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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 ...
[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.
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.
Babies receive a shot of vitamin K after birth to prevent life-threatening bleeding. But more parents are refusing the injection. The trend is alarming doctors.
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]
Fetal warfarin syndrome is a disorder of the embryo which occurs in a child whose mother took the medication warfarin (brand name: Coumadin) during pregnancy.Resulting abnormalities include low birth weight, slower growth, intellectual disability, deafness, small head size, and malformed bones, cartilage, and joints.
The compound is variously known as vitamin K 3 [7] and provitamin K 3. [8] Proponents of the latter name generally argue that the compound is not a real vitamin due to its artificial status (prior to its identification as a circulating intermediate) and its lack of a 3-methyl side chain preventing it from exerting all the functions (specifically, it cannot act as a cofactor for GGCX in vitro ...
The prothrombin time can be prolonged as a result of deficiencies in vitamin K, warfarin therapy, malabsorption, or lack of intestinal colonization by bacteria (such as in newborns). In addition, poor factor VII synthesis (due to liver disease ) or increased consumption (in disseminated intravascular coagulation ) may prolong the PT.