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ABSTRACT

Vitamin A deficiency (VAD) is the leading cause of preventable blindness in children and in pregnant women VAD causes night blindness. Vitamin A deficiency is a public health problem in more than half of all countries, especially in Africa and South-East Asia, hitting hardest young children and pregnant women in low-income countries. For maintenance of eye health, vitamin A is an important nutrient. Our body gets Vitamin A when we eat foods containing this vitamin. Lack of vitamin A causes eye diseases. Night Blindness is usually the first sign of Vitamin A deficiency. Night blindness is the inability or reduced ability to see in dim light or darkness. It sets in if light intensity goes below a certain level, for example, at the twilight level. It also refers to the condition in which the time it takes for the eyes to adapt to darkness is prolonged. Keyword : vitamin A deficiency, night blindness

INTRODUCTION
Vitamin A deficiency is a major public health problem in the developing world and the leading cause of irreversible blindness in children. To improve health and reduce the risk of blindness in developing countries, it is crucial for public health workers to be able to identify children who are suffering from vitamin A deficiency. Night Blindness is usually the sign of Vitamin A deficiency. In this case the lesions in eyes are most obvious. Normally, people does not consume balanced diet due to which Night Blindness occur. Mainly, Vitamin A is found in the diet in 2 forms. The dietary sources of Vitamin A is animal derived foods such as yolk of eggs, butter, whole milk, fish, liver, kidney. Plants and Vegetables derived, dietary source of Vitamin A include carrots, potatoes, pumpkins, mangoes, spinach, B-carotene. Deficiency of vitamin A in food may lead to development of night blindness. The main functions of Vitamin A, is that it helps in maintenance of normal vision in reduced light. This involves the synthesis of rhodopsin, a light sensitive pigment in the rods and cones of retina. This pigment then transforms the radiant energy into nerve impulses.

VITAMIN A DEFICIENCY
Vitamin A
Vitamin A is a vitamin which is needed by the retina of the eye in the form of a specific metabolite, the light-absorbing molecule retinal. This molecule is absolutely necessary for both scotopic and color vision. Vitamin A also functions in a very different role, as an irreversibly oxidized form retinoic acid, which is an important hormone-like growth factor for epithelial and other cells. Vitamin A is a fat-soluble vitamin.(1) Vitamin A plays a role in a variety of functions throughout the body, such as:

Vision The role of vitamin A in the vision cycle is specifically related to the retinal form. Within the eye, 11-cis-retinal is bound to rhodopsin (rods) and iodopsin (cones) at conserved lysine residues. As light enters the eye the 11-cis-retinal is isomerized to the all-"trans" form. The all-"trans" retinal dissociates from the opsin in a series of steps called bleaching. This isomerization induces a nervous signal along the optic nerve to the visual center of the brain. Upon completion of this cycle, the all-"trans"-retinal can be recycled and converted back to the 11-"cis"-retinal form via a series of enzymatic reactions.(2)

Gene transcription Immune function Embryonic development and reproduction Bone metabolism
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Haematopoiesis Skin health Antioxidant Activity

Recommended daily intake (Dietary Reference Intake) Life Stage Group Recommended Dietary Allowances (RDA) Adequate Intakes (AI*) g/day Infants 06 months 712 months Children 13 years 48 years Males 913 years 1418 years 19 - >70 years Females 913 years 1418 years 19 - >70 years Pregnancy <19 years 19 - >50 years 750 770 2800 3000 600 700 700 1700 2800 3000 600 900 900 1700 2800 3000 300 400 600 900 400* 500* 600 600 Upper Limit g/day

Vitamin A is found naturally in many foods likes liver (beef, pork, chicken, turkey, fish), carrot, broccoli leaf, sweet potato, butter , spinach, pumpkin ,collard greens, cantaloupe melon, egg, apricot, papaya mango, pea ,broccoli, etc. (3)

Vitamin A Deficiency
Vitamin A deficiency is estimated to affect millions of children around the world. Approximately 250,000-500,000 children in developing countries become blind each year owing to vitamin A deficiency, with the highest prevalence in Southeast Asia and Africa. According to the World Health Organization (WHO), vitamin A deficiency is under control in the United States, but in developing countries vitamin A deficiency is a significant concern. With the high prevalence of vitamin A deficiency, the WHO has implemented several initiatives for supplementation of vitamin A in developing countries. Epidemiology

Rare in the UK, but extremely common in developing countries especially Africa, Asia and Western Pacific.

Between 100 and 140 million children are vitamin A deficient, 250,000-500,000 of these children become blind every year, and half of these die within 12 months of losing their sight.

In pregnant women vitamin A deficiency occurs especially in the last trimester (demand by fetus and mother is highest).

Primary vitamin A deficiency Caused by prolonged dietary deficiency, particularly where rice is the staple food (doesn't contain carotene) that occurs among children and adults who do not consume an adequate intake of yellow and green vegetables, fruits and liver.

Vitamin A deficiency occurs with protein-energy malnutrition (marasmus or kwashiorkor) mainly because of dietary deficiency (but vitamin A storage and transport are also impaired).

Secondary vitamin A deficiency Occurs where there are problems in converting carotene to vitamin A, or reduced absorption, storage, or transport of vitamin A. This occurs in coeliac disease, tropical sprue, giardiasis, cystic fibrosis and other pancreatic disease, cirrhosis, duodenal bypass, chronic malabsorption of lipids, impaired bile production and release, low fat diets, and chronic exposure to oxidants, such as cigarette smoke. Vitamin A is a fat soluble vitamin and depends on micellar solubilization for dispersion into the small intestine, which results in poor utilization of vitamin A from low-fat diets. Zinc deficiency can also impair absorption, transport, and metabolism of vitamin A because it is essential for the synthesis of the vitamin A transport proteins and the oxidation of retinol to retinal. In malnourished populations, common low intakes of vitamin A and zinc increase the risk of vitamin A deficiency and lead to several physiological events. (4)

Presentation

Pathognomonic changes occur in the eye (usually bilateral although may be of differing degrees): night blindness, dry eyes, Bitot's spots (foamy patches on the white of the eye) and keratomalacia (thinning and ultimate ulceration of the cornea - colliquative necrosis). Bitot's spots are an important early sign, and can occur without clinical night blindness. If they are recognised and early Vitamin A replacement initiated complications and blindness can be prevented.

Other less specific changes include:


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Keratinisation of epithelia in the lung, gastrointestinal and urinary tract. Increased susceptibility to infection. Skin changes (follicular hyperkeratosis) are also common.

Since the unique function of retinyl group is the light absorption in retinylidene protein, one of the earliest and specific manifestations of vitamin A deficiency is impaired vision, particularly in reduced light - night blindness. Persistent deficiency gives rise to a series of changes, the most devastating of which occur in the eyes. Some other ocular changes are referred to as xerophthalmia. First there is dryness of the conjunctiva (xerosis) as the normal lacrimal and mucus secreting epithelium is replaced by a keratinized epithelium. This is followed by the build-up of keratin debris in small opaque plaques (Bitot's spots) and, eventually, erosion of the roughened corneal surface with softening and destruction of the cornea (keratomalacia) and total blindness. Other changes include impaired immunity, hypokeratosis (white lumps at hair follicles), keratosis pilaris and squamous metaplasia of the epithelium lining the upper

respiratory passages and urinary bladder to a keratinized epithelium. With relations to dentistry, a deficiency in Vitamin A leads to enamel hypoplasia.

Management

Good animal sources of vitamin A include liver, egg yolks, whole milk, animal butter and whole small fish (with liver intact). Animal sources, including vitamin A in breast milk, are more bioavailable than vegetable sources, which include carrots and other orange/yellow fruits and vegetables, and dark green leafy vegetables.

Drugs : Oral vitamin A palmitate in oil 20,000 g (60,000 IU) daily for 2 days and further dose after 7 to 10 days. If vomiting, then an intramuscular form is available.

Prognosis

Up to the stage of corneal xerosis (X2), prompt treatment can result in full preservation of sight without residual impairment (heals completely within a few weeks).

In the developing world, because severe degree of vitamin A deficiency is often accompanied by severe generalised malnutrition (PEM), death is the most likely outcome. Mortality in infants with severe vitamin A deficiency is up to 50%.

Only about 40% of patients with corneal xerophthalmia are alive one year later (25% are totally blind, and the remainder partially blind).

NIGHT BLINDNESS
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Definition Night blindness (nyctalopia) is the inability to see well at night or in poor light. It is not a disorder in itself, but rather a symptom of an underlying disorder or problem, especially untreated nearsightedness. (5) Causes & Symptoms Several different conditions and diseases can cause night blindness. These include:

Cataracts. This condition is characterized by a cloudiness of the lens. Congenital night blindness. This is an inherited, stable disease in which persons suffer from night blindness. Recent advances in gene mapping have identified several mutations responsible for this form of night blindness.

Liver conditions. Reduced night vision can be linked to poor liver functioning, due to a variety of conditions, which impairs vitamin A metabolism.

Macular degeneration. Degeneration of the macula retinae, a specialized region of the retina, can cause night blindness.

Retinitis pigmentosa. This is an inherited eye disease in which there is progressive deterioration of the photopigments of the photoreceptors, eventually resulting in blindness. The rods are destroyed early in the course of disease resulting in night blindness. Night blindness in children may be an early indicator of retinitis pigmentosa. Recent genetic studies have identified mutations related to retinitis pigmentosa on human chromosome 19.
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Vitamin A deficiency. Night blindness is commonly caused by a deficiency in vitamin A, in fact, it is one of the first indicators of vitamin A deficiency.

Xerophthalmia. This condition is characterized by dryness of the conjunctiva (the membrane that covers the eyelids and exposed surface of the eye) and cornea, light sensitivity, and night blindness. It is caused by vitamin A deficiency. Xerophthalmia rarely occurs in countries with adequate supplies of milk products.

Diagnosis Diagnosis begins with a detailed medical history regarding the night blindness. If the patient complains of difficulty seeing at night, ask when he first noticed the problem, severity of night blindness, when night blindness began, did it occur gradually or suddenly, is it intermittent or steadily worsening, is it worse at certain times or in certain conditions. Also, ask about other ocular symptoms, such as eye pain, blurred or halo vision, floaters or spots, and photophobia. Explore any history of glaucoma, cataracts, and familial degeneration of vision. If no ocular problems are apparent, briefly evaluate the patients nutritional status for vitamin A deficiency. Examine the eyes for ptosis, abnormal tearing, discharge, and conjunctival injection. Test visual acuity and visual fields in both eyes and, if trained and equipped, measure intraocular pressure. Check pupillary response, and evaluate extraocular muscle function by testing the six cardinal fields of gaze.

Types of Night Blindness

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1. Congenital Stationary Night Blindness: This type of night blindness, present at birth, can have varying causes often related to inherited disorders. 2. Progressive Night Blindness: As implied by the name, progressive night blindness continues to worsen. Causes can include factors such as vitamin A deficiency, disease, and toxic effects of drugs including quinine used to treat malaria and other conditions. 3. Night Blindness as Complication of Obesity Surgery: Individuals who undergo obesity surgery altering the way the body absorbs food can develop night blindness, primarily because nutrients such as vitamin A may be lacking if patients fail to use nutritional supplements following surgery. (6) Treatment Treatment for night blindness will depend upon its cause . Treatments generally include:

Taking vitamin A supplements Removal of the cataracts. Eating a diet with adequate amounts of Vitamin A may help prevent night blindness.

Night-blindness (middle) vs. normal sight (left and right)

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THE CORRELATION BETWEEN VITAMIN A DEFICIENCY AND NIGHT BLINDNESS

Vitamin A deficiency is a major public health problem in the developing world and the leading cause of irreversible blindness in children. Night blindness that occur due to Vitamin a deficiency is common in countries of South-East Africa, Central and South America. People most at risk are children between six months to six years, pregnant women, and lactating women. It was clear that womens risk of VAD is now well recognized, especially their high rates of night blindness. (7) Night Blindness is usually the first sign of Vitamin A deficiency. In this case the lesions in eyes are most obvious. Normally, people does not consume balanced diet due to which Night Blindness occur. So deficiency of such elements in food may lead to development of night blindness. The main functions of Vitamin A, is that it helps in maintenance of normal vision in reduced light. This involves the synthesis of rhodopsin, a light sensitive pigment in the rods and cones of retina. This pigment then transforms the radiant energy into nerve impulses. Night blindness is the inability or reduced ability to see in dim light or darkness. It also refers to the condition in which the time it takes for the eyes to adapt to darkness is prolonged. Night blindness, also called nyctalopia, is a symptom of several different diseases or conditions. All of the possible causes of night blindness are associated with the way in which the eye receives light rays. Light travels through the cornea and lens and lands on the retina at the back of the eye. The retina is composed of photoreceptors. Photoreceptors are specialized nerve cells that receive light rays and convert them into electrical signals, which are then transmitted to the brain, creating an image. (8)
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There are two types of photoreceptors, rods and cones. There are three million cones and 100 million rods in each eye. The two different photoreceptors are similar in structure, however, rods have a larger outer segment than cones. The outer segments of photoreceptors contain lightsensitive photopigments which change shape whenever light rays strike them. Rods contain the photopigments retinal and rhodopsin, whereas cones contain retinal and three different opsins. Rhodopsin is only able to discriminate between different degrees of light intensity, whereas the opsins of cones distinguish between light wavelengths in the red, blue, and green ranges. Hence, rods see only black and white, but cones see colors. Also, rods enable the eyes to detect motion and provide peripheral vision. Rods are responsible for vision in dim light, and cones are responsible for vision in bright light. The rods are spread throughout the retina, but the cones are only in the center of the retina. Vision in dim light or darkness is blurry because of the connections between the photoreceptors and the nerve cells which are linked to the brain. Each rod must share this connection to the brain with several other rods so the brain does not know exactly which rod produced the signal. Alternatively, vision in bright light is sharp because each cone has its own connection to the brain so the brain can determine exactly where on the retina the signal originated. Another feature of rods is that they must adapt to darkness. This is best exemplified by walking into a dark movie theater. At first, one can see very little. With time, vision improves and one is able to discern objects. Ultimately, one can see moderately well. This dark adaptation process occurs because of the chemical nature of rhodopsin. Rhodopsin is decomposed in bright light making the rods nonfunctional. In darkness, rhodopsin is regenerated faster than it can be

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decomposed. Dark adaptation takes about 1530 minutes and, when complete, increases light sensitivity by about 100,000 times. The diagram showing how vitamin A is used by the eye (9)

VISUAL PHYSIOLOGY
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The retina in our eyes contains two basic types of light sensors (photoreceptors), which form independent visual systems that are dedicated to special tasks:

Rods are primarily used for brightness and motion perception, as well as for night vision Cones are primarily used for color and daylight vision

Each eye has about 6.000.000 cones and 120.000.000 rods. People can distinguish about 200 different hues and about 100 levels of gray. (10)

Schematic rod (left) and cone (right) Photoreceptors. Electromagnetic radiation of wavelength between 400-700 nm initiates a chemical reaction in specialized retinal cells, the rods and cones, constituting a stimulus to nervous impulses which are transmitted and give rise to perception in the human visual cortex. The foveal part of the retina is predominantly occupied by cones which contain one of the three visual pigments and subserve colour vision. Rods contain a single visual pigment (rhodopsin)
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and increase in frequency from about 2 mm from the centre, maximum density being found between 3 and 6 mm from the fovea. Cone density decreases towards the periphery but extends to the ora serrata. The rods are far more numerous than the cones there being a total of 120 million rods and 6 million cones in each eye. (11) The light sensors are not evenly distributed across the retina. Cones are concentrated at the center of the retina, called macula or macula lutea (yellow spot). At the center of the macula is the fovea centralis, which has the highest cone density and therefore is critical in visual perception (ca. 150.000 receptors per square mm at maximum). Rods are absent from the central area of the retina. Their distribution reaches its peak at an angle of about 20 degrees from the center of the retina (ca. 160.000 receptors per square mm) and decreases to about half of it at about 60 degrees. The neurons from each eye form the two optic nerves that transmit visual information to the brain. Both optic nerves come together at the optic chiasm, where the information from the left sides of both eyes is combined and directed to the left side of the brain; the information of the right sides of the eyes is directed to the right side of the brain. As the images in the eyes are upside down, the information from the left half of the visual field is actually directed to the right side of the brain and vice versa. This combination of visual information is important for depth perception. Behind the optic chiasm, the optic nerve is called optic tract; it continues to the lateral geniculate nucleus and from there to the visual cortex, those areas of the brain, that process visual information.

CONCLUSION
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Vitamin A deficiency is estimated to affect millions of children around the world. Night blindness that occur due to Vitamin a deficiency is common in countries of South-East Africa, Central and South America.Vitamin A deficiency contributes to development of night blindness because of the nutrient's importance in maintaining the health of the eye's retina. The retina is well supplied with an important chemical substance called rhodopsin . Light falling on the retina brings about certain chemical changes in the rhodopsin and other substances present in the rods and cones. These changes occur very rapidly, but large quantities of vitamin A are needed to bring this about. If there is any marked deficiency of vitamin A, night blindness may occur. This can usually be corrected by administering suitable amounts of vitamin A in the diet.

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http://www.medicinenet.com. Accessed January 21,2010. 6. Vitamin A and Night Blindness. Literature reviews. Available at : http://www.healthvitaminsguide.com/deficiencies/night-blindness.htm. Accessed January 22,2010. 7. Ramakrishnan U, Hill ID. Assessment and control of vitamin A deficiency Disorders.J Nutr. 2002:132. 8. Night Blindness. Literature reviews. Available at : http://www.answers.com. Accessed January 22,2010. 9. Night Blindness. Literature reviews. Available at :

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http://www.sapdesignguild.org/vision_blindness.htm. Accessed January 25,2010. 11. Crick RP, Khaw PT. A Textbook of Clinical Ophthalmology : Examination at Function. 2nd ed. Singapore: World Scientific; 1997: p.237-8.

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