Vitamin A Deficiency AND Hypervitaminosis A: Presented by Dr. Pankaj Yadav

VITAMIN A DEFICIENCY
AND
HYPERVITAMINOSIS A
Presented by
Dr. PANKAJ YADAV
drpankajyadav05@gmail.com
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.
Active forms are retinol, retinaldehyde, and retinoic
acid
Plants synthesize the more complex carotenoids
which are cleaved to retinol by most animals and
stored 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 photosensitive
pigment in both rods (rhodopsin) & cones
(iodopsin), major difference lies in the nature of
protein bound
Needed in lysosomal membrane stability
Plays a role in keratinization, cornification, bone
development & cell growth & reproduction
Absorption of Vitamin A
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
Transport and Storage of
Vitamin A
Liver stores 90% of vitamin A in the body
Reserve is adequate for several months
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
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
The Visual Cycle
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 more
protective than supplements
Age-related macular degeneration
Cataracts
Acne
AML
Source of vitamin A
Colostrum
foods containing either preformed vitamin A
esters
- liver, milk,cheese,eggs or food products
fortified with vitamin A
or
carotenoid precursors (mainly beta-
carotene), such as green leaves, carrots, ripe
mangoes,eggs, and other orange-yellow
vegetables and fruits.
Source of vitamin A
fruit carotenoid Animal (micrograms/100gm)
sources(micrograms/100gm) Fatty fish liver oils
Mango (golden) 307 Halibut 900,000
Papaya (solo) 124 Cod 18,000
Cucurbita (mature pulp) 862 Shark 180,000
Buriti palm (pulp) 3,000 Dairy produce
Red palm oil 30,000 Butter 830
Carrot 2,000 Margarine, vitaminized 900
Dark green leafy vegetables Eggs 140
685
Milk 40
Tomato 100
Cheese, fatty type 320
Apricot 250
Liver of sheep and ox 15,000
Sweet potato, red and yellow
670 Beef, mutton, pork 04
Vitamin A requirement
Units of measuring vitamin A
Each g RAE corresponds to

1 g retinol,
2 g of -carotene in oil,
12 g 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
Prevalence of vitamin A
deficiency in South Asia (%)
Country sub clinical clinical
VAD (%) VAD (%)
Afghanistan 53 -
Bangladesh 28 0.7
Bhutan 32 0.7
INDIA 57 0.7
Nepal 33 1
Pakistan 35
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, 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 VADD,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
VITAMIN A DEFICIENCY
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 Bitots spots, to potentially
blinding stages of corneal xerosis, ulceration and
necrosis (keratomalacia)
2 biochemically determined concentrations of
retinol in plasma or serum
Classification of xerophthalmia
XNN ight blindness

X1A Conjunctival xerosis
X1BB itots spot
X2 Corneal xerosis
X3A Corneal ulceration/keratomalacia (< 1/3
corneal surface)
X3BCorneal ulceration/keratomalacia ( 1/3
corneal surface)
XSCorneal scar
XFXerophthalmic fundus
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 mol/l representing VAD , and
below 0.35 mol/l representing severe VAD.
a serum retinol concentration below a cutoff
of 1.05 mol/l has been proposed to reflect
low vitamin.
Criteria for assessing the
public
health significance of
Clinical (primary)
xerophthalmia
Night blindness (XN)* 1.0%
Bitots 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 mol/L (10
g/dL) 5.0%
Universal vitamin A distribution
schedule for preschool and
lactating mothers
Children 16 years
200,000 IU of vitaminA orally every 36 months.
Infants 611 months
100,000 IU of vitaminA orally every 36 months.
Lactating mothers
200,000 IU of vitaminA orally once: at delivery or
during the first 8 weeks 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
24 weeks later 100,000 IU 200,000 IU
Severe Protein-Energy Malnutrition (PEM)

Monthly until PEM resolves
100,000 IU 200,000 IU
Upper Level for Vitamin A
3000 g retinol
Hypervitaminosis A results from long-term
supplement use (2 4 x RDA)
Toxicity
Fatal dose (12 g)
HypervitaminosisA
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:
50-100 IU/dl)
Toxicity of Vitamin A
Acute short-term megadose (100 x

RDA); symptoms disappear when intake
stops
GI effects
Headaches
Blurred vision
Poor muscle coordination
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
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
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

Vitamin A Deficiency AND Hypervitaminosis A: Presented by Dr. Pankaj Yadav

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Vitamin A Deficiency AND Hypervitaminosis A: Presented by Dr. Pankaj Yadav

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VITAMIN A DEFICIENCY

Vitamin A deficiency (VAD) is a major

Not readily excreted

Vision (night, day, colour)

Age-related macular degeneration

Each g RAE corresponds to

Synergism between deficient dietary intake of

Xerophthalmia is the most specific VADD,and

XNN ight blindness

serum retinol concentrations in a population

Severe Protein-Energy Malnutrition (PEM)

Acute short-term megadose (100 x

long-term megadose; possible permanent

Teratogenic (may occur with as little as 3 x

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