Publication | Closed Access
Platelet and Fibrinogen Consumption in Man
494
Citations
41
References
1972
Year
Selective Platelet DestructionThrombosisThrombopoiesisCardiovascular DiseaseFibrinogen ConsumptionMedicineBlood PlateletPlatelet ConcentratesHematologyPathologyCombined PlateletHemostasisCoagulation SystemVascular BiologyCoagulopathyFibrinolysisStrokeAtherosclerosis
Measurements of platelet and fibrinogen turnover in 35 healthy subjects and 104 patients revealed three distinct consumptive processes of the hemostatic system. The study identified three consumptive patterns: combined platelet and fibrinogen loss in conditions such as venous thrombosis and cancer, reversible with heparin; selective platelet destruction in arterial thrombosis and related disorders, reversible by platelet inhibitors or steroids; and selective fibrinogen loss following urokinase infusion, characteristic of primary fibrinolytic syndromes.
Survival and turnover measurements of platelets and fibrinogen in 35 normal subjects and 104 selected patients defined three types of consumptive processes involving the hemostatic apparatus. The first, characterized by combined platelet and fibrinogen consumption, represents an exaggeration of the physiologic hemostatic response. It occurs in patients with venous thrombosis, tissue trauma, widespread cancer, obstetric complications, and bacteremia. The result of activation of the coagulation system, this process can be modified by heparin. The second, characterized by selective platelet destruction, appears to reflect platelet thrombus formation on abnormal surfaces in the arterial system, including prosthetic devices and arterial thrombosis, thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome, and vasculitis syndromes. This process is reversed by certain inhibitors of platelet function or adrenocortical steroid suppression of vascular inflammation. The third involves selective destruction of fibrinogen and follows the infusion of urokinase. Isolated fibrinogen destruction seems typical of primary fibrinolytic syndromes.
| Year | Citations | |
|---|---|---|
Page 1
Page 1