LEUKOCYTES IN CHRONIC VENOUS INSUFFICIENCY

The development of cutaneous trophic changes in chronic venous insuffi ciency Is linked to a complex microangiopathy whose central pathogenic event is subepidermal capillary destruction. Numerous studies, partic ularly those using classical and fluorescence cutaneous capillary micr oscopy, have demonstrated the causal effect of the microangiopathy. On a macrovascular point of view, it has been shown that ambulatory veno us hypertension, linked to varicose veins or to postthrombotic disease , is the main pathogenic factor leading to this microangiopathy and it s clinical consequences. The mechanism leading from macro-to microangi opathy remains, however, unknown. To date, the most plausible explanat ion of the skin capillary loss is the activation of leukocytes sequest rated in the cutaneous microcirculation during venous stasis. Several facts have been evidenced in this respect: the existence of a transien t sequestration of leukocytes in the microcirculation of the lower lim bs during orthostatic stasis; an increase of adhesion markers both on leukocytes and endothelial cells; and an increased production of leuko cyte degranulation enzymes and oxygen free radicals. Although these da ta are consistent, experimental evidence is still required for decisiv e proof for the leukocyte hypothesis.