Annual Review of Medicine Volume 59 2008 by C. Thomas Ed Caskey

By C. Thomas Ed Caskey

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Furthermore, purified FVIIa did not induce any signs of a general activation of the coagulation system in the same dog model. However, FVIIa might well be a major contributor to the hemostatic effectiveness of APCCs. FVIIa occurs in the normal circulation in a concentration corresponding to ∼1% of the total FVII protein mass (6). In the 1970s, very little was known about the roles of FVII/FVIIa and TF in the hemostatic process, and FVIIa as a hemostatic agent was a new concept. FVIIa was purified from human plasma and infused into two hemophilia patients who had FVIII inhibitors.

The majority of circulating TFPI is bound to plasma lipoproteins (9). Heparin releases the endothelial-cell-bound TFPI (3). Another pool of TFPI not released by heparin is bound to glycosylphosphatidylinositol (GPI), either directly (TFPI-beta) or indirectly (TFPI-alpha). Both forms of TFPI seem to be involved in the localization of TFPI to cell surfaces (9). TFPI has been found to enhance the TF-specific internalization and degradation of FVIIa, which requires the C-terminal domain of TFPI and FXa.

Inhibiting TFPI by adding a TFPI antibody was found to normalize the prolonged clotting time in plasma from hemophilia A and B patients, using a dilute prothrombin time assay (30). When TFPI is prevented from inhibiting the TF-FVIIa-FXa complex, thrombin generation in the absence of the prothrombinase complex is facilitated. org • TF-FVII Pathway and Therapeutic Opportunities 37 ANRV334-ME59-03 Table 1 ARI 16 December 2007 14:39 Summary of studies using FVIIai (32) Model system Results Annu. Rev.

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