Plasminogen activators, venous leg ulcers and reepithelialization.Int J Dermatol. 1995 Oct; 34(10):696-9.IJ
BACKGROUND AND OBJECTIVE
The pathogenesis of leg ulcers due to chronic venous hypertension (CVH) seems to be related to perivenular fibrin-film formation due to decreased cutaneous fibrinolytic activity dependent on reduced release of tissue-type plasminogen activator that leads to tissue anoxia and ulcer formation. The purpose of the work is a spectrophotometric evaluation of urokinase (UPA) at the edge, the floor and in the periulcerous skin of leg ulcers.
We examined a group of 10 patients with chronic leg ulcers caused by CVH. The biopsies from each patient were taken: (1) from the edge of the ulcer; (2) from the perilesional skin and (3) from the floor of the ulcer. Urokinase levels were evaluated in the same areas in 10 control subjects. The UPA activity was determined spectrophotometrically at 405 nm.
The results of our study showed that UPA is detectable in the center of the ulcer, on the edge, in the perilesional skin, as well as in the controls. Data are statistically significant. The highest levels of UPA are found at the edge of the ulcer; they were lower in the center and in the periulcerous skin.
A chemoattracting effect of UPA on human keratinocytes has been documented and this study showed significantly higher levels of UPA at the edge and on the floor of the ulcers, suggesting a possible role of an UPA gradient that could promote mobilization of keratinocytes from the edge to the floor, thus inducing reepithelialization. Moreover, UPA could play some role in neoangiogenesis and fibroblast chemoattraction, thus contributing in various ways to wound healing.