vitamins a deficiency.pdf

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STUDENT PROJECT

CHILDHOODS VITAMIN A DEFICIENCY

CREATED BY:

FARADILLA NOVITA ANGGREINI (0802005008)

MARIA CHRISMAYANI HINDOM (0802005018)

MADE UTARI RIMAYANTI (0802005025)

I GEDE CANDRA KARDANA NOPRASETYO (0802005035)

SUBA KAMARASAMY (0802005165)

NAGASANGKARI GOVINDASAMY (0802005171)

SUGANTHI CHANDIASEKHARA (0802005183)

JASVINJEET KAUR SIDHU (0802005184)

THINES RAMALINGAM (0802005189)

YUWANESWARY MANIAM (0802005204)

SGD B2.2 ENGLISH CLASS

5TH

SEMESTER

FACULTY OF MEDICINE UDAYANA UNIVERSITY

DENPASAR

2010


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PREFACE

We would like to say thanks to the Lord for His charity, because of Him, we can

finish this scientific writing as our student project on the time that have been

given to us.

Scientific writing based on the literatur titled Childhoods Vitamin A Deficiency

was made in order to complete and pass student project of endocrine system,

metabolism, and disorders block in 5th semester. Wishes that we can be able and

applicate our ability to compile scientific writing systematically which comes

from valid literatures.

In this chance, I would thank to:

1. dr. Ketut Suwetra, MS, AIF, Sp.GK as our block coordinator of ClinicalNutrition Block,

2. All the planners team and lecturers in Clinical Nutrition Block,3. dr. I Gusti Lanang Sidiarta, Sp.A (K) as our supervisor,4. dr. I Wayan Sumardika, M.Med.Ed as our facilitator, and5. All parties that have given supports for us in compiling this scientific

writing neither morally or materially.

We recognize that this writing still far away from perfection. Accordingly, we

wish more suggestions and critics for making this writing better. Finally, we also

hope this scientific writing can give positive contribution for the development of

knowledge, especially in medical field.

Denpasar, 22n of December 2010

Writers


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CONTENTS

Content Page

REPORT COVER ........................................................................................ i

PREFACE ..................................................................................................... ii

CONTENTS .................................................................................................. iii

FIGURE LISTS ............................................................................................ iv

TABLE LISTS .............................................................................................. iv

ABBREVIATIONS ...................................................................................... v

SECTION I INTRODUCTION .............................................................. 1

SECTION II CONTENTS REVIEW ...................................................... 3

2.1 Pathophysiology of Vitamin A Deficiency ................... 32.2 Clinical Manifestation of Vitamin A Deficiency ......... 42.3Nutritional Assessment for Vitamin A Deficiency ........ 7

2.3.1 Dietary Evaluation and Personal Histories ....... 7

2.3.2 Anthropometry ................................................. 8

2.3.3 Clinical Observation ......................................... 92.3.4 Biochemistry Test ............................................. 9

2.4 Evaluating Diagnosis for Vitamin A Deficiency .......... 112.4.1 Diagnosing Strategies ....................................... 11

2.4.2 Differential Diagnosis ...................................... 12

2.5Nutritional Management of Vitamin A Deficiency ..... 132.5.1 Adequate Intake Vitamin A for Primary Prevention 15

2.5.2 Treatment for Vitamin A Deficiency ............... 16

2.6 Complication and Prognosis of Vitamin A Deficiency . 18SECTION III SUMMARY ........................................................................ 20

REFERENCES ............................................................................................. 21


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FIGURELISTS

Figure 1. Spectrum of Vitamin A Deficiency Disorders .......................... 5

Figure 2. Ocular Manifestation of VAD. (A) Conjunctiva Xerosis,

(B) Bitots Spot, (C) Corneal Xerosis, (D) Corneal Ulcer,

(E) Corneal Scar, and (F) Follicular Hyperkeratosis ................. 6

TABLELISTS

Table 1. Selected Animal Sources of Vitamin A .................................... 14

Table 2. Selected Plant Sources of Vitamin A (from -carotene) ............ 15

Table 3. Recommended Dietary Allowances (RDA) for Vitamin A ....... 16

Table 4. Adequate Intakes (AIs) for Vitamin A for Infants ..................... 16


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ABBREVIATIONS

VAD = Vitamin A Deficiency

VADD = Vitamin A Deficiency Disorder

XN = Night Blindness

X1A = Conjuctiva Xerosis

X1B = Bitots Spot

X2 = Corneal Xerosis

X3 = Corneal Ulcer

XS = Corneal ScarXF = Xeropthalmic Fundus

RBP = Retinol Binding Protein

GI = Gastrointestinal

IBD = Inflammatory Bowel Disorder

WIC = Women, Infants, and Children

MAC = Mid Arm Circumference

TSF = Triceps Skin Fold

DXA = Dual-energy X-ray Absorptiometry

BMI = Body Mass Index

CBC = Complete Blood Count

WHO = World Health Organization

NHANES = National Health and Nutrition Examination Survey

IU = International Units

DV = Daily Value

RDA = Recommended Dietary Allowances

DRI = Dietary Reference Intakes

IOM = Institute of Medicine

RAE = Retinol Activity Equivalents

NID = National Immunization Days

PEM = Protein Energy Malnutrition
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SECTION I

INTRODUCTION

Vitamin A Deficiency (VAD) is a major public health nutrition problem in the

developing world. It especially affects young children, among whom deficiency

can cause xerophthalmia and lead to blindness, limit growth, weaken innate and

acquired host defenses, exacerbate infection and increase the risk of death (West,

2002). It is the underlying cause of 650,000 early childhood deaths and has

become recognized as an important problem among women of reproductive age in

many developing countries. Chronic vitamin A deficiency may increase the risksof complications and death during pregnancy and in the postpartum period

(Checkley et. al., 2010). Best available data suggest that 140 million preschool-

aged children and 7 million pregnant women suffer from VAD every year; 1,2-3

million children and significant numbers of women die unnecessarily, and another

4.4 million children and 6,2 million women suffer from xerophthalmia (West,

2002). Nearly half of all VAD and xerophthalmia occurs in South and Southeast

Asia (Sommer and Davidson, 2002).

It is widely accepted that VAD begins when liver stores of vitamin A fall below

20 g/g (0.07 mol/g). Serum retinol levels may still be within the homeostatically

regulated normal range. By convention, serum retinol levels 20 g/dL (0.70 mol/L)

are considered deficient, although in most well-nourished populations with

adequate stores, average serum retinol levels generally exceed 30 g/dL (1.05

mol/L) (Ballew et. al., 2001; Olmedilla et. al., 2001). One of the most common

ocular manifestation of VAD is xerophthalmia. These include night blindness(XN) through corneal ulceration and keratomalacia (X3) (Sommer and Davidson,

2002).

Whereas, Vitamin A Deficiency Disorder (VADD) as physiologic disturbance

secondary to VAD may be subclinical (e.g., impaired iron mobilization, disturbed

cellular differentiation, depressed immune response) or clinical (increased

infectious morbidity and mortality, growth retardation, anemia, xerophthalmia).

VADD begins long before the onset of xerophthalmia, although the prevalence


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and severity of these disorders, including increased mortality, increase with the

severity of deficiency (Sommer, 1997; Sommer and West, 1996).

In principle, eliminating VAD can be done through three programmatic

approaches: 1) attempt to increase the intake of naturally available foods rich in

vitamin A, such as eggs, papaya and red palm oil, by improving their availability

and use by the target population; 2) enrich commonly eaten foods, such as sugar

and cooking oil, with vitamin A; 3) distribute large-dose vitamin A supplements

among the target population (Schultink, 2002).


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SECTION II

CONTENTS REVIEW

2.1 Pathophysiology of Vitamin A Deficiency

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 retinol binding protein (RBP). The remaining vitamin A is deposited into

adipose tissue, the lungs, and the kidneys as retinyl esters, most commonly as

retinylpalmitate. 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 (Harrison,

2005).

VAD may be secondary to decreased ingestion, defective absorption and altered

metabolism, or increased requirements. Serum retinol concentration reflects an

individual's vitamin A status. 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. 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


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coexisting iron deficiency (Reddy, 2002). 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 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 (Harrison, 2005).

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. 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

(Reddy, 2002). 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 (Rothman et. al., 1995).

2.2 Clinical Manifestation of Vitamin A Deficiency

Ocular manifestation of vitamin A deficiency termed xeropthalmia.

Xerophthalmia results from instability of the pre corneal tear film, which can lead

to a dull corneal appearance and a superficial punctate keratopathy noted with the

use of fluorescein. This condition is classified into several stages (Figure 1 and 2)

(Schwartz, 2010):

- XN: Night blindness. Night blindness is the earliest and most commonsymptoms of vitamin A deficiency. Because of the essential role of

vitamin A in photoreceptor function.

- X1A: Conjuctiva xerosis. Conjunctival xerosis is typically found on thetemporal, interpalpebral, and bulbar conjunctivae. Characteristically, it


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is seen as a dry, granular patch that can exhibit thickening, wrinkling,

loss of pigmentation, and transparency.

- X1B: Bitots spot. Bitot spots are triangular, perilimbal, gray plaque s ofkeratinized conjunctival debris overlying an area of conjunctival

xerosis.

- X2: Corneal xerosis.- X3: Corneal ulcer. Corneal ulcerations can be partial or full thickness. Thus

it classified again to X3A and X3B. X3A is corneal ulceration < 1/3

corneal surface, and X3B is corneal ulceration 1/3 corneal surface.

The cormeal ulcarations or keratomalacia is a full-thickness liquefactive

necrosis of the cornea. Clinically, it is a sharply demarcated lesion with

an opaque, grayish yellow appearance. The stroma can slough, either

leaving a descemetocele or, in severe cases, causing perforation and

loss of the anterior chamber.

- XS: Corneal scar.- XF: Xeropthalmic fundus.

Figure 1. Spectrum of Vitamin A Deficiency Disorders (West, 2002).

The most distinctive clinical features of VAD are present in the ocular system;

however, numerous skin findings have also been reported such as dry-thicken skin

(toad skin), erythema, pruritus, broken fingernails, dry hair, follicular

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


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of keratin (Figure 2). Phrynoderma is characterized by red-brown follicular

papules that are approximately 2-6 mm in diameter, with a central keratotic

spinous plug. These lesions are usually found clustered around the bony

prominences of the elbows and the knees, although they may extend up the thighs

and the arms. 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.

Thus infections, such as measles, may precipitate a child into clinical VAD

(Ansstas, 2010).

Figure 2. Ocular Manifestation of VAD. (A) Conjunctiva Xerosis, (B) Bitots

Spot, (C) Corneal Xerosis, (D) Corneal Ulcer, (E) Corneal Scar, and

(F) Follicular Hyperkeratosis (Ansstas, 2010; Schwartz, 2010).

A B

C D

E F


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2.3 Nutritional Assessment of Vitamin A Deficiency

Nutritional assessment should allow for the early detection of both vitamin A

deficiencies and excesses. There is no single nutrition measurement that is best,

therefore, a combination of different measures is required. Growth is an important

indicator of health and nutritional status of a child. Several basic types of

activities for nutritional assessment of patient includes (Dugan, 2008):

2.3.1 Dietary Evaluation and Personal Histories

The dietary history provides information not only on the amount and quality

of food consumed, but also on the eating patterns and behaviours of the

family. This part of the nutritional assessment also provides information on

the number of meals, snacks, and beverages consumed; special foods eaten by

the child and family; vitamin and mineral supplements ingested regularly;

food allergies; intolerances; and unusual feeding behaviours. The child and

family are asked about psychosocial factors that impact on food selection and

intake, including family history, socio-economic status, and use of the Special

Supplemental Nutrition Program for Women, Infants, and Children (WIC)

and supplemental food programs, parent/caretakers perception of the childs

nutritional status, religious and cultural considerations (Dwyer, 1999).

The quantity and quality of dietary intake are assessed by prospective food

records (with weighed or estimated food portions), retrospective 24-hour

recalls (previous 24 hours or of a typical 24-hour period), or food frequency

questionnaires. The prospective food records are usually carried out for 3 to 7

days (including a combination of weekend and weekdays) and provide the

most accurate assessment of actual intake (Dugan, 2008). Obtaining the

medical history is central to the nutritional assessment. Past and present

medical information, including the duration of the current illness, relevant

symptoms, diagnostic tests and therapies (eg, chemotherapy, radiation), and

medications, is documented. Because nutritional abnormalities are often

associated with certain disease states, it is essential to identify underlying

medical conditions and the concomitant medication history. Medications can

cause nutritional deficiencies. For example, drugs such as cholestyramine


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cause malabsorption of vitamin A. The history of past growth patterns (with

previous growth charts, as possible), onset of puberty (for the child and other

biological family members), and a developmental history (including feeding

abilities) may also be included (Dugan, 2008).

2.3.2 Anthropometry

At a minimum, nutritional assessment of a child includes a measured weight,

length or height, and head circumference (birth to age 3 years), and these

measurements are followed over time to assess short- and long-term growth

and nutritional status. For children with chronic disease, a midarm

circumference (MAC) and triceps skinfold (TSF) thickness is also part of the

assessment to determine body fat and protein stores. In addition, a dual-

energy X-ray absorptiometry (DXA) scan may be added to more thoroughly

assess body composition (percent fat, lean body, and fat mass) and bone

mineral density (Dwyer, 1999).

a. Weight

Weight is a measure of overall nutritional status with age, sex, and

height/length required for optimal interpretation. Weight is determined using

a digital or beam balance scale. Weights are recorded to the nearest 0.01 kg in

infants and 0.1 kg in older children (Dwyer, 1999).

b. Height

A measure of stature is important for monitoring long-term nutritional status.

Recumbent length is measured using a length board for children from birth to

2 or 3 years. The measurement of length requires two individuals. It is

important as vitamin A deficiency leads to growth retardation in the bones

(Dugan, 2008).

c. Head Circumference

Head growth, primarily owing to brain development, is most rapid within the

first 3 years of life. Routine measurement of head circumference (the frontal

occipital circumference) is a component of the nutritional assessment in

children up to age 3 and longer in children who are at high nutritional risk.

Head circumference is a less sensitive indicator of short-term nutritional


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status than weight and height because brain growth is generally preserved in

cases of nutritional stress. Head circumference is not a helpful nutritional

status measure in children with hydrocephalus, microcephaly, and

macrocephaly (Dwyer, 1999).

d. Body Mass Index

The weight and height measures are used the patients body mass index

(BMI). This ratio is commonly used in evaluating obesity states in relations to

risk factors (Dwyer, 1999).

2.3.3 Clinical Observation

Clinical observation is usually combined with the indications gained from

measured vital signs and physical examinations.

a. Clinical ObservationVitamin A deficiency causes follicular hyperkeratosis and night blindness. It

also causes growth failure, formation of moulted teeth, urinary tract infection,

formation of calculi and also affects digestion of gastrointestinal tract

(Dwyer, 1999).

b. Vital Signs and Physical ExaminationsThis includes the pulse rate, respiration, temperature, and blood pressure

(Dwyer, 1999).

2.4.4 Biochemistry Test

a. Serum Retinol

Serum vitamin A appears in the form of retinol and retinol-binding protein

(RBP). Serum retinol levels remain constant until liver stores are severely

depleted or contain an excess amount. Low serum levels are seen in patients

with xerophthalmia. Normal serum vitamin A levels hit above 20 mcg/dL.

Levels between 10 and 19 mcg/dL depict marginally low stores and below 10

mcg/dL indicate a deficient state. Excessive intakes of vitamin A can result in

levels over 65 mcg/dL. Ingestion of vitamin A does no effect serum levels of

retinol and therefore fasting is not necessary before a test. However, serum

samples should be protected from bright light and hemolysis after being

obtained (Dugan, 2008).


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b. Serum Retinyl Ester

Less than 5% of vitamin A in the serum is in the form of retinyl esters. Levels

increase when the capacity of the liver to store vitamin A is exceeded.

Because ingestion of vitamin A immediately preceding a test can cause levels

of these esters to rise, a patient must fast prior to being tested (Dugan, 2008).

c. Serum Carotenoid

Levels of serum carotenoid reflect current intake. Serum carotenoid levels

may be useful as a secondary measure of vitamin A in populations that

consume carotenoids as their primary vitamin A source, but not very useful

for populations consuming primarily preformed vitamin A (Dugan, 2008).

d. Relative Dose Response

The relative dose response measure is a functional test that estimates vitamin

A in liver stores. In vitamin A deficiency, retinol-binding protein accumulates

in the liver as apo-RBP, a form that is not bound to retinol. When a dose of

vitamin A is administered, holo-RBP (protein bound to retinol) is released

from the liver and an increase in serum retinol is rapidly seen. Plasma is taken

at baseline, a dose of vitamin A is given, and a plasma sample is taken 5

hours later. The percentage change in serum retinol is then calculated. A

percent- change of 20% and higher indicates a deficient liver store of vitamin

A (Dugan, 2008).

e. Conjunctival Impression Cytology

The conjunctival impression cytology test is based on the lack of normal

goblet cells and the presence of enlarged epithelial cells in the conjunctiva of

vitamin-A deficient people. Cells are transferred from the conjunctiva to filter

paper, where they are stained and examined under a microscope (Dugan,

2008).

f. Rapid Dark Adaptation Test

This test is based on measurements of the time of occurrence of the Purkinje

shift. This refers to the peak wavelength sensitivity of the retina shifting from

red to the blue end of the spectrum during the transition from day vision to

night vision. The test has high sensitivity and specificity (Dugan, 2008).


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2.4 Evaluating Diagnosis for Vitamin A Deficiency

2.4.1 Diagnosing Strategies

The diagnosis of vitamin A deficiency is based on the history of dietary

intake of food or supplements containing vitamin A. Decrease in food

consumption such as margarine, fortified soy milk, egg yolk, liver, green and

orange vegetables will lead to vitamin A deficiency (Springhouse, 2005).

Besides that, clinical signs and symptoms that suggest vitamin A deficiency

maybe helpful in diagnosing this problem. Clinical signs and symptoms such

as night blindness, xerophthalmia, growth failure and keratinization of the

epithelium indicate this deficiency (Dugan, 2008).

The most common and accurate method in diagnosing vitamin A deficiency is

through laboratory studies. This includes (Springhouse, 2005):

a. Laboratory Studies (Springhouse, 2005):

A serum retinol study is a costly but direct measure using high-performance liquid chromatography. A value of less than 0.7 mg/L in

children younger than 12 years is considered low.

A serum Retinol Binding Protein (RBP) study is easier to perform andless expensive than a serum retinol study, because RBP is a protein and

can be detected by an immunologic assay. RBP is also a more stable

compound than retinol with respect to light and temperature. However,

RBP levels are less accurate, because they are affected by serum protein

concentrations and because types of RBP cannot be differentiated .

A zinc level is useful because zinc deficiency interferes with RBPproduction.

An iron panel is useful because iron deficiency can affect themetabolism of vitamin A.

Albumin levels are indirect measures of vitamin A levels. Obtain a complete blood count (CBC) with differential if anemia,

infection, or sepsis is a possibility.

An electrolyte evaluation and liver function studies should beperformed to evaluate for nutritional and volume status.


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b. Imaging Studies: In children, radiographic films of the long bones may

be useful when an evaluation is being made for bone

growth and for excessive deposition of periosteal bone

(Springhouse, 2005).

c. Procedures: Dark-adaptation threshold should be tested (Springhouse,

2005).

d. Confirming Diagnosis: A serum level of vitamin A that falls below 10

mcg/dl confirms the diagnosis. Levels between 10

and 19 mcg/dl are also considered low but the

patient is not likely to have developed significant

symptoms (Dwyer, 1999).

2.4.2 Differential Diagnosis

Most prominent symptoms that we can found in childrens with vitamin A

deficiency is Xerophtalmia, and Nyctalopia. Xerophthalmia is a term that

usually implies a destructive dryness of the conjunctival epithelium due to

dietary vitamin A deficiency which led to conjunctivitis. Other common

forms of dry eyes are associated with autoimmune diseases such as

Rheumatoid Arthritis and Sjogren's syndrome. Comparing with vitamin A

deficiency symptoms, Sjogrens syndrome affect all the glands not only tear

gland but also salivary gland and extraglandular glands. Infalmmation of

joints will be early symptoms of Rheumatoid Arthiritis where its

inflammation can progress to glands and organs if prolonged (Shiel, 2004).

The most common cause of Nyctalopia is retinitis pigmentosa, a disorder in

which the rod cells in the retina gradually lose their ability to respond to the

light. Childrens that suffering from this genetic condition have progressive

Nyctalopia and eventually their daytime vision may also be affected. Other

than vitamin A deficiency, X-linked congenital stationary night blindness is

another cause for Nyctalopia where the rods either do not work at all or work

very little since birth but the condition does not get worse (Irons, 2006).

Symptoms other than Xerophtalmia and Nyctalopia such as Follicular

hyperkeratosis is a skin condition characterized by excessive development of


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keratin in hair follicles resulting in rough, cone-shaped, elevated papules

whose openings are often closed with a white plug of sebum. Vitamin B

complex, vitamin C and vitamin E deficiences are the differential diagnosis

other than vitamin A deficiency. Vitamin A deficiency also impaired proper

growth and reproduction in childrens such as poor absorption of other

nutrients, glandular degeneration and sterility. Minerals such as zinc, folate

and iron deficiency also impaired growth and reproduction in childrens

(Anonim, 2008).

2.5 Nutritional Management of Vitamin A Deficiency

Lack of vitamin Aessential for the functioning of the immune systemcan lead

to irreversible blindness. But before that, a child deficient in vitamin A faces a 25

per cent greater risk of dying from common ailments, such as measles, malaria or

diarrhea (De Pee and West, 1996). World Health Organizations (WHO) goal is

the worldwide elimination of vitamin A deficiency (VAD) and its tragic

consequences, including blindness, disease and premature death. To successfully

combat VAD, short-term interventions and proper infant feeding must be backed

up by long-term sustainable solutions. The arsenal of nutritional well-being

weapons includes a combination of breastfeeding and vitamin A

supplementation, coupled with enduring solutions, such as promotion of vitamin

A-rich diets and food fortification (Bialostosky et. al., 2002).

In general, there are two categories of vitamin A in diet, depending on whether the

food source is an animal or a plant. Vitamin A found in foods that come from

animals is called preformed vitamin A. It is absorbed in the form of retinol, one of

the most usable (active) forms of vitamin A. Sources includes liver, whole milk,

and some fortified food products. Retinol can be made into retinal and retinoic

acid (other active forms of vitamin A) in the body (Institute of Medicine, 2001).

Vitamin A that is found in colorful fruits and vegetables is called provitamin A

carotenoid. They can be made into retinol in the body. Common provitamin A

carotenoids found in foods that come from plants are beta-carotene, alpha-

carotene, and beta-cryptoxanthin. Among these, beta-carotene is most efficiently
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made into retinol (Institute of Medicine, 2001). Alpha-carotene and beta-

cryptoxanthin are also converted to vitamin A, but only half as efficiently as beta-

carotene.

Retinol is found in foods that come from animals such as whole eggs, milk, and

liver (Ballew et. al., 2001). Most fat-free milk and dried nonfat milk solids sold in

the United States are fortified with vitamin A to replace the amount lost when the

fat is removed. Fortified foods such as fortified breakfast cereals also provide

vitamin A. Provitamin A carotenoids are abundant in darkly colored fruits and

vegetables. The 2000 National Health and Nutrition Examination Survey

(NHANES) indicated that major dietary contributors of retinol are milk,

margarine, eggs, beef liver and fortified breakfast cereals, whereas major

contributors of provitamin A carotenoids are carrots, cantaloupes, sweet potatoes,

and spinach (Harrison, 2005).

Table 1. Selected Animal Sources of Vitamin A (Department of Agriculture,

2004)

* IU = International Units.

** DV = Daily Value. DVs are reference numbers based on the Recommended

Dietary Allowances (RDAs). They were developed to help consumers

determine if a food contains a lot or a little of a nutrient. The DV for

vitamin A is 5,000.

Vitamin A in foods that come from animals is well absorbed and used efficiently

by the body. Vitamin A in foods that come from plants is not as well absorbed as

animal sources of vitamin A. Tables 1 and 2 suggest many sources of vitamin A

and provitamin A carotenoids (Department of Agriculture, 2004).
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Table 2. Selected Plant Sources of Vitamin A (from -carotene) (Department of

Agriculture, 2004)

2.5.1 Adequate Intake Vitamin A for Primary Prevention

Recommendations for vitamin A are provided in the Dietary ReferenceIntakes (DRIs) developed by the Institute of Medicine (IOM). DRI is the

general term for a set of reference values used for planning and assessing

nutrient intake in healthy people (Institute of Medicine, 2001). The RDA

recommends the average daily dietary intake level that is sufficient to meet

the nutrient requirements of nearly all (97% to 98%) healthy individuals in

each age and gender group (Department of Health and Human Services,

2004). In Table 3, RDAs for vitamin A are listed as micrograms (mcg) of

Retinol Activity Equivalents (RAE) to account for the different biological

activities of retinol and provitamin A carotenoids. Table 3 also lists RDAs for

vitamin A in International Units (IU), which are used on food and supplement

labels (1 RAE = 3.3 IU). Information is insufficient to establish an RDA for

vitamin A for infants. AIso have been established based on the amount of

vitamin A consumed by healthy infants fed breast milk (Table 4) (Institute of

Medicine, 2001).
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Table 3. Recommended Dietary Allowances (RDA) for Vitamin A (Institute

of Medicine, 2001)

Vitamin A for infant is a crucial component since the basis for lifelong health

begins in childhood. Maternal high supplementation benefits both mother and

breast-fed infant: high dose vitamin A supplementation of the lactating

mother in the first month postpartum can provide the breast-fed infant with an

appropriate amount of vitamin A through breast milk. However, high-dose

supplementation ofpregnant women should be avoided because it can cause

miscarriage and birth defects. Since breast milk is a natural source of vitamin

A, promoting breastfeeding is the best way to protect babies from VAD.

Planting these seeds between 6 months and 6 years of age can reduce

overall child mortality by a quarter in areas with significant VAD (Ross and

Gardner, 2001).

Table 4. Adequate Intakes (AIs) for Vitamin A for Infants (Institute of

Medicine, 2001)

2.5.2 Treatment for Vitamin A Deficiency

The goals of pharmacotherapy in vitamin A deficiency are to reduce

morbidity and to prevent complications. Treatment for subclinical VAD
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includes the consumption of vitamin Arich foods, such as liver, beef,

chicken, eggs, fortified milk, carrots, mangoes, sweet potatoes, and leafy

green vegetables (Department of Health and Human Services, 2004). For

VAD syndromes, treatment includes daily oral supplements, as follows:

a. children aged 3 years: 600 mcg (2000 IU) PO qd,b.children aged 4-8 years: 900 mcg (3000 IU) PO qd,c. children aged 9-13 years: 1700 mcg (5665 IU) PO qd,d.children aged 14-18 years: 2800 mcg (9335 IU) PO qd,therapeutic doses for severe disease include 60,000 mcg (200,000 IU) for at

least 2 d, which has been shown to reduce child mortality rates by 35-70%

(De Pee and West, 1996).

Decreasing night blindness requires the improvement of vitamin A status in at

risk populations. 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

bioavailable vitamin A (Department of Health and Human Services, 2004).

Fortification of food with vitamin A is costly, but can be done in wheat,

sugar, and milk. Consumption of yellow-orange fruits and vegetables rich in

carotenoids, specifically beta carotene, provides pro-vitamin A precursors

that will prevent VAD related night blindness (Bialostosky et. al., 2002).

As an oral form, the supplementation of vitamin A is effective for lowering

the risk ofmorbidity, especially from severe diarrhea, and reducing mortality

from measles and all-cause mortality. Some countries where vitamin A

deficiency is a public health problem address its elimination by including

vitamin A supplements available in capsule form with National Immunization

Days (NIDs) forpolio eradication ormeasles (Ballew et. al., 2001). When the

correct dosage is given, vitamin A is safe and has no negative effect on

seroconversion rates for Oral Polio Vaccine or measles vaccine. However,

because the benefit of vitamin A supplements is transient, children need them

regularly every four to six months. Since NIDs provide only one dose per

year, NIDs-linked vitamin A distribution must be complemented by other
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dose programs to maintain vitamin A in children (Ramakrishnan and Hill,

2002).

2.6 Complication and Prognosis of Vitamin A Deficiency

Vitamin A deficiency may leads to a lack of visual pigments, this reduces the

absorption of various wavelengths of light, resulting in blindness. Another

complication of vitamin A deficiency is poor eye adaptation to darkness

(nyctalopia). Other complications include dry skin and dry hair scaliness of the

skin because vitamin A deficiency causes the epithelial structures to become

stratified and keratinized. It can also result in acne. Some other complications of

vitamin A deficiency include: pruritus, broken fingernails, keratomalacia,

xerophthalmia, corneal perforation resulting in corneal opacity and blindness, and

follicular hyperkeratosis (phrynoderma) secondary to blockage of hair follicles

with plugs of keratin (Ramakrishnan and Hill, 2002).

Other signs of Vitamin A deficiency 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.

Due to immune system impairment the damaged epithelial structure often

becomes infected, for example, the conjunctivae of the eyes, the linings of the the

urinary tract nad the respiratory passages. Vitamin A is called the anti-infection

vitamin and its deficiency causes infection (Shiel, 2004).

Prognosis of vitamin A deficiency disorder is good if patients are treated when the

deficiency is subclinical. The prognosis for correcting night blindness is excellent.

Up to the stage of corneal xerosis (X2), prompt treatment can result in full

preservation of sight without residual impairment (heals completely within a few

weeks) (Ramsay et. al., 2001). In the developing world, because severe degree of

vitamin A deficiency is often accompanied by severe generalized malnutrition

(PEM), death is the most likely outcome (Ramsay et. al., 2001). Mortality in

infants with severe vitamin A deficiency is up to 50%. Only about 40% of patients

with corneal xerophthalmia are alive one year later (25% are totally blind and the

remainder partially blind) (McLaren and Frigg, 2001). Morbidity increases once
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blindness has progressed or an infection has been acquired. Irreversible conditions

include punctate keratopathy, keratomalacia, and corneal perforation. Ulcerations,

tissue death, and total blindness, caused by severe vitamin A deficiency, cannot be

treated with vitamin A (McLaren and Frigg, 2001).


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SECTION III

SUMMARY

Vitamin A is first absorbed in the intestine in the form of retinol. It is then

esterified into retinyl ester and transported into liver as chylomicron component.

In the body, 50-80% of vitamin A is stored in the liver, and the remaining is

deposited into adipose tissue, the lungs, and the kidneys. The term Vitamin A

deficiency (VAD) is a major public health nutrition problem in the developing

world which can cause xerophthalmia (blindness), growth retardation, and weaken

innate and acquired host defenses. Vitamin A Deficiency Disorder (VADD) isphysiologic disturbance secondary to VAD and may be subclinical or clinical.

VAD might be primary due to lack of intake, or secondary due to defective

absorption, metabolism and increased requirements of the substance. The most

distinctive clinical features of VAD are present in the ocular system, such as

xerophtalmia; however, numerous skin findings have also been reported such as

dry-thicken skin (toad skin), erythema, pruritus, broken fingernails, dry hair,

follicular hyperkeratosis (phrynoderma). Several basic types of nutritional

assessment of patient includes dietary evaluation and personal histories,

anthropometry, clinical observations and biochemistry test. The biochemistry test

includes retinol, retinyl esters and carotenoid plasma levels, relative dose

response, conjunctival impression cytology and rapid adaptation test. A serum

level of vitamin A that falls below 10 mcg/dl confirms the diagnosis. The goals of

pharmacotherapy in vitamin A deficiency are to reduce morbidity and to prevent

complications. The management of VAD include vitamin A supplementation and

treatment of underlying disease, in case of secondary VAD. Prognosis of vitamin

A deficiency disorder is good if patients are treated when the deficiency is

subclinical. Ulcerations, tissue death, and total blindness, caused by severe

vitamin A deficiency, cannot be treated with vitamin A.


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REFERENCES

Anonim. 2003. Follicular Hyperkeratosis. http://www.dermatology.org/hairnail

smucousmembranes/graphics/jpegs.jpg (Access on 14 December 2010).

Anonim. 2008. Vitamin and Mineral Deficiencies. http://www.gainhealth.org/

about-malnutrition/vitamin-and-mineral-deficiencies (Access on 12

December 2010).

Ansstas, G. 2010. Vitamin A Deficiency. http://emedicine.medscape.com/article/

126004-overview (Access on 7 December 2010).

Ballew, C., B. A. Bowman, A. L. Sowell, and C. Gillespie. 2001. Serum Retinol

Distributions in Residents of the United States: Third National Health and

Nutrition Examination Survey 19881994. American Journal of Clinical

Nutrition 73:586-593.

Bialostosky, K., J. D. Wright, J. Kennedy-Stephenson, M. McDowell, C. L.

Johnson. 2002.Dietary Intake of Macronutrients, Micronutrients, and Other

Dietary Constituents: United States 1988-1994. Vital and Health Statistics

11(245):6-99.

Checkley, W., K. P. West, R. A. Wise, M. R. Baldwin, L. Wu, S. C. LeClerq, et.al. 2010. Maternal Vitamin A Supplementation and Lung Function in

Offspring. New England Journal of Medicine 362(19):1784-1794.

De Pee, S. and C. E. West. 1996. Dietary Carotenoids and Their Role in

Combating Vitamin A Deficiency: A Review of the Literature. European

Journal of Clinical Nutrition 50(3):S38-S53.

Dugan, C. 2008. Clinical Assessment of Nutritional Status: Nutrition in

Pediatrics. New England Journal of Medicine 306:969-972.Dwyer, J. T. 1999. Nutritional Status Dietary Assessment. Encyclopedia of

Human Nutrition 1347-1357.

Harrison, E. H. 2005. Mechanisms of Digestion and Absorption of Dietary

Vitamin A. Annu Rev Nutr 25:5.1-5.18.

Institute of Medicine. 2001.Food and Nutrition Board: Dietary Reference Intakes

for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron,
http://www.dermatology.org/hairnail%20smucousmembranes/graphics/jpegs.jpghttp://www.dermatology.org/hairnail%20smucousmembranes/graphics/jpegs.jpghttp://www.gainhealth.org/%20about-malnutrition/vitamin-and-mineral-deficiencieshttp://www.gainhealth.org/%20about-malnutrition/vitamin-and-mineral-deficiencieshttp://emedicine.medscape.com/article/http://emedicine.medscape.com/article/http://www.gainhealth.org/%20about-malnutrition/vitamin-and-mineral-deficiencieshttp://www.gainhealth.org/%20about-malnutrition/vitamin-and-mineral-deficiencieshttp://www.gainhealth.org/%20about-malnutrition/vitamin-and-mineral-deficiencieshttp://www.dermatology.org/hairnail%20smucousmembranes/graphics/jpegs.jpghttp://www.dermatology.org/hairnail%20smucousmembranes/graphics/jpegs.jpghttp://www.dermatology.org/hairnail%20smucousmembranes/graphics/jpegs.jpg


27/28

22

Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington

D. C.: National Academy Press.

Irons, K. R. 2006. Understanding Nyctalopia (Night Blindness).

http://www.associatedcontent.com/article/88281/understanding_nyctalopia_

or_night_blindness.html?cat=70 (Access on 12 December 2010).

McLaren, D. S. and M. Frigg. 2001. Sight and Life Manual on Vitamin A

Deficiency Disorders (VADD) Second Edition. New York: Oxford

University Press.

Olmedilla, B., F. Granado, S. Southon, A. J. Wright, I. Blanco, E. Gil-Martinez,

et. al. 2001. Serum Concentrations of Carotenoids and Vitamins A, E, and C

in Control Subjects from Five European Countries. British Journal of

Nutrition 85: 227-238.

Ramakrishnan, U. and I. D. Hill. 2002. Assessment and Control of Vitamin A

Deficiency Disorders. The Journal of Nutrition 132:2947S-2953S.

Ramsay, A., N. A. Sabrosa, and C. E Pavesio. 2001. Bitot's Spots and Vitamin A

Deficiency in A Child from the UK. British Journal of Ophthalmology

85(3):372.

Reddy, V. 2002.History of the International Vitamin A Consultative Group 1975-

2000. The Journal of Nutrition 132(9):2852S-2856S.

Ross, A. C. dan E. M. Gardner. 2001. The Function of Vitamin A in Cellular

Growth and Differentiation, and Its Roles During Pregnancy and Lactation.

Adv Exp Med Biol 352:187-200.

Rothman, K. J., L. L. Moore, and M. R. Singer. 1995. Teratogenicity of High

Vitamin A Intake. New England Journal of Medicine (21):1369-1373.

Schultink, W. 2002. Use of Under Five Mortality Rate As an Indicator forVitamin A Deficiency in a Population. The Journal of Nutrition 132:2881S-

2883S.

Schwartz, R. 2010. Vitamin A Deficiency. http://emedicine.medscape.com/article

/1104441-overview (Access on 7 December 2010).

Shiel, W. C. 2004. Vitamin A Deficiency. http://www.medicinenet.com/

article.htm (Access on 12 December 2010).
http://www.associatedcontent.com/article/88281/understanding_nyctalopia_or_night_blindness.html?cat=70http://www.associatedcontent.com/article/88281/understanding_nyctalopia_or_night_blindness.html?cat=70http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=11277102http://emedicine.medscape.com/articlehttp://www.medicinenet.com/%20article.htmhttp://www.medicinenet.com/%20article.htmhttp://www.medicinenet.com/%20article.htmhttp://www.medicinenet.com/%20article.htmhttp://www.medicinenet.com/%20article.htmhttp://emedicine.medscape.com/articlehttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Abstract&list_uids=11277102http://www.associatedcontent.com/article/88281/understanding_nyctalopia_or_night_blindness.html?cat=70http://www.associatedcontent.com/article/88281/understanding_nyctalopia_or_night_blindness.html?cat=70


28/28

23

Sommer, A. and K. West. 1996. Vitamin A Deficiency: Health Survival and

Vision. New York: Oxford University Press.

Sommer, A. 1997. Clinical Research and the Human Condition: Moving from

Observation to Practice. Nat Med 10:1061-1063.

Sommer, A. and F. R. Davidson. 2002. Assessment and Control of Vitamin A

Deficiency: The Annecy Accords. The Journal of Nutrition 132:2845S-

2850S.

Springhouse. 2005. Vitamin A Deficiency. Professional Guide to Disease 8:928-

939.

U. S. Department of Agricultural Research Service. 2004. USDA National

Nutrient Database for Standard Reference, Release 17.

http://www.nal.usda.gov/fnic/foodcomp (Access on 8 December 2010).

U. S. Department of Health and Human Services. 2004. Advance Data from Vital

and Health Statistics: Dietary Intake of Selected Vitamins for the United

States Population: 1999-2000. Centers for Disease Control and Prevention

National Center for Health Statistics No.339.

West, K. P. 2002.Extent of Vitamin A Deficiency Among Preschool Children and

Women of Reproductive Age. The Journal of Nutrition 132:2857S-2866S.

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