A cell-based model of coagulation and the role of factor VIIa. Export

@article{citeulike:2873891, abstract = {Our cell-based model of haemostasis replaces the traditional 'cascade' hypothesis, and proposes that coagulation takes place on different cell surfaces in three overlapping steps: initiation, amplification, and propagation. In highlighting the importance of cellular control during coagulation, the cell-based model allows a more thorough understanding of how haemostasis works in vivo, and sheds light on the pathophysiological mechanisms behind certain coagulation disorders. For instance, this model proposes that haemophilia involves a failure of platelet-surface FXa generation, leading to a lack of platelet-surface thrombin production. Our data suggest that high-dose FVIIa is able to bind weakly to activated platelets, independently of tissue factor, in order to generate sufficient amounts of FXa to support a burst bf thrombin generation in the absence of FIXa/FVIIIa. The considerable success of high-dose recombinant FVIIa (rFVIIa; NovoSeven, Novo Nordisk, Copenhagen, Denmark) as a therapy for patients with haemophilia and inhibitors has led to its use in a growing number of alternative indications. We believe that even in the presence of the FIXa/FVIIIa complex, rFVIIa may be able to enhance both FXa and FIXa levels on the surface of activated platelets, thus increasing the production of thrombin.}, address = {Department of Pathology, Duke University Medical Center, Durham, North Carolina 27705, USA. Maureane.hoffman@med.va.gov}, author = {Hoffman, M.}, citeulike-article-id = {2873891}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/14697207}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=14697207}, issn = {0268-960X}, journal = {Blood reviews}, keywords = {10, coagulation, coagulopathy, rfviia}, month = {September}, posted-at = {2008-06-08 20:22:50}, priority = {2}, title = {A cell-based model of coagulation and the role of factor VIIa.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/14697207}, volume = {17 Suppl 1}, year = {2003} }

TY - JOUR ID - citeulike:2873891 L3 - citeulike-article-id:2873891 N2 - Our cell-based model of haemostasis replaces the traditional 'cascade' hypothesis, and proposes that coagulation takes place on different cell surfaces in three overlapping steps: initiation, amplification, and propagation. In highlighting the importance of cellular control during coagulation, the cell-based model allows a more thorough understanding of how haemostasis works in vivo, and sheds light on the pathophysiological mechanisms behind certain coagulation disorders. For instance, this model proposes that haemophilia involves a failure of platelet-surface FXa generation, leading to a lack of platelet-surface thrombin production. Our data suggest that high-dose FVIIa is able to bind weakly to activated platelets, independently of tissue factor, in order to generate sufficient amounts of FXa to support a burst bf thrombin generation in the absence of FIXa/FVIIIa. The considerable success of high-dose recombinant FVIIa (rFVIIa; NovoSeven, Novo Nordisk, Copenhagen, Denmark) as a therapy for patients with haemophilia and inhibitors has led to its use in a growing number of alternative indications. We believe that even in the presence of the FIXa/FVIIIa complex, rFVIIa may be able to enhance both FXa and FIXa levels on the surface of activated platelets, thus increasing the production of thrombin. JF - Blood reviews SN - 0268-960X AD - Department of Pathology, Duke University Medical Center, Durham, North Carolina 27705, USA. Maureane.hoffman@med.va.gov TI - A cell-based model of coagulation and the role of factor VIIa. VL - 17 Suppl 1 KW - 10 KW - coagulation KW - coagulopathy KW - rfviia AU - Hoffman, M PY - 2003/09// UR - http://view.ncbi.nlm.nih.gov/pubmed/14697207 ER -