422 VITAMIN K GROUP 



day of life. Adler^" attributes the entire process to a transient hepatic defect, 

 whereas Quick and Grossman^^ beheve that vitamin K becomes available 

 to the infant only after sufficient bacteria have developed in the bowel to 

 produce vitamin K. Sells and associates'^ found insufficient vitamin K in 

 human colostrum to maintain the baby's blood coagulability; however, 

 minimally adequate vitamin K was present in cow's milk. This might 

 explain the older observation^' that the prelacteal feedings of cow's milk 

 prevent hemorrhagic disease of the newborn. Sells' group- further found 

 that coagulability of the blood remained impaired as long as food (other 

 than aqueous glucose solution) was withheld from the infants. 



When vitamin K was found to prevent newborn hypoprothrombinemia, 

 it was anticipated that this hemorrhagic disease could be eliminated by 

 the simple expedient of routine prophylactic administration of vitamin K 

 to the baby or mother. Early, carefully controlled studies'^' '^ indicated 

 that this was overoptimistic but that some benefit was to be obtained. 

 Recently several reports'^ have questioned whether the routine use of 

 vitamin K is of any benefit. Since few clotting studies were carried out, 

 judgment should be reserved. The problem merits further careful study. 



b. Inhibition of Synthesis of Vitamin K by Intestinal Bacteria 



The most important source of vitamin K for the mammal is its own 

 intestinal bacteria,-^- ^"^ in particular, Escherichia coli}^ In the absence of 

 dietary vitamin K this source alone is usually sufficient to maintain a 

 normally coagulable blood. It is felt that the bacterial (farnesyl) vitamin'^^ 



2° B. Adler, Monatschr. Geburtschillfe u. Gyndkol. 118, 225 (1944). 



21 A. J. Quick and A. M. Grossman, Am. J. Med. Sci. 199, 1 (1940). 



22 R. L. Sells, S. A. Walker, and C. A. Owen, Proc. Soc. Exptl. Biol. Med. 47, 441 

 (1941). 



23 H. N. Sanford, H. J. Morrison, and L. Wyat, Am. J. Diseases Children 43, 569 

 (1932). 



2< L. M. Hellman, L. B. Shettles, and N. J. Eastman, Am. J. Obstet. Gynecol. 40, 844 

 (1940). 



25 E. L. Potter, Am. J. Obstet. Gynecol. 50, 235 (1945); H. N. Sanford, M. Kostalik, 

 and B. Blackmore, Am. J. Diseases Children 78, 686 (1949); J. D. Hay, F. P. Hud- 

 son, and T. S. Rodgers, Lancet I, 423 (1951). 



2" H. J. Almquist, Physiol. Revs. 21, 194 (1941). 



27 H. J. Almquist, C. F. Pentler, and E. Mecchi, Proc. Soc. Exptl. Biol. Med. 38, 336 

 (1938); H. J. Almquist and E. L. R. Stokstad, /. Biol. Chem. Ill, 105 (1935); H. R. 

 Butt and A. E. Osterberg, J. Nutrition 15, Suppl., 11 (1938). 



2^ S. Orla-Jensen, A. D. Orla-Jensen, H. Dam, and J. Glavind, Zentr. Bakt. Para- 

 sitenk. Abt. 2, 104, 202 (1941-1942) ; H. Dam and J. Glavind, Biochem. J. 32, Part 1, 

 1018 (1938). 



28a It is generally stated that the intestinal bacteria produce the farnesyl vitamin 

 [H. Dam, Med. Welt. 20, 958 (1951)]; however, Taveira reported the recovery of the 

 phytyl vitamin from £'sc/ierzc/jia co/i [M. Taveira, Ann. pharm.f rang. 9, 24:4: (1951)]. 



