The Reduction of Platelet Cofactor II (Autoprothrombin II) Activity with Anticoagulants

Summary

The total platelet cofactor activity in plasma and the platelet cofactor II activity in serum was measured. The normal variations are high. Some individuals have less serum platelet cofactor II than found in certain cases of PTC “deficiency”; and when the serum platelet cofactor II concentration was reduced to zero with the use of anticoagulants, there was no bleeding tendency observed. With the use of Sintrom and phenylindanedione, the total platelet cofactor activity of plasma was reduced and the platelet cofactor II activity of serum was reduced to near zero. With the latter drug platelet cofactor II of serum was still low 10 days after the drug was withdrawn. With Sintrom given intermittently the fluctuations in prothrombin concentration are noticeably more rapid than the changes in platelet cofactor II. In a preliminary study of other drugs, there were indications that platelet cofactor II concentration is not altered with some anticoagulants even though the prothrombin concentration is reduced. Apparently, the platelet cofactor II changes which occur are characteristic for each anticoagulant. The platelet cofactor I levels of the plasma are not appreciably, and most likely not at all altered by the drugs studied.

 

• References

• 1 Johnson S. A, Rutzky J, Schneider C. L, and Seegers W. H. Activation of purified prothrombin with hemophilic plasma. Proc. Internat. Soc. Hematol. 4 Congr. p. 373 1952
• 2 Verstraete M. De Vorming van Plasma Thromboplastine. 1955. Arscia Vitgaven; Brussels:
• 3 Verstraete M, and Vandenbroucke J. The thromboplastin generation test. Some practical modifications and study of the role of factors V and VII on the formation of plasma thromboplastin. Acta med. scand. 155: 37 1956;
• 4 Johnson S. A, and Seegers W. H. The reduction of autoprothrombin II activity with dicumarol. Circulation Research 4: 182 1956;
• 5 Naeye R. L. Plasma thromboplastin component: influence of coumarin compounds and vitamin K on its activity in serum. Proc. Soc. exp. Biol. (N. Y.) 91: 101 1956;
• 6 Sise H. S, Kimball D. M, and Adamis D. Plasma thromboplastin (PTC) deficiency produced by prolonged administration of prothrombopenic anticoagulants. Proc. Soc. exp. Biol. (N. Y.) 89: 31 1956;
• 7 Seegers W. H, Loomis E. C, and Vandenbelt J. M. Preparation of prothrombin products; Isolation of prothrombin and its properties. Arch. Biochem. 6: 85 1945;
• 8 Ware A. G, and Seegers W. H. Two-stage procedure for the quantitative determination of prothrombin concentration. Amer. J. clin. Path. 19: 471 1949;
• 9 Ware A. G, and Seegers W. H. Studies on prothrombin: purification, inactivation with thrombin, and activation with thromboplastin and calcium. J. biol. Chem. 174: 565 1948;
• 10 Seegers W. H. The purification of prothrombin. Record Chem. Progr. 13: 143 1952;
• 11 Schneider C. L, Claxton E. B, Hughes C. H, and Johnson S. A. Bovine platelets in large quantities, properties and activities concerned with hemostasis. Am. J. Physiol. 179: 237 1954;
• 12 Ware A. G, Guest M. M, and Seegers W. H. Fibrinogen: With special reference to its preparation and certain properties of the product. Arch. Biochem. 13: 321 1947;
• 13 Seegers W. H, and Smith H. P. Factors which influence the activity of purified thrombin. Am. J. Physiol. 137: 348 1942;
• 14 Johnson S. A, and Seegers W. H. Use of purified prothrombin in the study of hemophilia and plasma thromboplastin component (PTC deficiency). J. appi. Physiol. 6: 429 1954;
• 15 Biggs R, Douglas A. S, Maciarlane R. C, Dacie J. V, Pitney W. R, Merskey C, and O’Brien J. R. Christmas disease; a condition previously mistaken for hemophilia. Brit. med. J. 2: 1378 1952;
• 16 Aggeler P. M, White S. G, Glendening M. B, Page E. W, Leake T. B, and Bates G. Plasma thromboplastin component (PTC) deficiency: A new disease resembling hemophilia. Proc. Soc. exp. Biol. (N. Y.) 79: 692 1952;