Understanding of thrombin formation in vivo has been greatly enhanced by the development of a cell-based model of coagulation. In this model, all clotting is initiated by the combination of tissue factor and activated coagulation factor VII (FVIIa). The source of the tissue factor may be extravascular or intravascular. Once initial thrombin is formed, activated coagulation factors VIII and IX greatly accelerate the process, leading to a “thrombin burst.” This mechanism explains why deficiencies of factors VIII and IX lead to problematic clinical bleeding, whereas deficiencies of factors VII or XI may not.
The cell-based model of coagulation provides a good underlying theory supporting the therapeutic use of recombinant FVIIa. The use of this product is often guided by protocols and measurement of FVII activity levels. Thus the case report by Hood and Eby is timely, because requests for measurement of FVII activity are increasing with increasing use of recombinant FVIIa. The reported case emphasizes the use of recombinant human thromboplastin prothrombin time reagents in obtaining the best measurement of FVII activity. The algorithm reflects the need to tailor infusions of recombinant FVIIa to patient condition. Patients with congenital FVII deficiency and no history of bleeding will not need the amount of factor that a patient with coumadin-related intracerebral hemorrhage requires.
Good medical theory and knowledge leads to good medical diagnosis and treatment. Enhanced understanding of coagulation allows the development of therapies targeted to specific coagulation defects uncovered in the laboratory. Although laboratorians still must master the models of intrinsic and extrinsic clotting as a means to interpret laboratory tests, understanding gained from the new cell-based model of coagulation is indeed a welcome change.
Grant/Funding Support: None declared.
Financial Disclosures: None declared.
- © 2008 The American Association for Clinical Chemistry