Leukocytes in chronic venous insufficiency.

The development of cutaneous trophic changes in chronic venous insufficiency Is linked to a complex microangiopathy whose central pathogenic event is subepidermal capillary destruction. Numerous studies, particularly those using classical and fluorescence cutaneous capillary microscopy, have demonstrated the causal effect of the microangiopathy. On a macrovascular point of view, it has been shown that ambulatory venous hypertension, linked to varicose veins or to postthrombotic disease, is the main pathogenic factor leading to this microangiopathy and its clinical consequences. The mechanism leading from macro-to microangiopathy remains, however, unknown. To date, the most plausible explanation of the skin capillary loss is the activation of leukocytes sequestrated in the cutaneous microcirculation during venous stasis. Several facts have been evidenced in this respect: the existence of a transient sequestration of leukocytes in the microcirculation of the lower limbs during orthostatic stasis; an increase of adhesion markers both on leukocytes and endothelial cells; and an increased production of leukocyte degranulation enzymes and oxygen free radicals. Although these data are consistent, experimental evidence is still required for decisive proof for the leukocyte hypothesis.