In bromocarbamide intoxication in humans, as in rabbits, the predominant feature is the endothelial damage characterized by desquamation and vacuolisation, followed by interstitial oedema. Consumption coagulopathy, as observed in some cases of human bromocarbamide intoxication and also in our experimental model, can be prevented by anti-coagulant therapy with heparin and also, as could be shown in rabbits, with aggregation-inhibiting agents. These findings strongly suggest that consumption coagulopathy is only a secondary phenomenon which develops in the course of primary endothelial damage. Similarities in the histological findings of endothelial damage between bromocarbamide intoxication in humans and in rabbits and the so-called "Adalin purpura", which can be observed after chronic use of bromocarbamide, are discussed.