Similarity to Heparin of the Clotting Inhibitor in Acute Leucemia and the Significance of Hyperheparinemia in Estrapenic Cholinergic States

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Abstract
Evidence for the heparin identity of the anti-thrombin in 5 patients with acute leucosis and 2 with throm-botic cardiogenic shock was obtained. Addition of their plasmas to citrated normal plasma caused dissociation in the precipitation rates of filiar and gelatinous fibrin when the plasma was clotted by CaCl2-viper venom. In untreated citrated plasma, the opaque filiar fibrin component precipitates immediately prior to the formation of gelatinous fibrin, so that both components are dispersed uniformly through the resulting opaque clot. In the presence of 1 mg.% of herapin, gelatiniza- tion is delayed until retraction of the filiar fibrin has begun, so that both components of the clot can be distinguished. Dissociation is completed by 2 mg.% of heparin. Hyperheparin-emia of this extent cannot condition the hemorrhagic diathesis. Greater heparin concns. may be attained, since it is common practice in treating thrombophlebitis to give 100 mg. of heparin in 1 injn.. An explanation is attempted of the mechanism of hyperheparinemia arising during the estrapenic dys-crasias. Giving heparin to a subject with normal hemopoietic function is followed by decreased coagulability after which there is a hypercoagulable state. During such heparin rebound, thromboplastin markedly increases, whereas it decreases in the hemorrhagic phase of estrapenic hyperheparinemia. In thrombopenic forms of acute malignant hematolog-ic dyscrasias, even where coagulation time seems normal, the filiar fibrin component of the clot and clot retraction may both be absent. Since thromboplastin helps form the retractile filiar fibrin, its deficiency in these states is indicated. Elaboration of the major fraction of blood cholinesterase is a bone marrow function. This is true of the elaboration of the major fraction of the blood thromboplastin. Estrapenia connotes a depression of the hemopoietic marrow, which is usually inclusive. Thromboplastin deficiency may be related to the estrapenia in that the latter signifies panmyelophthisis, the marrow being unable to form thromboplastin because it forms few or none of its peripheropetal products. If heparin evokes and regulates the rate and extent of thromboplastin production by the marrow, there is an explanation of the origin of hyperheparinemia in marrow failure. Blood herapin will rise when blood thromboplastin is not available, a situation extant in the myelophthises.

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