Vitamin A deficiency

VITAMINS
 Vitamins are a class of organic compounds categorized as
essential nutrients.
 They are micronutrients.
 They DO NOT yield energy, but enable the body to use
other nutrients.
 The body generally CANNOT SYNTHESIZE THEM, so
they must be provided by food.
VITAMIN A

 Vitamin A consists of Retinol (pre-formed

vitamin), Retinal, Retinoic acid and ẞ-carotene
(pro-vitamin)
 Some of the ẞ-carotene is converted to retinol
in the intestinal mucosa
 I IU of Vit. A = 0.3 mcg of retinol (or 0.55 mcg
of retinol palmitate)
FUNCTIONS
 For NORMAL VISION in dim light.

 Maintaining the INTEGRITY AND NORMAL

FUNCTIONING of glandular and epithelial tissues which
lines intestinal, respiratory and urinary tracts as well as
skin and eyes.

 Supports GROWTH (skeletal growth)

 Enzymatic processing within the visual cycle begins with
delivery of vitamin A (all- trans -retinol) from the blood
circulation.
Functions continued..
 Retinol and retinoic acid function as STEROID
HORMONES. They regulate the protein synthesis thus
involved in cell growth and differentiation.

 SYNTHESIS of certain glycoproteins.

 Essential for the MAINTENANCE of proper immune

system

 CAROTENOIDS function as antioxidants and reduce the

risk of cancers. MAY protect against some epithelial cancers.
SOURCES
STORAGE
 Liver has an enormous capacity for storing Vit.A in the
form of retinol palmitate
 Under normal conditions, a well fed person has sufficient
Vit.A reserves to meet his needs for 6- 9months or more
 Free retinol is HIGHLY ACTIVE BUT TOXIC, so it is
transported in the blood stream by combining with retinol
binding protein (produced in the liver)
 So, in severe protein deficiency, sed production of retinol
binding protein prevents mobilization of liver retinol
reserves.
VITAMIN A DEFICIENCY
 Most susceptible populations:
 Preschool children with low F&V intake
 Urban poor
 Older adults
 Alcoholism
 Liver disease (limits storage)
 Fat malabsorption
VITAMIN A DEFICIENCY
 Vitamin A deficiency may result from :
 Dietary insufficiency of Vitamin A / Precursors
 Interference with absorption from intestines
 eg: diarrhoea, malabsorption syndrome, bile salt
deficiency
 Defect in the transport due to protein malnutrition –
‘Kwashiorkar’
 Defect in the storage due to diseases of liver
VITAMIN A DEFICIENCY
 Tissues chiefly affected –‘Epithelial’ principally which are
not normally keratinised
 Includes epithelium of respiratory tract, gastrointestinal
tract, genitourinary tract, eye & paraocular glands,
salivary glands, accessory glands of tongue & buccal
cavity and pancreas
 Fundamental change: Metaplasia of normal
nonkeratinised living cells into keratinising type of
epithelium
Deficiency-WHO statistics
 An estimated 250 million preschool children are
vitamin A deficient and it is likely that in vitamin A
deficient areas a substantial proportion of pregnant
women is vitamin A deficient.
 An estimated 250 000 to 500 000 vitamin Adeficient
children become BLIND EVERY YEAR, half of them
DYING within 12 months of losing their sight.
DEFICIENCY
OCULAR MANIFESTATIONS OF VITAMIN A
DEFICIENCY
 XEROPHTHALMIA:
 The term xerophthalmia was given by a joint WHO and USAID
committee in 1976 to cover all the ocular manifestations of
vitamin A deficiency
 including the structural changes affecting the conjunctiva,
cornea and retina and also the biophysical disorders of retinal
rods and cones functions.
WHO CLASSIFICATION (1982)
 XEROPHTHALMIA CLASSIFICATION(modified)
 XN Night blindness
 X1A Conjunctival xerosis
 X1B Bitot’s spots
 X2 Corneal xerosis
 X3A Corneal ulceration /keratomalacia affecting less than
1/3rd corneal surface
 X3B Corneal ulceration /keratomalacia affecting more than
1/3rd corneal surface
 XS Corneal scar due to xerophthalmia.
 XF Xerophthalmic fundus.
XN :NIGHT BLINDNESS(Nyctalopia)
 Earliest symptom of xerophthalmia in children
 Diminished visual acuity in ‘dim light’(Insufficient
adaptation to darkness)
 Defective rhodopsin function
X1A CONJUNCTIVAL XEROSIS
 Characterised by:
 One or more patches of dry, lustreless,nonwettable
conjunctiva.
 Interpalpebral conjunctiva(commonly temporal quadrants)
 Severe cases involves the entire bulbar conjunctiva.
 Desribed as ‘emerging like sand banks at receding tide’when
child ceases to cry
 Can lead to conjunctival thickening,wrinkling and
pigmentation.
X1B BITOT’S SPOTS
 Bilateral
 Bulbar conjunctiva in the interpalpebral area
 Commonly in temporal quadrant.
 Triangular greyish/silvery white spots/plaques.
 Firmly adherent to conjunctiva
 Foamy keratinised epithelium(corynebacterium xerosis)
X2 CORNEAL XEROSIS
 Dry lustreless appearance of cornea
 Earliest change is punctate keratopathy
 Begins in the lower nasal quadrant
 Bilateral punctate corneal epithelial erosions
 Can progress to epithelial defects
 Reversible on treatment
X3A & X3B CORNEAL ULCERATION
/KERATOMALACIA
 Stromal defects occur in late stages due to colliquative
necrosis leading to corneal ulceration ,softening
(melting) and destruction of cornea(keratomalacia)
 Corneal ulcers may be small or large
 Stromal defects involving less than 1/3rd cornea usually
heal leaving some useful vision
 Large stromal defects commonly result in blindness
XS CORNEAL SCAR
 Healing of stromal defects results in corneal scarring
 Size of the corneal scar depends on the size and density
of corneal defect.
XF XEROPHTHALMIC FUNDUS
 Uncommon in occurance
 Typical seed like lesions
 Whitish/yellow
 Raised
 Scattered uniformly over part of fundus
 At the level of optic disc.
 FFA reveals these dots to be focal retinal pigment epithelial defects
XF XEROPHTHALMIC FUNDUS
 Rarely these patients can present with scotomas corresponding
to the area of retinal involvement
 Respond to vitamin A therapy with scotoma disappearing in 1-
2 weeks and retinal lesions fading in 1-4 months.
VITAMIN A THERAPY
 Treatment schedules apply to all stages of active xerophthalmia
 1. Oral therapy (Recommended)

4
2) Parenteral therapy:
IN CASES OF
 severe disease
 unable to take oral feeds
 Repeated vomiting and diarrhoea
 malabsorption
Intramuscular injections of water miscible vit A preparation
Dose – 1,00,000 IU(Half the oral dose)
Local ocular therapy-

 Intense lubrication-instilled every 3-4 hours

 Topical retinoic acid
 Treatment of keratomalacia and corneal ulcer
 Treatment of corneal perforation
PROPHYLAXIS AGAINST XEROPHTHALMIA
 1.Short term approach -Periodic administration of vitamin
A supplements -WHO recommended ,universal
distribution schedule of vit A for prevention is as follows:
 2.Medium term approach- - fortification of food with Vit
A
 3. Long term approach-
 Promotion of adequate intake of Vit A rich foods in high risk
groups particularly preschool aged children on a periodic basis
and to mothers within 6-8 weeks after childbirth
 Other measures like nutritional education,social
marketing,home or community garden programs and measures
to improve food security.
HYPERVITAMINOSIS A
 Ingestion of large amounts of preformed vitaminA from
the diet,supplement intake or medications
 Acute:
 Single doses of >3,00,000 IU
 Headache,Blurred vision,nausea, vomiting, drowsiness ,
irritability i.e signs of raised ICP(Benign intracranial
hypertension)
 Serum vit A values-200-1000 IU/dl
Benign intracranial hypertension
 Increased intracranial pressure
 Idiopathic
 Headache (m.c),vomiting,pulsatile tinnitus
 Diplopia(compression of 6th nerve)
 Rarely compression of 3rd n 4th nerve
 Papillaedema
 visual field defects
 Long standing pappilledema leads to optic atrophy.
 Chronic – long-term megadose; possible permanent
damage ( >50,000 IU/day for several wks)
 Bone and muscle pain
 Loss of appetite
 Skin disorders
 Headache
 Dry skin
 Hair loss
 Increased liver size
 Manifestations reversible when vitamin A discontinued