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Introduction
• 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.
VITAMIN A
• Exits in 3 forms:
• all trans-retinol
• long chain fatty acyl ester of retinol (main
storage form)
• retinal (the active form in the retina)
• Retinoic acid is also considered to be
physiologically active
• Pro vitamin A or carotene can be
converted to retinol in vivo
Sources
Absorption
• Retinoids
• Retinyl esters broken down to free retinol in small
intestine - requires bile, digestive
enzymes, integration into micelles
• Once absorbed, retinyl esters reformed in
intestinal cells
• 90% of retinoids can be absorbed
• Carotenoids
• Absorbed intact, absorption rate much lower
• Intestinal cells can convert carotenoids to retinoids
• Approximately 80% is absorbed.
• It is passed along with fat through the
lymphatic system into blood stream.
• Absorption is poor in case of
diarrhea, jaundice and abdominal
disorder.
• Absorption increases if taken with fat.
• Vitamin A which is not absorbed is
excreted within 1 or 2 days in feces .
Transport
• Transported via chylomicrons from
intestinal cells to the liver
• Transported from the liver to target
tissue as retinol via retinol-binding
protein, which is bound to transthyretin
STORAGE
• The liver has enormous capacity to
store in the form of retinolpalmitate.
• under normal conditions a well-fed
person has sufficient Vitamin A
reserves to meet his need for 6 to
9months or more.
Excretion of Vitamin A
• Not readily excreted
• Some lost in urine
• Kidney disease and aging increase risk
of toxicity because excretion is impaired
Functions of vitamin A
• Vision (night, day, colour)
• Epithelial cell integrity against
infections
• Immune response
• Haematopoiesis
• Skeletal growth
• Fertility (male and female)
• Embryogenesis
Functions of Vitamin A:
Growth and Differentiation of
Cells
• Retinoic acid is necessary for cellular
differentiation
• Important for embryo
development, gene expression
• Retinoic acid influences
production, structure, and function of
epithelial cells that line the outside
(skin) and external passages (mucus
forming cells) within the body
Functions of Vitamin A:
Immunity
• Deficiency leads to decreased resistance
to infections
• Supplementation may decrease severity
of infections in deficient person
Functions of Vitamin A:
Vision
• Retinal is a necessary structural
component of rhodopsin or visual
purple, the light sensitive pigment
within rod and cone cells of the retina.
• If inadequate quantities of vitamin A
are present, vision is impaired.
Vision Cycle
The Visual Cycle
drpankajyadav05@gmail.com
• Role in Prevention of cardiovascular disease
• Antioxidant capabilities
• ≥5 servings/day of fruits and vegetables
• Role in Cancer prevention
• Antioxidant capabilities
• Lung, oral, and prostate cancers
• Studies indicate that vitamin A-containing foods are
more protective than supplements
• Other Roles in
• Age-related macular degeneration
• Cataracts
• Acne
• AML
Recommended daily allowances
(RDAs) for Vitamin A
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 carotenoids
Deficiency of Vitamin A
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 carriers
• Usually, Vitamin A Deficiency (VAD)
develops in an environment of ecological
social and economical deprivation
• Synergism between deficient dietary intake of
vitamin A coexists with severe
infections, such as measles, and frequent
infections causing diarrhoea and respiratory
diseases that can lower intake through
depressed appetite and absorption, and
deplete body stores of vitamin A through
excessive metabolism and excretion
Health consequences
• Xerophthalmia is the most specific
VAD, and is the leading preventable cause
of blindness in children throughout the
world
• Night blindness
• Anaemia can result from VAD in children
and women, likely due to multiple
apparent roles of vitamin A in supporting
iron mobilization and transport, and
hematopoiesis
Classification of xerophthalmia
• XN Night blindness
• X1A Conjunctival Xerosis
• X1B Bitot’s spot
• X2 Corneal Xerosis
• X3A Corneal
ulceration/keratomalacia (< 1/3
corneal surface)
• X3B Corneal
ulceration/keratomalacia (≥ 1/3
corneal surface)
• XS Corneal scar
• XF Xerophthalmic fundus
Night Blindness
• Lack of vitamin A causes
night blindness or inability to
see in dim light.
• night blindness occurs as a
result of inadequate pigment
in the retina.
• It also called tunnel vision.
• Night blindness is also found
in pregnant women in some
instances, especially during
the last trimester of
pregnancy when the vitamin
A needs are increased.
Night blindness
Bitot’s Spot
• These are foamy and
whitish cheese-like tissue
spots that develop
around the eye
ball, causing severe
dryness in the eyes.
• These spots do not affect
eye sight in the day light.
Conjunctival Xerosis
• Conjunctiva becomes
dry and non wettable.
• Instead of looking
smooth shiny it
appears muddy
&wrinkled.
Keratomalacia
• One of the major cause
for blindness in India.
• Cornea becomes soft
and may burst
• The process is rapid
• If the eye collapses
vision is lost.
Other Symptoms of VAD
• Alteration of skin and mucous membrane
• Hepatic dysfunction
• Headache
• Drowsiness
• Peeling of skin about the mouth and
elsewhere
Follicular hyperkeratosis
Assessing vitamin A status and
deficiency
• Two sets of indicators of VAD are commonly
used for population surveys:
1. clinically assessed eye signs.
Term xerophthalmia encompasses the
clinical spectrum of ocular manifestations of
VAD, from milder stages of night blindness
and Bitot’s spots, to potentially blinding
stages of corneal xerosis, ulceration and
necrosis (keratomalacia)
1. biochemically determined concentrations of
retinol in plasma or serum
Serum retinol concentrations
• Serum retinol concentrations in a
population constitutes the second major
approach to assessing vitamin
• A status in a population, with values
below a cut-off of 0.70 μmol/l representing
VAD , and below 0.35 μmol/l representing
severe VAD.
• A serum retinol concentration below a
cutoff of 1.05 μmol/l has been proposed to
reflect low vitamin.
Criteria for assessing the public
health significance of
Clinical (primXaeryr)ophthalmia
• 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 (10
μg/dL) 5.0%
Universal vitamin A distribution
schedule for preschool and
lactating mothers
• Children 1–6 years
200,000 IU of vitamin A orally every 3–6 months.
• Infants 6–11 months
100,000 IU of vitamin A orally every 3–6 months.
• Lactating mothers
200,000IU of vitamin A orally once at delivery or
during the first 8weeks postpartum if
breastfeeding or during the first 6 weeks if not
breast-feeding
Recommended Xerophthalmia
treatment schedule
6 -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 resolves
100,000 IU 200,000 IU
drpankajyadav05@gmail.com
Upper Level for Vitamin A
• 3000 μg retinol
• Hypervitaminosis A results from long-
term supplement use (2 –4 x RDA)
• Toxicity
• Fatal dose (12 g)
drpankajyadav05@gmail.com
Hypervitaminosis A
Acute Intoxication:
• Results when excessively large single
doses >300,000 IU ingested
• Infants: n/v, drowsiness or irritability
w/signs of increased ICP
• Adults:
drowsiness, irritability, headache &
vomiting
• Serum vitamin A values = 200-1000
IU/dl (N: 50
dr-
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Toxicity of Vitamin A
Acute toxicity
short-term megadose (100x RDA);
symptoms disappear when intake
stops
• GI effects
• Headaches
• Blurred vision
• Poor muscle coordination
drpankajyadav05@gmail.com
Chronic Intoxication
• Results when >50,000 IU/day ingested for several
wks or more
• Signs & symptoms in infants:
• Early are anorexia, pruritus, irritability, tender
swollen 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
discontinued
drpankajyadav05@gmail.com
Chronic Toxicity of Vitamin A
• long-term megadose; possible
permanent damage
• Bone and muscle pain
• Loss of appetite
• Skin disorders
• Headache
• Dry skin
• Hair loss
• Increased liver size
• Vomiting
drpankajyadav05@gmail.com
Toxicity of Vitamin A
• Teratogenic (may occur with as little as
3 x RDA of preformed vitamin A)
• Tends to produce physical defect on
developing fetus as a result of excess
vitamin A intake
• Spontaneous abortion
• Birth defects
drpankajyadav05@gmail.com
Thanking You

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Vitamin A presentation -.pptx

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  • 2. Introduction • 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.
  • 3. VITAMIN A • Exits in 3 forms: • all trans-retinol • long chain fatty acyl ester of retinol (main storage form) • retinal (the active form in the retina) • Retinoic acid is also considered to be physiologically active • Pro vitamin A or carotene can be converted to retinol in vivo
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  • 6. Absorption • Retinoids • Retinyl esters broken down to free retinol in small intestine - requires bile, digestive enzymes, integration into micelles • Once absorbed, retinyl esters reformed in intestinal cells • 90% of retinoids can be absorbed • Carotenoids • Absorbed intact, absorption rate much lower • Intestinal cells can convert carotenoids to retinoids
  • 7. • Approximately 80% is absorbed. • It is passed along with fat through the lymphatic system into blood stream. • Absorption is poor in case of diarrhea, jaundice and abdominal disorder. • Absorption increases if taken with fat. • Vitamin A which is not absorbed is excreted within 1 or 2 days in feces .
  • 8. Transport • Transported via chylomicrons from intestinal cells to the liver • Transported from the liver to target tissue as retinol via retinol-binding protein, which is bound to transthyretin
  • 9. STORAGE • The liver has enormous capacity to store in the form of retinolpalmitate. • under normal conditions a well-fed person has sufficient Vitamin A reserves to meet his need for 6 to 9months or more.
  • 10. Excretion of Vitamin A • Not readily excreted • Some lost in urine • Kidney disease and aging increase risk of toxicity because excretion is impaired
  • 11. Functions of vitamin A • Vision (night, day, colour) • Epithelial cell integrity against infections • Immune response • Haematopoiesis • Skeletal growth • Fertility (male and female) • Embryogenesis
  • 12. Functions of Vitamin A: Growth and Differentiation of Cells • Retinoic acid is necessary for cellular differentiation • Important for embryo development, gene expression • Retinoic acid influences production, structure, and function of epithelial cells that line the outside (skin) and external passages (mucus forming cells) within the body
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  • 15. Functions of Vitamin A: Immunity • Deficiency leads to decreased resistance to infections • Supplementation may decrease severity of infections in deficient person
  • 16. Functions of Vitamin A: Vision • Retinal is a necessary structural component of rhodopsin or visual purple, the light sensitive pigment within rod and cone cells of the retina. • If inadequate quantities of vitamin A are present, vision is impaired.
  • 19. • Role in Prevention of cardiovascular disease • Antioxidant capabilities • ≥5 servings/day of fruits and vegetables • Role in Cancer prevention • Antioxidant capabilities • Lung, oral, and prostate cancers • Studies indicate that vitamin A-containing foods are more protective than supplements • Other Roles in • Age-related macular degeneration • Cataracts • Acne • AML
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  • 22. 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 carotenoids
  • 24. 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 carriers
  • 25. • Usually, Vitamin A Deficiency (VAD) develops in an environment of ecological social and economical deprivation • Synergism between deficient dietary intake of vitamin A coexists with severe infections, such as measles, and frequent infections causing diarrhoea and respiratory diseases that can lower intake through depressed appetite and absorption, and deplete body stores of vitamin A through excessive metabolism and excretion
  • 26. Health consequences • Xerophthalmia is the most specific VAD, and is the leading preventable cause of blindness in children throughout the world • Night blindness • Anaemia can result from VAD in children and women, likely due to multiple apparent roles of vitamin A in supporting iron mobilization and transport, and hematopoiesis
  • 27. Classification of xerophthalmia • XN Night blindness • X1A Conjunctival Xerosis • X1B Bitot’s spot • X2 Corneal Xerosis • X3A Corneal ulceration/keratomalacia (< 1/3 corneal surface) • X3B Corneal ulceration/keratomalacia (≥ 1/3 corneal surface) • XS Corneal scar • XF Xerophthalmic fundus
  • 28. Night Blindness • Lack of vitamin A causes night blindness or inability to see in dim light. • night blindness occurs as a result of inadequate pigment in the retina. • It also called tunnel vision. • Night blindness is also found in pregnant women in some instances, especially during the last trimester of pregnancy when the vitamin A needs are increased.
  • 30. Bitot’s Spot • These are foamy and whitish cheese-like tissue spots that develop around the eye ball, causing severe dryness in the eyes. • These spots do not affect eye sight in the day light.
  • 31. Conjunctival Xerosis • Conjunctiva becomes dry and non wettable. • Instead of looking smooth shiny it appears muddy &wrinkled.
  • 32. Keratomalacia • One of the major cause for blindness in India. • Cornea becomes soft and may burst • The process is rapid • If the eye collapses vision is lost.
  • 33. Other Symptoms of VAD • Alteration of skin and mucous membrane • Hepatic dysfunction • Headache • Drowsiness • Peeling of skin about the mouth and elsewhere
  • 35. Assessing vitamin A status and deficiency • Two sets of indicators of VAD are commonly used for population surveys: 1. clinically assessed eye signs. Term xerophthalmia encompasses the clinical spectrum of ocular manifestations of VAD, from milder stages of night blindness and Bitot’s spots, to potentially blinding stages of corneal xerosis, ulceration and necrosis (keratomalacia) 1. biochemically determined concentrations of retinol in plasma or serum
  • 36. Serum retinol concentrations • Serum retinol concentrations in a population constitutes the second major approach to assessing vitamin • A status in a population, with values below a cut-off of 0.70 μmol/l representing VAD , and below 0.35 μmol/l representing severe VAD. • A serum retinol concentration below a cutoff of 1.05 μmol/l has been proposed to reflect low vitamin.
  • 37. Criteria for assessing the public health significance of Clinical (primXaeryr)ophthalmia • 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 (10 μg/dL) 5.0%
  • 38. Universal vitamin A distribution schedule for preschool and lactating mothers • Children 1–6 years 200,000 IU of vitamin A orally every 3–6 months. • Infants 6–11 months 100,000 IU of vitamin A orally every 3–6 months. • Lactating mothers 200,000IU of vitamin A orally once at delivery or during the first 8weeks postpartum if breastfeeding or during the first 6 weeks if not breast-feeding
  • 39. Recommended Xerophthalmia treatment schedule 6 -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 resolves 100,000 IU 200,000 IU drpankajyadav05@gmail.com
  • 40. Upper Level for Vitamin A • 3000 μg retinol • Hypervitaminosis A results from long- term supplement use (2 –4 x RDA) • Toxicity • Fatal dose (12 g) drpankajyadav05@gmail.com
  • 41. Hypervitaminosis A Acute Intoxication: • Results when excessively large single doses >300,000 IU ingested • Infants: n/v, drowsiness or irritability w/signs of increased ICP • Adults: drowsiness, irritability, headache & vomiting • Serum vitamin A values = 200-1000 IU/dl (N: 50 dr- pa 1 nk 0 aj0 yadI av U 05@ / gm d aill .c) om
  • 42. Toxicity of Vitamin A Acute toxicity short-term megadose (100x RDA); symptoms disappear when intake stops • GI effects • Headaches • Blurred vision • Poor muscle coordination drpankajyadav05@gmail.com
  • 43. Chronic Intoxication • Results when >50,000 IU/day ingested for several wks or more • Signs & symptoms in infants: • Early are anorexia, pruritus, irritability, tender swollen 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 discontinued drpankajyadav05@gmail.com
  • 44. Chronic Toxicity of Vitamin A • long-term megadose; possible permanent damage • Bone and muscle pain • Loss of appetite • Skin disorders • Headache • Dry skin • Hair loss • Increased liver size • Vomiting drpankajyadav05@gmail.com
  • 45. Toxicity of Vitamin A • Teratogenic (may occur with as little as 3 x RDA of preformed vitamin A) • Tends to produce physical defect on developing fetus as a result of excess vitamin A intake • Spontaneous abortion • Birth defects drpankajyadav05@gmail.com
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