[Serum levels of vascular endothelial growth factor in chronic hepatitis C patients treated with interferon alpha and ribavirin].

UNLABELLED

Liver fibrosis is a result of disturbed balance between extracellular matrix protein synthesis and degradation. Growth factors may play the meaningful role in pathogenesis of fibrosis. The aim of the study was the assessment of VEGF role in pathogenesis of fibrosis associated with chronic hepatitis C (CHC) and evaluation of the influence of antiviral therapy on VEGF levels depending on treatment results.

MATERIAL AND METHODS

Study group included 100 CHC patients with fibrosis (Scheuer: 1-4 points). Control group included 30 HCVAb-positive subjects with normal ALT, without fibrosis (Scheuer: 0 points). From all subjects blood samples were taken at the beginning of the study. From study group patients blood samples were also collected after the treatment with Rebetron.

RESULTS

There was no significant difference in VEGF levels between CHC group and control group. Significant negative correlation between VEGF levels and inflammatory activity (R = -0.40; p < 0.01) and fibrosis stage (R = -0.30; p < 0.05) was observed. After antiviral treatment significant elevation of VEGF occurred in responders (112.8 vs. 315.03 pg/ml; p < 0.05), but not in non-responders.

CONCLUSIONS

1. Progression of liver lesions is correlated with reduction of VEGF levels. 2. Good therapeutic effect is connected with the elevation of VEGF levels. 3. Angiogenesis stimulation by VEGF probably is an important element in regenerative processes accompanying fibrosis regression.