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ACC/SCN nutrition summary for policy-makers
Vitamin A deficiency
The statement on Vitamin A Deficiency on page 38 is one in a series being prepared by the Administrative Committee on Co-ordination's Sub-Committee on Nutrition for policy-makers and others interested in short, authoritative summaries of major nutrition problems and their prevention.
Single copies are available without charge from Dr. H.J.L. Burgess, Secretary, ACC Sub-Committee on Nutrition, c/o Food Policy and Nutrition Division, FAO, Via done Terme di Caracalla, 00100 Rome, Italy. The statements can be ordered in bulk at the prices indicated on the copy.
Additional summaries in this series will appear in future issues of the Food and Nutrition Bulletin.
Vitamin A deficiency
Vitamin A deficiency is the main cause of partial or complete blindness in young children in developing countries. Although blindness is by no means the only serious consequence of this deficiency, it is the most tragic and dramatic, particularly because means of prevention are available. Many of the affected children soon die due to continuing malnutrition, social neglect, infections, or accidents, but many also survive to live a handicapped life.
Vitamin A is essential for maintaining the integrity of epithelial tissues, including the skin and various mucous membranes. The most sensitive of these tissues appears to be the eye, and the word xerophthalmia derived from the Greek, meaning "dry eye," is used to describe the appearance in the early stage of the disease. The conjunctive loses its normal brilliance; it looks dry, thick wrinkled, and is sometimes hyperpigmented. During this phase a rapid cure can be brought about by administration of medicinal doses of vitamin A. Should the disease progress until the cornea has been affected with opacities or ulceration, the administration of vitamin A will lead to improvement, although scars may remain. If deterioration continues beyond this point, the cornea will rupture and the eye will collapse, leading to total blindness.
Interrelations with Other Diseases
Xerophthalmia or vitamin A deficiency is most often found in children who are also suffering from some degree of protein-energy deficiency. However, although protein-energy malnutrition may aggravate and hasten the irreversible damage to the eye, it is not directly responsible.
The second important interrelation is with infections. Even before the eyes are affected, vitamin A deficiency is believed to contribute to morbidity and mortality through lowering the body's resistance to infection. This association has been firmly established in animals, and there is a strong suspicion that the same mechanism operates in humans. Furthermore, an eye damaged by xerophthalmia is much more susceptible to serious infection, which greatly increases the risk of permanent scarring.
The Diagnosis of Vitamin A Deficiency
There are three ways by which vitamin A deficiency is
a. Reports by parents or guardians indicating that the child seems to have difficulty in seeing at night or in dim light. In countries where vitamin A deficiency is endemic, this "night blindness" is well recognized and usually there is a local term for the phenomenon
b. Clinical appearance of the eye, ranging from the early signs of "dry eye" already described, to the opaque or scarred cornea in the later stages.
c. Biochemical methods, whereby blood plasma vitamin A levels are measured.
Each of these methods has its limitations. Their combined use, however, gives a more complete and reliable assessment. The same techniques can be used to determine whether there is significant vitamin A deficiency in a community. Thus, if the earlier signs of xerophthalmia are seen in more than 2 per cent of children under five years of age, or if the plasma vitamin A is less than 10 µg per 100 ml in more than 5 per cent of the population at risk, a public health problem exists.
Extant of the Deficiency
Vitamin A availability is probably a problem in all tropical and semi-tropical regions to some extent. However, it is in the large Asian countries that it is most prevalent. It is estimated that at least 250,000 children go blind each year because of vitamin A deficiency.
Prevention of Vitamin A Deficiency
The best defense is an adequate intake of vitamin A or provitamin A in the normal diet. In particular, for the poor this will mean consumption of foods of vegetable origin that contain the pigment carotene, which is converted in the body to active vitamin A. Such foods include dark green leaves and orange and yellow fruits or vegetables. The diet of the rich will also include food of animal origin that may contain preformed vitamin A-for instance, liver and the fat component of milk and eggs. Because vitamin A can be stored in the human liver, it need not be eaten on a regular or daily basis.
When diets are inadequate, the possibility of fortifying certain foods should be considered. In industrialized countries, vitamin A is usually added to margarine and often to dry skim milk. In some Central American countries sugar is being fortified, and in the Philippines experiments with fortification of the flavoring agent monosodium glutamate (MSG) are being carried out. It is vitally important to fortify foods such as dry skim milk used in child feeding programs, especially in countries with known vitamin A deficiency problems.
The high-dose capsule
Where the problem is severe, where fortification is not feasible, or where it would take a long time to improve the basic diet, administration of high-dose capsules is useful as an interim measure. 200,000 international units (IU) of vitamin A (100,000 IU for infants) given orally in a single capsule will provide protection for three to six months. Distribution of such capsules is practised in India, Bangladesh, Indonesia, and the Philippines. However, while simple in principle, reaching all the young children in a large population every few months poses serious logistic problems. It is, therefore, difficult to maintain such campaigns for any length of time.
Every health service establishment should have a supply of high-dose capsules, so that at least children attending their MCH services can be protected. Because vitamin A is stored for long periods in the liver, there is potentially a risk of undesirable side effects should repeated high doses be given over a short period. Fortunately, in practice this has not been a serious problem, and children given high-dose capsules at intervals as close as two weeks apart have shown no ill effects
Control of infectious diseases through immunization and improved sanitation can play an important role in alleviating vitamin A deficiency problems. For instance, measles, which also affects the eye, can be particularly dangerous for children suffering from xerophthalmia.
Treatment of Severe Vitamin A Deficiency
The presence of active xerophthalmia in a child is a medical emergency, requiring the prompt administration of massive amounts of vitamin A. The best treatment for patients more than one year old is to inject one dose of 100,000 IU of water-miscible vitamin A intramuscularly. Where this is not available, a 200,000 IU capsule can be given orally. In either case, an additional 200,000 IU should be given orally on the following day to ensure adequate treatment and boost the liver reserves. The same dosage should be repeated two weeks later When the patient is less than one year old, the dosage should be reduced by half.
Xerophthalmia very rarely occurs in isolation and it is necessary also to attend to the child's other nutritional needs, particularly those for protein and energy, and to treat any infections.
Guidelines for the Eradication of Vitamin A Deficiency and Xerophthalmia, a Report of the International Vitamin A Consultative Group (IVACG) (1976) Available from the Nutrition Foundation, Inc., 489 Fifth Ave., New York, N.Y. 10016, USA.
Sommer, Alfred, Field Guide to the Detection and Control of Xerophthalmia (World Health Organization, Geneva, 1978).
Vitamin A Deficiency and Xerophthalmia, Report of a Joint WHO/USAID Meeting, WHO Tech. Rep. Ser. 590 (World Health Organization, Geneva, 1976).
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