The case history of a patient with moderate factor XII deficiency and recurrent deep vein thrombosis is described. A decreased resting fibrinolytic capacity suggests that ‘in vivo’ Hageman factor acts mainly as a promotor of clot dissolution. It further indicates that the in vitro demonstration of factor XII as an activator for other biochemical pathways might be of minor importance in vivo, as alternative pathways for activation of these systems exist.
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© 1980 S. Karger AG, Basel
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