74 THE H^MORRHAGIC DIATHESIS 



Taking up the points, then, in order : 



1. The defect is not in the fibrinogen, because it 

 is readily clotted if isolated and treated with throm- 

 bin. Moreover, when clot does at last form during 

 a haemorrhage, it is as firm and abundant as in 

 ordinary blood. 



2. The defect is not in the calcium salts, because 

 analysis shows no abnormality in quantity, and the 

 addition of these salts to drawn haemophiliac blood, 

 though it may hasten the time of clotting, does not 

 bring it to normal. 



3. The defect is not in the thrombokinase. Here 

 Sahli joins issue with Addis, because the addition of 

 washed leucocytes to haemophiliac blood rapidly 

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

 prothrombin as well as thrombokinase, 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 con- 

 centrated 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 believes 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 established that in the haemorrhagic diathesis it is 

 deficient not in quantity but only in character. He 



