An excerpt from www.merck.com

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 and guide differentiation of a variety of other tissues.

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 inversely related to age. 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.

Originally Posted by KP on thighs Has anyone here had their Vitamin A levels checked, is it possible to do? I found that a common symptoms of Vitamin A deficiency is: urinary tract infections plus Follicular hyperkeratosis of the skin. I used to have problems with urinary infections & KP is hyperkeratotic. I'd really love to know if others are Vitamin A deficient? I am going to call my doctor on Monday to see if I can be checked, apparently Vitamin A (retinol) is fat soluble sometimes you can you have enough Vitamin A but vitamin A storage and transport are defective. So it might be that my balance of protein-energy is not right. Another really freaky fact is that it binds with your DNA to regulate gene expression which seems to correspond with the theory that KP is genetic - sorry I'm not a specialist but this seems to make sense to me. Also I hate driving at night when I have to dim my lights for oncoming vehicles I feel it is so hard to see ( I wear glasses for driving but I am not made to wear them). Please let me know whether you have been tested. Thanks . I'll re-post after consulting my doctor, bear with me I work in an open-planned office & it is sometimes hard to juggle this. An excerpt from www.merck.com 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 http://a248.e.akamai.net/7/248/430/2...ages/sbeta.gif-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 and guide differentiation of a variety of other tissues. 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. Symptoms and Signs The severity of the effects of vitamin A deficiency is inversely related to age. 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.