Vitamin a deficiency HYPERVITAMINOSIS A

VITAMIN A DEFICIENCY
AND
HYPERVITAMINOSIS A
Presented by
Dr. PANKAJYADAV
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
sources(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 vegetables
685
 Tomato 100
 Apricot 250
 Sweet potato, red and yellow
670
 Animal (micrograms/100gm)
 Fatty fish liver oils
 Halibut 900,000
 Cod 18,000
 Shark 180,000
Dairy produce
 Butter 830
 Margarine, vitaminized 900
 Eggs 140
 Milk 40
 Cheese, fatty type 320
 Liver of sheep and ox 15,000
 Beef, mutton, pork 0–4

Vitamin A requirement


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

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 specificVADD,and
is the leading preventable cause of blindness
in children throughout the world
 Night blindness
 Anaemia can result fromVAD 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 ofVAD are commonly
used for population surveys:
1 clinically assessed eye signs.Term xerophthalmia
encompasses the clinical spectrum of ocular
manifestations ofVAD, from milder stages of
night blindness and Bitot’s 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 itot’s 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 μmol/l representing VAD , and
below 0.35 μmol/l representing severeVAD.
 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
xerophthalmia
Clinical (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 (10
μg/dL) 5.0%

Universal vitamin A distribution
schedule for preschool and
lactating mothers
 Children 1–6 years
200,000 IU of vitaminA orally every 3–6 months.
 Infants 6–11 months
100,000 IU of vitaminA orally every 3–6 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
 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

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)

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

ChronicIntoxication
 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 HYPERVITAMINOSIS A

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