Studies on Platelets: I. The Relationship of Platelet Agglutination to the Mechanism of Blood Coagulation

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Abstract
Expts. were conducted to establish the specificity of platelet agglutination by sera of patients with thrombocytopenic purpura. When saline-washed discrete platelets are added to sera of patients with hemophilia, or thrombocytopenia or even of healthy persons, provided they contain sufficient prothrombin activity, agglutination occurs. The agglutinating property of serum is directly proportional to the prothrombin activity in the serum; it is lost when serum is treated with tricalcium phosphate gel (which removes prothrombin and at least part of the accelerator agents), or Amberlite IR-100 (which removes Ca); it is gradually lost when prothrombin activity of serum disappears during storage. The agglutination of platelets suspended in serum with residual prothrombin activity is accompanied by the evolution of thrombin in the mixture. The appearance of thrombin can be clearly demonstrated when platelets are added to serum containing Ca, prothrombin and sufficient plasma prothrombin conversion factor (labile factor). Whether thrombin itself or other agents of the coagulation process (which may be activated by thrombin from unutilized precursors) are responsible for platelet agglutination cannot be stated with certainty. The agglutination of platelets in serum of patients with idiopathic thrombocytopenic purpura has been regarded as evidence that an immunologic or destructive mechanism is present in that condition. The results caution against considering agglutination of platelets by thrombocytopenic serum as prima facie evidence of such a mechanism. Passage of native serum through a Seitz filter does not assure the removal of prothrombin and, therefore, the occurrence of false positive results must be considered. The serum itself should be deprothrombinized with tricalcium phosphate gel or decalcified, before its ability to agglutinate platelets is studied.

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