PE12.4 | Vitamin E — Summary & Reflection

KEY TAKEAWAYS

Vitamin E (alpha-tocopherol) is the principal membrane-embedded antioxidant, protecting red cell membranes, myelin sheaths, and photoreceptors from lipid peroxidation. Dietary sources: vegetable oils, nuts, seeds. Absorption requires bile and chylomicrons (impaired in fat malabsorption).

Deficiency is rare in healthy term children but important in two groups: (1) premature infants — haemolytic anaemia, thrombocytosis, oedema at 4–6 weeks; exacerbated by iron (Fenton reaction); prevented by 25 IU/day from birth; (2) chronic fat malabsorption (abetalipoproteinaemia, cholestasis, CF) — spinocerebellar ataxia, peripheral neuropathy, pigmentary retinopathy; neurological damage may be irreversible; treat with water-soluble Vitamin E (TPGS) 15–25 IU/kg/day.

Diagnosis: serum alpha-tocopherol <3.5 mg/L in children; peripheral smear (acanthocytes); negative Coombs in haemolytic anaemia of prematurity. The interaction between Vitamin E and Vitamin C (regeneration of tocopheroxyl radical) illustrates antioxidant synergism.

REFLECT

Consider a 3-year-old child who has been jaundiced since birth and is referred from a district hospital with progressive difficulty walking and loss of reflexes. The parents are unaware that their child's chronic cholestasis — managed with only ursodeoxycholic acid — may have led to fat-soluble vitamin deficiency. What questions would you ask in the history to elicit fat malabsorption, and how would you assess Vitamin E status? Reflect on how a 'routine' nutritional supplement given from birth (25 IU/day of Vitamin E to premature infants) prevents a potentially serious blood disorder — a striking example of a cheap, targeted preventive intervention in neonatal care.