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VITAMIN E AND K (Fat Soluble Vitamin) – Dietary Sources, Clinical Features, Treatment and Prevention


Vitamin E is a tocopherol. Among the tocopherols alpha tocopherol is the most easily absorbed and biologically most active compound. All vegetable oils, wheat-germ, cotton seeds, egg yolk, butter and peas contain this vitamin and the average Indian diet contains the daily requirement which is 15 IU or 5 mg. Vitamin E which is a strong antioxidant prevents the peroxidation of cellular and subcellular membrane phospholipids. It is probably involved in preserving the integrity of cell membranes.

In cattle and poultry, vitamin E deficiency may lead to infertility. Nutritional deficiency of vitamin E is rare. Excess of free fatty acids in the diet increases the requirement for vitamin E. In premature infants fed on artificial diets containing iron and high concentrations of fatty acids, conditioned deficiency may develop, leading to the production of hemolytic anemia.

In doses of 400-800 mg, vitamin E acts as an effective antioxidant, thereby retarding the development of atheromatous changes in arteries.


This vitamin which is chemically a substituted naphthoquinone is present in adequate amounts in vegetable oils and green leafy vegetables as vitamin K1 (phytomenadione). Vitamin K comprises of several molecular forms that have a common 2-methyl-l, 4-naphthoquinone ring, but different side chains at the 3-position. In green leafy vegetables and legumes and vegetable oils such as rapeseed oil and soyabean oil vitamin K occurs as phylloquinone (old name K1).

Bacteria synthesize vitamin K which is named menaquinone (MK-n) which occurs in several molecular forms. Milk is a poor source. The colonic bacteria synthesize this vitamin (Vitamin K2) and this supplements the dietary source. Naturally occurring vitamin K is fat soluble. The synthetic form of this vitamin is vitamin K3 which is water-soluble. This can be given intramuscularly or intravenously, unlike the oily preparations which can be given only intramuscularly. Daily requirement is not clearly known, but is probably 1 μg/kg body weight. Body sources are limited and, therefore, signs of deficiency develop within 3 to 4 weeks of dietary deprivation. Oxidative phosphorylation processes which take place in cellular mitochondria require the presence of vitamin K. Vitamin K occurs in large amounts in liver and bone. In the liver it takes part in the synthesis of precursors for coagulation factors, protein C and protein S. Vitamin Kdependent coagulation factors (factors II, VII, IX and X) are produced in the inactive form by the liver, and vitamin K is required for their biological activation. The inhibitors of coagulation—Protein C and Protein S are also produced in the liver and these are also vitamin K dependent. Coumarins inhibit the enzyme vitamin K epoxide reductase and thereby inhibit further actions of Vitamin K.

Prothrombin (factor II) is synthesized in the liver as an inert precursor, termed protein induced by vitamin K absence (PIVKA). This is carboxylated to form prothrombin by the vitamin K dependent enzyme—gamma carboxylase. In the absence of vitamin K or after

administration of vitamin K antagonists such as coumarin PIVKA appears in the plasma.

Vitamin K is needed for the formation of several proteins concerned with calcium homeostasis. Vitamin K promotes the conversion of protein-bound glutamate residues to gamma-carboxy glutamate (Gla). Proteins containing Gla are present in several tissues such as bone, kidneys, placenta, pancreas, spleen and lungs.

Vitamin K also takes part in bone metabolism—both bone formation and resorption. Two of the important Vitamin K dependent proteins are osteocalcin and matrix Gla protein.

Vitamin K Deficiency

Vitamin K deficiency occurs in conditions associated with malabsorption of fat such as obstructive jaundice and malabsorption states. Prolonged treatment with broad spectrum antibiotics destroys the colonic bacteria which synthesize this vitamin. Deficiency manifests as mild or severe bleeding tendency occurring from injection sites, mucous membranes, and skin. Injections of vitamin K in doses of 5-10 mg corrects the defect, if hepatic parenchymal function is normal. In the presence of hepatic failure, vitamin K may not be effective.


Hemorrhage may develop in newborn infants occasionally. Prematurity predisposes to this condition. Vitamin K deficiency in the mother and anticoagulant medication aggravate this disorder. Hemorrhagic  tendency develops on the second or third day of delivery. This is due to exaggeration of the physiological hypoprothrombinemia which develops before the colon is colonized by bacteria.

A dose of 1 mg of vitamin K1 given intramuscularly to the baby brings about relief. Synthetic vitamin K is also effective. Larger doses have to be avoided since these lead to hemolysis. Administration of 5-10 mg vitamin K to the mother in late pregnancy abolishes this risk in the newborn.

Anticoagulant therapy Use of coumarin drugs or warfarin leads to alteration in the synthesis of coagulation factors. As a result proteins antigenically similar to factors II, VII, IX and X are produced but they lack the procoagulant properties. Excess of anticoagulants leads to hemorrhagic tendency.

Bleeding occurs from injection sites, urinary tract, gastrointestinal tract and uterus. Intramuscular injection of 10 mg vitamin K is usually effective. When the bleeding tendency is severe, large intravenous doses (50-75 mg) may be required. For severe cases transfusion of fresh blood or vitamin K-dependent coagulation factors may also be necessary.

VITAMIN E AND K (Fat Soluble Vitamin) – Dietary Sources, Clinical Features, Treatment and Prevention
VITAMIN E AND K (Fat Soluble Vitamin) – Dietary Sources, Clinical Features, Treatment and Prevention


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