The Correlation Between Vitamine a Deficiency and Xerophthalmia Among Children Under Five Years in Central Java

8/9/2019 The Correlation Between Vitamine a Deficiency and Xerophthalmia Among Children Under Five Years in Central Java

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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 ! 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 recogni"ed for its importance in promoting overall health and

survival of children.

#oung children in developed countries such as the $ndonesia are also susceptible to vitamin

A deficiency if their dietary intake of this essential vitamin is inade%uate. &hildren

especially in the toddler and preschool age groups should be screened for ade%uate intake of

vitamin A rich foods as part of their well child care. tudies in $ndonesia in 1((2 of 4)))

preschool children to identify dietary and other factors responsible for night blindness and

*erophthalmia found that children with even mild *erophthalmia died at a greater rate than

their peers without evidence of *erophthalmia. +he mortality rate was directly related to the

severity of the *erophthalmia. Additional studies in Asia and Africa yielded comparable

findings indicating a strong correlation between vitamin A deficiency even mild deficiencies

undetected by physical e*amination and the rate of infection and mortality in preschool age

children.

$n a survey in the ,epublic of the -arshall $slands involving 21 children aged 1/! years

serum retinol &0reactive protein &,3 and 10acid glycoprotein A53 were measured. 6f

21 children 24 .!73 had night blindness and 18! !.973 had serum retinol :).9)

;mol 4(.873 had elevated acute

phase proteins &, ?! mg


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1.2 PROBLEMS

@erophthalmia is disease that is caused by deficiency of vitamin A retinol3. eficiency of

vitamin A is occur in developing country such as $ndonesia. $n 1((2 many case are found in

$ndonesia especially at children.

$n this paper $ want to discuss about the correlation between deficiency vitamin A and

*erophthalmia disease. +he discussion about the definition prevention until the treatments of

the disease and the influence of lacking vitamin A on it. Bspecially this discussion will talk

about *erophthalmia disease among children under ! years in &entral Cava $ndonesia3 in

1((2.

1.3 LIMITATION OF PROBLEM

+he topics that $ will discuss in this paper are D

• Ehat is vitamin A deficiencyF

• Ehat is @erophthalmia diseaseF

• Eho is at risk of getting @eropthalmia diseaseF

• Ehy vitamin A deficiency can causes @erophthalmia diseaseF

• Gow do we prevent @eropthalmiaF

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 *erophthalmia disease. Hrom

this paper we can get more information about deficiency of vitamin A and *erophthalmia.

Iecause this paper tells us about the definition etiology signs and symptoms diagnosis

treatments and prevention. $t also discuss the correlation between vitamin A deficiency and

*erophthalmia especially among children under ! years old.

1.5 METHOD OF WRITING

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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

PREFACECONTENTCHAPTER I INTRODUCTION1.1 Background1. !roblems1." #imitation of problems1.$ %bjectives1.& 'ethod of (riting1.) *rame of +riting

CHAPTER II VITAMIN A.1 ,efinition

. 'etabolic fuction of vitamin A." ource of vitamin A.$ ,eficiency of vitamin A.& !athophysiology.) reatment and medication

CHAPTER III XEROPHTHALMIA DISEASE".1 ,efinition". /auses"." ign and ymptom".$ ,iagnosis".& herapy

CHAPTER IV THE CORRELATION BETWEEN VAD AND XEROPHTHALMIA

CHAPTER V CONCLUSIONBIBLIOGRAPH

CHAPTER II

VITAMIN A DEFICIENC

2.1 DEFINITION

+he word vitamin was originally derived from Hunk's term Jvital amine.J $n 1(12 he was

referring to &hristian Bijkman's discovery of an amine e*tracted from rice polishings that could

prevent beriberi. Hunk's recognition of the antiberiberi factor as vital for life was indeed accurate.

,esearchers have since found that vitamins are essential organic compounds that the human body

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cannot synthesi"e. Vitamins A K and B are classified as fat0soluble vitamins whereas others

are classified as water0soluble vitamins.

Vitamin A was the first fat0soluble vitamin to be discovered. Barly observations by ancient

Bgyptians recogni"ed that night blindness could be treated with consumption of liver. +wo

independent research teams 6sborne and -endel at #ale Lniversity and -c&ollum and avis at

the Lniversity of Eisconsin simultaneously discovered vitamin A in 1(1>. Vitamin A is made

up of a family of compounds called the retinoids. +he term retinoids includes all molecules

including synthetic molecules3 that are chemically related to retinol. +he 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. Gowever the o*idi"ed

metabolites retinaldehyde and retinoic acid are also biologically active compounds.,etinaldehyde 110cis3 is the essential form of vitamin A that is re%uired for normal vision

whereas retinoic acid is necessary for normal morphogenesis growth and cell differentiation.

Vitamin A also plays a role in iron utili"ation humoral immunity + cell/mediated immunity

natural killer cell activity and phagocytosis.

+here are essentially > forms of vitamin AD retinols beta carotenes and carotenoids. ,etinol also

known as preformed vitamin A is the most active form and is mostly found in animal sources of

food. Ieta carotene also known as provitamin A is the plant source of retinol from which

mammals make two0thirds of their vitamin A. &arotenoids the largest group of the > contain

multiple conjugated double bonds and e*ist in a free alcohol or in a fatty acyl0ester form.Vitamin

A is commercially available in esterified forms e.g. acetate palmitate3 since it is more stable as

an ester.

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2.2 METABOLIC FUNCTIONS OF VITAMIN A

Vitamin A plays a role in a variety of functions throughout the body such asD

• Vision.

• 5ene transcription.

• $mmune function.

• Bmbryonic development and reproduction.

• Ione metabolism.

• Gaematopoiesis.

• kin health.

• ,educing risk of heart disease.

• Antio*idant Activity.

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Vision

+he role of vitamin A in the vision cycle is specifically related to the retinal form. Eithin the eye

110cis0retinal is bound to rhodopsin rods3 and iodopsin cones3 at conserved lysine residues. As

light enters the eye the 110cis0retinal is isomeri"ed to the all0JtransJ form. +he all0JtransJ retinal

dissociates from the opsin in a series of steps called bleaching. +his isomeri"ation induces a

nervous signal along the optic nerve to the visual center of the brain. Lpon completion of this

cycle the all0JtransJ0retinal can be recycled and converted back to the 110JcisJ0retinal form via a

series of en"ymatic reactions. Additionally some of the all0JtransJ retinal may be converted to

all0JtransJ retinol form and then transported with an interphotoreceptor retinol0binding protein

$,I3 to the pigment epithelial cells. Hurther esterification into all0JtransJ retinyl esters allow

this final form to be stored within the pigment epithelial cells to be reused when needed. +he

final conversion of 110cis0retinal 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. 6nce retinol

has been taken up by a cell it can be o*idi"ed to retinal by retinol dehydrogenases3 and then

retinal can be o*idi"ed to retinoic acid by retinal o*idase3. +he 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. ,etinoic acid can bind to two different nuclear

receptors to initiate or inhibit3 gene transcriptionD the retinoic acid receptors ,A,s3 or the

retinoid J@J receptors ,@,s3. ,A, and ,@, must dimeri"e before they can bind to the MA.

,A, will form a heterodimer with ,@, ,A,0,@,3 but it does not readily form a homodimer

,A,0,A,3. ,@, on the other hand readily forms a homodimer ,@,0,@,3 and will form

heterodimers with many other nuclear receptors as well including the thyroid hormone receptor

,@,0+,3 the Vitamin > receptor ,@,0V,3 the pero*isome proliferator0activated receptor

,@,0A,3 and the liver J@J receptor ,@,0=@,3. +he ,A,0,@, heterodimer recogni"es

retinoid acid response elements ,A,Bs3 on the MA whereas the ,@,0,@, homodimer

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recogni"es retinoid J@J response elements ,@,Bs3 on the MA. +he other ,@, heterodimers

will bind to various other response elements on the MA. 6nce the retinoic acid binds to the

receptors and dimeri"ation has occurred the receptors undergo a conformational change that

causes co0repressors to dissociate from the receptors. &oactivators can then bind to the receptor

comple* which may help to loosen the chromatin structure from the histones or may interact

with the transcriptional machinery. +he receptors can then bind to the response elements on the

MA and upregulate or downregulate3 the e*pression of target genes such as cellular retinol0

binding protein &,I3 as well as the genes that encode for the receptors themselves.

Dermatology

Vitamin A appears to function in maintaining normal skin health. +he mechanisms behind

retinoid's therapeutic agents in the treatment of dermatological diseases are being researched. Hor

the treatment of acne the most effective drug is 1>0cis retinoic acid isotretinoin3. Although its

mechanism of action remains unknown it is the only retinoid that dramatically reduces the si"e

and secretion of the sebaceous glands. $sotretinoin reduces bacterial numbers in both the ducts

and skin surface. +his is thought to be a result of the reduction in sebum a nutrient source for the

bacteria. $sotretinoin reduces inflammation via inhibition of chemotatic responses of monocytes

and neutrophils. $sotretinoin also has been shown to initiate remodeling of the sebaceous glandsN

triggering changes in gene e*pression that selectively induces apoptosis. $sotretinoin is a

teratogen and its use is confined to medical supervision.

2.3 SOURCES OF VITAMIN A

Vitamin A is found naturally in many foodsD

• liver beef pork chicken turkey fish3 8!)) ;g 92273

•

carrot >! ;g (>73

• broccoli leaf )) ;g (7 3

• sweet potato 9)( ;g 9(73

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http://en.wikipedia.org/wiki/Teratogenhttp://en.wikipedia.org/wiki/Liverhttp://en.wikipedia.org/wiki/Carrothttp://en.wikipedia.org/wiki/Broccolihttp://en.wikipedia.org/wiki/Broccolihttp://en.wikipedia.org/wiki/Sweet_potatohttp://en.wikipedia.org/wiki/Sweet_potatohttp://en.wikipedia.org/wiki/Liverhttp://en.wikipedia.org/wiki/Carrothttp://en.wikipedia.org/wiki/Broccolihttp://en.wikipedia.org/wiki/Sweet_potatohttp://en.wikipedia.org/wiki/Teratogen


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• kale 81 ;g 9873

• butter 84 ;g 9873

• spinach 48( ;g !273

• leafy vegetables

• pumpkin >8( ;g 4173

• collard greens >>> ;g >973

• cantaloupe melon 18( ;g 1(73

• egg 14) ;g 1873

• apricot (8 ;g 1173

• papaya !! ;g 873

• mango > ;g 473

• pea > ;g 473

• broccoli >1 ;g >73

• winter s%uash

MoteD bracketed values are retinol e%uivalences and percentage of the adult male ,A per 1))g.

&onversion of carotene to retinol varies from person to person and bioavailability of carotene in

food varies.

2.4 VITAMIN A DEFICIENC

8

http://en.wikipedia.org/wiki/Kalehttp://en.wikipedia.org/wiki/Butterhttp://en.wikipedia.org/wiki/Spinachhttp://en.wikipedia.org/wiki/Leaf_vegetablehttp://en.wikipedia.org/wiki/Pumpkinhttp://en.wikipedia.org/wiki/Collard_greenshttp://en.wikipedia.org/wiki/Cantaloupe_melonhttp://en.wikipedia.org/wiki/Egg_(food)http://en.wikipedia.org/wiki/Apricothttp://en.wikipedia.org/wiki/Apricothttp://en.wikipedia.org/wiki/Papayahttp://en.wikipedia.org/wiki/Mangohttp://en.wikipedia.org/wiki/Peahttp://en.wikipedia.org/wiki/Winter_squashhttp://en.wikipedia.org/wiki/Recommended_Dietary_Allowancehttp://en.wikipedia.org/wiki/Kalehttp://en.wikipedia.org/wiki/Butterhttp://en.wikipedia.org/wiki/Spinachhttp://en.wikipedia.org/wiki/Leaf_vegetablehttp://en.wikipedia.org/wiki/Pumpkinhttp://en.wikipedia.org/wiki/Collard_greenshttp://en.wikipedia.org/wiki/Cantaloupe_melonhttp://en.wikipedia.org/wiki/Egg_(food)http://en.wikipedia.org/wiki/Apricothttp://en.wikipedia.org/wiki/Papayahttp://en.wikipedia.org/wiki/Mangohttp://en.wikipedia.org/wiki/Peahttp://en.wikipedia.org/wiki/Winter_squashhttp://en.wikipedia.org/wiki/Recommended_Dietary_Allowance


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$n the human body retinol is the predominant form and 110cis 0retinol is the active form.

,etinol0binding protein ,I3 binds vitamin A and regulates its absorption and metabolism.

Vitamin A is essential for vision especially dark adaptation3 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. $t functions as an

activator of gene e*pression by retinoid alpha0receptor transcription factor and ligand0dependent

transcription factor.

eficiency of vitamin A is found among malnourished elderly and chronically sick populations

in the Lnited tate but it is more prevalent in developing countries such as $ndonesia. Abnormal

visual adaptation to darkness dry skin dry hair broken fingernails and decreased resistance toinfections are among the first signs of vitamin A deficiency VA3.

+he risk of VA is increased in patients suffering from fat malabsorption cystic fibrosis sprue

pancreatic insufficiency $I or cholestasis as well as in persons who have undergone small0

bowel bypass surgery. +he risk is also increased in vegans refugees recent immigrants persons

with alcoholism and toddlers and preschool children living below the poverty line. +hese

patients should be advised to consume vitamin A.

ubclinical forms of VA 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. atients may have a recent history of increased infections infertility secondary to

impaired spermatogenesis or recent spontaneous abortion secondary to impaired embryonic

development. +he patient may also report increased fatigue as a manifestation of VA anemia.

igns and symptoms of vitamin A deficiency include the followingD

• Iitot spots 0 Areas of abnormal s%uamous cell proliferation and keratini"ation of the

conjunctiva can be seen in young children with VA.

• Ilindness due to retinal injury 0 Vitamin A has a major role in phototransduction. +he

cone cells are responsible for the absorption of light and for color vision in bright light.

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+he rod cells detect motion and are responsible for night vision. $n the rod cells of the

retina all0trans0retinol is converted into 110cis 0retinol which then combines with a

membrane0bound protein called opsin to yield rhodopsin.11 A similar type of reaction

occurs in the cone cells of the retina to produce iodopsin. +he visual pigments absorb

light at different wavelengths according to the type of cone cell they occupy. VA leads

to a lack of visual pigmentsN this reduces the absorption of various wavelengths of light

resulting in blindness.

• oor adaptation to darkness nyctalopia3

• ry skin

• ry hair

• ruritus

• Iroken fingernails

• Keratomalacia

• @erophthalmia

• &orneal perforation

• Hollicular hyperkeratosis phrynoderma3 secondary to blockage of hair follicles with

plugs of keratin.

• 6ther signs of VA include e*cessive deposition of periosteal bone secondary to reduced

osteoclastic activity anemia keratini"ation of mucous membranes and impairment of the

humoral and cell0mediated immune system.

.& !A0%!0I%#%2

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6nce ingested provitamins A are released from proteins in the stomach. +hese retinyl esters are

then hydroly"ed to retinol in the small intestine because retinol is more efficiently absorbed.

&arotenoids are cleaved in the intestinal mucosa into molecules of retinaldehyde which is

subse%uently reduced to retinol and then esterified to retinyl esters. +he 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. $n the body !)0)7 of vitamin A is

stored in the liver where it is bound to the cellular ,I. +he 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 mobili"ed from the liver to peripheral tissue by a process of deesterification of

the retinyl esters. $n blood vitamin A is bound to ,I which transports it as a comple* withtransthyretin. +he hepatic synthesis of ,I is dependent on the presence of "inc and amino acids

to maintain its narrow serum range of 4)0!) mcg


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human body whereas )0()7 of retinyl esters from animal proteins are absorbed. &arotenoid

absorption is affected by dietary factors including "inc deficiency abetalipoproteinemia and

protein deficiency.

Iecause vitamin A is a fat0soluble vitamin any 5$ diseases affecting the absorption of fats also

affect vitamin A absorption. atients with cystic fibrosis sprue pancreatic insufficiency

inflammatory bowel disorder $I3 or cholestasis as well as persons who have undergone

small0bowel bypass surgery are at increased risk for VA. +hese patients should be advised to

consume vitamin A.

6ne factor affecting the metabolism of vitamin A is alcoholism. Alcohol dehydrogenase

cataly"es the conversion of retinol to retinaldehyde which is then o*idi"ed to retinoic acid. +he

affinity of alcohol dehydrogenase to ethanol impedes the conversion of retinol to retinoic acid.

$ncreased re%uirements of vitamin A most commonly occur among sick children. +he American

Academy of ediatrics has recommended vitamin A supplementation for infants aged 8024

months who are hospitali"ed with measles and for all hospitali"ed children older than 8 months.

$n the 1(8)s the Eorld Gealth 6rgani"ation EG63 undertook the first global survey of

Vitamine A eficiency with associated *erophthalmia and complicated measles. $n 1(9> an

international vitamin A board was set up to alleviate global malnutrition.

+he EG6 and the Lnited Mations $nternational &hildren's Bmergency Hund LM$&BH3 have

issued joint statements recommending that vitamin A be administered to all children especially

those younger than 2 years who are diagnosed with measles. &oe*istent VA in young children

increases the risk of death. +he &ochrane atabase ystemic ,eview concluded that daily

treatment with 2))))) $L of vitamin A for at least 2 days reduces mortality rates.

regnant women do not re%uire increased vitamin A supplementation. $n fact the +eratology

ociety advocates that women be informed of the possible risk of cranial neural crest defects and

other malformations resulting from e*cessive use of vitamin A shortly before or during

pregnancy. +he recommended daily allowance ,A3 of )) mcg for all adult females is also

appropriate for pregnant women because their stores of vitamin A meet the fetal accretion rate.

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+he re%uirements for lactating women have been debated but the current ,A is 1>)) mcg in

the first 8 months and 12)) mcg in the second 8 months.

+he ,As of vitamin A for various age groups are as followsD

• $nfants aged 1 year or younger 0 >9! mcg

• &hildren aged 10> years 0 4)) mcg

• &hildren aged 408 years 0 !)) mcg

• &hildren aged 901) years 0 9)) mcg

• All males older than 1) years 0 1))) mcg

• All females older than 1) years 0 )) mcg

2.6 TREATMENT AND MEDICATION

TREATMENT

M!"#$%& $%'!(

+reatment for subclinical VA includes the consumption of vitamin A/rich foods such

as liver beef chicken eggs fortified milk carrots mangoes sweet potatoes and leafy green

vegetables.

Hor VA syndromes treatment includes daily oral supplements as followsD

• &hildren aged > years or younger 0 8)) mcg 2))) $L3

• &hildren aged 40 years 0 ()) mcg >))) $L3

• &hildren aged (01> years 0 19)) mcg !88! $L3

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• &hildren aged 1401 years 0 2)) mcg (>>! $L3

• All adults 0 >))) mcg 1)))) $L3

+herapeutic doses for severe disease include 8)))) mcg 2))))) $L3 which has been

shown to reduce child mortality rates by >!09)7.

D#!) (

• +he ietary 5uidelines for Americans from the L departments of Agriculture and

Gealth and Guman ervices recommend consumption of a variety of foods for a

comprehensive nutrient intake. Vitamin A / rich foods include the following.

o =iver

o Ieef

o &hicken

o Bggs

o Ehole milk

o Hortified milk

o &arrots

o -angoes

o 6range fruits

o weet potatoes

o pinach kale and other green vegetables

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• Bating at least ! 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 1)01!7 of the ,A of vitamin A.

MEDICATION

+he goals of pharmacotherapy are to reduce morbidity and to prevent complications

6$M5 $M+B,A&+$6M &6M+,A$M

$KA$

,B&AL+$6M

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Adult

>))) mcg 1)))) $L3 6 %d

evere diseaseD 8)))) mcg

2))))) $L3 6 for at least 2 d

&holestyramine

neomycin and

mineral oil may

decrease absorption

ocumented

hypersensitivity

N

hypervitaminosis AN pregnancy

if dose ?))

mcg yearsD 8)) mcg 2))) $L3 6

%d

40 yearsD ()) mcg >))) $L3 6

%d(01> yearsD 19)) mcg !88! $L3

6 %d

1401 yearsD 2)) mcg (>>! $L3

6 %d

evere diseaseD 8)))) mcg

2))))) $L3 6 for at least 2 d

Precautions

,isk of teratogenicity

increases in pregnant

women at doses ?))

mcg


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CHAPTER III

XEROPHTHALMIA DISEASE

3.1 D!*#+#)#,+

Xerophthalmia is a term that comes from the 5reek and means literally Jry ByesJ. +his is a

progressive medical condition in which the eye does not produce tears presenting e*treme

dryness and thickening of the conjunctiva due to decreased function of the tear or increased

evaporation of tears. +he cornea may be thickened and visual acuity may be decreased.

+his condition appears often as a result from disease locali"ed in the eye from a systemic

deficiency of vitamin A trauma or any condition in which the eyelids do not close completely.

@erophthalmia receives also other names such as @eroma ry Bye yndrome Keratitis icca

or Keratoconjunctivitis icca.

@erophthalmia usually occurs in people who are otherwise healthy but it is more common with

senior individuals because tear production decreases with age. $n a few rare cases it can be

associated with rheumatoid arthritis lupus erythematosis and other similar diseases common in

the elderly too. $t may also be caused by accident with thermal or chemical burns.

ymptoms and signs of this condition are dry eye ranging from a mild irritation and foreign body

sensation to severe discomfort with sensitivity to light.

Ehen @erophthalmia is due to vitamin A deficiency the condition begins with night blindness

and conjunctival *erosis dryness of the eye membranes3 and progresses to corneal *erosis

dryness of the cornea3 and in the late stages to keratomalacia softening of the cornea3. eries

of changes in the eye can lead to blindness.

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3.2 CAUSES OF XEROPHTHALMIA

@erophthalmia disease is caused by deficiency of vitamin A. Vitamin A deficiency is caused byD

• Absorption problems.

• eficiency of protein or "inc can reduce the amount of vitamin A released from the liver.

• $nterference with conversion of beta0carotene to retinol.

• =ow intake.

• Vitamin A storage problems.

3.3 SIGN AND SMPTOM

• Iitot's spots

• iarrhea

• ry eyes

• Hollicular hyperkeratosis 0 common areasD interior thighs and posterior arms

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• Keratini"ation

• =oss of bone

• =oss of both taste and smell

• =oss of tooth enamel

• Might blindness

• 6pacity

• ,educed immunity

• ,espiratory infections

• loughing 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. $ts 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

H,-! C%'! S//!0)#,+0

$mmunity vitamin A is necessary for maintaining the integrity of the mucus membranes3. $t is

necessary for differentiation of basal cells into mucus epithelial cells. $t is needed for growth and

development of enamel forming epithelial cells3 skeletal tissues and soft tissues. Vitamin A is

also necessary for humoral and cell0mediated immunity and for normal reproduction and

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lactation. ,etinyl esters from the diet are converted to retinal in the eye. ,etinal is then combined

with the protein opsin to form rhodopsin in the rods of the retina and iodopsin in the cones.

teroid hormone synthesis and cell differentiation also need vitamin A.

M#+"B," C,+0#"!'%)#,+0

Any eye disease is naturally distressing for the patient. +oday there is plenty that can be done to

alleviate this. $ncluding doses of vitamin A in the diet is one way of avoiding *erophthalmia. +he

worse thing to do is to assume that any disease is incurable. A positive attitude is necessary for

successful treatment. Avoid e*posures to the sun and perform slow neck rolls and other eye

e*ercises.

CHAPTER IV

THE CORRELATION BETWEEN VITAMIN A DEFICIENC AND

XEROPHTHALMIA AMONG CHILDREN UNDER 5 EARS IN CENTRAL

JAVA 12

+he most common cause of blindness in developing countries is vitamin A deficiency VA3.

+he Eorld Gealth 6rgani"ation EG63 estimates 1>. million children to have some degree of

visual loss related to VA. Might blindness and its worsened condition *erophthalmia are

markers of VA as VA can also lead to impaired immune function cancer and birth defects.

1((2 in &entral Cava $ndonesia3 found !)7 children under ! years old are suffer by

*erophthalmia disease.

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Might blindness *erophthalmia is the difficulty for the eyes to adjust to dim light. Affected

individuals are unable to distinguish images in low levels of illumination. eople with night

blindness have poor vision in the darkness but see normally when ade%uate light is present.

VA affects vision by inhibiting the production of rhodopsin the eye pigment responsible for

sensing low light situations. ,hodopsin is found in the retina and is composed of retinal an

active form of vitamin A3 and opsin a protein3. Iecause 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 inade%uate retinal to bind with opsin. Might blindness results.

Might blindness caused by VA has been associated with the loss of goblet cells in the

conjunctiva a membrane covering the outer surface of the eye. 5oblet cells are responsible for

secretion of mucus and their absence results in *erophthalmia a condition where the eyes fail to

produce tears. ead epithelial and microbial cells accumulate on the conjunctiva and form debris

that can lead to infection and possibly blindness.

ecreasing night blindness re%uires the improvement of vitamin A status in at risk populations.

upplements and fortification of food have been shown to be effective interventions. upplement

treatment for night blindness includes high doses of vitamin A 2))))) $L3 in the form of retinyl

palmitate to be taken by mouth which is administered two to four times a year. $ntramuscular injections are poorly absorbed and are ineffective in delivering sufficient bio0available vitamin

A. Hortification of food with vitamin A is costly but can be done in wheat sugar and milk.

Gouseholds may circumvent e*pensive fortified food by altering dietary habits. &onsumption of

yellow0orange fruits and vegetables rich in carotenoids specifically beta carotene provides pro0

vitamin A precursors that will prevent VA related night blindness.

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CHAPTER V

CONCLUTION

• +here are essentially > forms of vitamin AD retinols beta carotenes and carotenoids.

,etinol also known as preformed vitamin A is the most active form and is mostly

found in animal sources of food. Ieta carotene also known as provitamin A is the

plant source of retinol from which mammals make two0thirds of their vitamin A.

&arotenoids the largest group of the > contain multiple conjugated double bonds and

e*ist in a free alcohol or in a fatty acyl0ester form.

• +he role of vitamin A in the vision cycle is specifically related to the retinal form.

Eithin the eye 110cis0retinal is bound to rhodopsin rods3 and iodopsin cones3 at

conserved lysine residues. As light enters the eye the 110cis0retinal is isomeri"ed to

the all0JtransJ form. +he all0JtransJ retinal dissociates from the opsin in a series of

steps called bleaching. +his isomeri"ation induces a nervous signal along the optic

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nerve to the visual center of the brain. Lpon completion of this cycle the all0JtransJ0

retinal can be recycled and converted back to the 110JcisJ0retinal form via a series of

en"ymatic reactions. Additionally some of the all0JtransJ retinal may be converted to

all0JtransJ retinol form and then transported with an interphotoreceptor retinol0

binding protein $,I3 to the pigment epithelial cells. Hurther esterification into

all0JtransJ retinyl esters allow this final form to be stored within the pigment

epithelial cells to be reused when needed. +he final conversion of 110cis0retinal will

rebind to opsin to reform rhodopsin in the retina. ,hodopsin is needed to see black

and white as well as see at night. $t is for this reason that a deficiency in vitamin A

will inhibit the reformation of rhodopsin and lead to night blindness *erophthalmia3.

•+reatment for subclinical VA includes the consumption of vitamin A/richfoods such as liver beef chicken eggs fortified milk carrots mangoes sweet

potatoes and leafy green vegetables.

• Vitamin A is also necessary for humoral and cell0mediated immunity and for normal

reproduction and lactation. ,etinyl esters from the diet are converted to retinal in the

eye. ,etinal is then combined with the protein opsin to form rhodopsin in the rods of

the retina and iodopsin in the cones. teroid hormone synthesis and cell

differentiation also need vitamin A.

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BIBLIOGRAPH

1. =atham -ichael B. Human Nutrition in the Developing World (Fao Food and Nutrition

Paper). Hood O Agriculture 6rgani"ation of the Lnited. 1((9

2. Lnderwood Iarbara A. Vitamin A Deficiency Disorders: nternational !fforts to "ontrol

A Preventa#le $Po%&' & Nutr . 1>4D 2>1/2>8. 2))4.

>. tolt"fus ,C Gakimi - -iller KE et al. High dose vitamin A supplementation of

#reastfeeding ndonesian mothers: effects on the vitamin A status of mother and infant .

& Nutr& 123 43D 888/9!. 1((>

*& ME olomons - 6ro"co. Alleviation of Vitamin A deficiency +ith palm fruit and its

products. Asia ac C &lin Mutr. 2))>

!. ,oncone . ,erophthalmia secondary to alcoholinduced malnutrition. 6ptometry t.

=ouis -o.3 77 >3D 124/>>. 2))8

8. Available at D httpD


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Documents

The Correlation Between Vitamine a Deficiency and Xerophthalmia Among Children Under Five Years in Central Java