CHAPTER I

INTRODUCTION

1.1 BACKGROUND

Vitamin A deficiency is one of the world's top five major malnutrition problems estimated to
affect more than 124 million children worldwide . Vitamin A deficiency is known to occur in
developing countries, most commonly in children under 5 years of age. Vitamin A deficiency
has long been identified as the leading cause of pediatric blindness in the world but recently,
vitamin A has also been recognized for its importance in promoting overall health and
survival of children.
Young children in developed countries, such as the Indonesia, are also susceptible to vitamin
A deficiency if their dietary intake of this essential vitamin is inadequate. Children,
especially in the toddler and preschool age groups, should be screened for adequate intake of
vitamin A rich foods as part of their well child care. Studies in Indonesia in 1992 of 4000
preschool children to identify dietary and other factors responsible for night blindness and
xerophthalmia found that children with even mild xerophthalmia died at a greater rate than
their peers without evidence of xerophthalmia. The mortality rate was directly related to the
severity of the xerophthalmia. Additional studies in Asia and Africa yielded comparable
findings indicating a strong correlation between vitamin A deficiency even mild deficiencies
undetected by physical examination and the rate of infection and mortality in preschool age
children.
In a survey in the Republic of the Marshall Islands involving 281 children, aged 15 years,
serum retinol, C-reactive protein (CRP), and 1-acid glycoprotein (AGP) were measured. Of
281 children, 24 (8.5%) had night blindness and 165 (58.7%) had serum retinol <0.70
mol/L. Of 248 children with AGP and CRP measurements, 123 (49.6%) had elevated acute
phase proteins (CRP >5 mg/L and/or AGP >1000 mg/L).
1

1.2 PROBLEMS
Xerophthalmia is disease that is caused by deficiency of vitamin A (retinol). Deficiency of
vitamin A is occur in developing country such as Indonesia. In 1992 many case are found in
Indonesia especially at children.
In this paper, I want to discuss about the correlation between deficiency vitamin A and
xerophthalmia disease. The discussion about the definition, prevention until the treatments of
the disease and the influence of lacking vitamin A on it. Especially, this discussion will talk
about xerophthalmia disease among children under 5 years in Central Java (Indonesia) in
1992.
1.3 LIMITATION OF PROBLEM
The topics that I will discuss in this paper are :

What is vitamin A deficiency?

What is Xerophthalmia disease?

Who is at risk of getting Xeropthalmia disease?

Why vitamin A deficiency can causes Xerophthalmia disease?

How do we prevent Xeropthalmia?

1.4 OBJECTIVES
After reading this paper, the writer hopefully is successful on giving greater information
regarding to the correlation between vitamin A deficiency and xerophthalmia disease. From
this paper, we can get more information about deficiency of vitamin A and xerophthalmia.
Because this paper tells us about the definition, etiology, signs and symptoms, diagnosis,
treatments, and prevention. It also discuss the correlation between vitamin A deficiency and
xerophthalmia, especially among children under 5 years old.
1.5 METHOD OF WRITING
2

I look up these materials of Xerophthalmia disease and lacking vitamin A in many textbooks
in the library. I also collect many information and journals by using internet on-line.

1.6 FRAME OF WRITING

PREFACE
CONTENT
CHAPTER I INTRODUCTION
1.1
1.2
1.3
1.4
1.5
1.6

Background
Problems
Limitation of problems
Objectives
Method of writing
Frame of Writing

CHAPTER II VITAMIN A
2.1
2.2
2.3
2.4
2.5
2.6

Definition
Metabolic fuction of vitamin A
Source of vitamin A
Deficiency of vitamin A
Pathophysiology
Treatment and medication

CHAPTER III XEROPHTHALMIA DISEASE

3.1
3.2
3.3
3.4
3.5

Definition
Causes
Sign and Symptom
Diagnosis
Therapy

CHAPTER IV THE CORRELATION BETWEEN VAD AND XEROPHTHALMIA

CHAPTER V CONCLUSION
BIBLIOGRAPHY

CHAPTER II
VITAMIN A DEFICIENCY

2.1 DEFINITION
The word vitamin was originally derived from Funk's term "vital amine." In 1912, he was
referring to Christian Eijkman's discovery of an amine extracted from rice polishings that could
prevent beriberi. Funk's recognition of the antiberiberi factor as vital for life was indeed accurate.
Researchers have since found that vitamins are essential organic compounds that the human body
3

cannot synthesize. Vitamins A, D, K, and E are classified as fat-soluble vitamins, whereas others
are classified as water-soluble vitamins.
Vitamin A was the first fat-soluble vitamin to be discovered. Early observations by ancient
Egyptians recognized that night blindness could be treated with consumption of liver. Two
independent research teams, Osborne and Mendel at Yale University and McCollum and Davis at
the University of Wisconsin, simultaneously discovered vitamin A in 1913. Vitamin A is made
up of a family of compounds called the retinoids. The term retinoids includes all molecules
(including synthetic molecules) that are chemically related to retinol. The retinoid designation
resulted from finding that vitamin A had the biologic activity of retinol, which was originally
isolated from the retina. Vitamin A, in the strictest sense, refers to retinol. However, the oxidized
metabolites, retinaldehyde and retinoic acid, are also biologically active compounds.
Retinaldehyde (11-cis) is the essential form of vitamin A that is required for normal vision,
whereas retinoic acid is necessary for normal morphogenesis, growth, and cell differentiation.
Vitamin A also plays a role in iron utilization, humoral immunity, T cellmediated immunity,
natural killer cell activity, and phagocytosis.
There are essentially 3 forms of vitamin A: retinols, beta carotenes, and carotenoids. Retinol, also
known as preformed vitamin A, is the most active form and is mostly found in animal sources of
food. Beta carotene, also known as provitamin A, is the plant source of retinol from which
mammals make two-thirds of their vitamin A. Carotenoids, the largest group of the 3, contain
multiple conjugated double bonds and exist in a free alcohol or in a fatty acyl-ester form.Vitamin
A is commercially available in esterified forms (e.g., acetate, palmitate) since it is more stable as
an ester.

2.2 METABOLIC FUNCTIONS OF VITAMIN A

Vitamin A plays a role in a variety of functions throughout the body, such as:

Vision.

Gene transcription.

Immune function.

Embryonic development and reproduction.

Bone metabolism.

Haematopoiesis.

Skin health.

Reducing risk of heart disease.

Antioxidant Activity.

Vision
The role of vitamin A in the vision cycle is specifically related to the retinal form. Within the eye,
11-cis-retinal is bound to rhodopsin (rods) and iodopsin (cones) at conserved lysine residues. As
light enters the eye the 11-cis-retinal is isomerized to the all-"trans" form. The all-"trans" retinal
dissociates from the opsin in a series of steps called bleaching. This isomerization induces a
nervous signal along the optic nerve to the visual center of the brain. Upon completion of this
cycle, the all-"trans"-retinal can be recycled and converted back to the 11-"cis"-retinal form via a
series of enzymatic reactions. Additionally, some of the all-"trans" retinal may be converted to
all-"trans" retinol form and then transported with an interphotoreceptor retinol-binding protein
(IRBP) to the pigment epithelial cells. Further esterification into all-"trans" retinyl esters allow
this final form to be stored within the pigment epithelial cells to be reused when needed. The
final conversion of 11-cis-retinal will rebind to opsin to reform rhodopsin in the retina.
Gene transcription

Vitamin A, in the retinoic acid form, plays an important role in gene transcription. Once retinol
has been taken up by a cell, it can be oxidized to retinal (by retinol dehydrogenases) and then
retinal can be oxidized to retinoic acid (by retinal oxidase). The conversion of retinal to retinoic
acid is an irreversible step, meaning that the production of retinoic acid is tightly regulated, due
to its activity as a ligand for nuclear receptors. Retinoic acid can bind to two different nuclear
receptors to initiate (or inhibit) gene transcription: the retinoic acid receptors (RARs) or the
retinoid "X" receptors (RXRs). RAR and RXR must dimerize before they can bind to the DNA.
RAR will form a heterodimer with RXR (RAR-RXR), but it does not readily form a homodimer
(RAR-RAR). RXR, on the other hand, readily forms a homodimer (RXR-RXR) and will form
heterodimers with many other nuclear receptors as well, including the thyroid hormone receptor
(RXR-TR), the Vitamin D3 receptor (RXR-VDR), the peroxisome proliferator-activated receptor
(RXR-PPAR) and the liver "X" receptor (RXR-LXR). The RAR-RXR heterodimer recognizes
retinoid acid response elements (RAREs) on the DNA whereas the RXR-RXR homodimer
6

recognizes retinoid "X" response elements (RXREs) on the DNA. The other RXR heterodimers
will bind to various other response elements on the DNA. Once the retinoic acid binds to the
receptors and dimerization has occurred, the receptors undergo a conformational change that
causes co-repressors to dissociate from the receptors. Coactivators can then bind to the receptor
complex, which may help to loosen the chromatin structure from the histones or may interact
with the transcriptional machinery. The receptors can then bind to the response elements on the
DNA and upregulate (or downregulate) the expression of target genes, such as cellular retinolbinding protein (CRBP) as well as the genes that encode for the receptors themselves.
Dermatology

Vitamin A appears to function in maintaining normal skin health. The mechanisms behind
retinoid's therapeutic agents in the treatment of dermatological diseases are being researched. For
the treatment of acne, the most effective drug is 13-cis retinoic acid (isotretinoin). Although its
mechanism of action remains unknown, it is the only retinoid that dramatically reduces the size
and secretion of the sebaceous glands. Isotretinoin reduces bacterial numbers in both the ducts
and skin surface. This is thought to be a result of the reduction in sebum, a nutrient source for the
bacteria. Isotretinoin reduces inflammation via inhibition of chemotatic responses of monocytes
and neutrophils. Isotretinoin also has been shown to initiate remodeling of the sebaceous glands;
triggering changes in gene expression that selectively induces apoptosis. Isotretinoin is a
teratogen and its use is confined to medical supervision.
2.3 SOURCES OF VITAMIN A
Vitamin A is found naturally in many foods:

liver (beef, pork, chicken, turkey, fish)

(6500 g 722%)

carrot

(835 g 93%)

broccoli leaf

(800 g 89% )

sweet potato

(709 g 79%)

kale

(681 g 76%)

butter

(684 g 76%)

spinach

(469 g 52%)

leafy vegetables

pumpkin

(369 g 41%)

collard greens

(333 g 37%)

cantaloupe melon

(169 g 19%)

egg

(140 g 16%)

apricot

(96

g 11%)

papaya

(55

6%)

mango

(38

4%)

pea

(38

4%)

broccoli

(31

3%)

winter squash

Note: bracketed values are retinol equivalences and percentage of the adult male RDA per 100g.
Conversion of carotene to retinol varies from person to person and bioavailability of carotene in
food varies.
2.4 VITAMIN A DEFICIENCY

In the human body, retinol is the predominant form, and 11-cis -retinol is the active form.
Retinol-binding protein (RBP) binds vitamin A and regulates its absorption and metabolism.
Vitamin A is essential for vision (especially dark adaptation), immune response, bone growth,
reproduction, the maintenance of the surface linings of the eyes, epithelial cell growth and repair,
and the epithelial integrity of the respiratory, urinary, and intestinal tracts. Vitamin A is also
important for embryonic development and the regulation of adult genes. It functions as an
activator of gene expression by retinoid alpha-receptor transcription factor and ligand-dependent
transcription factor.
Deficiency of vitamin A is found among malnourished, elderly, and chronically sick populations
in the United State, but it is more prevalent in developing countries such as Indonesia. Abnormal
visual adaptation to darkness, dry skin, dry hair, broken fingernails, and decreased resistance to
infections are among the first signs of vitamin A deficiency (VAD).
The risk of VAD is increased in patients suffering from fat malabsorption, cystic fibrosis, sprue,
pancreatic insufficiency, IBD, or cholestasis, as well as in persons who have undergone smallbowel bypass surgery. The risk is also increased in vegans, refugees, recent immigrants, persons
with alcoholism, and toddlers and preschool children living below the poverty line. These
patients should be advised to consume vitamin A.
Subclinical forms of VAD may not cause any symptoms, but the risk of developing respiratory
and diarrheal infections is increased, the growth rate is decreased, and bone development is
slowed. Patients may have a recent history of increased infections, infertility secondary to
impaired spermatogenesis, or recent spontaneous abortion secondary to impaired embryonic
development. The patient may also report increased fatigue, as a manifestation of VAD anemia.
Signs and symptoms of vitamin A deficiency include the following:

Bitot spots - Areas of abnormal squamous cell proliferation and keratinization of the
conjunctiva can be seen in young children with VAD.

Blindness due to retinal injury - Vitamin A has a major role in phototransduction. The
cone cells are responsible for the absorption of light and for color vision in bright light.
9

The rod cells detect motion and are responsible for night vision. In the rod cells of the
retina, all-trans-retinol is converted into 11-cis -retinol, which then combines with a
membrane-bound protein called opsin to yield rhodopsin.11 A similar type of reaction
occurs in the cone cells of the retina to produce iodopsin. The visual pigments absorb
light at different wavelengths, according to the type of cone cell they occupy. VAD leads
to a lack of visual pigments; this reduces the absorption of various wavelengths of light,
resulting in blindness.

Poor adaptation to darkness (nyctalopia)

Dry skin

Dry hair

Pruritus

Broken fingernails

Keratomalacia

Xerophthalmia

Corneal perforation

Follicular hyperkeratosis (phrynoderma) secondary to blockage of hair follicles with

plugs of keratin.

Other signs of VAD include excessive deposition of periosteal bone secondary to reduced
osteoclastic activity, anemia, keratinization of mucous membranes, and impairment of the
humoral and cell-mediated immune system.

2.5 PATHOPHYSIOLOGY

10

Once ingested, provitamins A are released from proteins in the stomach. These retinyl esters are
then hydrolyzed to retinol in the small intestine, because retinol is more efficiently absorbed.
Carotenoids are cleaved in the intestinal mucosa into molecules of retinaldehyde, which is
subsequently reduced to retinol and then esterified to retinyl esters. The retinyl esters of retinoid
and carotenoid origin are transported via micelles in the lymphatic drainage of the intestine to the
blood and then to the liver as components of chylomicrons. In the body, 50-80% of vitamin A is
stored in the liver, where it is bound to the cellular RBP. The remaining vitamin A is deposited
into adipose tissue, the lungs, and the kidneys as retinyl esters, most commonly as retinyl
palmitate.
Vitamin A can be mobilized from the liver to peripheral tissue by a process of deesterification of
the retinyl esters. In blood, vitamin A is bound to RBP, which transports it as a complex with
transthyretin. The hepatic synthesis of RBP is dependent on the presence of zinc and amino acids
to maintain its narrow serum range of 40-50 mcg/dL. Through a receptor-mediated process, the
retinol is taken up by the peripheral tissues from the RBP-transthyretin complex.
VAD may be secondary to decreased ingestion, defective absorption and altered metabolism, or
increased requirements. An adult liver can store up to a year's reserve of vitamin A, whereas a
child's liver may have enough stores to last only several weeks. Serum retinol concentration
reflects an individual's vitamin A status. Because serum retinol is homeostatically controlled, its
levels do not drop until the body's stores are significantly limited. The serum concentration of
retinol is affected by several factors, including RBP synthesis in the liver, infection, nutritional
status, and the existing level of other nutrients, such as zinc and iron.
In zinc deficiency, impaired synthesis of proteins occurs with rapid turnover (eg, RBP). In turn,
this impairment affects retinol transport by RBP from the liver to the circulation and to other
tissues. The mechanism by which iron affects vitamin A metabolism has not been identified, but
randomized, double-blind studies have shown that vitamin A supplementation alone is not
sufficient to improve VAD in the presence of coexisting iron deficiency.
The bioavailability of the carotenoids varies; this availability depends on absorption and on their
yield of retinol. Only 40-60% of ingested beta carotene from plant sources is absorbed by the
11

human body, whereas 80-90% of retinyl esters from animal proteins are absorbed. Carotenoid
absorption is affected by dietary factors, including zinc deficiency, abetalipoproteinemia, and
protein deficiency.
Because vitamin A is a fat-soluble vitamin, any GI diseases affecting the absorption of fats also
affect vitamin A absorption. Patients with cystic fibrosis, sprue, pancreatic insufficiency,
inflammatory bowel disorder (IBD), or cholestasis, as well as persons who have undergone
small-bowel bypass surgery, are at increased risk for VAD. These patients should be advised to
consume vitamin A.
One factor affecting the metabolism of vitamin A is alcoholism. Alcohol dehydrogenase
catalyzes the conversion of retinol to retinaldehyde, which is then oxidized to retinoic acid. The
affinity of alcohol dehydrogenase to ethanol impedes the conversion of retinol to retinoic acid.
Increased requirements of vitamin A most commonly occur among sick children. The American
Academy of Pediatrics has recommended vitamin A supplementation for infants aged 6-24
months who are hospitalized with measles and for all hospitalized children older than 6 months.
In the 1960s, the World Health Organization (WHO) undertook the first global survey of
Vitamine A Deficiency with associated xerophthalmia and complicated measles. In 1973, an
international

vitamin

board

was

set

up

to

alleviate

global

malnutrition.

The WHO and the United Nations International Children's Emergency Fund (UNICEF) have
issued joint statements recommending that vitamin A be administered to all children, especially
those younger than 2 years, who are diagnosed with measles. Coexistent VAD in young children
increases the risk of death. The Cochrane Database Systemic Review concluded that daily
treatment with 200,000 IU of vitamin A for at least 2 days reduces mortality rates.
Pregnant women do not require increased vitamin A supplementation. In fact, the Teratology
Society advocates that women be informed of the possible risk of cranial neural crest defects and
other malformations resulting from excessive use of vitamin A shortly before or during
pregnancy. The recommended daily allowance (RDA) of 800 mcg for all adult females is also
appropriate for pregnant women, because their stores of vitamin A meet the fetal accretion rate.
12

The requirements for lactating women have been debated, but the current RDA is 1300 mcg in
the first 6 months and 1200 mcg in the second 6 months.
The RDAs of vitamin A for various age groups are as follows:

Infants aged 1 year or younger - 375 mcg

Children aged 1-3 years - 400 mcg

Children aged 4-6 years - 500 mcg

Children aged 7-10 years - 700 mcg

All males older than 10 years - 1000 mcg

All females older than 10 years - 800 mcg

2.6 TREATMENT AND MEDICATION

TREATMENT
Medical care:
Treatment for subclinical VAD includes the consumption of vitamin Arich foods, such
as liver, beef, chicken, eggs, fortified milk, carrots, mangoes, sweet potatoes, and leafy green
vegetables.
For VAD syndromes, treatment includes daily oral supplements, as follows:

Children aged 3 years or younger - 600 mcg (2000 IU)

Children aged 4-8 years - 900 mcg (3000 IU)

Children aged 9-13 years - 1700 mcg (5665 IU)

13

Children aged 14-18 years - 2800 mcg (9335 IU)

All adults - 3000 mcg (10,000 IU)

Therapeutic doses for severe disease include 60,000 mcg (200,000 IU), which has been
shown to reduce child mortality rates by 35-70%.
Diet :

The Dietary Guidelines for Americans, from the US departments of Agriculture and
Health and Human Services, recommend consumption of a variety of foods for a
comprehensive nutrient intake. Vitamin A rich foods include the following.
o Liver
o Beef
o Chicken
o Eggs
o Whole milk
o Fortified milk
o Carrots
o Mangoes
o Orange fruits
o Sweet potatoes
o Spinach, kale, and other green vegetables

14

Eating at least 5 servings of fruits and vegetables per day is recommended in order to
provide a comprehensive distribution of carotenoids.

A variety of foods, such as breakfast cereals, pastries, breads, crackers, and cereal grain
bars, are often fortified with 10-15% of the RDA of vitamin A.

MEDICATION
The goals of pharmacotherapy are to reduce morbidity and to prevent complications

DOSING

INTERACTION

CONTRAIND
IKASI

15

PRECAUTION

Adult
3000 mcg (10,000 IU) PO qd
Severe disease: 60,000 mcg
(200,000 IU) PO for at least 2 d

Cholestyramine,

Documented

neomycin, and

hypersensitivity

mineral oil may

decrease absorption

hypervitaminosi

Pregnancy
A - Fetal risk not
revealed in controlled
studies in humans

s A; pregnancy
(if dose >800
mcg/d)
Pediatric
3 years: 600 mcg (2000 IU) PO

Precautions
Risk of teratogenicity

qd

increases in pregnant

4-8 years: 900 mcg (3000 IU) PO

women at doses >800

qd

mcg/d (not

9-13 years: 1700 mcg (5665 IU)

recommended);

PO qd

parenteral vitamin A in

14-18 years: 2800 mcg (9335 IU)

infants of low birth

PO qd

weight may be

Severe disease: 60,000 mcg

associated with

(200,000 IU) PO for at least 2 d

thrombocytopenia, renal
dysfunction,
hepatomegaly,
cholestasis, ascites,
hypotension, and
metabolic acidosis (EFerol syndrome)

16

CHAPTER III
XEROPHTHALMIA DISEASE

3.1 Definition
Xerophthalmia is a term that comes from the Greek and means literally "Dry Eyes". This is a
progressive medical condition in which the eye does not produce tears, presenting extreme
dryness and thickening of the conjunctiva due to decreased function of the tear or increased
evaporation of tears. The cornea may be thickened and visual acuity may be decreased.
This condition appears often as a result from disease localized in the eye, from a systemic
deficiency of vitamin A, trauma, or any condition in which the eyelids do not close completely.
Xerophthalmia receives also other names such as Xeroma, Dry Eye Syndrome, Keratitis Sicca,
or Keratoconjunctivitis Sicca.
Xerophthalmia usually occurs in people who are otherwise healthy but it is more common with
senior individuals because tear production decreases with age. In a few rare cases, it can be
associated with rheumatoid arthritis, lupus erythematosis, and other similar diseases common in
the elderly too. It may also be caused by accident with thermal or chemical burns.
Symptoms and signs of this condition are dry eye ranging from a mild irritation and foreign body
sensation to severe discomfort with sensitivity to light.
When Xerophthalmia is due to vitamin A deficiency, the condition begins with night blindness
and conjunctival xerosis (dryness of the eye membranes) and progresses to corneal xerosis
(dryness of the cornea), and, in the late stages, to keratomalacia (softening of the cornea). Series
of changes in the eye can lead to blindness.

17

3.2 CAUSES OF XEROPHTHALMIA

Xerophthalmia disease is caused by deficiency of vitamin A. Vitamin A deficiency is caused by:

Absorption problems.

Deficiency of protein or zinc can reduce the amount of vitamin A released from the liver.

Interference with conversion of beta-carotene to retinol.

Low intake.

Vitamin A storage problems.

3.3 SIGN AND SYMPTOM

Bitot's spots

Diarrhea

Dry eyes

Follicular hyperkeratosis - common areas: interior thighs and posterior arms

18

Keratinization

Loss of bone

Loss of both taste and smell

Loss of tooth enamel

Night blindness

Opacity

Reduced immunity

Respiratory infections

Sloughing of epithelial cells of cornea

3.4 DIAGNOSIS
Vitamin A blindness is both the easiest and the cheapest major nutritional illness to cure. Vitamin
A is probably the most important of all vitamins. Its great importance is demonstrated
dramatically in that, more than nay other vitamin, deficiencies of Vitamin A are still widespread
throughout the world and involve millions of persons, especially children.
3.5 TREATMENT
Home Care Suggestions
Immunity (vitamin A is necessary for maintaining the integrity of the mucus membranes). It is
necessary for differentiation of basal cells into mucus epithelial cells. It is needed for growth and
development of enamel (forming epithelial cells), skeletal tissues, and soft tissues. Vitamin A is
also necessary for humoral and cell-mediated immunity, and for normal reproduction and
19

lactation. Retinyl esters from the diet are converted to retinal in the eye. Retinal is then combined
with the protein opsin to form rhodopsin in the rods of the retina and iodopsin in the cones.
Steroid hormone synthesis and cell differentiation also need vitamin A.
Mind/Body Considerations
Any eye disease is naturally distressing for the patient. Today there is plenty that can be done to
alleviate this. Including doses of vitamin A in the diet is one way of avoiding xerophthalmia. The
worse thing to do is to assume that any disease is incurable. A positive attitude is necessary for
successful treatment. Avoid exposures to the sun and perform slow neck rolls and other eye
exercises.

CHAPTER IV
THE CORRELATION BETWEEN VITAMIN A DEFICIENCY AND
XEROPHTHALMIA AMONG CHILDREN UNDER 5 YEARS IN CENTRAL
JAVA, 1992

The most common cause of blindness in developing countries is vitamin A deficiency (VAD).
The World Health Organization (WHO) estimates 13.8 million children to have some degree of
visual loss related to VAD. Night blindness and its worsened condition, xerophthalmia, are
markers of VAD, as VAD can also lead to impaired immune function, cancer, and birth defects.
1992, in Central Java (Indonesia) found 50% children under 5 years old are suffer by
xerophthalmia disease.

20

Night blindness, xerophthalmia is the difficulty for the eyes to adjust to dim light. Affected
individuals are unable to distinguish images in low levels of illumination. People with night
blindness have poor vision in the darkness, but see normally when adequate light is present.
VAD affects vision by inhibiting the production of rhodopsin, the eye pigment responsible for
sensing low light situations. Rhodopsin is found in the retina and is composed of retinal (an
active form of vitamin A) and opsin (a protein). Because the body cannot create retinal in
sufficient amounts, 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 results.
Night blindness caused by VAD has been associated with the loss of goblet cells in the
conjunctiva, a membrane covering the outer surface of the eye. Goblet cells are responsible for
secretion of mucus, and their absence results in xerophthalmia, a condition where the eyes fail to
produce tears. Dead epithelial and microbial cells accumulate on the conjunctiva and form debris
that can lead to infection and possibly blindness.
Decreasing night blindness requires the improvement of vitamin A status in at risk populations.
Supplements and fortification of food have been shown to be effective interventions. Supplement
treatment for night blindness includes high doses of vitamin A (200,000 IU) in the form of retinyl
palmitate to be taken by mouth, which is administered two to four times a year. Intramuscular
injections are poorly absorbed and are ineffective in delivering sufficient bio-available vitamin
A. Fortification of food with vitamin A is costly, but can be done in wheat, sugar, and milk.
Households may circumvent expensive fortified food by altering dietary habits. Consumption of
yellow-orange fruits and vegetables rich in carotenoids, specifically beta carotene, provides provitamin A precursors that will prevent VAD related night blindness.

21

CHAPTER V
CONCLUTION

There are essentially 3 forms of vitamin A: retinols, beta carotenes, and carotenoids.
Retinol, also known as preformed vitamin A, is the most active form and is mostly
found in animal sources of food. Beta carotene, also known as provitamin A, is the
plant source of retinol from which mammals make two-thirds of their vitamin A.
Carotenoids, the largest group of the 3, contain multiple conjugated double bonds and
exist in a free alcohol or in a fatty acyl-ester form.

The role of vitamin A in the vision cycle is specifically related to the retinal form.
Within the eye, 11-cis-retinal is bound to rhodopsin (rods) and iodopsin (cones) at
conserved lysine residues. As light enters the eye the 11-cis-retinal is isomerized to
the all-"trans" form. The all-"trans" retinal dissociates from the opsin in a series of
steps called bleaching. This isomerization induces a nervous signal along the optic

22

nerve to the visual center of the brain. Upon completion of this cycle, the all-"trans"retinal can be recycled and converted back to the 11-"cis"-retinal form via a series of
enzymatic reactions. Additionally, some of the all-"trans" retinal may be converted to
all-"trans" retinol form and then transported with an interphotoreceptor retinolbinding protein (IRBP) to the pigment epithelial cells. Further esterification into
all-"trans" retinyl esters allow this final form to be stored within the pigment
epithelial cells to be reused when needed. The final conversion of 11-cis-retinal will
rebind to opsin to reform rhodopsin in the retina. Rhodopsin is needed to see black
and white as well as see at night. It is for this reason that a deficiency in vitamin A
will inhibit the reformation of rhodopsin and lead to night blindness (xerophthalmia).

Treatment for subclinical VAD includes the consumption of vitamin Arich

foods, such as liver, beef, chicken, eggs, fortified milk, carrots, mangoes, sweet

potatoes, and leafy green vegetables.

Vitamin A is also necessary for humoral and cell-mediated immunity, and for normal
reproduction and lactation. Retinyl esters from the diet are converted to retinal in the
eye. Retinal is then combined with the protein opsin to form rhodopsin in the rods of
the retina and iodopsin in the cones. Steroid hormone synthesis and cell
differentiation also need vitamin A.

23

BIBLIOGRAPHY

1. Latham, Michael E. Human Nutrition in the Developing World (Fao Food and Nutrition
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