770 XII. VITAMINS K 



prothrombin in damaged livers. ^-^"--^ On the other hand, when large 

 doses of vitamin K are administered prior to exposure of animals to chloro- 

 form, a protective action on the liver can be noted.-™ When the adminis- 

 tration of vitamin K, parenterally or orally, is inel'fective in causing a 

 production of prothrombin, it is generally considered that the hypopro- 

 thrombinemia results from failure of the liver tissue to synthesize the pro- 

 thrombin, rather than from faiku'e of the supply of vitamin K.-^''-'^- A 

 mild hepatic insufficiency such as that resulting from fever, ^^^ anesthesia, ^^^ 

 or traumatic injury of the liver,'"" may be sufficient to interfere with its 

 ability to synthesize prothrombin. Anticoagulant drugs also exert their 

 effect through a direct action upon the liver. 



(^) Symptoms of Avitaminosis K 



The effect of vitamin K deficiency on animals is simple, consisting in a 

 single abnormality, namely a reduction of plasma prothrombin. As a 

 result of this decrease, the clotting time of the blood is greatly prolonged. 

 This condition frequently causes subcutaneous and intramuscular hemor- 

 rhage, which usually results in the death of the animal. 



In the case of man the picture is somewhat similar. Certain complica- 

 tions, such as a poor intestinal absorption, due to intestinal diseases, to 

 occlusion of the bile duct, or to liver injury, as well as a deficiency in 

 vitamin K in the diet, may cause this condition. In fact, in the case of 

 man and of animals, with the exception of the fowl, avitaminosis K seldom 

 occurs solely as a result of lack of vitamin K in the diet. In the human, 

 vitamin K deficiency is most frequently observed in the newborn and in 

 adults with biliary obstruction. 



8. Hypervitaminosis K 



Although symptoms of a true hypervitaminosis K have not been dem- 

 onstrated comparable to those occurring when excessive amounts of 

 vitamins A or D are ingested, there is evidence of toxicity when large 



227 S. J. WUson, Proc. Soc. Exptl. Biol. Med., 4i, 559-561 (1939). 



228 F. J. Pohle and J. K. Stewart, /. Clin. Invest., 19, 365-372 (1940). 



229 R. Kark and A. W. Souter, Lancet, 1940, 1, 1149-1153. 



230 M. A. Pessagno, Dia vied., 22, 1264 (1950); cited by W. H. Sebrell, Jr., and R. S. 

 Harris, The Vitamins, Vol. II, Acad. Press, New York, 1954, p. 427. 



231 P. N. Unger, S. Shapiro, and S. Schwalb, /. Clin. Invest., 27, 39-47 (1948\ 



232 P. N. Unger, M. Weiner, and S. Shapiro, Am.. J. Clin. Pathol, 18, 835-851 (1948). 



233 R. K. Richards, Science, 97, 313 (1943). 



234 S. C. Cullen, S. E. Ziffern, R. B. Gibson, and H. P. Smith, /. Am. Med. Assoc, 115, 

 991-994(1940). 



