Vitamin A and

Xerophthalmia
-Jayashree Iyer
Roll No. 43
 Vitamin A
O It is an essential fat soluble vitamin occurring in 2
forms.
Preformed Pro-vitamin A

• Retinoids (retinal, retinol, • Carotenoids

retinoic acid)
• Found in animal products
• Must be converted to
retinoid form
• Intestinal cells can split
carotene into 2
molecules of retinoids.
• Found in plant products

O Vitamin A deficiency is the most common cause of non-

accidental blindness worldwide.
Recommended daily allowance
O Unit of activity is retinal equivalent(RE)/International
Units(IU)
O 1 RE = 1 mcg retinol = 6 mcg beta-carotene
O 1 IU= 0.3 mcg retinol = 0.6 mcg beta-carotene

1. Infants children: 400-600 mcg/day

2. Adults: 600-800 mcg/day
3. Pregnancy and lactation: 1000-1200 mcg/day
 Absorption of Vitamin A
O Dietary vitamin A from animal sources is available in
the form of retinyl esters.
O Retinyl esters Retinol + Fatty acids by
pancreatic hydrolases in the small intestine.
O Absorption of retinol requires presence of bile salts
and digestive enzymes.
O In the intestinal cells, retinol is converted back to retinyl
esters and secreted with chylomicrons.

Carotene
O β-carotene dioxygenase Retinaldehyde Retinol
 Transport and Storage of
Vitamin A
O Liver stores 90% of vitamin A in the body
O Reserve is adequate for 6-9 months
O Transported via chylomicrons from intestinal
cells to the liver
O Transported from the liver to target tissue as
retinol via retinol-binding protein
 Excretion of Vitamin A
O Not readily excreted
O Some lost in urine
O Kidney disease and aging increase risk of
toxicity because excretion is impaired
 Functions of Vitamin A
O Normal vision
O Maintains normal epithelial and glandular
function
O Supports skeletal growth
O Powers up immune system and prevents
infections
O Embryonic development and regulation of adult
genes
 Wald’s Visual Cycle
O It is the biological conversion of a photon into an
electrical signal in the retina.
O Processing of visual input begins in the retina with
detection of light by photoreceptor cells – the rods and
cones.
O Rods and cones contain chemicals that decompose on
exposure to light and thus, excite the nerve fibres leading
from the eye.
O The photo sensitive chemical present in rods is rhodopsin
and in cones there are various iodopsins/colour pigments.
O Vit. A is necessary to form rhodopsin (in rods, night
vision) and iodopsins (in cones, color vision).
O In the retina, retinaldehyde functions as the prosthetic
group for the light sensitive opsin proteins, forming
rhodopsin and iodopsins.
O The absorption of light by rhodopsin causes
isomerization of retinaldehyde from 11-cis to all-trans
form, and a conformational change in opsin.
O This results in the release of retinaldehyde from the
protein, and the initiation of a nerve impulse.
O The key to initiation of the visual cycle is the
availability of 11-cis-retinaldehyde, and hence
vitamin A.
 Deficiency of Vitamin A
Most susceptible Consequences:
populations: O Night blindness
O Preschool children with
O Decreased mucus production
low F&V intake
O Decreased immunity
O Urban poor
O Bacterial invasion of the eye
O Older adults
O Conjunctival xerosis
O Alcoholism
O Bitot’s spots
O Liver disease (limits
O Xerophthalmia
storage)
O Irreversible blindness
O Fat malabsorption
O Follicular hyperkeratosis
O Poor growth
 Xerophthalmia
O It is a term given to cover all the ocular
manifestations of vit. A deficiency, including the
structural changes affecting the conjunctiva,
cornea and retina and also the biophysical
disorders of retinal rods and cones.
O Etiology
1. Dietary deficiency of vit. A
2. Defective absorption of vit. A from gut
 WHO Classification (1982)
O XN: Night blindness
O X1A: Conjunctival xerosis
O X1B: Bitot’s spots
O X2: Corneal xerosis
O X3A: Corneal ulceration/keratomalacia affecting less
than 1/3rd corneal surface
O X3B: Corneal ulceration/keratomalacia affecting more
than 1/3rd corneal surface
O XS: Corneal scar due to xerophthalmia
O XF: Xerophthalmic fundus.
 XN: Night blindness(Nyctalopia)
O Earliest symptom of xerophthalmia in children
O Diminished visual acuity in dim light (insufficient adaptation
to darkness)
O Defective rhodopsin function.
 X1A: Conjunctival Xerosis
O One or more patches of dry, lustreless, non-wettable
conjunctiva
O Interpalpebral conjunctiva(commonly temporal quadrants)
O Severe cases involve entire bulbar conjunctiva
O Described as ‘emerging like sand banks at receding tide’
when child stops crying.
O Associated with conjunctival thickening, wrinkling and
pigmentation.
 X1B: Bitot’s Spots
O Bilateral
O Bulbar conjunctiva in the interpalpebral area
O Commonly in temporal quadrant
O Triangular greyish/silvery white spots/plaques
O Firmly adherent to conjunctiva
O Foamy keratinized epithelium(corynebacterium
xerosis)
 X2: Corneal xerosis
O Dry lustreless appearance of cornea
O Earliest change is punctate keratopathy
O Begins in lower nasal quadrant
O Bilateral punctate corneal epithelial erosions
O Can progress to epithelial defects
O Reversible on treatment
 X3A and X3B: Corneal
ulceration/keratomalacia
O Stromal defects occur in late stages due to colliquative
necrosis leading to corneal ulceration,
softening(melting) and destruction of
cornea(keratomalacia)
O Corneal ulcers maybe small or large
O Stromal defects involving less than 1/3rd cornea
usually heal leaving some useful vision
O Large stromal defects commonly result in blindness
 Small ulcers Large ulcers

O 1-3mm O More than 3mm

O Occur peripherally O Occur centrally
O Circular O Involve entire cornea
O Steep margins and O Leads to blindness
sharply demarcated
 XS: Corneal Scar
O Healing of stromal defects leads to corneal
scarring
O Size of corneal scar depends on size and
density of corneal defect
XF: Xerophthalmic fundus
O Uncommon
O Typical seed like lesions
O Whitish/yellow
O Raised
O Scattered uniformly over part of fundus
O At the level of optic disk
O FFA reveals these dots to be focal retinal
pigment epithelial defects
 Vitamin A therapy
O Treatment schedules apply for all stages of
active xerophthalmia.
1. Oral therapy(recommended)
2. Parenteral therapy - in cases of:
O Severe disease
O Unable to take oral feed
O Repeated vomitting and diarrhea
O Malabsorption

Intramuscular injections of water miscible vitamin A

preparation.
Dose: 1,00,000 IU(half the oral dose)
 Prophylaxis
O Dietary modification by promoting adequate
intake of Vit. A rich foods such as green leafy
vegetables.
O Fortification of foods such as dairy products
with Vit. A.
O Supplementation of single large doses of
Vitamin. A on periodic basis scheduled as
follows.
 Hypervitaminosis A
O 3000 μg retinol
O Hypervitaminosis A results from long-term
supplement use (2-4 x RDA)
O Fatal dose (12 g)
O Teratogenic (may occur with as little as 3 x
RDA of preformed vitamin A)
O Tends to produce physical defects in
developing fetus
O Spontaneous abortion
O Birth defects
 Toxicity of Vitamin A
Acute: Chronic:
Short-term megadose (100 Long-term megadose;
possible permanent
x RDA); symptoms damage.
disappear when intake O Bone and muscle pain
stops. O Loss of appetite
O Headaches O Skin disorders
O Blurred vision O Headache
O Dry skin
O Poor muscle coordination
O Hair loss
O Increased liver size
O Vomiting
Thank you.