Araştırma Makalesi

Alkalen reflü gastritli hastalarda gastrik mukozal değişiklikler ve Helicobacter pylori enfeksiyonu

Cilt: 25 Sayı: 2 29 Ağustos 2017
  • Enver Akbaş
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Gastric mucosal changes and Helicobacter pylori infection in patients with alkaline reflux gastritis

Abstract

Background and Aims: We tried to evaluate the frequency of Helicobacter pylori infection, foveolar hyperplasia, intestinal metaplasia, and gastric mucosal atrophy of the antrum in patients with alkaline reflux gastritis (bile reflux gastritis) by comparing these patients with a control group comprised of individuals without bile reflux gastritis. We also sought to interpret the results of the irritating effects of bile on the gastric mucosa. Materials and Methods: One hundred and fifteen of 220 patients presenting to our hospital and diagnosed as having alkaline reflux gastritis were included as the patient group, and 105 patients without bile reflux gastritis were included as the control group in our study. The presence of concentrating or precipitated bile in the gastric mucosa abundantly and observation of mucosal hyperemia and edema was considered to be alkaline reflux gastritis. Biopsies were taken from both patient and control groups, and the presence of intestinal metaplasia, foveolar hyperplasia, atrophy, and Helicobacter pylori in the tissue was investigated. Results: The rates of observation of intestinal metaplasia in the control group and the bile reflux gastritis group were found to be 9.5% and 10.1%; respectively. No statistically significant difference was determined between the groups regarding the rate of observation of intestinal metaplasia. The rate of observation of atrophy was found to be 7.6% and 10.1% in the control group and in the bile reflux gastritis group, respectively. No statistically significant difference was determined between the groups regarding the rate of observation of atrophy. In addition, histopathological investigation revealed foveolar hyperplasia was observed at a rate of 4.3% in patients with bile reflux gastritis, and 2.9% in the control group. The difference between these rates was not statistically significant. While the rate of observation of Helicobacter pylori in the control group was 80.0%, it was determined to be 60.6% in the bile reflux gastritis group. In addition, this rate in the bile reflux gastritis group was less than the group without bile reflux gastritis and was found to be statistically significant. Conclusion: The frequency of foveolar hyperplasia, intestinal metaplasia, and gastric mucosal atrophy of the antrum in patients with alkaline reflux gastritis was found to be similar to patients without bile reflux gastritis. The frequency of Helicobacter pylori infection in patients with bile reflux gastritis was determined to be significantly less than the control group. This condition might result from unsuitability of the alkaline medium for Helicobacter pylori caused by bile in the gastric mucosa.

 

Key words: Bile reflux gastritis, Helicobacter pylori, foveolar hyperplasia, intestinal metaplasia, antral gastric atrophyBackground and Aims: We tried to evaluate the frequency of Helicobacter pylori infection, foveolar hyperplasia, intestinal metaplasia, and gastric mucosal atrophy of the antrum in patients with alkaline reflux gastritis (bile reflux gastritis) by comparing these patients with a control group comprised of individuals without bile reflux gastritis. We also sought to interpret the results of the irritating effects of bile on the gastric mucosa. Materials and Methods: One hundred and fifteen of 220 patients presenting to our hospital and diagnosed as having alkaline reflux gastritis were included as the patient group, and 105 patients without bile reflux gastritis were included as the control group in our study. The presence of concentrating or precipitated bile in the gastric mucosa abundantly and observation of mucosal hyperemia and edema was considered to be alkaline reflux gastritis. Biopsies were taken from both patient and control groups, and the presence of intestinal metaplasia, foveolar hyperplasia, atrophy, and Helicobacter pylori in the tissue was investigated. Results: The rates of observation of intestinal metaplasia in the control group and the bile reflux gastritis group were found to be 9.5% and 10.1%; respectively. No statistically significant difference was determined between the groups regarding the rate of observation of intestinal metaplasia. The rate of observation of atrophy was found to be 7.6% and 10.1% in the control group and in the bile reflux gastritis group, respectively. No statistically significant difference was determined between the groups regarding the rate of observation of atrophy. In addition, histopathological investigation revealed foveolar hyperplasia was observed at a rate of 4.3% in patients with bile reflux gastritis, and 2.9% in the control group. The difference between these rates was not statistically significant. While the rate of observation of Helicobacter pylori in the control group was 80.0%, it was determined to be 60.6% in the bile reflux gastritis group. In addition, this rate in the bile reflux gastritis group was less than the group without bile reflux gastritis and was found to be statistically significant. Conclusion: The frequency of foveolar hyperplasia, intestinal metaplasia, and gastric mucosal atrophy of the antrum in patients with alkaline reflux gastritis was found to be similar to patients without bile reflux gastritis. The frequency of Helicobacter pylori infection in patients with bile reflux gastritis was determined to be significantly less than the control group. This condition might result from unsuitability of the alkaline medium for Helicobacter pylori caused by bile in the gastric mucosa.


Keywords

Kaynakça

  1. KAYNAKLAR 1-Niemelä S. Duodenogastric reflux in patients with upper abdominal complaints or gastric ulcer with particular reference to reflux-associated gastritis. Scand J Gastroenterol Suppl 1985; 115:1 2-Karttunen T, Niemelä S. Campylobacter pylori and duodenogastric reflux in peptic ulcer disease and gastritis. Lancet 1988; 1:118. 3-Stein HJ, Smyrk TC, DeMeester TR, et al. Clinical value of endoscopy and histology in the diagnosis of duodenogastric reflux disease. Surgery 1992; 112:796. 4-Niemelä S, Karttunen T, Heikkilä J, Lehtola J. Characteristics of reflux gastritis. Scand J Gastroenterol 1987; 22:349. 5- Nakamura M, Haruma K, Kamada T, et al. Duodenogastric reflux is associated with antral metaplastic gastritis. Gastrointest Endosc 2001; 53:53. 6-Davenport HW. Destruction of the gastric mucosal barrier by detergents and urea. Gastroenterology 1968; 54:175. 7- Orchard R, Reynolds K, Fox B, et al. Effect of lysolecithin on gastric mucosal structure and potential difference. Gut 1977; 18:457. 8-Eastwood GL. Effect of pH on bile salt injury to mouse gastric mucosa. A light- and electron-microscopic study. Gastroenterology 1975; 68:1456. 9-Loffeld RJ, Loffeld BC, Arends JW, et al. Retrospective study of Campylobacter-like organisms in patients undergoing partial gastrectomy. J Clin Pathol 1988; 41:1313. 10-Karttunen T, Niemelä S. Campylobacter pylori and duodenogastric reflux in peptic ulcer disease and gastritis. Lancet 1988; 1:118. 11-Dempsey DT, Mercer DW, Deb B, et al. Adaptive cytoprotection of gastric surface epithelial cells against injury by physiologic concentrations of bile acid. Surgery 1990; 108:348. 12-Dixon MF. Reflux gastritis. Acta Gastroenterol Belg. 1989 May-Aug;52(3-4):292-6. 13-Cai J, Jia BQ. Clinical characteristics of bile reflux gastritis. Zhonghua Nei Ke Za Zhi. 1989 Feb;28(2):89-92, 126.

Ayrıntılar

Birincil Dil

Türkçe

Konular

-

Bölüm

Araştırma Makalesi

Yazarlar

Enver Akbaş Bu kişi benim
Medipol Üniversitesi, Tıp fakültesi, esenler Sağlık ve Uygulama Merkezi, İstanbul
0000-0002-3486-1787
Türkiye

Yayımlanma Tarihi

29 Ağustos 2017

Gönderilme Tarihi

25 Eylül 2017

Kabul Tarihi

3 Haziran 2017

Yayımlandığı Sayı

Yıl 2017 Cilt: 25 Sayı: 2

Kaynak Göster

APA
Akbaş, E. (2017). Alkalen reflü gastritli hastalarda gastrik mukozal değişiklikler ve Helicobacter pylori enfeksiyonu. Endoskopi Gastrointestinal, 25(2), 29-31. https://doi.org/10.17940/endoskopi.339832
AMA
1.Akbaş E. Alkalen reflü gastritli hastalarda gastrik mukozal değişiklikler ve Helicobacter pylori enfeksiyonu. Endoskopi Gastrointestinal. 2017;25(2):29-31. doi:10.17940/endoskopi.339832
Chicago
Akbaş, Enver. 2017. “Alkalen reflü gastritli hastalarda gastrik mukozal değişiklikler ve Helicobacter pylori enfeksiyonu”. Endoskopi Gastrointestinal 25 (2): 29-31. https://doi.org/10.17940/endoskopi.339832.
EndNote
Akbaş E (01 Ağustos 2017) Alkalen reflü gastritli hastalarda gastrik mukozal değişiklikler ve Helicobacter pylori enfeksiyonu. Endoskopi Gastrointestinal 25 2 29–31.
IEEE
[1]E. Akbaş, “Alkalen reflü gastritli hastalarda gastrik mukozal değişiklikler ve Helicobacter pylori enfeksiyonu”, Endoskopi Gastrointestinal, c. 25, sy 2, ss. 29–31, Ağu. 2017, doi: 10.17940/endoskopi.339832.
ISNAD
Akbaş, Enver. “Alkalen reflü gastritli hastalarda gastrik mukozal değişiklikler ve Helicobacter pylori enfeksiyonu”. Endoskopi Gastrointestinal 25/2 (01 Ağustos 2017): 29-31. https://doi.org/10.17940/endoskopi.339832.
JAMA
1.Akbaş E. Alkalen reflü gastritli hastalarda gastrik mukozal değişiklikler ve Helicobacter pylori enfeksiyonu. Endoskopi Gastrointestinal. 2017;25:29–31.
MLA
Akbaş, Enver. “Alkalen reflü gastritli hastalarda gastrik mukozal değişiklikler ve Helicobacter pylori enfeksiyonu”. Endoskopi Gastrointestinal, c. 25, sy 2, Ağustos 2017, ss. 29-31, doi:10.17940/endoskopi.339832.
Vancouver
1.Enver Akbaş. Alkalen reflü gastritli hastalarda gastrik mukozal değişiklikler ve Helicobacter pylori enfeksiyonu. Endoskopi Gastrointestinal. 01 Ağustos 2017;25(2):29-31. doi:10.17940/endoskopi.339832