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Newborn infants have low stores of vitamin K, and human breast milk has low concentrations of the vitamin. This combination can lead to vitamin K deficiency and later onset bleeding. Vitamin K deficiency leads to the risk of blood coagulation problems due to impaired production of clotting factors II, VII, IX, X, protein C and protein S by the ...
Cell-free DNA can be used the determine the Rh antigen of the fetus when the mother is Rh negative. Blood is taken from the mother during the pregnancy, and using PCR, can detect the K, C, c, D, and E alleles of fetal DNA. This blood test is non-invasive to the fetus and is an easy way of checking antigen status and risk of HDN.
[2] [3] Vitamin K injections are administered to newborns as a preventative measure to reduce the risk of hemorrhagic disease of the newborn (HDN). [ 4 ] [ 5 ] The coagulation pathway helps the body stop active bleeds by using vitamin K dependent clotting factors (factors II, VII, IX, and X) which are synthesized by the liver.
Newborn infants are a special case. Plasma vitamin K is low at birth, even if the mother is supplemented during pregnancy, because the vitamin is not transported across the placenta. Vitamin K deficiency bleeding (VKDB) due to physiologically low vitamin K plasma concentrations is a serious risk for premature and term newborn and young infants.
American Academy of Pediatrics has issued guidelines for managing this disease, which can be obtained for free. National Institute for Health and Care Excellence (NICE) has issued guidelines for the recognition and treatment of neonatal jaundice in the United Kingdom .
Vitamin K is a family of structurally similar, fat-soluble vitamers found in foods and marketed as dietary supplements. [1] The human body requires vitamin K for post-synthesis modification of certain proteins that are required for blood coagulation ("K" from Danish koagulation, for "coagulation") or for controlling binding of calcium in bones and other tissues. [2]
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Vitamin K 1-deficiency may occur by disturbed intestinal uptake (such as would occur in a bile duct obstruction), by therapeutic or accidental intake of a vitamin K 1-antagonist such as warfarin, or, very rarely, by nutritional vitamin K 1 deficiency. As a result, Gla-residues are inadequately formed and the Gla-proteins are insufficiently active.