, et al. Prevalence of Helicobacter pylori, gastric myoelectrical activity, gastric mucosal changes and dyspeptic symptoms before and after laparoscopic cholecystectomy. Hepatogastroenterology 2004; 51: 485–490
  • Referans5: Itoh M, et al. Antibacterial action of bile acids against Helicobacter pylori and changes in its ultrastructural morphology: effect of unconjugated dihydroxy bile acid. J Gastroenterol 1999; 34: 571–576
  • Referans6: Bode G, et al. Polymorphism in Helicobacter pylori--a key function in recurrence of infection? Med Klin (Munich) 1992; 87: 179–184
  • Referans7: Graham DY. Bile acid therapy for Helicobacter pylori [letter]. Aliment Pharmacol Ther 1992; 6: 653
  • Referans8: Hanninen ML. Sensitivity of Helicobacter pylori to different bile salts. Eur J Clin Microbiol Infect Dis 1991; 10: 508-518
  • Referans9: Farsakh NA, et al. Prevalence of Helicobacter pylori in patients with gall stones before and after cholecystectomy: a longitudinal study. Gut 1995; 36: 675-678
  • Referans10: Gunn A, Keddie N. Some clinical observations on patients with gallstones. Lancet 1972; 2: 239–241.
  • Referans11: Sobala GM, et al. Bile reflux and intestinal metaplasia in grastic mucosa. J Clin Pathol 1993; 46: 235-240.
  • Referans12: Kellosalo J, et al. Effect of biliary tract procedures on duodenogastric reflux and the gastric mucosa. Scand J Gastroenterol 1991; 26: 1272- 1278.
  • Referans13: Tewari SN, et al. The prevelance of Campylobacter pylori gastritis: A study of symptomatic nonulcer dyspepsia and bile gastritis. J Clin Gastroenterol 1989; 11: 271-277.
  • Referans14: Taşkin V, et al. The effect of duodenogastric reflux on Helicobacter pylori presence and gastric histopathologic changes. Turk J Gastroenterol. 2003; 14: 239- 242.
  • Referans15: Karttunen T, Niemelä S. Campylobacter pylori and duodenogastric reflux in peptic ulcer disease and gastritis. Lancet 1988; 1: 118.
  • Referans16: Caldwell MT, et al. Helicobacter pylori infection increases following cholecystectomy. Ir J Med Sci 1995; 164: 52–55.
  • Referans17: Ladas SD, et al. Helicobacter pylori may induce bile reflux: link between H pylori and bile induced injury to gastric epithelium. Gut 1996; 38:15- 18
  • Referans18: Amieva M, Peek RM, Jr. Pathobiology of Helicobac¬ter pylori-induced Gastric Cancer. Gastroenterology 2016; 150: 64-78.
  • Referans19: Fuchs KH, et al. Variability in the composition of physiologic duodenogastric reflux. J Gastrointest Surg. 1999; 3: 389–396.

Alkalen Reflü Gastritin İntragastrik pH ve Helicobacter Pylori Kolonizasyonu Üzerine Etkisi

Yıl 2020, Cilt: 4 Sayı: 1, 24 - 28, 30.04.2020

Öz

Amaç: Alkalen reflü gastrit ile Helicobacter pylori ilişkisi hâlen belirsizdir. Duodenogastrik reflü
sonucu mideye kaçan safra ve pankres sıvılarının mide mukozasında kimyasal irritasyon ve pH
değişikliklerine yol açtığı düşünülmektedir. Ancak intragastrik pH değişikliklerinin Helicobacter
pylori üzerine etkisi ve duodenum içeriğinin intragastrik pH’ya etkisi bilinmemektedir. Bu çalışmada
alkalen reflü gastrit hastalarında intragastrik pH ile Helicobacter pylori varlığı arasındaki ilişki
araştırılmıştır.


Gereç ve Yöntemler: Çalışmaya gastroskopide alkalen reflü gastrit tespit edilen (n=30) ve kontrol
grubu için antral gastrit tanısı alan hastalar (n=35) dahil edildi. Tüm hastalardan gastroskopi
esnasında mide içerisinden alınan sıvı örneğinden pH çalışıldı ve antrumdan alınan örnekten
üreaz testi yapıldı.


Bulgular: Alkalen reflü gastrit olgularında ortalama intragastrik pH kontrol grubu ile benzerdi
(Sırasıyla 3,43±1,94, 3,2±2,02, p=0,504). Hem Alkalen reflü gastrit grubunda hem de kontrol
grubunda üreaz testi pozitifliği oranları benzerdi (p=0,461). Her iki grupta intragastrik pH’nın alkali
veya asidik olması üreaz testi pozitifliği ile ilişkili değildi.


Sonuç: Alkalen reflü gastriti hastalarında da intragastrik pH’nın asidik olduğunu ve hem
duodenogastrik safra reflüsünün hem de intragastrik pH değişiklikliklerinin Helicobacter pylori
kolonozisyonu üzerine etkisi olmadığını düşünüyoruz.

Kaynakça

  • Referans1: 1. Fein M, et al. Fiberoptic technique for 24-hour bile reflux monitoring. Standards and normal values for gastric monitoring. Dig Dis Sci 1996; 41: 216- 225.
  • Referans2: Hyun JJ, et al. Correlation Between Bile Reflux Gastritis and Biliary Excreted Contrast Media in the Stomach. J Comput Assist Tomogr 2017; 41: 696–701.
  • Referans3: O’Connor HJ, et al. Campylobacter like organisms and reflux gastritis. J Clin Pathol 1986; 39: 531-534
  • Referans4: Gad Elhak N, et al. Prevalence of Helicobacter pylori, gastric myoelectrical activity, gastric mucosal changes and dyspeptic symptoms before and after laparoscopic cholecystectomy. Hepatogastroenterology 2004; 51: 485–490
  • Referans5: Itoh M, et al. Antibacterial action of bile acids against Helicobacter pylori and changes in its ultrastructural morphology: effect of unconjugated dihydroxy bile acid. J Gastroenterol 1999; 34: 571–576
  • Referans6: Bode G, et al. Polymorphism in Helicobacter pylori--a key function in recurrence of infection? Med Klin (Munich) 1992; 87: 179–184
  • Referans7: Graham DY. Bile acid therapy for Helicobacter pylori [letter]. Aliment Pharmacol Ther 1992; 6: 653
  • Referans8: Hanninen ML. Sensitivity of Helicobacter pylori to different bile salts. Eur J Clin Microbiol Infect Dis 1991; 10: 508-518
  • Referans9: Farsakh NA, et al. Prevalence of Helicobacter pylori in patients with gall stones before and after cholecystectomy: a longitudinal study. Gut 1995; 36: 675-678
  • Referans10: Gunn A, Keddie N. Some clinical observations on patients with gallstones. Lancet 1972; 2: 239–241.
  • Referans11: Sobala GM, et al. Bile reflux and intestinal metaplasia in grastic mucosa. J Clin Pathol 1993; 46: 235-240.
  • Referans12: Kellosalo J, et al. Effect of biliary tract procedures on duodenogastric reflux and the gastric mucosa. Scand J Gastroenterol 1991; 26: 1272- 1278.
  • Referans13: Tewari SN, et al. The prevelance of Campylobacter pylori gastritis: A study of symptomatic nonulcer dyspepsia and bile gastritis. J Clin Gastroenterol 1989; 11: 271-277.
  • Referans14: Taşkin V, et al. The effect of duodenogastric reflux on Helicobacter pylori presence and gastric histopathologic changes. Turk J Gastroenterol. 2003; 14: 239- 242.
  • Referans15: Karttunen T, Niemelä S. Campylobacter pylori and duodenogastric reflux in peptic ulcer disease and gastritis. Lancet 1988; 1: 118.
  • Referans16: Caldwell MT, et al. Helicobacter pylori infection increases following cholecystectomy. Ir J Med Sci 1995; 164: 52–55.
  • Referans17: Ladas SD, et al. Helicobacter pylori may induce bile reflux: link between H pylori and bile induced injury to gastric epithelium. Gut 1996; 38:15- 18
  • Referans18: Amieva M, Peek RM, Jr. Pathobiology of Helicobac¬ter pylori-induced Gastric Cancer. Gastroenterology 2016; 150: 64-78.
  • Referans19: Fuchs KH, et al. Variability in the composition of physiologic duodenogastric reflux. J Gastrointest Surg. 1999; 3: 389–396.
Toplam 19 adet kaynakça vardır.

Ayrıntılar

Birincil Dil Türkçe
Konular Sağlık Kurumları Yönetimi
Bölüm Araştırma Makalesi
Yazarlar

Süleyman Kargın 0000-0003-4597-8654

Nisa Çetin Kargın 0000-0002-3819-2402

Yayımlanma Tarihi 30 Nisan 2020
Kabul Tarihi 29 Nisan 2020
Yayımlandığı Sayı Yıl 2020 Cilt: 4 Sayı: 1

Kaynak Göster

Vancouver Kargın S, Çetin Kargın N. Alkalen Reflü Gastritin İntragastrik pH ve Helicobacter Pylori Kolonizasyonu Üzerine Etkisi. Med J West Black Sea. 2020;4(1):24-8.

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