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Diagnosing vitamin A deficiency and toxicity
Evaluating persons with intestinal malabsorption of lipids
Evaluating individuals with motor and sensory neuropathies for vitamin E deficiency
Monitoring vitamin E status of premature infants requiring oxygenation
The level of vitamin A in the plasma or serum is a reflection of the quantities of vitamin A and carotene ingested and absorbed by the intestine (carotene is converted to vitamin A by intestine absorptive cells and hepatocytes).
Vitamin A plays an essential role in the function of the retina (adaptation to dim light), is necessary for growth and differentiation of epithelial tissue, and is required for growth of bone, reproduction, and embryonic development. Together with certain carotenoids, vitamin A enhances immune function, reducing the consequences of some infectious diseases.
Degenerative changes in eyes and skin are commonly observed in vitamin A deficiency. Poor adaptation of vision to darkness (night blindness) is an early symptom that may be followed by degenerative changes in the retina. In developing countries, vitamin A deficiency is the principal preventable cause of blindness. Severe or prolonged deficiency leads to dry eye (xerophthalmia) that can result in corneal ulcers, scarring, and blindness. Another important consequence of inadequate intake is acquired immunodeficiency disease, with an increased incidence of death related to infectious diseases. In patients with HIV, vitamin A deficiency is associated with increased disease progression and mortality.
Vitamin A in excess can be toxic. In particular, chronic vitamin A intoxication is a concern in normal adults who ingest >15 mg per day, and in children who ingest >6 mg per day of vitamin A over a period of several months. Manifestations are various and include dry skin, cheilosis, glossitis, vomiting, alopecia, bone demineralization and pain, hypercalcemia, lymph node enlargement, hyperlipidemia, amenorrhea, and features of pseudotumor cerebri with increased intracranial pressure and papilledema. Liver fibrosis with portal hypertension and bone demineralization may also result. Congenital malformations, like spontaneous abortions, craniofacial abnormalities, and valvular heart disease have been described in pregnant women taking vitamin A in excess. Consequently, in pregnancy, the daily dose of vitamin A should not exceed 3 mg.
Vitamin E contributes to the normal maintenance of biomembranes, the vascular system, and the nervous systems; and provides antioxidant protection for vitamin A. The level of vitamin E in the blood plasma or serum after a 12- to 14-hour fast reflects the individual's reserve status.
Currently, the understanding of the specific actions of vitamin E is very incomplete. The tocopherols (vitamin E and related fat-soluble compounds) function as antioxidants and free-radical scavengers, protecting the integrity of unsaturated lipids in the biomembranes of all cells and preserving retinol from oxidative destruction. Vitamin E is known to promote the formation of prostacyclin in endothelial cells and to inhibit the formation of thromboxanes in thrombocytes, thereby minimizing the aggregation of thrombocytes at the surface of the endothelium. Those influences on thrombocyte aggregation may be of significance in relation to risks for coronary atherosclerosis and thrombosis.
Deficiency of vitamin E in children leads to reversible motor and sensory neuropathies; this problem also has been suspected in adults. Premature infants who require an oxygen-enriched atmosphere are at increased risk for bronchopulmonary dysplasia and retrolental fibroplasia. Supplementation with vitamin E has been shown to lessen the severity of, and may even prevent, those problems. In addition, low blood levels of vitamin E may be associated with abetalipoproteinemia, presumably as a result of a lack of the ability to form very low-density lipoproteins and chylomicrons in the intestinal absorptive cells of affected persons.
Vitamin E toxicity has not been established clearly. Chronically excessive ingestion has been suspected as a cause of thrombophlebitis, although this has not been definitively verified.
Deficiencies of vitamins A and E may arise from poor nutrition or from intestinal malabsorption. Persons, especially children, at risk include those with bowel disease, pancreatic disease, chronic cholestasis, celiac disease, cystic fibrosis, and intestinal lymphangiectasia. Infantile cholangiopathies that may lead to malabsorption of vitamins A and E include intrahepatic dysplasia and rubella-related embryopathy.
VITAMIN A (RETINOL)
0-6 years: 11.3-64.7 mcg/dL
7-12 years: 12.8-81.2 mcg/dL
13-17 years: 14.4-97.7 mcg/dL
> or =18 years: 32.5-78.0 mcg/dL
VITAMIN E (ALPHA-TOCOPHEROL)
0-17 years: 3.8-18.4 mg/L
> or =18 years: 5.5-17.0 mg/L
Significant deficiency: <3.0 mg/L
Significant excess: >40 mg/L
The World Health Organization recommendations supplementation when vitamin A levels fall below 20.0 mcg/dL. Severe deficiency is indicated at levels <10.0 mcg/dL. Vitamin A values >120.0 mcg/dL suggest hypervitaminosis A and associated toxicity.
Vitamin E (alpha-tocopherol):
-Values that indicate need for supplementation:
-Premature: <2.0 mg/L
-Neonate: <2.0 mg/L
-Child (3 months): <3.0 mg/L
-Child (2 years): <3.0 mg/L
-Adults: <3.0 mg/L
-Values that indicate significant excess:
-Adults: >40.0 mg/L
Testing of nonfasting specimens or the use of vitamin supplementation can result in elevated plasma vitamin concentrations. Reference values were established in patients who were fasting.
Acute ethanol ingestion may result in increased serum vitamin A levels.
1. Ball GFM: Vitamins: their role in the human body. Oxford, Blackwell Publishing, 2004, pp 133-187, 234-255
2. Ross AC: Vitamin A and Carotenoids. In Modern Nutrition in Health and Disease. 10th edition. Edited by ME Shils, M Shike, AC Ross, et al. Philadelphia, Lippincott Williams and Wilkins, 2006, pp 351-375
3. Traber MG: Vitamin E. In Modern Nutrition in Health and Disease.10th edition. Edited by ME Shils, M Shike, AC Ross, et al. Philadelphia, Lippincott Williams and Wilkins, 2006, pp 434-441