The refractory form of gastroesophageal reflux disease: clinical and endoscopical, functional and morphofunctional criteria
Abstract
Aim of investigation. To estimate activity of cells of diffuse endocrine system of the esophagus at patients with refractory form of gastroesophageal reflux disease (GERD).
Material and methods. Twenty three patients with the refractory form of gastroesophageal reflux disease (RFGERD), 100 patients of GERD who responded to treatment, including 60 of those with non-erosive form of endoscopically positive GERD (NFGERD), 40 — with erosive form of GERD (EFGERD) and 14 patients with Barret’s esophagus (BE) were investigated. Groups of comparison included 30 patients with chronic H. pyloriassociated gastritis and 20 generally healthy patients. Contents of nephro-endocrine cells in mucosa of the esophagus, producing nitric oxide synthase, endothelin-1, melatonin, neurotensin and р53 was determined by immunehistochemical method.
Results. In contrast to NFGERD and EFGERD, at RFGERD higher grade of hyperplasia of esophageal neuroendocrine cells secreting neurotensin, and esophageal epithelial cells expressing р53 was observed.
Conclusions. Disorders of functional activity of neuroendocrinal cells of esophageal mucosa, producing neurotensin, and epithelial cells of the esophagus expressing р53, can act as a factor promoting development of refractory forms of GERD.
About the Authors
M. A. OsadchukRussian Federation
A. M. Osadchuk
Russian Federation
D. V. Balashov
Russian Federation
I. M. Kvetnoy
Russian Federation
References
1. Ивашкин В.Т. Диагностика и лечение гастроэзофагеальной рефлюксной болезни: Пособие для врачей, руководителей органов управления здравоохранением и лечебно-профилактических учреждений. – М., 2005. – 30 с.
2. Осадчук М.А., Калинин. А.В., Липатова Т.Е. и др. Роль диффузной нейроэндокринной системы в патогенезе и исходе гастроэзофагеальной рефлюксной болезни // Рос. журн. гастроэнтерол. гепатол. колопроктол. – 2007. – Т. 17, № 3. – С. 35–39.
3. Abdel-Latif M.M., Duggan S., Reynolds J.V., Kelleher D. Inflammation and esophageal carcinogenesis // Curr. Opin. Pharmacol. – 2009. – Vol. 9, N 4. – Р. 334–342.
4. Dent J., Armstrong D., Delaney D.C. Symptom evaluation in reflux disease: Proceedings of a workshop held in Marrakech, Morocco // Gut. – 2004. – Vol. 53. – P. 1–65.
5. Fujiwara Y., Higuchi K., Yamamori K. et al. Pathogenesis and treatment of refractory gastroesophageal reflux disease in Japanese patients // Nippon Rinsho. – 2004. – Vol. 62, N 8. – P. 1510–1515.
6. Lee K.M., Lee J.S., Jung H.S. et al. Late reactivation of sonic hedgehog by Helicobacter pylori results in population of gastric epithelial cells that are resistant to apoptosis: Implication for gastric carcinogenesis // Cancer Lett. – 2009. – Vol. 18. – P. 345–351.
7. Park W., Vaezi M.F. Esophageal impedance recording: clinical utility and limitations // Curr. Gastroenterol. Rep. – 2005. – Vol. 7, N 3. – Р. 182–189.
8. Richter J.E. Role of the gastric refluxate in gastroesophageal reflux disease: Acid, weak acid and bile // Am. J. Med. Sci. – 2009. – Vol. 8. – P. 63–69.
9. Solaymani-Dodaran M., Logan R.F.A., West J. et al. Risk of esophageal cancer in Barrett’s esophagus and gastroesophageal reflux // Gut. – 2004. – Vol. 53. – P. 1070–1074.
10. Vaezi M.F. Refractory GERD: acid, nonacid, or not GERD? // Am. J. Gastroenterol. – 2004. – Vol. 99, N 6. – P. 981–988.
11. Velasco M.J., Ortiz V., Ponce J. Gastroesophageal reflux disease refractory to esomeprazole // Gastroenterol. Hepatol. – 2005. – Vol. 28, N 2. – P. 65–77.
12. Wojtuń S., Gil J., Jałocha Ł. et al. Gastroesophageal reflux disease – diagnosis and management // Pol. Merkur. Lekarski. – 2009. – Vol. 155. – Р. 512–516.
Review
For citations:
Osadchuk M.A., Osadchuk A.M., Balashov D.V., Kvetnoy I.M. The refractory form of gastroesophageal reflux disease: clinical and endoscopical, functional and morphofunctional criteria. Russian Journal of Gastroenterology, Hepatology, Coloproctology. 2011;21(2):30-36. (In Russ.)