Consumption-Coagulopathy

Abstract

9 cases of consumption-coagulopathy were described.
These included 3 cases of carcinomatosis and 2 cases of acute promyelocytic leukemia. In the remaining 4 cases, the initial courses were mycotic infection, paroxysmal nocturnal hemoglobinuria, infectious mononucleosis and liver cirrhosis, respectively.
The clot promoting substances, which were probably active intermediate products of clotting system, were demonstrated in 3 cases. Autopsy was done in 6 cases, and disseminated intravascular thrombi were observed in only 2 cases without evidences of increased fibrinolysis. No hemostatic effect was observed with the administration of synthetic fibrinolytic inhibitors, whereas a marked inhibition in fibrinolytic activity was observed following intravenous infusion of small doses of heparin.
From these data, it is postulated that some clinical conditions such as increased fibrinolysis and decreased platelet adhesiveness in the early stage of myocardial infarction may be accounted for by the mechanism similar to consumption-coagulopathy.
The relationship between hypercoagulability and consumption-coagulopathy is discussed.