Intravascular coagulation in acute leukemia: clinical and subclinical abnormalities.

were found to have evidence of a generalized hemostatic disorder. These patients could be divided into three groups. The first group consisted of three patients with increased fibrinogen catabolism without clinical or laboratory evidence of intravascular coagulation. The second group of five patients had laboratory evidence of intravascular coagulation without clinically evident bleeding or thrombosis. The third group of seven patients developed symptomatic intravascular coagulation characterized by bleeding, renal failure, and poor response to platelet transfusions. Laboratory evidence for intravascular coagulation in these patients included falling plasma fibrinogen and factor V levels and elevated serum levels of fibrinogen degradation products. Heparin therapy resulted in clinical improvement in all seven patients. Rising plasma fibrinogen and factor V levels correlated with a beneficial clinical response to heparin. Increased fibrinogen catabolism, asymptomatic intravascular coagulation, and symptomatic intravascular coagulation form part of a spectrum of generalized hemostatic disorders in acute leukemia.