138 THE HiEMORRHAGIC DIATHESIS 



3. The defect is not in the thromhokinase. Here 

 Sahli joins issue with Addis, because the addition of 

 washed leucocytes to hasmophihac blood rapidly 

 causes it to clot. These may, however, bring in 

 prothrombin as well as thromhokinase, and Addis 

 shows that solutions of thrombokinase, derived by 

 crushing up testis in saline, have far less effect on 

 haemophiliac than on normal blood unless very concen- 

 trated extracts are used. Again, there is just as much 

 thrombokinase in the serum of a bleeder, squeezed 

 out after coagulation, as in that of a normal person. 



4. It is in the prothrombin that the defect lies. A 

 very little normal plasma, or a few washed corpuscles 

 from a normal person, restore the coagulation power 

 forthwith. 



Addis beheves that he has directly proved the 

 point by the adoption of the following method for 

 isolating the prothrombin, and at the same time he 

 has estabhshed that in the haemorrhagic diathesis it is 

 deficient not in quantity but only in character. He 

 prepared a solution of fibrinogen from normal or 

 haemophiliac plasma in the ordinary way by precipi- 

 tating it by passing a stream of carbon dioxide through 

 plasma kept from clotting by citrate or oxalate. 

 Fibrinogen so obtained, as Mellanby shows, always 

 carries with it prothrombin, and in the presence of 

 calcium salts and thrombokinase would liberate 

 thrombin. Addis, however, added instead a trace of 

 thrombin, which clotted the fibrinogen and left its 

 prothrombin in solution. When a trace of prothrombin 

 so obtained from a normal blood was added to haemo- 

 phihac blood, this promptly coagulated. (The criticism 



