Xerophthalmia vitamin

All cases of PEM without obvious eye lesions, on admission, should be given vitamin A in a prophylactic oral dose of 110 mg retinyl palmitate or 66 mg retinyl acetate (200,000 lU) because of low reserves of this vitamin, xerophthalmia may be precipitated when growth is stimulated during recovery. 

In humans, vitamin A deficiency manifests itself in the following ways night blindness, xerophthalmia, Bitot s spots, and corneal involvement and ulceration. Changes in the skin have also been observed. Although vitamin A deficiency is seen in adults, the condition is particularly harmful in the very young. Often, this results from malnutrition (56). 

The key experiments leading to the identification of vitamin D were those of Mellanby (1918-1919) using puppies. When they were fed on bread, skimmed milk, linseed oil, yeast (to give B vitamins), and orange juice (vitamin C) the puppies developed rickets. When cod-liver oil and/or butter were added, rickets was prevented. The distinction between the effects of vitamin A and the anti-rachitic factor was aided by the sensitivity of vitamin A to oxidation. Aerated (oxidized) cod-liver oil no longer cured xerophthalmia but its anti-rachitic properties were unaffected (McCollum, 1922). 

In the absence of sufficient vitamin A, one consequence is a vision defect termed night blindness or, more technically, xerophthalmia. The rod cells in the retina are largely responsible for vision in low light. If they have too little retinal, they cannot do their job and night blindness, the inability to see in low light, results. If the condition persists, it is characterized by extreme dryness of the conjunctiva and can result in permanent blindness. 

World Health Organization (1984). Prevention and control of vitamin A deficiency and Xerophthalmia. WHO 37th World Health Assembly, agenda item 20.A37/A. Conference paper No. 6. 

In Southeast Asia, an estimated 5 million children develop an eye disease known as xerophthalmia due to vitamin A dehciency every year. Of these, 0.25-0.5 million will eventually go blind. Vitamin A dehciency is also correlated with a weakened immune system and consequentially an increased susceptibility to potentially fatal afflictions, including diarrhea, respiratory diseases, and childhood diseases such as measles. According to statistics compiled by UNICEF, improved vitamin A nutrition could be expected to prevent approximately 1-2 million deaths a year among children aged 1-4, and an additional 0.25-0.5 million deaths during later childhood. 

Avitaminosis A results in the loss of night vision nyctalopia). Furthermore, the removal of vitamin A from the diet causes the cornea of the eye to dry out xerophthalmia). However, excessive intake of vitamin A can result in severe and even fatal toxicity. 

It is indicated in night blindness, vitamin A deficiency (in infants, in pregnancy, lactation, malabsorption syndrome), for prophylaxis of vitamin A deficiency, acne, ichthyosis, psoriasis, xerophthalmia, Bitot s spots (especially children). 

Impotence Night blindness Retardation of growth Xerophthalmia Increased visuel threshold Dryness of cornea Yes FAT-SOLUBLE p-Carotene not acutely toxic, but supplementation is hot recommended Excess vitamin A can increase incidence of fractures... 

Vitamin A (retinol, retinal, retinoic acid—the three active forms of vitamin A, and p-carotene) function in the maintenance of reproduction, vision, promotion of growth, differen tiation and maintenance of epithelial tissues, and gene expression. A deficiency of vitamin A results in impotence, night blindness, retardation of growth, and xerophthalmia. Large amounts of vitamin A are toxic and can result in an increased incidence of frac tures. 

Vitamin A is necessary for growth and reproduction, resistance to infection, maintenance and differentiation of epithelial tissues, stability and integrity of membrane structures, and the process of vision. In terms of the last function, vitamin A is a component of rhodopsin or visual purple, a photosensitive pigment in the eye that is needed for vision in dim light. An early mild clinical symptom of vitamin A deficiency is night blindness a severe deficiency of this fat-soluble vitamin results in xerophthalmia, an eye condition leading to blindness. 

DeLuca, L. M., Glover, J., Heller, J., Olson, J. A. and Underwood, B. 1979. Guidelines for the Eradication of Vitamin A Deficiency and Xerophthalmia. VI. Recent Advances in the Metabolism and Function of Vitamin A and Their Relationship to Applied Nutrition. Nutrition Foundation, New York. 

The principal physiological functions of tins vitamin include growth, production of visual purple, maintenance of skin and epithelial cells, resistance to infection, gluconeogenesis. mucopolysaccharide synthesis, bone development, maintenance of myelin and membranes, maintenance of color and peripheral vision, maintenance of adrenal cortex and steroid hormone synthesis, Specific vitamin A deficiency diseases include xerophthalmia, nyctalopia, hemeralopia, keratomalacia, and hyperkeratosis. 

In 1912, Hopkins reported a factor m milk needed for the growth of rats. In 1913, Osborne and Mendel demonstrated that milk factor is fat soluble, and present in other fats also, McCollum and Davis, in 1913-1915, identified milk factor (fat-soluble A) in butter and egg yolk. In 1917, McCollum and Simmonds found xerophthalmia in rats due to lack of fat-soluble A. In 1920, Drummond renamed fat-soluble A, vitamin A. In 1930, Moore determined that carotene is a precursor of vitamin A. See also . During 1930-1937, Karrer et al, isolated and synthesized vitamin A. In 1935, Wald reported visual purple in retina to be a complex of protein and vitamin A. 

Vitamin A, a fat-soluble vitamin, is indicated for severe vitamin A deficiency with xerophthalmia. (See the section Importance of Vitamin A in Human Nutrition. )... 

The symptoms of vitamin D deficiency disease has been documented in 16th century literature. A clear picture of the basis for the disease and methods of treatment were unclear until the experiments by Sir Edward Mellanby (3,4). In the early 1920 s, cod liver oil was known to cure rickets and xerophthalmia. The name vitamin D was given to... 

Vitamin A deficiency is characterized by xerophthalmia, follicular hyperkeratosis (phrynoderma), and generalized xerosis.29 In hypervitaminosis A the skin becomes dry, rough, pruritic, and scaly and the lips become cracked. 

Because of the potential teratogenic effects of high-dose vitamin A, caution must be taken in the treatment of severe vitamin A deficiency among pregnant women as well as women of reproductive age. Women of reproductive age should be treated with 200,000 IU only when they display active corneal xerophthalmia. For... 

Clinical signs of vitamin A deficiency (xerophthalmia) are often diagnosed together with infections such as pneumonia and diarrhea. Why ... 

WHO, UNICEF, IVACG Task Force Vitamin A Supplements. A Guide to Their Use In the Treatment and Prevention of Vitamin A Deficiency and Xerophthalmia. 2nd ed. World Health Organization, Geneva, 1997. 

The discovery, isolation and final synthesis of a whole group of new compounds essential to health in a balanced diet was another triumph of the chemist. These compounds called vitamins A, Ba or G, C, D, E, K, and several others closely associated with vitamin Ba, such as niacin, pantothenic acid, inositol, para-amino benzoic acid, choline, pyndoxine (Be), biotin (H), folic acid and Bn, prevent deficiency diseases such as xerophthalmia (an eye disease), beriberi, pellagra, scurvy, rickets, sterility (in rats), excessive bleeding and so forth. Professors Elmer V. McCollum and Herbert M. Evans, and Joseph Goldberger were among the early American pioneers in this field of research. Drugs, anaesthetics, and medicines like procaine, cyclopropane, dramamme, ephedrine, aspirin, phenace-tin, urotropin, veronal, quinine, and strychnine have been synthesized to alleviate the pains of mankind. The essential... 

Retinol (= Vitamin A)] (carotene) E.V McCollum showed xerophthalmia in rats due to Vitamin A deficiency... 

Protein-energy malnutrition results in functional vitamin A deficiency, with very low circulating levels of the vitamin and development of clinical signs of xerophthalmia (Section 2.4). The condition is unresponsive to the administration of vitamin A and often occurs despite adequate liver reserves of retinol. The problem is one of impaired synthesis of RBP in the liver and hence a... 

A mild infection, such as measles, commonly triggers the development of xerophthalmia in children whose vitamin A status is marginal. In addition to functional deficiency as a result of impaired synthesis of RBP (Section 2.2.3) and transthyretin in response to infection, there may be a considerable urinary loss of vitamin A because of increased renal epithelial permeability and proteinuria, permitting loss of retinol bound to RBP-transthyretin. The American Academy of Pediatrics Committee on Infectious Diseases (1993) recommended vitamin A supplements for aU children who have been hospitalized with measles. 

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