Intravascular Coagulation in Acute Leukemia: Clinical and Subclinical Abnormalities

Abstract

Fifteen patients with acute leukemia 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.

Roles of protein C, protein S, and antithrombin III in acute leukemia

“…The occurrence of various coagulation abnormalities in acute leukemia is well established [1,2]. Hemorrhage is the most common hemostatic disorder in patients with acute leukemia, and thrombosis is a rarer complication.…”

“…Hemorrhage is the most common hemostatic disorder in patients with acute leukemia, and thrombosis is a rarer complication. Disseminated intravascular coagulation (DIC) is responsible for the majority of cases with clinically significant bleeding or thrombosis [1]. These abnormalities demonstrate different degrees of blood-clotting activation and characterize the so-called ''hypercoagulable state'' in these subjects.…”

Acute promyelocytic leukemia—clinical management of 15 patients

“…In the majority of cases the most marked abnormality in these values occurred on the second or third day of chemotherapy, but major abnormalities were noted as late as day 5 While prolongation of the PT occurred in all cases with therapy, three patients had no further fall in fibrinogen levels with treatment ( Table 11). Heparin infusions were continued for a mean of nine days (range, [4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19] and were discontinued when clinical bleeding stopped and the coagulation parameters returned towards normal after the administration of effective chemotherapy. In ten of the 13 patients surviving through initial induction therapy the PT had returned to normal by day 12, though in one patient it took 31 days for the value to revert to normal, and in two patients with disease considered resistant to therapy the PT remained prolonged (Table 11).…”

Factors and inhibitors of blood coagulation and fibrinolysis in acute nonlymphoblastic leukaemia

“…The most serious haemorrhages are seen in acute promyelocytic leukaemia (1-4), which constitutes 13% of acute nonlymphoblastic leukaemia (ANLL) in adults (5). The coagulation disturbances in promyelocytic leukaemia have been attributed both to disseminated intravascu-lar coagulation (DIC) (1)(2)(3)(4)(5)(6)(7)(8) and to primary (9) and secondary (8,10) fibrinolysis. Since both the factors of coagulation and fibrinolysis and their inhibitors are expected to be consumed in DIC and since new reliable methods for determining these inhibitors have recently been developed (11) we have investigated the disturbances of coagulation and fibrinolysis with special reference to the protease inhibitors in patients with ANLL.…”