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3 Vitamin A Deficiency
3 Vitamin A Deficiency
VITAMIN A DEFICIENCY
Epidemiology
Global:-
140 -150 million under 5 children are at risk
Sources of vitamin A
Liver, fish (cod) liver oils,
refers to all-trans-retinol
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The aldehyde form of vitamin A is retinal and functions
in vision.
The physiologically most important vitamin A
0 – 6 month = 400Ug/day
1 -3 yrs = 300ug/day
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Vit A Deficiency
Deficiency could result from
Low dietary intake
Increased requirement during
Illness-
infections, malabsorptions…
Pregnancy
Lactation
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VAD – clinical manifestations
Ophthalmic
Insidiouse & rarely occur before 2 yr
Night blindness
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VAD – clinical manifestations
Ophthalmic
Keratomalacia – irreversible wrinkling cloudiness of
cornea blindness
Corneal xerosis
Corneal ulceration
Photophobia
secreting epithelium.
Repiratory, genitourinary – squamous metaplasia
increased infections
The combination of defective epithelial barriers to
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VAD - diagnosis
Clinical
Biochemical
Infants = 20-50ug/dl
Older children = 30- 225ug/dl
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VAD- treatment & prevention
Treatment supplementation for different diseases
dose
On days 1, 2, & 14 in case of measles
/xerophthalmia/
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VAD- treatment & prevention
Optimal breast feeding
Vitamin A supplementation
mother
3 doses of 25,000 IU in the 1st 3 mo of age –for the
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VAD – treatment…
Supplementation as part of immunization schedule
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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.