Klinicheskaia meditsina · 2015
[DIFFUSE NEUROENDOCRINE SYSTEM OF THE STOMACH AND CHARACTERISTICS OF PROLIFERATION IN REALIZATION OF CORREA'S CASCADE IN DISEASES ASSOCIATED WITH HELICOBACTER PYLORI].
СтатьяНазвание и аннотация: Оригинал на русском
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Svistunov A A, Kireeva N V, Osadchuk M A, Kvetnoy I M
Аннотация
AIM: To study the role of the vascular endothelial growth factor (VEGF), Ki-67, BCL-2, and endocrine cells (EC) of gastric mucosa producing somatostatin (SS), glucagon (GL), and pancreatic polypeptide (PP) in diseases associated with Helicobacter pylori. To use the data obtained to develop early diagnostic criteria for the progress of structural changes in gastric mucosa of the patients with stomach ulcer disease [SUD), chronic atrophic gastritis (CAG), gastric adenomatous polyps (GAP), and gastric cancer (GC) before and after surgical intervention and eradication of H. pylori.
MATERIALS AND METHODS: We examined 104 patients with gastric pathology associated with Helicobacter pylori including 30 with SUD, 30 with CAG, 20 with GAP and CAG, 24 with stage II noncardia GC. The effectiveness of the treatment was evaluated 2 months after alleviation of inflammation in the stomachfollowing polypectomy in case of GAP or gastrectomy in case of GC. Material for immunohistochemical studies was taken from the fundus. Monoclonal antibodies against VEGF SS, GL, PP Ki-67, BCL-2 (1:100, Novocastra) were used. Histobacterioscopy was conducted using antral mucosal smears stained by the Romanowsky-Giemsa procedure.
RESULTS: Exacerbation of SUD was accompanied by a decrease in the number of epithelial cells and EC producing VEGF glucagon (GL), and pancreatic polypeptide (PP) with the increase in the number of SS-secreting EC along with intensification of proliferative processes determined from the number of Ki-67 and BCL-2 immunopositive epithelial cells. CAG and GC were associated with persistence of H. pylori, hyperplasia of EC producing VEGF glucagon (GL), pancreatic polypeptide (PP) and hypoplasia of SS-secreting EC along with high proliferative activity of epitheliocytes expressed via Ki-67 and BCL-2.
CONCLUSION: Endothelial growth factor (VEGF), somatostatin (SS), glucagon (GL), and pancreatic polypeptide (PP) are of importance for the prognostication of development and clinical course of diseases associated with Helicobacter pylori since their pathological properties are realized either directly or indirectly through H. pylori, Ki-67 and BCL-2. Eradication of H. pylori does not result in the disappearance of intestinal metaplasia.
MATERIALS AND METHODS: We examined 104 patients with gastric pathology associated with Helicobacter pylori including 30 with SUD, 30 with CAG, 20 with GAP and CAG, 24 with stage II noncardia GC. The effectiveness of the treatment was evaluated 2 months after alleviation of inflammation in the stomachfollowing polypectomy in case of GAP or gastrectomy in case of GC. Material for immunohistochemical studies was taken from the fundus. Monoclonal antibodies against VEGF SS, GL, PP Ki-67, BCL-2 (1:100, Novocastra) were used. Histobacterioscopy was conducted using antral mucosal smears stained by the Romanowsky-Giemsa procedure.
RESULTS: Exacerbation of SUD was accompanied by a decrease in the number of epithelial cells and EC producing VEGF glucagon (GL), and pancreatic polypeptide (PP) with the increase in the number of SS-secreting EC along with intensification of proliferative processes determined from the number of Ki-67 and BCL-2 immunopositive epithelial cells. CAG and GC were associated with persistence of H. pylori, hyperplasia of EC producing VEGF glucagon (GL), pancreatic polypeptide (PP) and hypoplasia of SS-secreting EC along with high proliferative activity of epitheliocytes expressed via Ki-67 and BCL-2.
CONCLUSION: Endothelial growth factor (VEGF), somatostatin (SS), glucagon (GL), and pancreatic polypeptide (PP) are of importance for the prognostication of development and clinical course of diseases associated with Helicobacter pylori since their pathological properties are realized either directly or indirectly through H. pylori, Ki-67 and BCL-2. Eradication of H. pylori does not result in the disappearance of intestinal metaplasia.