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Vitamin A Deficiency


Vitamin A (retinol) is fat soluble and is found mainly in fish liver oils, liver, egg yolks, butter, and cream. Green leafy and yellow vegetables contain beta-carotene and other pro-vitamin carotenoids, which are converted to retinal in the mucosal cells of the small intestine.

Retinal is reduced to retinol, then esterified. Most of the body's vitamin A is stored in the liver as retinyl palmitate. It is released into the circulation as retinol bound to retinol binding protein and prealbumin (transthyretin).

The 11-cis isomer of retinal (vitamin A aldehyde) combines with opsin to form rhodopsin, the prosthetic group of photoreceptor pigments in the retina.

In somatic (non-germ or body) cells, retinol is converted to retinoic acid, which combines with receptors that bind to DNA and regulate gene expression to maintain epithelial tissues and guide differentiation of a variety of other tissues.

Proportions of retinol and beta-carotene, are as follows:

1 USP U equals 1 IU;

1 IU equals 0.3 µg of retinol;

1 µg of beta-carotene equals 0.167 µg of retinol.

Other pro-vitamin carotenoids are half as active as beta-carotene.

Growth retardation is a common sign in children.

Inadequate intake or utilization of vitamin A can cause impaired dark adaptation and night blindness; xerosis of the conjunctiva and cornea; xerophthalmia and keratomalacia; keratinization of lung, GI tract, and urinary tract epithelia; increased susceptibility to infections; and sometimes death. Follicular hyperkeratosis of the skin is common.

Bitot's spots (superficial foamy patches composed of epithelial debris and secretions on the exposed bulbar conjunctiva) occur in advanced deficiency.


Primary vitamin A deficiency is usually caused by prolonged dietary deprivation. It is endemic in areas where rice, devoid of carotene, is the staple, such as southern and eastern Asia.

Secondary vitamin A deficiency may be due to inadequate conversion of carotene to vitamin A or to interference with absorption, storage, or transport of vitamin A. Interference with absorption or storage is likely in celiac disease, sprue, cystic fibrosis, pancreatic disease, duodenal bypass, congenital partial obstruction of the jejunum, obstruction of the bile ducts, giardiasis, and cirrhosis.

Vitamin A deficiency is common in protein-energy malnutrition (marasmus or kwashiorkor), principally because the diet is deficient but also because vitamin A storage and transport are defective.

Conventional Labs

Plasma retinol levels fall after liver stores are exhausted.

The normal range is 20 to 80 µg/dL (0.7 to 2.8 µmol/L);

10 to 19 µg/dL (0.35 to 0.66 µmol/L) is low,

< 10 µg/dL (< 0.35 µmol/L) is deficient.





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