Preservision Areds (beta-carotene/ascorbic acid/vitE ac/zinc oxide/cupric oxide)

Vitamin E activity is generally expressed in USP or International Units which are equivalent; the International Unit of vitamin E is no longer officially recognized but continues to be used in the labeling of some preparations. It should be noted that vitamin E preparations are historically and incorrectly labeled as d- or dl-alpha-tocopherol and their respective esters. Vitamin E compounds include the all racemic (all rac)-alpha-tocopherol (dl-alpha-tocopherol (RRR-, RRS-, RSR-, RSS-, SSS-, SRS-, SSR-, and SRR-) or synthetic) form and its esters and the RRR-alpha-tocopherol (d-alpha-tocopherol or natural) form and its esters, and any of these compounds may be present in fortified foods and vitamin preparations.

One unit of vitamin E equals the biologic activity of 1 mg of all rac-alpha-tocopheryl acetate (dl-alpha-tocopheryl acetate), 1.12 mg of all rac-alpha-tocopheryl succinate (dl-alpha-tocopheryl acid succinate), 910 mcg of all rac-alpha-tocopherol (dl-alpha-tocopherol), 735 mcg of RRR-alpha-tocopheryl acetate (d-alpha-tocopheryl acetate), 830 mcg of RRR-alpha-tocopheryl succinate (d-alpha-tocopheryl acid succinate), and 670 mcg of RRR-alpha-tocopherol (d-alpha-tocopherol). However, because the USP potency unit for vitamin E was defined before studies showed a lack of human activity for the 2S-stereoisomers, the National Academy of Sciences (NAS) Food and Nutrition Board recommended in 2000 that the current equivalency defined in the USP standard be redefined based on the R-stereoisomeric forms of alpha-tocopherol, which are the forms that are active in humans. According to the NAS definition, each USP unit of vitamin E is equivalent to the biologic activity of 450 mcg of the synthetic all rac-alpha-forms of tocopherol and its esters or 670 mcg of the RRR-alpha-forms of tocopherol and its esters.

To avoid toxicity, dietary intake of vitamin A should be estimated and considered when determining the dosage of the vitamin. Vitamin A activity is expressed in terms of the equivalent amount of retinol (i.e., as retinol equivalents (RE) or retinol activity equivalents (RAE)) and is expressed also in USP units or International Units (IU, units). USP units and International Units are equivalent. One USP vitamin A unit is the specific biologic activity of 0.3 mcg of all-trans-retinol; one retinol equivalent (RE) is the specific biologic activity of 1 mcg of all-trans-retinol; one retinol activity equivalent (RAE) is equal to 1 mcg of all-trans-retinol, 12 mcg of all trans-beta-carotene, or 24 mcg of other provitamin A carotenoids. The use of RAE is preferred when calculating and reporting the amount of total vitamin A in mixed foods or assessing the amount of dietary and supplemental vitamin A consumed.

Ascorbic acid is usually administered orally. When oral administration is not feasible or when malabsorption is suspected, the drug may be administered IM, IV, or subcutaneously. When given parenterally, utilization of the vitamin reportedly is best after IM administration and that is the preferred parenteral route.

Vitamin E is usually administered orally. When oral administration is not feasible or when malabsorption is suspected, the drug may be given parenterally as a component of a multivitamin injection. Some clinicians use water-miscible oral vitamin E preparations in patients with malabsorption syndromes.

Vitamin A usually is administered orally. Oral vitamin A capsules containing high strengths (e.g., 50,000 units) no longer are commercially available in the US; however, high-strength oral capsules and solutions may be available from various organizations (e.g., United Nations Children's Fund (UNICEF), the International Dispensary Association (IDA)) for treatment of deficiencies in developing countries. When oral administration is not feasible or when malabsorption is present, the drug may be given IM.

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Concurrent administration of more than 200 mg of ascorbic acid per 30 mg of elemental iron increases absorption of iron from the GI tract; however, most individuals are able to absorb orally ingested iron adequately without concurrent administration of ascorbic acid.

Increased urinary excretion of ascorbic acid and decreased excretion of aspirin occur when the drugs are administered concurrently.

Salicylates inhibit uptake of ascorbic acid by leukocytes and platelets. As a result, leukocyte and plasma concentrations of ascorbic acid are decreased to concentrations slightly higher than those associated with tissue depletion of the vitamin; however, there is no evidence to date that salicylate therapy precipitates ascorbic acid deficiency. Although concomitant administration of ascorbic acid supplements in patients receiving salicylates increases plasma ascorbic acid concentrations, leukocyte ascorbic acid concentrations are not increased and tissue stores of the vitamin may not be increased. Therefore, routine administration of ascorbic acid supplements to patients receiving salicylates is not warranted; however, patients receiving high dosages of salicylates who exhibit any signs or symptoms of ascorbic acid deficiency should be evaluated for such a deficiency.

Ascorbic acid has reportedly decreased the anticoagulant effect of warfarin; however, other investigators have failed to show this effect. Concurrent administration of ascorbic acid and fluphenazine reportedly resulted in decreased fluphenazine plasma concentration. Acidification of the urine following administration of ascorbic acid may result in altered excretion of other drugs.

Vitamin E may increase the absorption, utilization, and storage of vitamin A and may protect against hypervitaminosis A; however, these effects are controversial.

Vitamin E in dosages of greater than 10 units/kg daily may delay the response to iron therapy in children with iron-deficiency anemia, and low-birthweight infants treated with iron supplements may develop vitamin E-deficiency hemolytic anemia.

Vitamin E or one of its metabolites reportedly may have anti-vitamin K effects; patients receiving oral anticoagulants may be at risk of hemorrhage after large doses of vitamin E. In normal healthy individuals, vitamin E caused no change in blood clotting.

Excessive use of mineral oil may decrease the absorption of vitamin E.

Orlistat may result in decreased GI absorption of fat-soluble vitamins such as vitamin E. At least 2 hours should elapse between (before or after) any orlistat dose and vitamin E administration; administering fat-soluble vitamins at bedtime may be a convenient time. Although the manufacturer of orlistat recommends that a vitamin supplement containing fat-soluble vitamins (A, D, E and K) be used during orlistat therapy, such vitamin concentrations in clinical studies with the drug remained within the normal range for most patients despite decreases, and vitamin supplementation was only occasionally needed.

There are no contraindication interactions for this drug.

There are no severe interactions for this drug.

There are no moderate interactions for this drug.

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There are no contraindication contraindications for this drug.

There are no severe contraindications for this drug.

There are no moderate contraindications for this drug.

There is no enhanced messaging for this drug.

There are no severe adverse reactions for this drug.

There are no less severe adverse reactions for this drug.

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Vitamin E has not been shown to be teratogenic. There is no evidence that vitamin E requirements in pregnant women differ from women who are not pregnant. (See Dosage: Dietary and Replacement Requirements, under Dosage and Administration.)

Vitamin A is teratogenic in animals; malformations of the CNS, eye, palate, and urogenital tract have been described in several species. Adequate and well-controlled studies in humans are not available. A limited number of reports of human fetal malformations (e.g., cranial neural crest defects) following maternal ingestion of large dosages of vitamin A (10,000 units or more daily) during or both before and during pregnancy suggest potential teratogenicity, at least at high dosages. The use of vitamin A in excess of the US RDA generally is contraindicated in women who are or may become pregnant. (See Dietary and Replacement Requirements in Dosage and Administration: Dosage.)If vitamin A is used during pregnancy or if the patient becomes pregnant while receiving the drug, the patient should be apprised of the potential fetal hazard. It also has been suggested that women of reproductive age should limit their intake of dietary sources (e.g., liver) containing high concentrations of vitamin A; beta-carotene, a precursor of vitamin A, has not been shown to be teratogenic and may be considered as a source of vitamin A supplementation in such women. Dosages exceeding the RDA may be necessary in women of childbearing age with vitamin A deficiency. There is some evidence suggesting that dosages up to 10,000 units daily or up to 25,000 units weekly may be used safely in women of childbearing age (13-49 years of age), and such dosages are recommended in those with active xerophthalmia. Even higher dosages may be necessary if active corneal lesions are present. (See Vitamin A Deficiency under Dosage and Administration: Dosage.)

Vitamin A is distributed into milk. Unless the maternal diet is inadequate, infants can usually obtain sufficient vitamin A from nursing, at least for the first 6 months of life. The effect of large maternal dosages of vitamin A on nursing infants is not known.

For information on the currently recommended RDAs of vitamin A for pregnant and lactating women, see Dietary and Replacement Requirements, under Dosage and Administration: Dosage.

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