Abstract

Vitamin K is required for carboxylation of a number of calcium-binding proteins including the coagulation factors II, VII, IX and X; the anticoagulant proteins C and S; other proteins in kidney, dentin and lung and osteocalcin in bone. When there is deficiency of vitamin K, inactive, uncarboxylated forms of the clotting proteins (descarboxy-proteins or PIVKA's Proteins formed In Vitamin K Absence) circulate and are a much more sensitive measure of deficiency than the prothrombin time. There are two natural sources of vitamin K, plants and bacteria. Plants produce phylloquinone, also called vitamin K1. Bacteria produce a range of related compounds, the menaquinones or vitamins K2. The naturally occurring K vitamins are fat soluble and absorption from the small intestine is dependant on the presence of bile salts and pancreatic lipases. Dietary vitamin K~ is certainly the main, if not the only, source in human infants; contrary to what is commonly taught, colonic absorption of bacterially-produced menaquinones is unproven. The maternal:fetal gradient for vitamin K1 across the placenta may be as high as 40: 1, which explains the very low cord blood concentrations. The infant who is formula fed from birth is at an immediate advantage regarding vitamin K (though perhaps in no other way) because he can drink until satisfied and the milk contains a high concentration of the vitamin (about 50 gg/1 in most formulae); by contrast, the breast fed baby has a meagre supply of milk in the early days and the vitamin K content is only about 2 ~tg/1. Delay in establishing feeding, especially by breast, may precipitate vitamin K deficiency in the early days of life and it is the breast

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