Vitamin a deficiency HYPERVITAMINOSIS A


Published on

Vitamin A deficiency (VAD) is a major nutritional concern in poor societies, especially in lower income countries like INDIA.
Vitamin A is an essential nutrient needed in small amounts for the normal functioning of the visual system, and maintenance of cell function for growth, epithelial integrity, red blood cell production, immunity and reproduction.

Published in: Health & Medicine
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Vitamin a deficiency HYPERVITAMINOSIS A

  2. 2. Introduction Vitamin A deficiency (VAD) is a majornutritional concern in poor societies,especially in lower income countries likeINDIA. Vitamin A is an essential nutrient needed insmall amounts for the normal functioning ofthe visual system, and maintenance of cellfunction for growth, epithelial integrity, redblood cell production, immunity
  3. 3.  Active forms are retinol, retinaldehyde, and retinoicacid Plants synthesize the more complex carotenoidswhich are cleaved to retinol by most animals andstored in the liver as retinyl palmitate N retinol plasma values: 15-30 mcg/dl in infants &30-90 mcg/dl in adults Retinal is the prosthetic group of photosensitivepigment in both rods (rhodopsin) & cones(iodopsin), major difference lies in the nature ofprotein bound Needed in lysosomal membrane stability Plays a role in keratinization, cornification, bonedevelopment & cell growth &
  4. 4. Absorption of Vitamin A Retinoids Retinyl esters broken down to free retinol in smallintestine - requires bile, digestive enzymes,integration into micelles Once absorbed, retinyl esters reformed in intestinalcells 90% of retinoids can be absorbed Carotenoids Absorbed intact, absorption rate much lower Intestinal cells can convert carotenoids to
  5. 5. Transport and Storage ofVitamin A Liver stores 90% of vitamin A in the body Reserve is adequate for several months Transported via chylomicrons from intestinalcells to the liver Transported from the liver to target tissue asretinol via retinol-binding protein, which isbound to
  6. 6. Excretion of Vitamin A Not readily excreted Some lost in urine Kidney disease and aging increase risk oftoxicity because excretion is
  7. 7. Functions of vitamin A Vision (night, day, colour) Epithelial cell integrity against infections Immune response Haematopoiesis Skeletal growth Fertility (male and female)
  8. 8. Functions of Vitamin A:Growth and Differentiation ofCells• Retinoic acid is necessary for cellulardifferentiation• Important for embryo development, geneexpression• Retinoic acid influences production,structure, and function of epithelial cells thatline the outside (skin) and external passages(mucus forming cells) within the
  9. 9. Functions of Vitamin A:Immunity Deficiency leads to decreased resistance toinfections Supplementation may decrease severity ofinfections in deficient
  10. 10. The Visual
  11. 11.  Prevention of cardiovascular disease Antioxidant capabilities ≥5 servings/day of fruits and vegetables Cancer prevention Antioxidant capabilities Lung, oral, and prostate cancers Studies indicate that vitamin A-containing foods are moreprotective than supplements Age-related macular degeneration Cataracts Acne
  12. 12. Source of vitamin A Colostrum foods containing either preformed vitamin Aesters- liver, milk,cheese,eggs or food productsfortified with vitamin Aor carotenoid precursors (mainly beta-carotene), such as green leaves, carrots, ripemangoes,eggs, and other orange-yellowvegetables and
  13. 13. Source of vitamin A fruit carotenoidsources(micrograms/100gm) Mango (golden) 307 Papaya (solo) 124 Cucurbita (mature pulp) 862 Buriti palm (pulp) 3,000 Red palm oil 30,000 Carrot 2,000 Dark green leafy vegetables685 Tomato 100 Apricot 250 Sweet potato, red and yellow670 Animal (micrograms/100gm) Fatty fish liver oils Halibut 900,000 Cod 18,000 Shark 180,000Dairy produce Butter 830 Margarine, vitaminized 900 Eggs 140 Milk 40 Cheese, fatty type 320 Liver of sheep and ox 15,000 Beef, mutton, pork 0–
  14. 14. Vitamin A requirement
  15. 15. Units of measuring vitamin A Each μg RAE corresponds to 1 μg retinol, 2 μg of β-carotene in oil, 12 μg of "dietary" beta-carotene, One International Unit (I.U.) = 0.3 mcg. of retinol = 0.6 mcg. of beta-carotene = 1.2 mcg. of other total mixed
  16. 16. Prevalence of vitamin Adeficiency in South Asia (%) Country sub clinical clinicalVAD (%) VAD (%) Afghanistan 53 - Bangladesh 28 0.7 Bhutan 32 0.7 INDIA 57 0.7 Nepal 33 1 Pakistan
  17. 17. High risk group Infancy Childhood Pregnancy Lactation Urban poor Older adults Alcoholism Liver disease (limits storage) Fat malabsorption Increased excretion as in cancer & UTI Low protein intake resulting in deficient
  18. 18.  Usually,VAD develops in an environment ofecological social and economical deprivation Synergism between deficient dietary intake ofvitamin A coexists with severe infections, such asmeasles, and frequent infections causingdiarrhoea and respiratory diseases that can lowerintake through depressed appetite andabsorption, and deplete body stores of vitamin Athrough excessive metabolism and
  19. 19. Health consequences Xerophthalmia is the most specificVADD,andis the leading preventable cause of blindnessin children throughout the world Night blindness Anaemia can result fromVAD in children andwomen,likely due to multiple apparent rolesof vitamin A in supporting iron mobilizationand transport, and
  20. 20. VITAMIN A
  21. 21. Assessing vitamin A status anddeficiency Two sets of indicators ofVAD are commonlyused for population surveys:1 clinically assessed eye signs.Term xerophthalmiaencompasses the clinical spectrum of ocularmanifestations ofVAD, from milder stages ofnight blindness and Bitot’s spots, to potentiallyblinding stages of corneal xerosis, ulceration andnecrosis (keratomalacia)2 biochemically determined concentrations ofretinol in plasma or
  22. 22. Classification of xerophthalmia XNN ight blindness X1A Conjunctival xerosis X1BB itot’s spot X2 Corneal xerosis X3A Corneal ulceration/keratomalacia (< 1/3corneal surface) X3BCorneal ulceration/keratomalacia (≥ 1/3corneal surface) XSCorneal scar XFXerophthalmic
  23. 23. Serum retinol concentrations serum retinol concentrations in a populationconstitutes the second major approach toassessing vitamin A status in a population, with values below acut-off of 0.70 μmol/l representing VAD , andbelow 0.35 μmol/l representing severeVAD. a serum retinol concentration below a cutoffof 1.05 μmol/l has been proposed to reflectlow
  24. 24. Criteria for assessing thepublichealth significance ofxerophthalmiaClinical (primary) Night blindness (XN)* 1.0% Bitot’s spot (X1B) 0.5% Corneal xerosis and/or ulceration/keratomalacia(X2 + X3A + X3B) 0.01% Xerophthalmia-related corneal scars (XS) 0.05%Biochemical (supportive) Serum retinol (vitaminA) < 0.35 μmol/L (10μg/dL)
  25. 25. Universal vitamin A distributionschedule for preschool andlactating mothers Children 1–6 years200,000 IU of vitaminA orally every 3–6 months. Infants 6–11 months100,000 IU of vitaminA orally every 3–6 months. Lactating mothers200,000 IU of vitaminA orally once: at delivery orduring the first 8 weeks postpartum ifbreastfeeding or during the first 6 weeks if
  26. 26. Recommended xerophthalmiatreatment schedule6 -12 months > 1 yr Immediately 100,000 IU 200,000 IU Next day 100,000 IU 200,000 lU 2–4 weeks later 100,000 IU 200,000 IU Severe Protein-Energy Malnutrition (PEM)Monthly until PEM resolves100,000 IU 200,000
  27. 27. Upper Level for Vitamin A 3000 μg retinol Hypervitaminosis A results from long-termsupplement use (2 – 4 x RDA) Toxicity Fatal dose (12 g)
  28. 28. HypervitaminosisAAcute Intoxication: Results when excessively large single doses>300,000 IU ingested Infants: n/v, drowsiness or irritability w/signsof increased ICP Adults: drowsiness, irritability, headache &vomiting Serum vitamin A values = 200-1000 IU/dl (N:50-100 IU/dl)
  29. 29. Toxicity of Vitamin A Acute – short-term megadose (100 xRDA); symptoms disappear when intakestops GI effects Headaches Blurred vision Poor muscle
  30. 30. ChronicIntoxication Results when >50,000 IU/day ingested for several wksor more Signs & symptoms in infants: Early are anorexia, pruritus, irritability, tenderswollen bones w/motion limitation Alopecia, seborrhea, cheilosis & peeling of palms &soles Hepatomegaly & hypercalcemia observed Craniotabes & hyperostosis of long bones Elevated serum vit A levels confirms diagnosis Reversible manifestations when vitamin A
  31. 31. Chronic Toxicity of Vitamin A long-term megadose; possible permanentdamage Bone and muscle pain Loss of appetite Skin disorders Headache Dry skin Hair loss Increased liver size
  32. 32. Toxicity of Vitamin A Teratogenic (may occur with as little as 3 xRDA of preformed vitamin A) Tends to produce physical defect on developingfetus as a result of excess vitamin A intake Spontaneous abortion Birth
  33. 33.