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In vitamin E deficiency due to digestive malabsorption in paediatric patients with congenital chronic cholestasis or hereditary chronic cholestasis, from birth (full term newborns) up to 18 years of age.

How it works

Vitamin E's anti-atherogenic activity involves the inhibition of the oxidation of LDL and the accumulation of oxLDL in the arterial wall. It also appears to reduce oxLDL-induced apoptosis in human endothelial cells. Vitamin E inhibits protein kinase C (PKC) activity. The inhibition of PKC results in inhibition of smooth muscle cell proliferation, which is involved in atherogenesis.Vitamin E's antithrombotic and anticoagulant activities involves the downregulation of the expression of intracellular cell adhesion molecule(ICAM)-1 and vascular cell adhesion molecule(VCAM)-1 which lowers the adhesion of blood components to the endothelium. Vitamin E upregulates the expression of cytosolic phospholipase A2 and cyclooxygenase (COX)-1 which in turn enhances the release of prostacyclin. Prostacyclin is a vasodilating factor and inhibitor of platelet aggregation and platelet release. Vitamin E has also been found in culture to decrease plasma production of thrombin, a protein which binds to platelets and induces aggregation. A metabolite of vitamin E called vitamin E quinone or alpha-tocopheryl quinone (TQ) is a potent anticoagulant. This metabolite inhibits vitamin K-dependent carboxylase, which is a major enzyme in the coagulation cascade. Many disorders of the nervous system are caused by oxidative stress. Vitamin E protects against this stress, thereby protecting the nervouse system.

Common side effects

Necrotizing enterocolitis, Bleeding due to vitamin k deficiency, Blurred vision, Diarrhoea, Fatigue, Flatulence, Headache, Increased creatinine level in blood, Stroke


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Content on this page was last updated on 28 September, 2016, by Dr. Varun Gupta (MD Pharmacology)