COAGL'LATIOX OF HLOOI) 321 



After phosphorus poisoning the blood may become non-coagula- 

 ble, whicli Jacoby*^ ascribed to an absence of fibrinogen in the blood, 

 because of a fibrinogen-destroying ferment in the liver. Doyon^^ has 

 made a similar finding in chloroform necrosis of the liver, but he at- 

 tributes especial importance to an excess of antithrombin liberated 

 from the liver in these conditions. Whipple has also found a de- 

 crease in fibrinogen with chloroform necrosis and cirrhosis of the 

 liver. ^^ In other instances of decreased coagulability the fibrinogen 

 is present, generally in normal amounts. After death the blood be- 

 comes incoagulable because the fibrinogen is destroyed through a 

 process similar to that of fibrinolysis;*^ this fibrinolysis may be com- 

 plete as early as ten hours after death. The other proteins of the 

 blood do not seem to be correspondingly attacked. Thrombokinase 

 is also scanty in cadaver blood, but there seem to be no coagulation- 

 inhibiting substances present. In anaphylactic shock the coagula- 

 bility is reduced or abolished, associated with which is a leucopenia.^° 



Whipple^^ states that the antithrombin-prothrombin balance in the 

 blood is in delicate equilibrium, but preserved by strong factors of 

 safety. The prothrombin factor is rarely involved, most notably in 

 melena neonatorum and aplastic anemia, and such conditions may be 

 relieved by injecting normal blood, through the added prothrombin. 

 The antithrombin factor is often excessive in hemorrhagic conditions, 

 especially with hepatic injury, or it may be lowered and lead to throm- 

 bosis from relatively slight injuries. Obviously the injection of nor- 

 mal blood will harm rather than help patients with hemorrhage due 

 to excessive antithrombin. Antithrombin is often found increased in 

 diseases of the blood-forming organs, e. g., leukemia, possibly as a 

 reaction to the products of disintegration of corpuscles; and hence 

 hemorrhagic tendencies are noted in these diseases. In icterus the 

 notable tendency to hemorrhage seems to depend upon the binding of 

 the calcium of the blood. by the bile pigments,^^ and administration 

 of calcium may bring the coagulation time back to normal with a cor- 

 responding decrease in the hemorrhagic tendency. 



Pfeiffer^^ estimated the fibrin content of the- blood in disease, and 

 found it increased in diseases with leucocytosis (pneumonia, rheuma- 

 tism, erysipelas, scarlet fever), except leukemia, where it was normal; 



"Zeit. physiol. Chem., 1900 (30), 175; also Doyon et al, Compt. Rend. Soc. 

 Biol., 1905 (58), 493. 



"Compt. Rend. Soc. Biol., 1905 (58), 704; Jour. phys. et path., 1912 (14), 

 229. 



«8 Bull. Johns Hopkins Hosp., 1913 (24), 207. 



8' Morawitz, Hofmeister's Beitr., 1906 (8), 1. 



^° The incoagulability of menstrual blood is ascribed to a lack of fibrin ferment 

 by Bell (Jour. Path, and Bact., 1914 (18), 462) and to an excess of antithrombin 

 by Dienst (Miinch. med. Woch., 1912 (51), 2799). 



"1 Arch. Int. Med., 1913 (12), 637. 



" Lee and Vincent, Arch. Int. Med., 1915 (16), 59. 



»3 Zeit. klin. Med., 1897 (33), 214; Cent. f. inn. Med., 1898 (19), 1. 



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