Thromb Haemost 1959; 3(04): 578-587
DOI: 10.1055/s-0038-1654413
Originalarbeiten — Original Articles — Travaux Originaux
Schattauer GmbH

Studies on the Fate of Coagulation Factors during the Clotting of Normal and Pathological Blood[*]

Cecil Hougie
1   Department of Clinical Pathology, University of Virginia Hospital, Charlottesville
› Author Affiliations
Further Information

Publication History

Publication Date:
12 June 2018 (online)

 

Summary

In a mild case of Stuart factor (SF) deficiency and in a patient with hemophilia B (factor IX deficiency) consumption of AHF (factor VIII) was normal but was abnormal in more severe examples of these diseases. This finding reconciles previously conflicting reports. Factor V utilisation was abnormal in moderately severe cases of SF deficiency, hemophilia A and hemophilia B but normal in mild cases of SF deficiency and hemophilia B. A mild case of hemophilia A was not studied. These findings would be expected from the modern concept of blood coagulation. However, the findings with respect to AHF are equally well explained if AHF is destroyed by some intermediate product of blood coagulation, such as thrombin, appearing at the time of the appearance of fibrin.

The concentration of SF was found to remain constant during the clotting of both normal blood and blood deficient in factor VIL

The concentration of factor VII during the coagulation of normal blood remained constant until the appearance of fibrin. The concentration then increased, but this finding was not consistently obtained. No abnormality in the fate of factor VII during the clotting of blood deficient in SF was found.


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* This investigation was supported by grant H-3536 from the Nat. Heart Inst., N.I.H. Public Health Service, USA.


  • References

  • 1 Alexander B, Goldstein R, Rich L, Le Bolloch A. G, Diamond L. K, Borges W. Congenital Afibrinogenemia: A study of some basic aspects of coagulation. Blood 1954; 9: 843
  • 2 Barnett C. P. Hemorrhagic diathesis due to factor VII deficiency. A. M. A. Arch. intern. Med 1957; 99: 280
  • 3 Bergsagel D. E, Biggs R. The Christmas factor. Rev. Hémat 1955; 10: 354
  • 4 Bergsagel D. E, Hougie C. Intermediate stages in the formation of blood thromboplastin. Brit. J. Haematol 1956; 2: 113
  • 5 Biggs R, Douglas A. S, Macfarlane R. G. The initial stages of blood coagulation. J. Physiol. (Lond.) 1953; 122: 528
  • 6 Douglas A. S. Antihemophilic Globulin Consumption during blood coagulation. Blood 1956; 11: 423
  • 7 Douglas A. S. Factor V consumption during blood coagulation. Brit. J. Haematol 1956; 2: 153
  • 8 Ferguson J. H, Rierson H. A, Johnston Jr C. L. Factors in Thrombin and Thromboplastin formation. Proc. Soc. exp. Biol. (N. Y.) in press.
  • 9 Fisch U, Duckert F. Some aspects of kinetics of the first stages of blood thromboplastin formation. Thromb. Diath. haem 1957; 3: 497
  • 10 Graham J. B, Barrow E. M, Hougie C. Stuart clotting defect II. Genetic aspects of a new hemorrhagic state. J. clin. Invest 1957; 36: 497
  • 11 Hougie C. The role of factor V in the formation of blood thromboplastin. J. Lab. clin. Med 1957; 50: 16
  • 12 Hougie C, Barrow E. M, Graham J. B. Stuart clotting defect. I. Segregation of a hereditary hemorrhagic state from the heterogenous group heretofore called “stable factor” (SPCA, proconvertin, factor VII) deficiency. J. clin. Invest 1957; 36: 485
  • 13 Hougie C. The reactions of factor V and SF with brain. Proc. Soc. exp. Biol. (N.Y.) 1959; 101: 132
  • 14 Johnston Jr C. L, Ferguson J. H, O’Hanlon F. A, Black W. L. The fate of factor VII and Stuart factor during the clotting of normal blood. Thromb. Diath. haem 1959; 3: 36
  • 15 Koller F. Der heutige Stand der Gerinnungsforschung. Thromb. Diath. haem 1958; 2: 407
  • 16 Macfarlane R. G. Blood coagulation with particular reference to the early stages. Physiol. Rev 1956; 36: 479
  • 17 Marcacci M, Ioria S. Rapporti frail fattore Stuart e la scomparsa dell’ attivita AHF durante la coagulazione. La Sintesi 1957; 1: 601
  • 18 Penick G. D. Some factors that influence utilization of antihemophilic activity during clotting. Proc. Soc. exp. Biol. (N. Y.) 1957; 96: 277
  • 19 Rizza C. R, Walker W. The inactivation of antihemophilic globulin by thrombin. Transactions of the 6th Congress of the European Society of Haematology. 1957: 173
  • 20 Rodman Jr N. F, Barrow E. M, Graham J. B. Diagnosis and control of the hemophiloid states with the partial thromboplastin time (PTT) test. Amer. J. clin. Path 1958; 29: 525
  • 21 Soulier J. P, Wartelle O, Ménaché D. Hageman trait and PTA deficiency; the role of contact of blood with glass. Brit. J. Haematol 1959; 5: 121
  • 22 Soulier J. P, Gobbi F, Larrieu M. J. Séparation-du fibrinogène et du facteur antihemophilique A. Rev. Hémat 1957; 12: 481
  • 23 Surgenor D. M. Some properties of a reaction mechanism analogous to thrombin formation. Thromb. Diath. haem 1959; 3: 227

  • References

  • 1 Alexander B, Goldstein R, Rich L, Le Bolloch A. G, Diamond L. K, Borges W. Congenital Afibrinogenemia: A study of some basic aspects of coagulation. Blood 1954; 9: 843
  • 2 Barnett C. P. Hemorrhagic diathesis due to factor VII deficiency. A. M. A. Arch. intern. Med 1957; 99: 280
  • 3 Bergsagel D. E, Biggs R. The Christmas factor. Rev. Hémat 1955; 10: 354
  • 4 Bergsagel D. E, Hougie C. Intermediate stages in the formation of blood thromboplastin. Brit. J. Haematol 1956; 2: 113
  • 5 Biggs R, Douglas A. S, Macfarlane R. G. The initial stages of blood coagulation. J. Physiol. (Lond.) 1953; 122: 528
  • 6 Douglas A. S. Antihemophilic Globulin Consumption during blood coagulation. Blood 1956; 11: 423
  • 7 Douglas A. S. Factor V consumption during blood coagulation. Brit. J. Haematol 1956; 2: 153
  • 8 Ferguson J. H, Rierson H. A, Johnston Jr C. L. Factors in Thrombin and Thromboplastin formation. Proc. Soc. exp. Biol. (N. Y.) in press.
  • 9 Fisch U, Duckert F. Some aspects of kinetics of the first stages of blood thromboplastin formation. Thromb. Diath. haem 1957; 3: 497
  • 10 Graham J. B, Barrow E. M, Hougie C. Stuart clotting defect II. Genetic aspects of a new hemorrhagic state. J. clin. Invest 1957; 36: 497
  • 11 Hougie C. The role of factor V in the formation of blood thromboplastin. J. Lab. clin. Med 1957; 50: 16
  • 12 Hougie C, Barrow E. M, Graham J. B. Stuart clotting defect. I. Segregation of a hereditary hemorrhagic state from the heterogenous group heretofore called “stable factor” (SPCA, proconvertin, factor VII) deficiency. J. clin. Invest 1957; 36: 485
  • 13 Hougie C. The reactions of factor V and SF with brain. Proc. Soc. exp. Biol. (N.Y.) 1959; 101: 132
  • 14 Johnston Jr C. L, Ferguson J. H, O’Hanlon F. A, Black W. L. The fate of factor VII and Stuart factor during the clotting of normal blood. Thromb. Diath. haem 1959; 3: 36
  • 15 Koller F. Der heutige Stand der Gerinnungsforschung. Thromb. Diath. haem 1958; 2: 407
  • 16 Macfarlane R. G. Blood coagulation with particular reference to the early stages. Physiol. Rev 1956; 36: 479
  • 17 Marcacci M, Ioria S. Rapporti frail fattore Stuart e la scomparsa dell’ attivita AHF durante la coagulazione. La Sintesi 1957; 1: 601
  • 18 Penick G. D. Some factors that influence utilization of antihemophilic activity during clotting. Proc. Soc. exp. Biol. (N. Y.) 1957; 96: 277
  • 19 Rizza C. R, Walker W. The inactivation of antihemophilic globulin by thrombin. Transactions of the 6th Congress of the European Society of Haematology. 1957: 173
  • 20 Rodman Jr N. F, Barrow E. M, Graham J. B. Diagnosis and control of the hemophiloid states with the partial thromboplastin time (PTT) test. Amer. J. clin. Path 1958; 29: 525
  • 21 Soulier J. P, Wartelle O, Ménaché D. Hageman trait and PTA deficiency; the role of contact of blood with glass. Brit. J. Haematol 1959; 5: 121
  • 22 Soulier J. P, Gobbi F, Larrieu M. J. Séparation-du fibrinogène et du facteur antihemophilique A. Rev. Hémat 1957; 12: 481
  • 23 Surgenor D. M. Some properties of a reaction mechanism analogous to thrombin formation. Thromb. Diath. haem 1959; 3: 227