Two cases are described of factor VII deficiency in the blood of healthy female beagles. The diagnosis was established on the basis of: (i) prolonged Quick's one-stage prothrombin and 'Thrombotest' times, both corrected by the addition of 10 per cent by volume of normal canine serum; (ii) normal Russell's viper venom time and thromboplastin generation test; and (iii) reduced factor VII activity compared with plasma from a normal dog. Attention is drawn to some implications of inherited bloodcoagulation disorders not associated with physical evidence of bleeding. According to the theory proposed by Macfarlane (1964), there are in man two principal blood-coagulation mechanisms, intrinsic and extrinsic, whereby plasma prothrombin is activated to thrombin, which in turn converts plasma fibrinogen to fibrin. The production of intrinsic prothrombin activator, or thromboplastin as it is sometimes called, depends on a sequence of enzymeproenzyme reactions derived from the interaction of plasma-coagulation factors and blood platelets. The extrinsic pathway requires the presence of tissue extracts with thromboplastic activity, and incorporates a plasma coagulation factor not required in the intrinsic pathway. This coagulation factor is referred to as factor VII. A description of the properties of this factor is given by Biggs & Macfarlane (1962). Either congenital or acquired absence of one or more of the coagulation factors from the plasma results in haemostatic failure. Biggs & Macfarlane (1962) record ten cases of spontaneous deficiency of factor VII in the human and regard it as a rare defect. It may occur alone or in combination with reduced factors II and X in liver disease, vitamin K deficiency, or following anticoagulant treatment with coumarin derivatives (Biggs & Macfarlane, 1966). An inherited condition resembling factor VII deficiency was discovered in beagles in Canada by Mustard, Secord, Hoeksema, .Downie & Rowsell (1962).
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