ORIGINAL ARTICLES   

International Angiology 1998 March;17(1):49-52

Copyright © 2000 EDIZIONI MINERVA MEDICA

language: English

Levels of the inhibitor of PMN-Elastase in venous blood reflowing from chronically affected veins: the role of venous stasis

Signorelli S. *, Arpaia G., Cimminiello C., Pennisi G. *, Borsetto M. **, Mazzullo M. ***, Bonfardeci C., Andreozzi G. M. *

From the Vascular and Thrombotic Pathology, II Medical Department, S. Carlo Borromeo Hospital, Milan, Italy * Department of Internal Medicine ”A. Francaviglia“ Chair of Angiology, University of Catania, Italy ** Vascular Surgery Department, S. Donato Hospital, Italy *** Department of Internal Medicine, Hospital of Lecco, Italy.

Background. Attention has recent­ly been paid to the cell and bio­chem­i­cal dis­or­ders ­involved in chron­ic ­venous insuf­fi­cien­cy (CVI) and to their pos­sible rela­tion­ship to the endo­the­li­um.
Methods. In the ­present study, car­ried out in 14 ­patients with CVI, we eval­u­at­ed the lev­els of the inhib­i­tor of elas­tase (I-EL) gen­er­at­ed by poly­mor­pho­nu­cle­ate cells in the blood reflow­ing from affect­ed super­fi­cial veins of legs both at rest and after pro­longed ­venous sta­sis (1 hour in stand­ing posi­tion).
Results. We eval­u­at­ed the I-EL both as per­cent­age of activ­ity (base­line 82.3±24.5%; after sta­sis 100.7±37.8%) and as abso­lute val­ues (0.67±0.26 U/ml; after sta­sis 0.79± 0.39 U/ml). In blood sam­ples taken after ­venous sta­sis we found a ten­den­cy ­toward a trap­ping of white blood cells and an ­increase of the haem­a­toc­rit over base­line. The dif­fer­ence in the per­cent­ag­es of activ­ity of I-EL was sta­tis­ti­cal­ly sig­nif­i­cant, but only a trend was ­observed for the abso­lute val­ues.
Conclusions. We ­believe that the typ­i­cal haemo­dy­nam­ic dis­or­ders of ­patient with CVI ­increased by pro­longed ­venous sta­sis can mod­i­fy the func­tion of white blood cells, which are close­ly ­linked with ­venous hyper­ten­sion, thus play­ing an impor­tant role in the path­o­gen­e­sis of skin ­ulcers.