It is now well established that prothrombin is continuously formed in the normal liver in the presence of adequate vitamin K. In 1938 Warner1 observed that partial hepatectomy in the rat resulted in a decrease in the prothrombin content of the blood. Warren and Rhoads2 reported in 1939 that after hepatectomy in dogs the plasma prothrombin fell to less than 20 per cent of normal within twelve to eighteen hours. Other evidence implicating the liver as a site of prothrombin production has been presented by many workers.3 These investigators produced damage to the liver by giving animals various hepatoxins and observed a fall in plasma prothrombin.
There is also ample evidence at hand which points to the liver as the source of prothrombin in man. In patients with hepatic disease the prothrombin level is frequently down, and the giving of vitamin K to these patients either does