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Vitamin A deficiency
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Vitamin A deficiency : ウィキペディア英語版
Vitamin A deficiency

Vitamin A deficiency (VAD) is a lack of vitamin A in humans. It is common in poorer countries but rarely seen in more developed countries. Nyctalopia (night blindness) is one of the first signs of VAD. Xerophthalmia, keratomalacia, and complete blindness can also occur since Vitamin A has a major role in phototransduction.
Vitamin A deficiency is the leading cause of preventable childhood blindness and is critical to achieving Millennium Development Goal 4 to reduce child mortality.〔 Approximately 250,000 to 500,000 malnourished children in the developing world go blind each year from a deficiency of vitamin A, approximately half of whom die within a year of becoming blind. The United Nations Special Session on Children in 2002 set a goal of the elimination of VAD by 2010.
The prevalence of night blindness due to VAD is also high among pregnant women in many developing countries. VAD also contributes to maternal mortality and other poor outcomes in pregnancy and lactation.
VAD also diminishes the ability to fight infections. In countries where children are not immunized, infectious diseases like measles have higher fatality rates. As elucidated by Alfred Sommer, even mild, subclinical deficiency can also be a problem, as it may increase children's risk of developing respiratory and diarrheal infections, decrease growth rate, slow bone development, and decrease likelihood of survival from serious illness.
VAD is estimated to affect approximately one third of children under the age of five around the world.〔World Health Organization, Global prevalence of vitamin A deficiency in populations at risk 1995–2005, WHO global database on vitamin A deficiency.〕 It is estimated to claim the lives of 670,000 children under five annually.〔Black RE et al., Maternal and child undernutrition: global and regional exposures and health consequences, The Lancet, 2008, 371(9608), p. 253.〕 Approximately 250,000–500,000 children in developing countries become blind each year owing to VAD, with the highest prevalence in Southeast Asia and Africa. According to the World Health Organization (WHO), VAD is under control in the United States, but, in developing countries, VAD is a significant concern. Globally, 65% of all children aged 6 to 59 months received two doses of vitamin A in 2013, fully protecting them against VAD (80% in the least developed countries).
==Signs and symptoms==
The common cause of blindness in developing countries is VAD. The World Health Organization (WHO) estimates 13.8 million children to have some degree of visual loss related to VAD.〔J S Rahi, S Sripathi, C E Gilbert, A Foster. Childhood blindness due to VAD in India: regional variations. Archives of Disease in Childhood. 72: 330–333, 1995.〕 Night blindness and its worsened condition, xerophthalmia, are markers of VAD, as it can also lead to impaired immune function, cancer, and birth defects. Collections of keratin in the conjunctiva, known as Bitot's spots, are also seen. Imtiaz's sign is the earliest ocular sign of VAD. Conjunctival epithelial defects occur around lateral aspect of the limbus in subclinical stage of VAD. These conjunctival epithelial defects are not even visible on a biomicroscope, but they take up black stain and become readily visible after instillation of kajal (surma); this is called "Imtiaz's sign".〔http://www.paramountbooks.com.pk/LoginIndex.asp?title=Concise-Ophthalmology-(pb)-2014&Isbn=9789696370017&opt=3&sUBcAT=06〕
Night blindness is the difficulty for the eyes to adjust to dim light. Affected individuals are unable to distinguish images in low levels of illumination. People with night blindness have poor vision in the darkness, but see normally when adequate light is present.
VAD affects vision by inhibiting the production of rhodopsin, the eye pigment responsible for sensing low light situations. Rhodopsin is found in the retina and is composed of retinal (an active form of vitamin A) and opsin (a protein). Because the body cannot create retinal in sufficient amounts, a diet low in vitamin A will lead to a decreased amount of rhodopsin in the eye, as there is inadequate retinal to bind with opsin. Night blindness results.
Night blindness caused by VAD has been associated with the loss of goblet cells in the conjunctiva, a membrane covering the outer surface of the eye. Goblet cells are responsible for secretion of mucus, and their absence results in xerophthalmia, a condition where the eyes fail to produce tears. Dead epithelial and microbial cells accumulate on the conjunctiva and form debris that can lead to infection and possibly blindness.〔Underwood, Barbara A. Vitamin A Deficiency Disorders: International Efforts to Control A Preventable “Pox.” J. Nutr. 134: 231S–236S, 2004.〕
Decreasing night blindness requires the improvement of vitamin A status in at-risk populations. Supplements and fortification of food have been shown to be effective interventions. Supplement treatment for night blindness includes high doses of vitamin A (200,000 IU) in the form of retinyl palmitate to be taken by mouth, which is administered two to four times a year.〔Sommer A, Muhilal, Tarwotjo I, Djunaedi E and Glover J (1980b) Oral versus intramuscular vitamin A in the treatment of xerophthalmia. Lancet 1: 557–559.〕 Intramuscular injections are poorly absorbed and are ineffective in delivering sufficient bio-available vitamin A. Fortification of food with vitamin A is costly, but can be done in wheat, sugar, and milk.〔Arroyave G, Mejia LA and Aguilar JR (1981) The effect of vitamin A fortification of sugar on the serum vitamin A levels of preschool Guatemalan children: a longitudinal evaluation. J. Nutr. 34: 41–49.〕 Households may circumvent expensive fortified food by altering dietary habits. Consumption of yellow-orange fruits and vegetables rich in carotenoids, specifically beta-carotene, provides pro-vitamin A precursors that will prevent VAD related night blindness.

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