Vitamin A deficiency diseases

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Vitamin A deficiency (VAD) is a global problem. Vitamin A deficiency is a serious, but preventable nutritional disease. Infants, young children and pregnant and lactating women are
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the most vulnerable groups for developing vitamin A hypovitaminosis. Vitamin A deficiency in children causes severe visual impairment and the risk of childhood diseases like diarrhoea and measles.

Even, subclinical Vitamin A deficiency can increase child's risk of developing respiratory diseases and intestinal infections and diseases. It decreases the growth rate and bone development. The likelihood of survival and recovery from serious diseases is highly reduced. All these ophthalmic and general health problems can easily corrected with minimal cost by certain changes in the food habits.

The major cause of vitamin A deficiency is inadequate intake through food. Iron or zinc deficiency can affect vitamin A uptake. Alcoholism and frequent infections can deplete the micronutrient in the body. The common symptoms of vitamin A deficiency are night blindness and xerophthalmia related diseases. Vitamin A deficiency treatment is by administering oral or injectable forms of the supplements.
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World status of Vitamin A deficiency

According to World Health Organization estimates, 250 million preschool children suffer from vitamin A avitaminosis and related diseases.
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.
An estimated 250 000 to 500 000 vitamin A-deficient children become blind every year, half of them dying within 12 months of losing their sight.

Vitamin A deficiency diseases

Vitamin A avitaminosis leads to several ophthalmic manifestations, including, xerophthalmia, night blindness, Bitot's spots, conjunctival xerosis, corneal xerosis, ulceration and necrosis of the cornea (keratomalacia). Other risk factors and diseases associated with the hypovitaminosis are, decreased immunity, hematopoietic cell alterations, nutritional anemia, hyperglycemia and reduced insulin secretion and infective diseases like severe measles.

Xerophthalmia

Xerophthalmia literally means dryness in eyes. In ophthalmology, the term xerophthalmia refers to the spectrum of ocular changes due to systemic vitamin A deficiency. Xerophthalmia may affect any age group, but preschool children, adolescents and pregnant women are the worst affected. The ocular manifestations are observed on retina, conjunctiva and cornea.

Night blindness

Rod photoreceptor cells in the retina of the eye are responsible for vision under low levels of illumination. Rod photoreceptor cells are entirely responsible for night vision. Rhodopsin is a photoreceptive pigment present within the photoreceptor cell comprising a large protein called opsin and an organic molecule called retinal. The stimulation of retinal by light causes it change from existing 11-cis-retinal form to all-trans-retinal form. This structural change leads to a cascade of events ending in visual phototransduction and neurotransmission.

The retinal component of rhodopsin is derived from vitamin A and its insufficiency causes loss of the pigment in the rod cells. The dark adaptation is impaired and night blindness occurs. Treatment with vitamin A supplementation may restore the vision in a few days.

Conjunctival xerosis

Conjunctival xerosis is the earliest sign of hypovitaminosis. Structural changes and loss of goblet cells in the conjunctiva take place leading to dry, non-wettable and rough patches. The conjunctiva gets thickened, wrinkled and pigmented. Keratinized epithelial cells may form cheesy matter and accumulate above the conjunctival surface as “Bitot's spots”. The pigmentation of conjunctiva gives a clouded appearance to the eye. When treated with supplements of vitamin A, the Bitot's spots begin to regress within two to five days and the xerosis resolves after sometime.

Corneal xerosis

Corneal xerosis sets in initially as superficial depressions in the cornea. With the progress of the condition stromal edema develops, and the cornea appears hazy, granular, and pebbly upon examination. Treatment, even at this stage, leads to complete recovery within one to two weeks with no scarring. Forming of corneal ulcers causes permanent destruction of part or all of the corneal stroma. Superficial ulcers may heal without much scarring. Deep ulcers and perforation of the cornea, even after healing may cause visual impairment.

Keratomalacia

Keratomalacia is rare extreme stage of xerophthalmia, affecting the full thickness of of cornea with rapid progressive necrosis (death) of the corneal tissue. The necrotic tissue may slough off, leaving a gaping ulcer and extrusion of intraocular contents. The globe of the eye may get permanently distorted or lost. Blindness is inevitable and treatment with vitamin A supplements may save the other eye and life.

Decreased immunity and diseases

Vitamin A, in the retinoic acid form, plays an important role in gene transcription. The transcription process and cell replication of T-killer cells require retinoids. In the event of vitamin A avitaminosis, proliferation and replication processes get suppressed, contributing to fewer number of T-killer cells and lymphocytes available to take on pathogens. With suppressed immunity, measles, respiratory diseases and diarrhoea attack with severity.

Another outcome of vitamin A avitaminosis is the keratinization of the skin and of the mucous membranes in the respiratory, gastrointestinal and urinary tracts leading to infections and diseases. The skin gets thickened, dry, scaly and there is thickening of hair follicles. de Azevedo Paiva A et al. reported that 'vitamin A had an effect on the recruitment of T and B lymphocytes to the circulation of children with hypovitaminosis A and anemia.'

Hyperglycemia?

Trasino SE et al. in their study 'Vitamin A Deficiency Causes Hyperglycemia and Loss of Pancreatic β-Cell Mass' on adult mice, published in The Journal of Biological Chemistry (2015 Jan 16;290(3):1456-73), reported that "vitamin A (all-trans-retinol) (VA) is required both for the maintenance of pancreatic β-cell and α-cell mass and for glucose-stimulated insulin secretion in adult mice. Dietary VA deprivation (VAD) causes greatly decreased pancreatic vitamin A levels, hyperglycemia, and reduced insulin secretion."
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References:
1.West KP Jr. Vitamin A deficiency disorders in children and women. Food Nutr Bull. 2003 Dec;24(4 Suppl):S78-90.
2.de Azevedo Paiva A, Rondó PH, Rehder Vaz-de-Lima L, de Freitas Oliveira C, Ueda M, Gonçalves-Carvalho C, Reinaldo LG. The impact of vitamin A supplementation on the immune system of vitamin A-deficient children. Int J Vitam Nutr Res. 2010 Jun;80(3):188-96.
3.Fernanda B. Michelazzo, Julicristie M. Oliveira, Juliana Stefanello, Liania A. Luzia, Patricia H. C. Rondó. The Influence of Vitamin A Supplementation on Iron Status. Nutrients. 2013 Nov; 5(11): 4399–4413.
4.McLaren DS, Kraemer K. Interaction of vitamin A and other micronutrients. World Rev Nutr Diet. 2012;103:101-5.
5.Trasino SE, Benoit YD, Gudas LJ. Vitamin A Deficiency Causes Hyperglycemia and Loss of Pancreatic β-Cell Mass. J Biol Chem. 2015 Jan 16;290(3):1456-73.
6.de Pee S, Dary O. Biochemical indicators of vitamin A deficiency: serum retinol and serum retinol binding protein. J Nutr. 2002 Sep;132(9 Suppl):2895S-2901S.
7.Huiming Y1, Chaomin W, Meng M. Vitamin A for treating measles in children. Cochrane Database Syst Rev. 2005 Oct 19;(4):CD001479.
8.http://www.who.int/nutrition/topics/vad/en/
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