Bibliotheca haematologica最新文献

A computer analysis of the coagulation laboratory records at the first department of Hokkaido University Hospital over a three-year period (1979-1981) was performed on 553 patients with presumptive intravascular coagulation. It is indicated that the most important diagnostic tests for DIC were Fbg, FDP, and AT III. DIC may have developed not only in patients with reduced Fbg but also in patients with normal or elevated Fbg. It is necessary to estimate the actual situations in the patients with DIC by utilizing sequential laboratory tests. In DIC, SDS-PAGE patterns of Fbg indicated the marked reduction of LMW Fbg, and the activated fibrin formation must be caused by the high affinity of thrombin for HMW Fbg. Changes in the immunoprecipitative second peak of AT III may indicate the binding of different serine proteases to AT III in DIC. Rapid and simple diagnostic tests for DIC are clinically required. An analysis of the TEG pattern using normal plasma mixed with the patient's plasma can indicate the presence of procoagulant activity in patient plasma. Such a laboratory test using TEG is the most useful and rapid diagnostic test in DIC. An anticoagulant effect of heparin therapy is determined by APTT and heparin levels. The antithrombotic effect of heparin therapy is determined by FPA as an immediate index and by Fbg, FDP, and AT III as a slow index.

Figure 5 summarizes the three different phases in the pathophysiology of disseminated intravascular coagulation exemplified by the effect of endotoxin. During the first phase, the coagulation system is activated to generate soluble fibrin. Fibrin kept in solution by fibrinogen or fibrinolytic degradation products can be cleared from the circulating blood. If the amount of soluble fibrin exceeds a certain threshold, soluble fibrin may precipitate or polymerize to fibrin clots. At this state, active fibrinolysis breaks down the precipitated fibrin to fibrinolytic degradation products preventing the preservation of fibrin. If the capacity of the fibrinolytic system is exhausted, or if fibrinolysis is inhibited, fibrin clots may be preserved, causing cell damage, as for instance bilateral renal cortical necrosis.

Microthrombi in 43 untreated and 26 treated cases of DIC were studied histologically and immunohistochemically. In the untreated cases, four types of microthrombi (intraluminal microthrombi with or without fibroblastic and/or smooth muscle cell reaction) were identified. Microthrombi in the former three types showed various degrees of thrombolysis. Failure of thrombolysis seemed to lead the organization of microthrombi. These morphological findings were considered to indicate the course of DIC and the degree of disappearance of the microthrombi in DIC. Microthrombi in the hepatic sinusoids and glomerular capillaries were studied with special reference to the removal processes of the microthrombi. Pathogenesis of renal cortical necrosis in DIC was also discussed. The number of microthrombi was markedly decreased by heparin and gabexate mesilate treatment. The incidences of microthrombi in the liver, kidney, lung, and heart were compared in the two treated groups.

Disseminated intravascular coagulation (DIC) occurs most frequently during the newborn period. Some clinical and laboratory criteria are available for the diagnosis of DIC in adults. However, they are not necessarily applicable in the diagnosis of DIC in newborn infants since the physiological state of coagulation during the newborn period differs from that in adults. We therefore reviewed 74 cases of DIC in newborns, including 34 cases at our own newborn care units. Criteria for the diagnosis of DIC in newborn infants were established.

Levels of prekallikrein and HMW kininogen that had increased during pregnancy decreased with start of labor. The role of the kinin-forming system with oxytocin in the mechanism of labor was suggested from the results of decreased prekallikrein and HMW kininogen, appearance of a free kallikrein-like enzyme during labor, and from the case of arrested labor in which both prekallikrein and HMW kininogen were markedly decreased. Prekallikrein was markedly decreased in patients with acute obstetrical DIC and severe toxemia of pregnancy. The excessive activation of prekallikrein in DIC seemed to be of help for understanding such clinical signs as shock, abnormal labor, and increased permeability in obstetrical DIC.