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Summary and conclusionsThe value of fibrinolytic enhancement with an anabolic steroid (stanozolol) combined with elastic stockings in treating venous lipodermatosclerosis was assessed in a six-month double-blind cross-over trial. Thirty-four legs of 23 patients in whom other treatments had failed were studied. The patients were randomly divided into two groups who were treated with either stanozolol plus elastic stockings or placebo plus elastic stockings for three months, and then vice versa. Treatment with or without stanozolol caused the area of lipodermatosclerosis to decrease, but the rate of healing when patients took stanozolol was double that when they took the placebo, and this was assumed to be biologically important. Stanozolol also reduced the incidence of extravascular fibrin detected in skin biopsy specimens. The elastic stockings with placebo produced significant decreases in leg volume, ankle circumference, and skin thickness.Stanozolol is valuable in treating intractable lipodermatosclerosis, giving relief of pain and reducing induration, inflammation, tenderness, and pigmentation. IntroductionWe have described the apparent bcneficial effect on venous lipodermatosclcrosis (liposclerosis; the changes in the skin and subcutancous changes commonly knowvn as "the postphlcbitic lcg") of stimulating blood fibrinolytic activity wvith the anabolic

The changes in foot vein pressure during exercise have been measured in 30 normal legs and 109 legs with varicose veins or postphlebitic changes and correlated with the number of capillaries visible in a histological section of skin from the ulcer-bearing area. There was a significant correlation between the inability of the calf pump to reduce foot vein pressure during exercise and the number of capillaries in the skin. It is suggested that the increased number of capillaries secondary to venous hypertension during exercise may be the prime cause of the nutritional abnormalities that eventually cause a venous ulcer.

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An increased number of skin capillaries has been found in human skin subjected to sustained venous hypertension. To investigate this observation, venous hypertension was produced in the hind limb of Greyhounds by fashioning an arteriovenous (AV) fistula between the femoral vessels. This caused an increase in the number of capillaries in the skin of the lower leg. The capillary permeability of normal legs and legs subjected to chronic venous hypertension was then studied by observing the movement of radioactive molecules from the plasma to the fluid within Guyton capsules. Fibrinogen, a large molecule, leaked out of the capillaries significantly faster in the limbs with a high venous pressure and an enlarged capillary bed. It is suggested that the increase in the size and permeability of the dermal skin capillaries secondary to prolonged venous hypertension is the cause of lipodermatosclerosis and venous ulceration.