Gastric mucosal changes and Helicobacter pylori infection in patients with alkaline reflux gastritis

Yıl 2017, Cilt: 25 Sayı: 2, 29 - 31, 29.08.2017

Enver Akbaş

https://doi.org/10.17940/endoskopi.339832

Öz

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.

Anahtar Kelimeler

Bile reflux gastritis, Helicobacter pylori, foveolar hyperplasia, intestinal metaplasia, antral gastric atrophy

Alkalen reflü gastritli hastalarda gastrik mukozal değişiklikler ve Helicobacter pylori enfeksiyonu

Öz

Giriş ve Amaç: Alkalen reflü gastriti (safra reflüsü
gastriti) olan hastalarda, Helicobacter pylori enfeksiyonu, foveolar
hiperplazi, intestinal metaplazi ve antral gastrik mukozal atrofinin sıklığını,
safra gastriti olmayan kontrol grubu ile karşılaştırıp safranın gastrik
mukozaya irritan etkisinin sonuçlarını değerlendirmeye çalıştık. Gereç ve Yöntem: Hastanemize başvuran 220
hastadan alkalen reflü gastrit tesbit edilen 115 tanesi vaka grubu, mide
mukozasında safra reflüsü gastriti olmayan 105 hasta ise kontrol grubu olarak
alındı. Mide mukozasında bol miktarda konsantre veya presipite safra varlığı
ile mukozal hiperemi ve ödemin endoskopik olarak görülmesi alkalen reflü
gastrit olarak kabul edildi. Her iki hasta grubunda da biyopsiler alındı ve
dokuda intestinal metaplazi, foveolar hiperplazi, atrofi ve Helicobacter pylori
varlığı araştırıldı. Bulgular: Kontrol grubu vakalarda intestinal metaplazi
görülme oranı %9,5, safra gastriti grubunda intestinal metaplazi görülme oranı
%10,1 bulunmuştur. Gruplar arasında intestinal metaplazi görülme oranları
bakımından istatistiksel olarak anlamlı farklılık saptanmamıştır. Kontrol
grubunda atrofi görülme oranı %7,6, safra gastriti grubunda atrofi görülme oranı
%10,1 bulunmuştur. Gruplar arasında atrofi görülme oranları bakımından
istatistiksel olarak anlamlı farklılık saptanmamıştır. Histopatolojik
incelemede foveolar hiperplazi safra gastriti olan hastalarda %4,3 oranında
görülürken, kontrol grubu vakalarda %2,9 oranında görülmekte olup aradaki fark
istatistiksel olarak anlamlı değildir. Kontrol grubu vakalarda Helicobacter
pylori görülme oranı %80,0 iken, safra gastriti grubunda %60,6 saptanmıştır.
Safra gastriti grubunda Helicobacter pylori görülme oranının, safra gastriti
olmayan gruptan düşük olması istatistiksel olarak anlamlı bulunmuştur. Sonuç: Alkalen reflü gastriti olan
hastalarda, foveolar hiperplazi, intestinal metaplazi ve antral gastrik mukozal
atrofi sıklığı safra gastriti olamayan hastalar ile benzer bulundu.
Helicobacter pylori enfeksiyonu ise safra reflüsü gastrit olan hastalarda
kontrol grubu hastalara göre belirgin olarak daha düşük bulundu. Bu durum;
safranın gastrik mukozada oluşturduğu alkali ortamın Helicobacter pylori için
uygun bir vasat olmamasından kaynaklanıyor olabilir.

Anahtar Kelimeler

Safra reflüsü gastriti, Helicobacter pylori, foveolar hiperplazi, intestinal metaplazi, antral gastrik atrofi

Kaynakça

• 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.