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• W2069126087 startingPage "1739" @default.
• W2069126087 abstract "SummarySeveral physiological antithrombotic proteins—including antithrombin, protein C, protein S, tissue factor pathway inhibitor, and components of the fibrinolytic system—act as inhibitors at strategic sites in the coagulation cascade to maintain normal blood fluidity under normal circumstances. The molecular basis of specific inherited hypercoagulable states has been recently elucidated. With the description of resistance to activated protein C, which is the commonest coagulation defect associated with thrombophilia, a specific primary hypercoagulable state can be identified in over 50% of patients with thrombophilia. Although the prevalence in the normal population of some prothrombotic mutations is remarkably high, most affected individuals do not have clinical thrombotic complications, so it is likely that clinically apparent hypercoagulable states result from multigene interactions, and that clinical episodes of thrombosis are precipitated by acquired prothrombotic insults in patients with an inherited predisposition to thrombosis." @default.
• W2069126087 created "2016-06-24" @default.
• W2069126087 creator A5039526598 @default.
• W2069126087 date "1994-12-01" @default.
• W2069126087 modified "2023-09-23" @default.
• W2069126087 title "Hypercoagulable states: molecular genetics to clinical practice" @default.
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• W2069126087 doi "https://doi.org/10.1016/s0140-6736(94)92888-6" @default.
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