ENDOTHELIAL DYSFUNCTION IN ULCERATIVE COLITIS AND POSSIBILITIES FOR ITS CORRECTION DURING TREATMENT

Abstract

Introduction. The prevalence and severity of ulcerative colitis (UC) make it a relevant issue in the modern world. 
According to current data, the disease has a complex pathogenesis involving reactions from various functional systems of 
the body. One such system is the vascular endothelium, whose condition and relationship with UC progression and treatment 
outcomes remain poorly studied. 
Aim: To determine the characteristics of vascular endothelial function in relation to the clinical course of ulcerative colitis 
during treatment. 
Materials and methods: A total of 68 patients with UC, categorized based on disease activity and treatment regimen, 
and 80 clinically healthy individuals in the control group were examined. Several endothelial function parameters were 
analyzed: the number of circulating endothelial cells (CECs), levels of nitric oxide (NO) metabolites and endothelin-1 in the 
blood, and the degree of endothelium-dependent vasodilation. The frequency and timing of relapses were assessed over a 
one-year prospective observation period. 
Results: Significant differences in endothelial function indicators were observed between the main and control groups 
(endothelin-1 activity increased by 119.5%, p<0.01; CEC levels increased by 88.4%, p<0.001). Among subgroups of patients 
categorized by disease activity, significant differences in CEC levels were identified, but no notable variations in other 
endothelial function parameters were observed. In comparison with the control group, minimal disease activity did not show 
significant deviations. During treatment, differences between clinical groups were found only in CEC levels, which decreased 
by 18.8% (p=0.043). In patients with moderate disease activity, remission rates were significantly higher when endothelial 
function was targeted, and remission was achieved faster. Differences in favor of Group 1 were 50.8% (t=0.032, p<0.05) for 
remission rate and 46.3% (p=0.013) for remission duration. 
Conclusions:  
1. The progression of UC is associated with endothelial dysfunction, characterized by an imbalance between vasodilatory 
and vasoconstrictive factors, reduced vasodilation, and damage to the endothelial layer of the vascular wall. 
2. There is a correlation between disease activity and the severity of endothelial dysfunction, with greater dysfunction 
observed at higher activity levels, suggesting a pathogenic role of endothelial dysfunction in UC. 
3. Pharmacological treatment can reduce the degree of endothelial dysfunction, with effects persisting over an extended period.