Medicine:Vitamin A deficiency

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Short description: Disease resulting from low vitamin A concentrations in the body
Prevalence of vitamin A deficiency, 1995-2005

Vitamin A deficiency (VAD) or hypovitaminosis A is a lack of vitamin A in blood and tissues.[1] It is common in poorer countries, especially among children and women of reproductive age, but is rarely seen in more developed countries.[1] Vitamin A plays a major role in phototransduction, so this deficiency impairs vision, often presenting with nyctalopia (night blindness).[1] In more severe VAD cases, it can progress to xerophthalmia, keratomalacia, and complete blindness.[1]

Vitamin A deficiency is the leading cause of preventable childhood blindness worldwide and is a major cause of childhood mortality.[1] Each year, approximately 250,000 to 500,000 malnourished children in the developing world go blind from a VAD, with about half of whom dying within a year of losing their sight.[2] Addressing VAD has been a critical focus of global health initiatives, including Sustainable Development Goal 2: to end hunger, achieve food security and improved nutrition and promote sustainable agriculture.[3]

In pregnant women, VAD is associated with a high prevalence of night blindness and poor maternal health outcomes including an increased risk of maternal mortality and complications during pregnancy and lactation.[4][5][6][7] VAD also affects the immune system and diminishes the body's ability to fight infections.[1] In countries where children are not immunized, VAD is linked to higher fatality rates from infectious diseases such as measles.[1] Even mild, subclinical deficiency can also be a problem, as it may increase children's risk of developing respiratory and diarrheal infections, decrease growth, impair bone development, and reduce their likelihood of surviving serious illnesses.[6]

Globally, VAD is estimated to affect about one-third of children under the age of five, causing an estimated 670,000 deaths in children under five annually.[8][9] It is most prevalent in sub-Saharan Africa (48 percent) and South Asia (44 percent).[8] Although VAD is well-managed in many high income nations, it remains a significant concern in resource-poor settings. Public health interventions, such as vitamin A supplementation, reached 59% of targeted children in 2022, highlighting the ongoing need for comprehensive efforts to combat VAD.[8]

Signs and symptoms

Vitamin A deficiency is the most common cause of blindness in developing countries. The WHO estimated in 1995 that 13.8 million children had some degree of visual loss related to VAD.[10] Night blindness and its worsened condition, xerophthalmia, are markers of Vitamin A deficiency; collections of keratin in the conjunctiva, known as Bitot's spots, and ulceration and necrosis of cornea keratomalacia can be seen. Conjunctival epithelial defects occur around lateral aspect of the limbus in the subclinical stage of VAD. These conjunctival epithelial defects are not 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".[11]

Night blindness

Main article: Nyctalopia

A process called dark adaptation typically causes an increase in photopigment amounts in response to low levels of illumination. This occurs to an enormous magnitude, increasing light sensitivity by up to 100,000 times its sensitivity in normal daylight conditions. VAD affects vision by inhibiting the production of rhodopsin, the photopigment 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).

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.[12]

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 massive 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.[13] Intramuscular injections are poorly absorbed and are ineffective in delivering sufficient bioavailable vitamin A. Fortification of food with vitamin A is costly, but can be done in wheat, sugar, and milk.[14] Households may circumvent expensive fortified food by altering dietary habits. Consumption of yellow-orange fruits and vegetables rich in carotenoids, specifically beta-carotene, provides provitamin A precursors that can prevent VAD-related night blindness. However, the conversion of carotene to retinol varies from person to person and bioavailability of carotene in food varies.[15][16]

Infection

Along with poor diet, infection and disease are common in many developing communities.[1] Infection depletes vitamin A reserves which in turn make the affected individual more susceptible to further infection.[1] Increased incidence of xerophthalmia has been observed after an outbreak of measles, with mortality correlated with severity of eye disease.[1] In longitudinal studies of preschool children, susceptibility to disease increased substantially when severe VAD was present.[1] While VAD can make measles worse, Vitamin A supplements do not prevent measles, high doses may be dangerous, and vaccines remain the most effective was to prevent the disease.[17]

The reason for the increased infection rate in vitamin A deficient individuals is that killer T-cells require the retinol metabolite retinoic acid to proliferate correctly.[1] Retinoic acid is a ligand for nuclear retinoic acid receptors that bind the promoter regions of specific genes,[18] thus activating transcription and stimulating T cell replication.[1] Vitamin A deficiency will often entail deficient retinol intake, resulting in a reduced number of T-cells and lymphocytes, leading to an inadequate immune response and consequently a greater susceptibility to infections.[1] In the presence of dietary deficiency of vitamin A, VAD and infections reciprocally aggravate each other.[1]

Causes

In addition to dietary problems, other causes of VAD are known. Iron deficiency can affect vitamin A uptake. Other causes include conditions that affect intestinal absorption of vitamin A, including fibrosis, pancreatic insufficiency (including alcoholic pancreatitis), inflammatory bowel disease, and small-bowel bypass surgery.[19] These patients represent a majority of cases of vitamin A deficiency in economically developed nations, but not in developing nations.[20] Protein energy malnutrition is often seen in VAD. This is because suppressed synthesis of retinol binding protein (RBP) due to protein deficiency leads to reduced retinol uptake.[21]

In addition to its effects on the pancreas which can cause malabsorption, alcohol can cause a form of vitamin A deficiency localized to the human eye. Retinol requires retinol dehydrogenase to be converted to retinaldehyde; retinol dehydrogenase is the same enzyme as alcohol dehydrogenase. In people with chronic alcohol abuse, alcohol may compete with retinol for this enzyme, depriving the eye of the active form of retinol.[22]

Certain medications are known to decrease intestinal absorption of vitamin A and may cause or contribute to a deficiency. These medications include the antibiotic neomycin, bile acid sequestrants, and mineral oil.[22]

Diagnosis

Initial assessment may be made based on clinical signs of VAD.[22] The most common sign of VAD is night blindness, but VAD might also present with conjunctival xerosis, Bitot spots (foamy lesions), corneal xerosis, or corneal ulcerations.[23]

A VAD deficiency diagnosis is confirmed with laboratory findings. Several methods of assessing bodily vitamin A levels are available, with plasma retinol levels being the most common method of assessing VAD in individuals.[24] A plasma or serum retinol level below 0.70 μmol/L suggests subclinical vitamin A deficiency in both children and adults, while a level below 0.35 μmol/L indicates a severe deficiency of vitamin A.[24]

Other biochemical assessments include measuring serum retinol levels, serum zinc, plasma retinol ester levels, plasma and urinary retonioic acid levels, and vitamin A in breast milk.[22][24] While liver biopsies are regarded as the gold standard for assessing total body vitamin A, they are rarely used outside of research settings because of the risks associated with the procedure.[23] Additionally, conjunctival impression cytology can be used to assess the presence of xerophthalmia which is strongly correlated with VAD status (and can be used to monitor recovery progress).[22][25]

Vitamin A sources

This section is an excerpt from Vitamin A § Sources[ edit ]

Prevention and treatment

Treatment of VAD can be undertaken with both oral vitamin A and injectable forms, generally as vitamin A palmitate.

  • High dose vitamin A supplementation has been proven to be an effective and cost effective treatment.[26] Current World Health Organization guidance recommends biannual vitamin A supplementation for children aged 6 to 59 months in areas with high levels of retinol deficiency.[27] Children aged 6-12 months should receive a dose of 100,000 IU and children aged 1-5 years should receive a dose of 200,000 IU each time.[26] This significantly reduces the risk of morbidity, especially from severe diarrhea, and reduces mortality from measles and all-cause mortality.[26] Vitamin A supplementation of children under five who are at risk of VAD has been found to reduce all‐cause mortality by 12 to 24%.[26]
  • Side effects of vitamin A supplements are rare. Vitamin A toxicity is a rare concern associated with high levels of vitamin A over prolonged periods of time. Symptoms may include nausea, vomiting, headache, dizziness, irritability, blurred vision, and a lack of muscle coordination.[28] However, when administered in the correct dose, vitamin A is generally safe and effective.[26]
  • The World Health Organization also recommends vitamin A supplementation during pregnancy and lactation in areas where VAD is prevalent.[29] Maternal high supplementation benefits both mother and breast-fed infant: high-dose vitamin A supplementation of the lactating mother in the first month postpartum can provide the breast-fed infant with an appropriate amount of vitamin A through breast milk.[29] It also reduces the risk of infection, night blindness, and anemia in the mother.[29] However, vitamin A supplementation in developed countries and high-dose supplementation of pregnant women should be avoided because it can cause miscarriage and birth defects.[30]

Although synthetic vitamin A supplementation is a useful and effective treatment for VAD, a 2017 review (updated in 2022) reported that synthetic vitamin A supplementation may not be the best long‐term solution for vitamin A deficiency, but rather food fortification, improved food distribution programs, and crop improvement, such as for fortified rice or vitamin A-rich sweet potato, may be more effective in eradicating vitamin A deficiency.[31]

  • Food fortification is also useful for improving VAD. A variety of oily and dry forms of the retinol esters, retinyl acetates, and retinyl palmitate are available for food fortification of vitamin A. Margarine and oil are the ideal food vehicles for vitamin A fortification. They protect vitamin A from oxidation during storage and prompt absorption of vitamin A. Beta-carotene and retinyl acetate or retinyl palmitate are used as a form of vitamin A for vitamin A fortification of fat-based foods. Fortification of sugar with retinyl palmitate as a form of vitamin A has been used extensively throughout Central America. Cereal flours, milk powder, and liquid milk are also used as food vehicles for vitamin A fortification.[32][33]
  • In addition to adding synthetic vitamin A to foods, researchers have explored fortifying foods such as rice and corn through genetic engineering.
    • Research on rice began in 1982, and the first field trials of golden rice cultivars were conducted in 2004.[34][35] The result was "Golden Rice", a variety of Oryza sativa rice produced through genetic engineering to biosynthesize beta-carotene, a precursor of retinol, in the edible parts of rice.[36][37] In May 2018, regulatory agencies in the United States, Canada, Australia and New Zealand concluded that Golden Rice met food safety standards.[38] On 21 July 2021, the Philippines became the first country to officially issue the biosafety permit for commercially propagating Golden Rice.[39][40] In 2023, however, the Supreme Court of the Philippines ordered the agriculture department to stop commercial propagation of golden rice in relation to a petition filed by MASIPAG (a group of farmers and scientists), who claimed that golden rice poses risk to the health of consumers and to the environment.[41]
    • Researchers at the U.S. Agricultural Research Service have been able to identify genetic sequences in corn that are associated with higher levels of beta-carotene, the precursor to vitamin A. They found that breeders can cross certain variations of corn to produce a crop with an 18-fold increase in beta-carotene.[42]
  • Dietary diversification can also reduce risk of VAD. Non-animal sources of vitamin A like fruits and vegetables contain pro-vitamin A and account for greater than 80% of intake for most individuals in the developing world. The increase in consumption of vitamin A-rich foods of animal origin such as liver, milk, cheese, or eggs, also has beneficial effects on VAD.[43]

Public health initiatives

Some countries where VAD is a public-health problem address its elimination by including vitamin A supplements available in capsule form with national immunization days (NIDs) for polio eradication or measles. When the correct dosage is given, vitamin A is safe and has no negative effect on seroconversion rates for oral polio or measles vaccines.[44] Additionally, the delivery of vitamin A supplements, during integrated child health events such as child health days, has helped ensure high coverage of vitamin A supplementation in a large number of least developed countries. Child health events enable many countries in West and Central Africa to achieve over 80% coverage of vitamin A supplementation.[45] According to UNICEF data, in 2013 worldwide, 65% of children between the ages of 6 and 59 months were fully protected with two high-dose vitamin A supplements.Since NIDs provide only one dose per year, NIDs-linked vitamin A distribution must be complemented by other programs to maintain vitamin A in children.[46][47]

Global efforts to support national governments in addressing VAD are led by the Global Alliance for Vitamin A (GAVA), which is an informal partnership between Nutrition International, Helen Keller International, UNICEF, WHO, and CDC. About 75% of the vitamin A required for supplementation of preschool-aged children in low- and middle-income countries is supplied through a partnership between Nutrition International and UNICEF, with support from Global Affairs Canada.[2] An estimated 1.25 million deaths due to vitamin A deficiency have been averted in 40 countries since 1998.[2]

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 "Vitamin A". Micronutrient Information Center, Linus Pauling Institute, Oregon State University, Corvallis. January 2015. http://lpi.oregonstate.edu/mic/vitamins/vitamin-A. 
  2. ↑ 2.0 2.1 2.2 "Micronutrient Deficiencies: Vitamin A". World Health Organization. https://www.who.int/nutrition/topics/vad/en/index.html. 
  3. ↑ "Goal 2 | Department of Economic and Social Affairs". https://sdgs.un.org/goals/goal2#targets_and_indicators. 
  4. ↑ "WHO Vitamin A deficiency | Micronutrient deficiencies". https://www.who.int/nutrition/topics/vad/en/. 
  5. ↑ Latham, Michael E. (1997). Human Nutrition in the Developing World (Fao Food and Nutrition Paper). Food & Agriculture Organization of the United. ISBN 92-5-103818-X. 
  6. ↑ 6.0 6.1 Sommer, Alfred (1995). Vitamin a Deficiency and Its Consequences: A Field Guide to Detection and Control. Geneva: World Health Organization. ISBN 92-4-154478-3. 
  7. ↑ "A world fit for children". http://www.unicef.org/worldfitforchildren/files/A-RES-S27-2E.pdf. 
  8. ↑ 8.0 8.1 8.2 "Vitamin A Deficiency in Children" (in en-US). https://data.unicef.org/topic/nutrition/vitamin-a-deficiency/#_ftn1. 
  9. ↑ Black RE et al., Maternal and child undernutrition: global and regional exposures and health consequences, The Lancet, 2008, 371(9608), p. 253.
  10. ↑ "Childhood blindness due to VAD in India: regional variations". Archives of Disease in Childhood 72 (4): 330–33. 1995. doi:10.1136/adc.72.4.330. PMID 7763066. 
  11. ↑ "Untitled Document". http://www.paramountbooks.com.pk/LoginIndex.asp?title=Concise-Ophthalmology-(pb)-2014&Isbn=9789696370017&opt=3&sUBcAT=06. 
  12. ↑ Underwood, Barbara A. Vitamin A Deficiency Disorders: International Efforts to Control A Preventable "Pox." J. Nutr. 134: 231S–236S, 2004.
  13. ↑ "Oral versus intramuscular vitamin A in the treatment of xerophthalmia". Lancet 1 (8168 Pt 1): 557–559. 1980b. doi:10.1016/S0140-6736(80)91053-3. PMID 6102284. 
  14. ↑ "The effect of vitamin A fortification of sugar on the serum vitamin A levels of preschool Guatemalan children: a longitudinal evaluation". J. Nutr. 34 (1): 41–49. 1981. doi:10.1093/ajcn/34.1.41. PMID 7446457. 
  15. ↑ "Recent knowledge about intestinal absorption and cleavage of carotenoids" (in fr). Annales de Biologie Clinique 63 (2): 165–177. 2005. PMID 15771974. 
  16. ↑ "Spinach or carrots can supply significant amounts of vitamin A as assessed by feeding with intrinsically deuterated vegetables". The American Journal of Clinical Nutrition 82 (4): 821–828. 2005. doi:10.1093/ajcn/82.4.821. PMID 16210712. 
  17. ↑ "3 things parents need to know-about measles and vitamin A". National Federation for Infectious Diseases. April 30, 2020. https://www.nfid.org/resource/3-things-parents-need-to-know-about-measles-and-vitamin-a/. 
  18. ↑ Cunningham, T.J.; Duester, G. (2015). "Mechanisms of retinoic acid signalling and its roles in organ and limb development". Nat. Rev. Mol. Cell Biol. 16 (2): 110–123. doi:10.1038/nrm3932. PMID 25560970. 
  19. ↑ "Vitamin A Deficiency Clinical Presentation: History, Physical, Causes". http://emedicine.medscape.com/article/126004-clinical#b5. 
  20. ↑ Suter, Paolo M. (2022). "Chapter 333: Vitamin and Trace Mineral Deficiency and Excess". Harrison's principles of internal medicine (21st ed.). New York: McGraw Hill. ISBN 978-1-264-26850-4. 
  21. ↑ (Combs, 1991).
  22. ↑ 22.0 22.1 22.2 22.3 22.4 Bates, C J (1 January 1999). "Diagnosis and detection of vitamin deficiencies" (in en). British Medical Bulletin 55 (3): 643–657. doi:10.1258/0007142991902529. ISSN 0007-1420. PMID 10746353. 
  23. ↑ 23.0 23.1 "Xerophthalmia - EyeWiki" (in en). https://eyewiki.org/w/index.php?title=Xerophthalmia&oldid=109090. 
  24. ↑ 24.0 24.1 24.2 "Vitamin A deficiency" (in en). https://www.who.int/data/nutrition/nlis/info/vitamin-a-deficiency. 
  25. ↑ "Diagnosis and Treatment of Vitamin A Deficiency: Workup". https://www.medscape.org/viewarticle/724972_4. 
  26. ↑ 26.0 26.1 26.2 26.3 26.4 Imdad, Aamer; Mayo-Wilson, Evan; Herzer, Kurt; Bhutta, Zulfiqar A (2017-03-10). Cochrane Developmental, Psychosocial and Learning Problems Group. ed. "Vitamin A supplementation for preventing morbidity and mortality in children from six months to five years of age" (in en). Cochrane Database of Systematic Reviews 2017 (11). doi:10.1002/14651858.CD008524.pub3. PMID 28282701. 
  27. ↑ Patil, Shraddha; Zamwar, Udit M; Mudey, Abhay (2023-11-18). "Etiology, Epidemiology, Pathophysiology, Signs and Symptoms, Evaluation, and Treatment of Vitamin A (Retinol) Deficiency" (in en). Cureus 15 (11). doi:10.7759/cureus.49011. ISSN 2168-8184. PMID 38111435. 
  28. ↑ Olson, Jazmine M.; Ameer, Muhammad Atif; Goyal, Amandeep (2024), "Vitamin A Toxicity", StatPearls (Treasure Island (FL): StatPearls Publishing), PMID 30422511, https://www.ncbi.nlm.nih.gov/books/NBK532916/, retrieved 2024-12-16 
  29. ↑ 29.0 29.1 29.2 McCauley, Mary E; van den Broek, Nynke; Dou, Lixia; Othman, Mohammad (2015-10-27). Cochrane Pregnancy and Childbirth Group. ed. "Vitamin A supplementation during pregnancy for maternal and newborn outcomes" (in en). Cochrane Database of Systematic Reviews 2016 (3). doi:10.1002/14651858.CD008666.pub3. PMID 26503498. 
  30. ↑ "High dose vitamin A supplementation of breast-feeding Indonesian mothers: effects on the vitamin A status of mother and infant". J. Nutr. 123 (4): 666–675. 1993. doi:10.1093/jn/123.4.666. PMID 8463867. 
  31. ↑ Imdad, Aamer; Mayo-Wilson, Evan; Haykal, Maya R.; Regan, Allison; Sidhu, Jasleen; Smith, Abigail; Bhutta, Zulfiqar A. (16 March 2022). "Vitamin A supplementation for preventing morbidity and mortality in children from six months to five years of age". The Cochrane Database of Systematic Reviews 2022 (3). doi:10.1002/14651858.CD008524.pub4. ISSN 1469-493X. PMID 35294044. 
  32. ↑ Guidelines on Food Fortification With Micronutrients. Geneva: World Health Organization. 2006. ISBN 92-4-159401-2. 
  33. ↑ Food and Agriculture Organization of the United Nations (1996). Food Fortification: Tech & Quality Control (Food & Nutrition Papers). Bernan Assoc. ISBN 92-5-103884-8. 
  34. ↑ FAQ: Who invented Golden Rice and how did the project start? Goldenrice.org.
  35. ↑ LSU AgCenter Communications (2004). "'Golden Rice' Could Help Reduce Malnutrition". http://www.lsuagcenter.com/news_archive/2004/October/Headline+News/Golden+Rice+Could+Help+Malnutrition.htm. 
  36. ↑ "From disagreements to dialogue: unpacking the Golden Rice debate". Sustain Sci 13 (5): 1469–82. 2018. doi:10.1007/s11625-018-0577-y. PMID 30220919. Bibcode: 2018SuSc...13.1469K. 
  37. ↑ "Engineering the provitamin A (beta-carotene) biosynthetic pathway into (carotenoid-free) rice endosperm". Science 287 (5451): 303–5. January 2000. doi:10.1126/science.287.5451.303. PMID 10634784. Bibcode: 2000Sci...287..303Y. 
  38. ↑ "Golden Rice meets food safety standards in three global leading regulatory agencies" (in en-gb). International Rice Research Institute – IRRI. http://irri.org/news/media-releases/golden-rice-meets-food-safety-standards-in-three-global-leading-regulatory-agencies. 
  39. ↑ "Philippines OKs GMO 'golden rice'". https://www.philstar.com/headlines/2021/07/24/2114742/philippines-oks-gmo-golden-rice. 
  40. ↑ "Filipinos soon to plant and eat Golden Rice" (in en-US). 23 July 2021. https://www.philrice.gov.ph/filipinos-soon-to-plant-and-eat-golden-rice/. 
  41. ↑ Ordoñez, John Victor D. (20 April 2023). "SC issues Writ of Kalikasan vs Golden Rice, Bt eggplant - BusinessWorld Online". https://www.bworldonline.com/top-stories/2023/04/20/517938/sc-issues-writ-of-kalikasan-vs-golden-rice-bt-eggplant/. 
  42. ↑ "A New Approach that Saves Eyesight and Lives in the Developing World". USDA Agricultural Research Service. May 2010. https://www.ars.usda.gov/news-events/news/research-news/2010/a-new-approach-that-saves-eyesight-and-lives-in-the-developing-world/. 
  43. ↑ "childinfo.org: Vitamin A Deficiency". http://www.childinfo.org/areas/vitamina/. 
  44. ↑ Rahman, Mohammad M.; Alvarez, Jose O.; Mahalanabis, Dilip; Wahed, Mohammad A.; Islam, Mohammad A.; Unicomb, Leanne; Habte, Demissie; Fuchs, George J (1998-07-01). "Effect of vitamin A administration on response to oral polio vaccination". Nutrition Research 18 (7): 1125–1133. doi:10.1016/S0271-5317(98)00094-3. ISSN 0271-5317. https://linkinghub.elsevier.com/retrieve/pii/S0271531798000943. 
  45. ↑ "Vitamin A Deficiency and Supplementation UNICEF Data". http://data.unicef.org/nutrition/vitamin-a.html. 
  46. ↑ "Distribution of vitamin A during national immunization days". https://www.who.int/vaccines-documents/DocsPDF/www9836.pdf. 
  47. ↑ "WHO Vitamin A supplementation". https://www.who.int/vaccines/en/vitamina.shtml. 

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