THE H^EMORRHAGIC DIATHESIS 73 



Another abnormality in the blood is a frequent 

 deficiency in polymorphonuclear leucocytes. 



We may take it that the rival theory, that of the 

 undue fragility of the vessel walls, is now definitely 

 abandoned. Morawitz and Lossen have both shown 

 that the cedema obtained by dry-cupping is no 

 greater in haemophiliacs than it is in normal 

 individuals. 



So far, then, there is substantial agreement. 

 When we seek to go further, and to inquire just which 

 we are to blame of the various elements that take 

 part in regulating the coagulation of the blood, the 

 problem becomes complicated. 



Theoretically, the delay might be due to : 



(1) Deficient quantity or quality of the fibrinogen ; 



(2) Deficiency or excess of calcium salts ; (3) De- 

 ficient quantity or quality of the thrombokinase ; 



(4) Deficient quantity or quality of the prothrombin ; 



(5) Excess of antithrombin. 



In the examination of these factors we follow the 

 researches of Addis. The main point to determine 

 is whether the delay is in the first or the second of 

 the two reactions involved, that is, in the conversion 

 of prothrombin into thrombin, or in the conversion 

 of fibrinogen into fibrin. It proves that the former 

 is at fault ; the latter is quite normal. Haemophiliac 

 fibrinogen is as readily clotted by normal or by 

 haemophiliac thrombin as is normal fibrinogen, and 

 normal fibrinogen is easily clotted by thrombin from 

 a bleeder. But the haemophiliac blood must stand 

 a long time before any prothrombin is converted into 

 thrombin. 



