Abstract
Von Willebrand factor, tumor necrosis factor-α levels and portal bloodstream were examined in 47 patients with liver cirrhosis and 8 apparently healthy persons. The increase of von Willebrand factor and tumor necrosis factor-α levels were found to lead to the development of erosive-ulcerative lesions of gastric mucosa. The abnormalities of portal resistance, von Willebrand factor and TNF-α are interrelated data which play a certain role in occurrence of erosive-ulcerative lesions of gastric mucosa in patients with liver cirrhosis.
Highlights
Congestive phenomena in the vascular system in case of portal hypertension, especially pronounced in the microcirculation, hypoxia, stasis, erythrocyte aggregation, and endotoxemia result in disorders of the erythrocyte morphofunctional properties in liver cirrhosis patients and vasculopathy [8]
The analysis of the results of the research showed that von Willebrandfactor (vWF) increase in the blood plasma was observed in all the liver cirrhosis (LC) patients: in the 1st group of patients up to 10,94±1,55 IU/ml (р
The analysis of portal vein resistance showed that congestive index (CI) increased in all patients with liver cirrhosis: in the 1st group of patients up to 0,055±0,005 (р>0,05), the 2nd group – up to 0,11±0,01 (р
Summary
Congestive phenomena in the vascular system in case of portal hypertension, especially pronounced in the microcirculation, hypoxia, stasis, erythrocyte aggregation, and endotoxemia result in disorders of the erythrocyte morphofunctional properties in liver cirrhosis patients and vasculopathy [8]. Endothelial cells lesion leads to von Willebrandfactor (vWF) release – a multimeric glycoprotein participating in platelet adhesion and aggregation, promoting formation of microclots and further disturbance of microcirculation [6]. Intensified release of vWF in vitro is observed under the action of various stimuli including mechanical injury, endotoxins, histamine, complement complex as well as cytokines [4]. Increased TNF-α production promotes inhibition of the vascular smooth muscles reaction to restricting stimuli, causing hypoxia and sludge-phenomenon, intensifying local and systemic microcirculatory disorders, activating inflammatory process. TNF-α level increase results in disturbance of mitochondrial respiration and apoptosis stimulation [5]
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