title: Circulating endothelial cells in venous blood as a marker of endothelial damage in chronic venous insufficiency: improvement with venoruton.
abstract: Damage to endothelial cells is common in vascular disorders and in reactions associated with transplantation. An elevated number of circulating endothelial cells indicates the extent of endothelial damage in a variety of disorders. In chronic venous insufficiency (CVI), the number of endothelial cells is abnormally increased, and this can be considered an important indication of endothelial damage. A group of 23 subjects with two levels of CVI (severe and very severe with previous ulcerations) with an increased endothelial cell count (seen by microscopy) was studied and treated for 4 weeks with oral Venoruton (0-[beta-hydroxyethyl]-rutosides) (1 g/day) to evaluate the effects of treatment on the circulating endothelial cells in blood taken from a peripheral leg vein. The controls comprised two groups with comparable age and sex distribution, one of healthy individuals and one of CVI subjects. After 4 weeks, a significant decrease was noted in endothelial cells both in subjects with CVI and in those with very severe CVI with previous ulcerations. This study suggests that endothelial cells may play a significant role in venous disease, being both an indication of severe disease and a further problem in itself. The use of Venoruton appears to decrease the number of circulating endothelial cells. This suggests an important role of this compound in protecting the endothelium and offers new potentially important therapeutic options that are not limited only to venous disease.
authors.affiliation: Irvine2 Vascular Lab and Physiology, Department of Biomedical Sciences, G D'Annunzio, University, Chieti-Pescara, Italy.
authors.forename: Maria Rosaria
authors.initials: MR
authors.lastname: Cesarone
authors.forename: Gianni
authors.initials: G
authors.lastname: Belcaro
authors.forename: Luciano
authors.initials: L
authors.lastname: Pellegrini
authors.forename: Andrea
authors.initials: A
authors.lastname: Ledda
authors.forename: Giulia
authors.initials: G
authors.lastname: Vinciguerra
authors.forename: Andrea
authors.initials: A
authors.lastname: Ricci
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Gizzi
authors.forename: Edmondo
authors.initials: E
authors.lastname: Ippolito
authors.forename: Filiberto
authors.initials: F
authors.lastname: Fano
authors.forename: Mark
authors.initials: M
authors.lastname: Dugall
authors.forename: Giovanni
authors.initials: G
authors.lastname: Acerbi
authors.forename: Marisa
authors.initials: M
authors.lastname: Cacchio
authors.forename: Andrea
authors.initials: A
authors.lastname: Di Renzo
authors.forename: Morio
authors.initials: M
authors.lastname: Hosoi
authors.forename: Stefano
authors.initials: S
authors.lastname: Stuard
authors.forename: Marcello
authors.initials: M
authors.lastname: Corsi
mesh_terms: D001775:Blood Circulation; D002452:Cell Count; D002908:Chronic Disease; D042783:Endothelial Cells / Q000187:drug effects* / Q000473:pathology; D004730:Endothelium, Vascular / Q000473:pathology*; D005260:Female; D006801:Humans; D006896:Hydroxyethylrutoside / Q000031:analogs & derivatives* / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D014662:Vasoconstrictor Agents / Q000627:therapeutic use*; D014689:Venous Insufficiency / Q000473:pathology*
chemical_list: D006896:Hydroxyethylrutoside; D014662:Vasoconstrictor Agents; C005865:troxerutin