Disease Information for Avitaminosis A

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 -carotene and other provitamin 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 cells, retinol is converted to retinoic acid, which combines with receptors that bind to DNA and regulate gene expression to maintain epithelial tissues; Primary vitamin A deficiency is usually caused by prolonged dietary deprivation; It is endemic in areas, such as southern and eastern Asia, where rice, devoid of carotene, is the staple; 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; The severity of the effects of vitamin A deficiency is worse in young; Growth retardation is a common sign in children; this 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; rod dysfunction, can be detected by dark adaptometry, rod scotometry, or electroretinography (these tests require cooperative subjects); Dysfunction of the retina is followed by changes in the structure and function of epithelial cells; Xerosis of the bulbar conjunctiva consists of drying, thickening, wrinkling, and muddy pigmentation; the cornea becomes xerotic, infiltrated, and hazy at an early stage; Keratomalacia rapidly supervenes with liquefaction of part or all of the cornea, leading to rupture, with extrusion of the eye contents and subsequent shrinking of the globe (phthisis bulbi), or to anterior bulging (corneal ectasia and anterior staphyloma) and blindness; Bitot"s spots (superficial foamy patches composed of epithelial debris and secretions on the exposed bulbar conjunctiva) occur in advanced deficiency; Severe Vitamin A deficiency, in children, mortality can be 50% or more; Plasma retinol levels fall after liver stores are exhausted; Plasma levels of vitamin A and RBP also fall in acute infections; Secondary infection may complicate the corneal changes; Trial with therapeutic doses of vitamin A assists in the diagnosis----------[Merck Manual 17th]-----

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