Vitamin E deficiency plays a significant role in human nutrition, and premature infants lacking vitamin E may develop hemolytic anemia.

bubble_chart Pathogenesis

Vitamin E is a fat-soluble vitamin widely present in foods, with abundant amounts found in vegetable oils, seeds, nuts, egg yolks, and green leafy vegetables. Due to the hydroxyl group on its molecular ring, which can provide hydrogen to bind with free radicals and O^-₂, free radicals have an oxidizing effect on the polyunsaturated fatty acids in cell membrane structures. Vitamin E is highly susceptible to oxidation, thereby neutralizing this oxidizing effect, making it an extremely effective antioxidant. In the body, vitamin E works alongside other antioxidants, such as glutathione peroxidase, to maintain the integrity of biological membranes. For example, it protects the unsaturated fatty acids in red blood cell membranes from oxidative damage, preventing red blood cell destruction and hemolysis. It may also play a role in nucleic acid metabolism. The esters formed by the combination of vitamin E and fatty acids lack antioxidant properties. In premature infants, if the diet contains a higher proportion of unsaturated fatty acids, the requirement for vitamin E increases relatively.

Low birth weight infants fed with infant formula containing excessively high levels of polyunsaturated fatty acids show a significantly lower incidence of related conditions when breastfed, as breast milk maintains an appropriate ratio of polyunsaturated fatty acids to vitamin E. Very low birth weight premature infants have poorer absorption of fats and fat-soluble vitamins. Additionally, if iron intake is excessively high, the demand for vitamin E increases accordingly to protect the lipids in cell membranes from oxidation. Vitamin E deficiency can also occur in conditions such as intestinal malabsorption, cystic fibrosis of the pancreas, and biliary obstruction.

bubble_chart Diagnosis

Hemoglobin levels are mostly between 60-100g/L, with reticulocytes grade I elevated. Peripheral blood smears show acanthocytes and contracted red blood cells. Platelet counts may increase. Bone marrow examination reveals multinucleated erythroblasts. Diagnosis is confirmed by measuring plasma vitamin E levels; a level below 12 μmol/L (0.5 mg/dL) supports the diagnosis. After oral vitamin E administration, it remains in the bloodstream for 1-2 days, so plasma levels should be measured at least 3 days after intake. Alternatively, the sensitivity of the patient's red blood cells to hemolysis upon exposure to hydrogen peroxide can be tested to indirectly confirm vitamin E deficiency.

Initially, 10 mg/day can be administered, and after blood changes occur, it can be reduced to 5 mg/day as a maintenance dose. For chronic fat malabsorption or gallbladder stasis, water-soluble vitamin E should be taken orally or administered via intramuscular injection. However, care must be taken not to exceed the dosage, as exceeding 15 mg/kg per day can lead to increased serum creatine kinase activity, elevated urinary creatine excretion, and muscle weakness in pediatric patients. There have been reports of fatalities resulting from intravenous administration at standard doses.

bubble_chart Prevention

The recommended intake of vitamin E for normal infants can be found in Appendix 3 of Chapter 3. For those fed with milk, it is approximately 0.05 mg/d, while for those fed with other foods, it is about 1.5 mg/d. For premature infants weighing less than 1500g and children with fat malabsorption, it is advisable to use water-soluble vitamin E at 5 mg/d to prevent deficiency.