Vitamin E, Serum
CPT CODE:
- 84446
USEFUL FOR:
Evaluation of individuals with motor and sensory neuropathies
Monitoring vitamin E status of premature infants requiring oxygenation
Evaluation of persons with intestinal malabsorption of lipids
SPECIMEN REQUIRED:
Draw blood in a plain, red-top tube(s) following an overnight (12-14 hour) fast (infants - draw prior to next feeding). (Serum gel tube is not acceptable.) Spin down and send 2 mL of serum frozen in amber vial (Supply T192) to protect from light. Note: Vitamin A, vitamin E and carotene analysis can be performed on 1 tube. However, the total volume of serum sent must be = or >4 mL. Aliquot 3 mL into an amber vial (Supply T192) to protect from light and label for carotene. Pour the remaining serum into an amber vial (Supply T192) to protect from light and label for vitamin A and/or vitamin E. Send both vials frozen.
TRANSPORT TEMPERATURE:
Frozen\Refrig <24 hrs OK\Ambient NO
CLINICAL INFORMATION:
Vitamin E contributes to the normal maintenance of biomembranes, the vascular system, and the nervous system, and provides antioxidant protection for vitamin A. The level of vitamin E in the 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 atthe 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 andsensory 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 retrolentalfibroplasia; supplementation with vitamin E has been shown to lessenthe severity of, and may even prevent, those problems.
Deficiencies of vitamin E may arise from poor nutrition orfrom intestinal malabsorption. At-risk persons, especially children, include those with bowel disease, pancreatic disease, chroniccholestasis, celiac disease, cystic fibrosis, and intestinal lymphangiectasia. Infantile cholangiopathies that may lead to malabsorption of vitamin E include intrahepatic and extrahepatic biliary atresia, paucity of intrahepatic bile ducts, arteriohepatic dysplasia, and rubella-related embryopathy. 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 implicated as a cause of thrombophlebitis, although this has not been definitively verified.
CLINICAL INTERPRETATION:
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): <4.0 mg/L Adult: <4.0 mg/L Values that indicate significant excess: Adult: >40.0 mg/L
REFERENCE VALUES:
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








