Acquired Thrombophilia: A Hitherto Unrecognized Procoagulant‐Antithrombin Imbalance

Inherited, acquired and iatrogenic ‘diseases of low antithrombin activity’ share a common denominator: each is associated with an increased tendency toward, or incidence of, thrombosis. This suggested the possibility that these diseases constituted a distinct pathogenetic entity. Molecular models and clinical studies suggested 3 interrelated phenomena: increased serum procoagulants; decreased antithrombin; a tendency to thrombosis. The term ‘Acquired Thrombophilia’ is proposed to designate pre‐thrombotic and thrombotic individuals presenting this non‐inherited combination of laboratory and clinical findings. The antithrombin clotting time is shown to be inversely related to the level of circulating serine procoagulants, directly related to the level of antithrombin, and results from a procoagulant‐antithrombin inter‐molecular reaction. Patients with Acquired Thrombophilia have ‘turned‐on’ or excessive procoagulants resulting in ‘turned‐off’ or tightly bound antithrombin molecules.