THE COAGULATION DEFECT IN SWEET CLOVER DISEASE AND IN THE HEMORRHAGIC CHICK DISEASE OF DIETARY ORIGIN

Publisher Website
Google Scholar
Abstract
A quantitative method for the determination of prothrombin was developed on the basis that the clotting time of recalcified oxalated plasma to which an excess of thromboplastin has been added is directly dependent on the concn. of prothrombin. A study of the prothrombin in sweet clover disease showed that a marked decrease in this clotting factor occurs in a few days after the toxic hay is fed, and that the hemorrhagic tendency runs parallel with the reduction in prothrombin. Transfusion with citrated blood greatly increases the concn. of prothrombin and causes an improvement in the condition, but the effect is of short duration. Injection of defibrinated blood does not increase the prothrombin content of the blood. Alfalfa is effective both in preventing and curing the disease. When chicks are fed a diet (Almquist''s) lacking vitamin K, a marked reduction in prothrombin occurs, and when it drops below 10% a distinct hemorrhagic tendency can be observed. In chicks the production of prothrombin requires the intake of a precursor, vitamin K. In sweet clover disease, it appears that a toxic principle rapidly destroys prothrombin. To replace this loss the animal requires an accessory food factor which appears to be abundant in alfalfa, but this unknown constituent is not vitamin K, for it is not extractable with ether. The author presents the possibility that the hemorrhagic diathesis of obstructive jaundice may be due to a deficiency of the vitamin required by the body for the production of prothrombin since the patients in which this condition develops are generally given an inadequate diet, and lack bile in the intestines, which tends to cause a poor absorption of fat soluble substances such as vitamin K.

This publication has 8 references indexed in Scilit: