FITSUM D

VITAMIN A DEFICIENCY
Epidemiology
Global:-
140 -150 million under 5 children are at risk

≈ 500, 000 preschool children become blind each year

 50% die within 1 year of loosing sight

Africa :-
Highest prevalence

1% preschool children are clinically affected

18 – 37% of children are sub clinically affected

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VAD – epidemio…
Ethiopia
Prevalence is 27%

Associated mortality is 17%

Sources of vitamin A
Liver, fish (cod) liver oils,

egg yolk, fortified margarines and fortified milk;

carotenoids from plants: green vegetables, yellow

fruits and vegetables
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 VAD…
Vitamin A:-
 Is a subclass of a family of lipid-soluble heat stable

refers to all-trans-retinol

obtained from plants in the form of provitamin-A

carotenoids: α-, β-, and γ-carotenes and β-

cryptoxanthin
Teratogenic effects if given in 1st TM of pregnancy

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The aldehyde form of vitamin A is retinal and functions

in vision.
The physiologically most important vitamin A

metabolite is retinoic acid.

functions as a ligand for specific nuclear transcription

factors  Regulates genes involved in cell division,

differentiation, & death
Absorption, Transport, Metabolism, Storage
Adequate lipid and protein within the meal

Provitamins-A vitamin A molecules in the small

intestine by carotene cleavage enzyme dioxygenase

Esterification of vitamin A to retinyl palmitate for

incorporation into chylomicrons  lymph &

circulation to the liver for storage or to other tissues.
Retinol-binding protein (RBP) & thyroid hormone

transport protein, transthyretin.

Malnutrition, particularly protein deficiency, 

impaired synthesis of retinol transport protein

vitamin A deficiency.
If vitamin A is provided in the absence of RBP, vitamin

A is transported to the tissues via chylomicrons &

alleviates the symptoms of vitamin A deficiency.
Function and Mechanism of Action
Required throughout the life cycle

Systemic functions mediated at the gene level by all-

trans-retinoic acid (RA), which is a ligand for the

retinoid receptors: RARs and RXRs.
Regulates many genes that are involved in the cell

division, cell death, & cell differentiation.

Function…
Reproduction, growth, embryonic & fetal
development, & bone development
Respiratory, gastrointestinal, hematopoietic, &
immune functions.
Nongenomic role in vision –
Component of retinal pigment- iodoppsin /cone cells/ &
rhdopsin /rod cells/
Ability of the vitamin A molecule to photoisomerize
(change shape when exposed to light).
Fetal development of the eye
 VAD…
Daily intake

0 – 6 month = 400Ug/day

6-12 month = 500ug/day

1 -3 yrs = 300ug/day

4-8 yrs =400ug/day….

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 Vit A Deficiency
Deficiency could result from
Low dietary intake
Increased requirement during
Illness-
infections, malabsorptions…
Pregnancy

Lactation

Fastly growing child (6 mo -5 yrs)

Disorders associated with fat malabsorption

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VAD – clinical manifestations
Ophthalmic
Insidiouse & rarely occur before 2 yr

Conjunctival Xerosis - dry

Xerophthamlmia- dry, scaly layers of cells

Night blindness

Bitot spot - dry silver –gray plaque on

bulbarconjunctiva due to keratinization

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VAD – clinical manifestations
Ophthalmic
Keratomalacia – irreversible wrinkling cloudiness of
cornea  blindness
Corneal xerosis
Corneal ulceration
Photophobia

Advanced xerophthalmia with an opaque, dull cornea

and some damage to the iris in a 1 yr old boy
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 VAD c/m…
Impairment of the humoral & cell mediated immune

system via direct and indirect effects on the phagocytes

& T cells
Non-specific dermatological problems
Dry & scaly skin

Phrynoderma (follicular hyperkeratosis)

Destruction of hair follicles & their replacement

with mucus-secreting glands.

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Intestines & Respiratory tract – disruption of mucus-

secreting epithelium.
Repiratory, genitourinary – squamous metaplasia 

increased infections
The combination of defective epithelial barriers to

infection, low immune response, and lowered response

to inflammatory stress  poor growth
Other clinical signs of vitamin A deficiency include
poor overall growth,
anemia,
mental retardation, and
increased intracranial pressure, with wide separation
of the cranial bones at the sutures.
There may be vision problems due to bone overgrowth
causing pressure on the optic nerve
 VAD c/m…
Classification
Primary signs
X1A – conjunctival xerosis
X1B – conj. Xerosis + bitot’s spot
X2A – corneal xerosis
X3A – keratomalacia/corneal ulcer – involves <1/3 cornea
X3B – keratomalacia involving >1/3 of cornea
Secondary signs
xN – night blindness
xF – xerophthalmic fundus /white/
xS – sequalae of corneal ulcer

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VAD - diagnosis
Clinical

Biochemical

Normal retinol in plasma

Infants = 20-50ug/dl
Older children = 30- 225ug/dl

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 VAD- treatment & prevention
Treatment supplementation for different diseases

Pneumonia, Persistent diarrheal disease – one

dose
On days 1, 2, & 14 in case of measles

On days 1, 2, 14, 30 in cases of eye problems

/xerophthalmia/

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 VAD- treatment & prevention
Optimal breast feeding
Vitamin A supplementation

200,000 IU in the 1st 8 wks post partum – for the

mother
3 doses of 25,000 IU in the 1st 3 mo of age –for the

infant. (Note: 1 IU = 0.3 μg retinol)

Infants 6 to 11 months 100,000 Once

Children 12 to 59 months 200,000 Q 4 to 6 months

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VAD – treatment…
Supplementation as part of immunization schedule

6 -12 month = 100,000IU

> 12 month = 200,000IU

Food diversification & forification

VITAMIN A FOR HEALTHY BODY &

GOOD SIGHT

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Hypervitaminosis A
Chronic hypervitaminosis A results from excessive
ingestion of vitamin A for several weeks or months.
Toxicity can be induced in adults and children with
chronic daily intakes of 15,000 /50,000 IU / ug and 6,000
ug , respectively.
Fatal dose = 12gm
Symptoms subside rapidly on withdrawal.
Signs of subacute or chronic toxicity can include
headache; vomiting; anorexia; dry, itchy desquamating
skin; seborrheic cutaneous lesions; fissuring at the
corners of the mouth; alopecia and/or coarsening of the
hair; bone abnormalities; swelling of the bones;
enlargement of the liver and spleen; diplopia;
increased intracranial pressure; irritability; stupor;
limited motion; and dryness of the mucous
membranes. In addition, desquamation of the palms
and the soles of the feet is common.
Radiographs show hyperostosis affecting several long
bones, especially in the middle of the shafts.
Serum levels of vitamin A are elevated.
Hypercalcemia and/or liver cirrhosis may be present.
Hypervitaminosis A is distinct from cortical
hyperostosis
In young children  vomiting and bulging fontanels.
An affected child has anorexia, pruritus, and a lack of
weight gain.
Acute hypervitaminosis A toxicity has occurred in
infants in developing countries after ingestion of very
large amounts of vitamin A during vaccine
administration.
Symptoms include nausea, vomiting, and drowsiness;
less-common symptoms include diplopia, papilledema,
cranial nerve palsies, and other symptoms suggesting
pseudotumor cerebri.
Severe congenital malformations occur in infants of
mothers who consumed therapeutic doses (0.5-1.5
mg/kg) of oral 13-cis-retinoic acid during the 1st
trimester of pregnancy for treatment of acne or
cancer. These malformations result in a high
incidence (>20%) of spontaneous abortions and birth
defects.
Excessive intake of carotenoids is not associated with
toxicity but can cause yellow coloration of the skin
that disappears when intake is reduced; this disorder
(carotenemia) is especially likely to occur in children
with liver disease, diabetes mellitus, or
hypothyroidism and in those who do not have
enzymes that metabolize carotenoids.