Blindness, vitamin A deficiency

In this period, the empirical healing of certain diseases by foods was estabUshed. Examples (3) were the treatment of night blindness (vitamin A deficiency) with hver ia many cultures over centuries, of beriberi (vitamin deficiency) by use of unpoHshed rice by the Japanese navy, of scurvy (vitamin C deficiency) by citms fmits ia the British navy or piae needle extracts by North American natives, and pellagra (niacia deficiency) by a dietary shift away from corn-based foods ia many countries. Other, nondietary empirical treatments iavolved, eg, exposure of children ia northern latitudes to sunlight to cute tickets (vitamin D deficiency) (4). 

On a vitamin A-deficient diet, mucus-secreting tissues become keratinized. This condition tends to occur in the trachea, the skin, the saUvary glands, the cornea, and the testes. When this occurs in the cornea, it can be followed by blindness. Vitamin A deficiency is the principal cause of blindness in the very young. This problem is particularly acute in the third world (8). 

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). 

In this period, the empirical healing of certain diseases by foods was established. Examples (3) were the treatment of night blindness (vitamin A deficiency) with liver in many cultures over centuries, of beriberi (vitamin deficiency) by use of unpolished rice by the Japanese navy, of scurvy (vitamin C... 

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). 

Patients with vitamin A deficiency may report visual disturbances, night blindness, and dry skin. 

A deficiency of vitamin A results in night blindness. A chronic deficiency results in a thickening of membranes in the cornea which, if untreated, can lead to blindness through perforation of the cornea and loss of the lens. It is estimated that half a million children develop blindness due to vitamin A deficiency every year. Refeeding malnourished children can produce a deficiency of vitamin A (see below). 

Very low reserves of vitamin A. This leads to an important effect of refeeding. The requirement for vitamin A increases when the children are supphed with protein so that they can quickly become vitamin A deficient, resulting in blindness (see above). Hence, the vitamin must be administered with the protein. 

Vitamin A deficiency can result from insufficient dietary intake, from malabsorption and it has been recognized that also malfunction of RAR-receptors can lead to symptoms of vitamin A deficiency. These symptoms include skin lesions, night blindness, corneal ulcerations and conjunctivitis and poor bone remodeling. Vitamin A deficiency associated with malnutrition is wide spread in large parts of the world and may be fatal in infants and young children suffering from kwashiorkor or marasmus. 

L B. Supplement with vitamin A. Vitamin A deficiency symptoms include night blindness that can lead to corneal ulceration. This deficiency can occur in patients with impaired liver storage or fat malabsorption. Dairy products, such as milk, are a good source of vitamin A. (3-Carotene, a vitamin A precursor, is found in pigmented vegetables, such as carrots. When a deficiency is diagnosed, it is appropriate to treat the patient with a supplement rather than to rely on increased consumption of vitamin A-rich foods. A patient with pancreatic disease and malabsorption syndrome will need parenteral supplementation. 

A deficiency of vitamin A leads to vision defects, e.g. night blindness. Vitamin A is quite unstable and sensitive to oxidation and light. Excessive... 

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. 

The fortification of these milk products with vitamin A is endorsed by the American Medical Association, with the concurrence of the Food and Nutrition Board, National Academy of Sciences, National Research Council and the Expert Panel on Food Safety and Nutrition of the Institute of Food Technologists (AMA 1982). The fortification of dried skim milk with vitamin A is viewed by the World Health Organization and the Food and Agricultural Organization (WHO 1977) as an important measure to combat vitamin A deficiency in developing countries, where 20,000 to 100,000 children yearly develop blindness from a lack of vitamin A in their diets (DeLuca et al. 1979). 

A strikingly early symptom of vitamin A deficiency is night blindness. A variety of other symptoms include dry skin and hair, conjunctivitis of the eyes, retardation of growth, and low resistance to infection. The skin symptoms are particularly noticeable in the internal respiratory passages and alimentary canal lining. About 0.7 mg/day of vitamin A is required by an adult. The content of vitamin A in foods is often expressed in terms of international units 1.0 mg of retinol equals 33331.U. 

Vitamin A, as retinal, has a clearly established role in vision (Chapter 23) and apparently has a specialized function in reproduction. In vitamin A deficiency no sperm cells are formed in males, and fetal resorption occurs in females. Rats deprived of vitamin Abut fed retinoic acid become blind and sterile but otherwise appear healthy.e bb Evidently either the alcohol or the aldehyde has an essential function in reproduction, whereas bone growth and maintenance of mucous secretions requires only retinoic acid. Indeed, retinoic acid is 100 to 1000 times more active than other forms of vitamin A in these differentiation functions.1 ... 

It is well established that vitamin A deficiency (VAD) is a public health problem in more than ioo countries, especially in Africa and Southeast Asia, hitting hardest young children and pregnant women. Worldwide, over 124 million children are estimated to be vitamin A deficient. Many of these children go blind or become ill from diarrhea, and nearly eight million preschool age children die each year as the result of this deficiency. The World Health Organization estimates that improved vitamin A nutritional status could prevent the deaths of 1.3—2.5 million late-infancy and preschool age children each year (Humphrey et al. 1992). The heartache of losing a child to a preventable disease is not one commonly encountered in the developed world. 

Cystic fibrosis patients are usually advised to take more than the recommended daily amounts of these vitamins in order to prevent deficiency. A common problem associated with poor absorption of fat-soluble vitamins is deficiency of vitamin K. Vitamin K is required by the liver to produce many blood coagulation factors. Part of the problem for cystic fibrosis patients is their chronic antibiotic therapy, which decreases the bacterial population of the colon colonic bacteria synthesize vitamin K. Vitamin K deficiency leads to prolonged blood-clotting time. Vitamin D deficiency could cause rickets in a child or osteomalacia in adults. Vitamin A deficiency leads to night blindness, skin and other ocular defects. 

Vitamin A-deficient experimental animals fail to grow adults are blind and sterile, with testicular degeneration in males and keratinization of the uterine epithelium in females. Although deficient female animals wUl conceive, and the fetuses will implant, formation of the placenta is impaired and the fetuses are resorbed. Epithelia in general are hyperplastic and keratinized, and there is impaired cellular immunity with increased susceptibility to infection. Both retinol and retinoic acid are required for gestation in the rat in deficient animals, retinoic acid alone will not prevent fetal resorption after about day 10 of gestation (WeUik and DeLuca, 1995 WeUik et al., 1997). 

Vitamin A deficiency is a major problem of children under five in developing countries, being the single most common preventable cause of blindness. Table 2.1 shows the prevalence of vitamin A deficiency in different regions of the world. The increased susceptibility to infection and impairment of immune responses in vitamin A deficiency causes significant childhood mortality. A number of trials of vitamin A supplementation in areas of endemic deficiency show a 20% to 35% reduction in child mortality. 

---