Eksperimental'naia i klinicheskaia gastroenterologiia = Experimental & clinical gastroenterology · 2010
[Capillary collusion of gastric mucosa in patients with Helicobacter pylori gastritis and portal hypertension].
СтатьяНазвание и аннотация: Оригинал на русском
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Kovaleva O I, Khomeriki S G, Zhukov A G, Koviazina I O, Golovanova E V
Аннотация
INTRODUCTION: Prominent mucosal vasodilatation mediated by increased production of nitric oxide is thought to be manifestation of portal hypertensive gastropathy (PHG) in patients with chronic diffuse liver diseases. Recently was shown that Helicobacter pylori (Hp) infection could stimulate nitric oxide activity.
AIM: To investigate if chronic Hp infection is involved in development of gastric mucosal capillary dilatation in patients with PHG.
METHODS: The study was performed on 56 patients with PHG evaluated by upper endoscopy. The gastric biopsy was obtained from antrum and corpus. Hp status was assessed by rapid urease test and histology. Gastric mucosal capillary network (GMCN) assessed on histological sections immunostained for CD34, specific marker for endothelial cells. Nikon-CP995 camera and digital image analyzing system (DMI-1) was used for morphometry.
RESULTS: Marked vasodilatation was observed in antrum mucosa of Hp- patients with PHG and Hp+ patients without PHG (p < 0.05), relative volume of vessels was also increased, but number of vessels was not changed significantly. The relative volume and number of vessels in corpus mucosa were significantly higher in Hp- with PHG and Hp+ without PHG (p < 0.01). The mean size of vessels in corpus mucosa was decreased in Hp- with PHG (p < 0.05), but was not changed in Hp+ patients. Morphometric parameters in Hp+ with PHG was not changed significantly as compared to Hp+ without PHG or Hp- patients.
CONCLUSION: Hp provokes the same morphometric changes in GMCN as PHG. Hp may be one of factors important for regulation of GMCN function and structure. No additive effect between Hp infection and PHG on GMCN was observed in patients with PHG.
AIM: To investigate if chronic Hp infection is involved in development of gastric mucosal capillary dilatation in patients with PHG.
METHODS: The study was performed on 56 patients with PHG evaluated by upper endoscopy. The gastric biopsy was obtained from antrum and corpus. Hp status was assessed by rapid urease test and histology. Gastric mucosal capillary network (GMCN) assessed on histological sections immunostained for CD34, specific marker for endothelial cells. Nikon-CP995 camera and digital image analyzing system (DMI-1) was used for morphometry.
RESULTS: Marked vasodilatation was observed in antrum mucosa of Hp- patients with PHG and Hp+ patients without PHG (p < 0.05), relative volume of vessels was also increased, but number of vessels was not changed significantly. The relative volume and number of vessels in corpus mucosa were significantly higher in Hp- with PHG and Hp+ without PHG (p < 0.01). The mean size of vessels in corpus mucosa was decreased in Hp- with PHG (p < 0.05), but was not changed in Hp+ patients. Morphometric parameters in Hp+ with PHG was not changed significantly as compared to Hp+ without PHG or Hp- patients.
CONCLUSION: Hp provokes the same morphometric changes in GMCN as PHG. Hp may be one of factors important for regulation of GMCN function and structure. No additive effect between Hp infection and PHG on GMCN was observed in patients with PHG.