|DATE||Friday, March 03|
|AUTHOR||Dr. Carlos Orozco (BSc, MSc, ND, MD, PhD, FPAMS)|
Vitamin K is a fat-soluble vitamin. The “K” is derived from the German word “koagulation”. Coagulation refers to blood clotting, because vitamin K is essential for the functioning of several proteins involved in blood clotting (1).
The K vitamins exist naturally as K1 (phylloquinone) in green vegetables and K2 (menaquinone) produced by intestinal bacteria and K3 is synthetic menadione. When administered, vitamin K3 is alkylated to one of the vitamin K2 forms of menaquinone.
The major function of the K vitamins is in the maintenance of normal levels of the blood clotting proteins, factors II, VII, IX, X and protein C and protein S, which are synthesized in.
the liver as inactive precursor proteins. Conversion from inactive to active clotting factor requires a posttranslational modification of specific glutamate (E) residues. This modification is a carboxylation and the enzyme responsible requires vitamin K as a cofactor. The resultant modified E residues are g-carboxyglutamate (gla) (4). This process is most clearly understood for factor II, also called preprothrombin. Prothrombin is modified preprothrombin. The gla residues are effective calcium ion chelators. Upon chelation of calcium, prothrombin interacts with phospholipids in membranes and is proteolysed to thrombin through the action of activated factor X (Xa).
Although vitamin K-dependent gamma-carboxylation occurs only on specific glutamic acid residues in a small number of proteins, it is critical to the calcium-binding function of those proteins (5,6).
The ability to bind calcium ions (Ca2+) is required for the activation of the 7 vitamin K-dependent clotting factors in the coagulation cascade. The term, coagulation cascade, refers to a series of events, each dependent on the other that stops bleeding through clot formation. Vitamin K-dependent gamma-carboxylation of specific glutamic acid residues in those proteins makes it possible for them to bind calcium. Factors II (prothrombin), VII, IX, and X make up the core of the coagulation cascade. Protein Z appears to enhance the action of thrombin (the activated form of prothrombin) by promoting its association with phospholipids in cell membranes. Protein C and protein S are anticoagulant proteins that provide control and balance in the coagulation cascade. Because uncontrolled clotting may be as life threatening as uncontrolled bleeding, control mechanisms are built in to the coagulation cascade. Vitamin K-dependent coagulation factors are synthesized in the liver. Consequently, severe liver disease results in lower blood levels of vitamin K-dependent clotting factors and an increased risk of uncontrolled bleeding (hemorrhage) (7).
Signs and Symptoms of Deficiency
Deficiency of vitamin K may cause of be associated with birth defects (underdeveloped nose, mouth and mid face, shortened fingers, flat nasal bridge), bone abnormalities, cognitive impairment, decreased vitality, eye hemorrhage, easy bruising, gastrointestinal bleeding, haematomas, lower bone density, hip fractures, hypo prothromobinemia, increased clotting time, mitral valve collapse, mucosal bleeding, nose bleeds, osteoporosis, osteopenia, premature aging.
Deficiency symptoms as related to metabolic action result in: