A familial hemorhagic diathesis due to an antithrombin.

IN A REVIEW published in 1955 Alexander’ stated that he knew of no well documented case of disturbed hemostasis in which excessive antithrombin activity had been the pthnary disorder. In 1955 Chevalier et al.2 reported briefly on three patients in whom purpura was accompanied by an increased capacity of serum to destroy thrombin during incubation at 37 C.; in at least one of these patients the hemostatic defects were accompaniments of an acute febrile episode. Loeliger and Hers3 have described chronic antithrombinemia in a case of rheumatoid arthritis with marked hypergammaglobulinemia. More recently, the occurrence of circulating antithrombins has been described in many disease states.4’5 We report now on a familial hemorrhagic diathesis in which increased antithrobin activity was an isolated defect.