VITAMIN E DEFICIENCY

Vitamin E is a group of natural fat-soluble compounds- #945;-tocoferols.

Physiology: Vitamin E is an important antioxidant (free-radical scavenger), consequently considered as protective against severe inflammatory and neoplastic pathologies.

RDA of Vitamin E is ~5-10 mg of -tocoferol equivalent/ day (1 mg = 1.5 IU), higher in preterms and adolescents (10-15 mg/day).

Dietary sources: Vitamin E is widely distributed in vegetable oils, fats and nuts, specially those rich in polyunsaturated fatty acids. Whole wheat, egg yolk and milk products are also rich sources of Vitamin E.

Vitamin E Deficiency

Etiology: Vitamin E deficiency is mainly seen in: (a) preterms due to poor stores, (b) chronic liver disease,

(c) Malabsorption syndrome, and (d) high iron states, e.g. in hemolytic anemia.

Clinically vitamin E deficiency has been implicated in:

• Hemolytic anemia in preterms (at 6-10 weeks)

• Edema in kwashiorkor

• Degenerative neuropathy in biliary atresia or chro­nic liver disease, presenting as ataxia, peripheral neuropathy and posterior-column abnormalities

• Retinopathy of prematurity

Treatment: Though exact role and dose of vitamin E is not established, daily oral supplementation of 5-25 IU in high-risk children, e.g. preterms or those with chronic liver disease may prevent or reverse clinical abnormalities.

6.6 VITAMIN K DEFICIENCY

Vitamin K is a fat-soluble vitamin with very important role in hemostasis (coagulation) and to some extent, in bone metabolism.

Physiology: Vitamin K is essential for normal coagulation, via: (a) hepatic synthesis of FII, VII, IX and X, (b) activity of anticoagulant protein C and S, platelet stimulating factors, and (c) activity of osteocalcin—a calcium-binding protein.

Sources: Vitamin K available in 3 forms: natural fat­soluble vitamin K₁ in dietary sources, endogenously synthesized vitamin K₂ in gut by normal bacterial flora, and water-soluble synthetic preparations (vitamin K₃ or menadione).

Vitamin K₁ is present in animal foods, beans, green vegetables and milk, though major requirement is fulfilled by endogenous intestinal synthesis.

RDA of vitamin K is ~2-3 #956;g#8725;day in infants, 30-60 #956;g/ day in children and 60-120 #956;g#8725;day in adolescents.

Vitamin K deficiency is seen in:

• Breastfed newborns due to low vitamin K content in breast milk.

• Altered gut flora after chronic diarrhea or prolonged antibiotic therapy, due to reduced gut synthesis.

• Defective utilization in chronic liver disease or during drug therapy, e.g. dicoumarol and aspirin.

Clinically vitamin K deficiency commonly manifests as hemorrhagic disease of newborn (Ch 12.17.1), though in older children, it may present as bleeding from multiple sites.

Diagnosis depends on clinical suspicion, increased prothrombin time and elevated PIVKA-II levels (proteins induced in vitamin K absence), with normal range of 17-50 mAU/ml.

Treatment: Therapeutic vitamin K preparations are available as fat-soluble vitamin K1 or aqueous synthetic analogues (menadione). Hemorrhagic manifestations may be rapidly controlled with 5 mg of any of these preparations (preferably aqueous), given parenterally. However, large doses of synthetic analogues may precipitate hemolysis in G6PD deficiency and in preterms. Blood/plasma transfusions is necessary in severe bleeding.

Prevention: Single oral or intramuscular vitamin K administration (1.0 mg) at birth is enough to prevent hemorrhagic disease in newborn, while periodic supple­mentation is necessary in chronic liver diseases and other deficiency states.

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