Anda di halaman 1dari 28

STUDENT PROJECT

CHILDHOODS VITAMIN A DEFICIENCY

CREATED BY: FARADILLA NOVITA ANGGREINI MARIA CHRISMAYANI HINDOM MADE UTARI RIMAYANTI I GEDE CANDRA KARDANA NOPRASETYO SUBA KAMARASAMY NAGASANGKARI GOVINDASAMY SUGANTHI CHANDIASEKHARA JASVINJEET KAUR SIDHU THINES RAMALINGAM YUWANESWARY MANIAM SGD B2.2 ENGLISH CLASS 5TH SEMESTER (0802005008) (0802005018) (0802005025) (0802005035) (0802005165) (0802005171) (0802005183) (0802005184) (0802005189) (0802005204)

FACULTY OF MEDICINE UDAYANA UNIVERSITY DENPASAR 2010

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 Clinical Nutrition 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, and 5. 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, 22nd of December 2010

Writers

ii

CONTENTS
Content REPORT COVER PREFACE CONTENTS Page ........................................................................................ i ii

.....................................................................................................

.................................................................................................. iii ............................................................................................ iv .............................................................................................. iv ...................................................................................... .............................................................. ...................................................... ................... ......... ........ ....... v 1 3 3 4 7 7 8 9 9

FIGURE LISTS TABLE LISTS

ABBREVIATIONS SECTION I

INTRODUCTION

SECTION II CONTENTS REVIEW

2.1 Pathophysiology of Vitamin A Deficiency

2.2 Clinical Manifestation of Vitamin A Deficiency 2.3 Nutritional Assessment for Vitamin A Deficiency 2.3.1 Dietary Evaluation and Personal Histories 2.3.2 Anthropometry

................................................. ......................................... .............................................

2.3.3 Clinical Observation 2.3.4 Biochemistry Test

2.4 Evaluating Diagnosis for Vitamin A Deficiency 2.4.1 Diagnosing Strategies 2.4.2 Differential Diagnosis

.......... 11

....................................... 11 ...................................... 12 ..... 13

2.5 Nutritional Management of Vitamin A Deficiency

2.5.1 Adequate Intake Vitamin A for Primary Prevention 15 2.5.2 Treatment for Vitamin A Deficiency ............... 16 . 18

2.6 Complication and Prognosis of Vitamin A Deficiency SECTION III SUMMARY REFERENCES

........................................................................ 20

............................................................................................. 21

iii

FIGURE LISTS
Figure 1. Figure 2. Spectrum of Vitamin A Deficiency Disorders .......................... 5

Ocular Manifestation of VAD. (A) Conjunctiva Xerosis, (B) Bitots Spot, (C) Corneal Xerosis, (D) Corneal Ulcer, (E) Corneal Scar, and (F) Follicular Hyperkeratosis ................. 6

TABLE LISTS
Table 1. Table 2. Table 3. Table 4. Selected Animal Sources of Vitamin A .................................... 14 ............ 15 ....... 16

Selected Plant Sources of Vitamin A (from -carotene)

Recommended Dietary Allowances (RDA) for Vitamin A Adequate Intakes (AIs) for Vitamin A for Infants

..................... 16

iv

ABBREVIATIONS
VAD VADD XN X1A X1B X2 X3 XS XF RBP GI IBD WIC MAC TSF DXA BMI CBC WHO NHANES IU DV RDA DRI IOM RAE NID PEM = Vitamin A Deficiency = Vitamin A Deficiency Disorder = Night Blindness = Conjuctiva Xerosis = Bitots Spot = Corneal Xerosis = Corneal Ulcer = Corneal Scar = Xeropthalmic Fundus = Retinol Binding Protein = Gastrointestinal = Inflammatory Bowel Disorder = Women, Infants, and Children = Mid Arm Circumference = Triceps Skin Fold = Dual-energy X-ray Absorptiometry = Body Mass Index = Complete Blood Count = World Health Organization = National Health and Nutrition Examination Survey = International Units = Daily Value = Recommended Dietary Allowances = Dietary Reference Intakes = Institute of Medicine = Retinol Activity Equivalents = National Immunization Days = Protein Energy Malnutrition

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 risks of complications and death during pregnancy and in the postpartum period (Checkley et. al., 2010). Best available data suggest that 140 million preschoolaged 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

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).

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

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 common symptoms of vitamin A deficiency. Because of the essential role of vitamin A in photoreceptor function. - X1A: Conjuctiva xerosis. Conjunctival xerosis is typically found on the temporal, interpalpebral, and bulbar conjunctivae. Characteristically, it

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 of keratinized conjunctival debris overlying an area of conjunctival xerosis. - X2: - X3: Corneal xerosis. 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: - XF: Corneal scar. 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

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).

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 deciencies. For example, drugs such as cholestyramine

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 dualenergy 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 rst 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

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 Observation Vitamin 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 Examinations This 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).

10

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).

11

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 highperformance 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 and less 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 RBP production.

An iron panel is useful because iron deficiency can affect the metabolism 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 be performed to evaluate for nutritional and volume status.

12

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 glan ds 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

13

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 A essential for the functioning of the immune system can 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, alphacarotene, and beta-cryptoxanthin. Among these, beta-carotene is most efficiently

14

made into retinol (Institute of Medicine, 2001). Alpha-carotene and betacryptoxanthin are also converted to vitamin A, but only half as efficiently as betacarotene. 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).

15 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 Reference Intakes (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).

16

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 of pregnant 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

17 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 of morbidity, 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) for polio eradication or measles (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

18

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

19

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).

20

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) is physiologic 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.

21

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 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, (Access on 12

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 19752000. 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 for Vitamin A Deficiency in a Population. The Journal of Nutrition 132:2881S2883S. 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).

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 132:2845S2850S. Springhouse. 2005. Vitamin A Deficiency. Professional Guide to Disease 8:928939. 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.