Pericapillary fibrin in the ulcer-bearing skin of the leg: the cause of lipodermatosclerosis and venous ulceration

• Published in: BMJ 1982-10, Vol.285 (6348), p.1071-1072
• Main Authors: Burnand, K G, Whimster, I, Naidoo, A, Browse, N L
• Format: Article
• Language: English
• Subjects: Biopsies; Capillaries; Clinical Research; Female; Fibrin - metabolism; Humans; Hypertension; Leg Ulcer - metabolism; Legs; Male; Oxygen; Saphenous vein; Scleroderma, Localized - metabolism; Skin; Skin - blood supply; Skin - metabolism; Specimens; Varicose Ulcer - metabolism; Varicose veins; Veins
• ISSN: 0007-1447; 0267-0623; 0959-8138; 1468-5833
• DOI: 10.1136/bmj.285.6348.1071

Forty-one biopsy specimens, taken from the ulcer-bearing skin of 41 legs of 21 patients attending the varicose vein clinic, were selectively stained for fibrin with phosphotungstic acid haemotoxylin before being blindly assessed,. Layers of fibrin were found surrounding the dermal capillaries in all 26 legs with lipodermatosclerosis. None of the specimens from the 15 legs with clinically normal skin contained fibrin. There was also an increased number of dermal capillaries cut in cross section per high powered field in 24 of the 26 legs with lipodermatosclerosis compared with two of the 15 legs with normal skin (p less than 0.001). The mean reduction in foot vein pressure during exercise was significantly less in the 26 limbs with pericapillary fibrin than in the other 15 limbs (p less than 10(-6). Lipodermatosclerosis is synonymous with pericapillary fibrin deposition and is associated with, and probably secondary to, both a persistently raised venous pressure and an increase in the size of the dermal capillary bed. This extravascular deposition of fibrin probably stimulates tissue fibrosis and blocks the diffusion of oxygen to the overlying epidermis, producing cellular death and venous ulceration.