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Vitamin -A Deficiency
Khushboo Goyal
Enrolment No. - 141302544

Introduction

Impact of Vitamin A Deficiency

Disorder on Worldwide Public Health
Extent of Vitamin A deficiency
250 million preschool-age children have
subclinical vitamin A deficient
7.2 million pregnant women

3 million people with clinical Xerophthalmia

300, 000 people blind from Xerophthalmia

Impact of Vitamin A Intervention on Child Survival

is significant and is well understood

Improvement of vitamin A status in young

child populations leads to a reduction in allcause mortality rates of about 23%.
United Nations, 1993

Improved vitamin A nutriture would be

expected to prevent approximately 1.3-2.5
million deaths annually among children aged
under 5 years.
Bulletin of WHO, 1992
However, Mechanisms involved in disease are still poorly
understood

Impact of Vitamin A Deficiency on Child Mortality

Research shows that Vitamin A deficiency accentuates child mortality rates

2 Clinical
Manifestations

WHO criteria of a public health problem of

Xerophthalmia

Night Blindness

(XN)

Bitots Spots

(X1B)

Corneal Xerosis/ Ulceration/ Keratomalcia

Corneal Scar
Plasma retinal of <0.35mol/l (10 g/dl

(X2, X3A, X3B)

(XS)

In > 1%
In > 0.5%
In >0.01%
In > 0.05%

In > 5%

However, Mechanisms involved in disease are still poorly understood

Untreated Vitamin-A Deficiency may lead to Night

Blindness, Xerophthalmia, Keratomalacia and
eventually complete blindness
Percent with Serum Vitamin A:

<10
g/dL

10-19
g/dL

Normal Children

252

Children with night-blindness

or Bitots spots

325

30

55

15

Children with corneal

xerophthalmia

98

75

24

37

Serum vitamin A levels in a sample of Indonesian children with and

without ocular lesions. Conversion factor SI units(mol/L)= x 0.035

>20
g/dL

55

Symptoms

Imtiaz's sign is the earliest ocular sign of VAD.

Conjunctival epithelial defects occur around lateral

aspect of the limbus in subclinical stage of VAD. These
are not even visible on a biomicroscope, but they take up
black stain and become readily visible after instillation
of kajal (surma); this is called "Imtiaz's sign"

Night Blindness
results from prolonged deficiency of Vit- A

VAD affects vision by

inhibiting the production of
rhodopsin, the eye pigment
responsible for sensing low
light situations. A diet low
in vitamin A will lead to a
decreased amount of
rhodopsin in the eye, as
there is inadequate retinal to
bind with opsin.

Night blindness and its worsened condition, Xerophthalmia, are

markers of VAD. It can also lead to impaired immune function,
cancer, and birth defects. Collections of keratin in the conjunctiva,
known as Bitot's spots, are also seen.

Causes of
Deficiency

Factors that may Affect Plasma Vitamin A or

Retinol Levels
Liver disease decreases plasma retinal levels, probably
as a result of a combination of decreased synthesis and
secretion of RBP.
Protein-energy malnutrition decreases RBP production
because of a limited supply of protein substrate.
Consequently hepatic release of vitamin A is impaired
resulting in decreased serum retinol levels
Zinc deficiency decreases plasma retinol levels via its
. the synthesis of RBP.
role in

Stress decreases plasma retinol levels.

Estrogens, either endogenous or those used in

contraceptive agents, increase plasma retinol and RBP
apparently as a result of incresed mobilization of
Vitamin A from the liver
Cystic fibrosis is associated with a defect in the
transport of vitamin A from the hepatic stores to the
periphery resulting in decreased levels of circulating
retinol and RBP.

Infections and parasitic infections lower plasma

retinol levels.

Low fat diets impair absorption of vitamin A, lowering

plasma retinol concentrations.

Functions

Functions of Vitamin - A
Vision (night, day, colour)
Epithelial cell integrity against infections
Immune response

Haemopoiesis
Skeletal growth
Fertility (male and female)
Embryogenesis

Prevention

Prevention using periodic oral supplementation

Infants <6 Months
Non-Breast fed infants
Breast fed infants whose mothers have not
received supplemental Vitamin A

Infants 6 12 Months
Every 4 6 months

Children >12 Months

Every 4 6 months

Mothers
Within 8 weeks of delivery

Dosage

50,000
IU

100,000
IU
200,000
IU
200,000
IU

Prevention by consuming Vitamin- A rich diet

on a regular basis

Poultry

Milk & Milk Products

Corn / Maize

Non-animal sources of vitamin A which contain pre-formed vitamin A

account for greater than 80% of intake in the developing world.
The increase in consumption of vitamin A-rich foods of animal origin in
addition to fruits and vegetables has beneficial effects on VAD.
Corn contains high levels of beta-carotene, the precursor to vitamin A

Diagnosis

Tests of Vitamin A Status

Subclinical
Relative dose-response test
Serum retinol
Decreased
Status

Retinal rod function

Conjunctival impression
cytology (CIC)

Clinical
Night blindness
Conjunctival and corneal eye
signs

Preliminary Assessment of Vitamin A status

of a population
can be performed using

Interviews by structured questionnaires

Chart Reviews

Search for clinically active cases

Search for old, healed, disease

Collection of existing data on dietary intake

Collection of data on Serum Vitamin A levels

Treatment

Treatment Schedule (Orally)

Age

Dosage

<6 months

50, 000 IU

6 months-12 months

100, 000 IU

> 12 months

200, 000 IU

The same dosage must be administered the next

day as well as after an interval of 2 weeks

Treatment should also include a suitable diet plan.

The following are the representative values of Vitamin-A in different
foodstuffs