Vitamin a Deficiency... Dr Castro

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    VITAMIN A DEFICIENCY

    &

    IRON DEFICIENCY ANEMIA:

    A GLOBAL HEALTH CONCERN

    Rebecca Abiog Castro, MD

    P i tri tr nt r l H t l N triti n

    UST Hospital

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    Vitamin A Deficiency (VAD):

    Definition:

    It is the tissue concentration of vitamin A low

    is no evidence of clinical xeropthalmia.

    WHO 1998

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    VITAMIN A DEFICIENCY (VAD):A PUBLIC HEALTH PROBLEM

    Major nutritional concern in poor societies,

    especially in developing countries

    Assessed by measuring the prevalence of deficiencyin a population, represented by:

    specific biochemical markers (low serum retinol)

    clinical indicators of status (xerophthalmia)

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    A GLOBAL HEALTH CONCERN

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    VITAMIN A DEFICIENCY (VAD):A PUBLIC HEALTH PROBLEM

    Global prevalence of vitamin A deficiency in populations at risk 19952005WHO Global Database on Vitamin A Deficiency

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    LOCAL DATA:

    VAD IN THE PHILIPPINES

    4 in every 10 children or 38%, of 0-5 years of age;

    2 out of every 10 or 22% ofpregnant and 16% of lactating mothers,

    had deficient to low plasma retinol levels in 1998;

    Considering the economic situation from 1998 to the present, the

    vitamin A deficiency problem is not expected to decline, and may

    be getting worse.

    6th National Nutrition Survey FNRI, DOST

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    PHILIPPINE DATA: VAD

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    Vitamin A (called retinol in mammals) is a fat-soluble vitamin

    Beta-carotene is converted to vitamin A in the body: 6 mg of beta-

    VITAMIN A

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    The daily recommended dietary allowance (RDA) is expressed as retinol

    activity equivalents (RAEs; 1 RAE = 1 g all-trans-retinol;)

    Retinol Activity Equivalents based on age:

    infants 01 yr : 400500 g

    3 yr : 300 g

    VITAMIN A

    48 yr : 400 g

    913 yr : 600 g

    Boys 1418 yr of age and men: 900 g; Girls 1418 of age and women: 700 g

    During pregnancy: 750770 g

    during lactation: 12001300

    g

    A daily tolerable upper level of vitamin A for adults is 3,000 g of preformed

    vitamin

    Nelson Textbook of Pediatrics, 18th edition

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    Vitamin A: Functions

    Vision

    Epithelial differentiation Growth

    Reproduction

    Pattern formation during embryogenesis Bone development

    Hematopoiesis

    Brain development

    Immune system function

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    VITAMIN A: METABOLISM

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    Vitamin A: Absorption and Bioavailability

    70 90% of vitamin A from the diet is absorbed in the intestine

    Within the intestinal lumen: vitamin is incorporated into a micelle

    and absorbed across the brush border into the enterocytes

    Greater than 90% of the retinol store within the body enters as

    retinyl esters that are subsequently found within the lipid portion of

    the chylomicron

    Absorption: very rapid (maximum absorption occurring 2-6 hours

    after digestion)

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    Within the enterocyte:

    precursors of vitamin A(carotenoids) are converted to

    active forms of the vitamin;

    VITAMIN A:Absorption & Bioavailability

    Newly formed products &

    precursors packaged into

    chylomicrons and readied for

    transport throughout the body

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    Transport

    After leaving the enterocytes, chylomicrons( carry retinyl esters,

    carotenoids, and unesterfired retinol, triglycerides) are circulatedfirst through the lymphaticgeneral circulation

    VITAMIN A:

    a ex ra- epa c ce s:

    chylomicrons release triglycerides

    vitamin A remains within the chylomicron and is incorporated into a

    chylomicron remnant

    The chylomicron remnant then travels back to the liver where it is

    taken up and further metabolized or stored.

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    Vitamin A:Storage

    Approximately 50 to 85% of the total body retinol are stored in the

    liver when vitamin A status is adequate;

    90% of the retinol is stored in the form of retinyl esters inside

    hepatic stellate (star-shaped) cells along with droplets of lipid (fat-soluble)

    Retinol returning to the liver is re-esterfied before storage

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    Once hepatic stellate cells are saturated with all the retinol they can

    hold, hypervitaminosis can result;

    Precursor to vitamin A, beta-carotene, can be stored in adipose cells

    VITAMIN A:Storage

    o a epo s roug ou e o y;

    Excess beta-carotene supplementation carotenemia

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    Vitamin A: Excretion

    The kidneys are the main paths of RBP and retinol excretion from

    the body

    Achieved mainly via renal catabolism and glomerular filtration

    Those persons suffering from renal disease often experience

    elevated serum levels of RBP and retinol and therefore must be

    more aware of vitamin A toxicity.

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    Main underlying cause of VAD: diet that is chronicallyinsufficient in vitamin A

    VITAMIN A DEFICIENCY (VAD): A PUBLIC HEALTH PROBLEM

    CAUSE

    Can lead to lower body stores and fail to meet

    physiologic needs (e.g. support tissue growth, normal

    metabolism, resistance to infection)

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    Low vitamin A intake during nutritionallydemanding periods in life greatly raises the risk of

    vitamin A deficiency disorders (VADD):

    VITAMIN A DEFICIENCY (VAD): A PUBLIC HEALTH PROBLEM

    CAUSE

    Infancy Childhood

    Pregnancy

    Lactation

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    Vitamin A deficiency: due to chronic failure to eat sufficient

    amounts of vitamin A or beta-carotene blood-serum level

    of vitamin A defined range

    VITAMIN A Deficiency: Clinical Features

    e a-caro ene s a orm o pre-v am n rea y conver e o

    vitamin A in the body

    Night blindness is the first symptom of vitamin A deficiency

    Prolonged and severe vitamin A deficiency can produce total

    and irreversible blindness

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    Vitamin A deficiency: Clinical manifestations

    Associated with the requirement of this vitamin for the

    maintenance of epithelial functions:

    GI tractdiarrhea

    Respiratory tractbronchial obstruction

    Genito-urinary tract

    Squamous metaplasia of the renal pelvis,ureters and vagina may lead to increased infections in,

    hematuria and pyuria.

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    Vitamin A Deficiency: Clinical manifestations

    Skin dry, scaly, hyperkeratotic patches, commonly on the

    arms, legs, shoulders, and buttocks.

    Eye night blindness, xerophthalmia, bitot spots

    , ,

    Others:

    poor overall growth,

    susceptibility to infections Anemia

    Apathy

    mental retardation

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    o spo xerop a m a

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    Vitamin A Deficiency: Diagnosis

    Clinical manifestations:

    Night blindness

    Xeropthalmia (Bitots spot, keratomalacia)

    Dark adaptation tests assess early-stage vitamin A

    deficiency

    Vitamin A levels (NV:2060 g/dL)

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    Treatment

    Sign of vitamin A deficiency Treatment: < 6 months: 150,000 IU X 3 = 450,000 IU

    6-12 months: 100,000 IU x 3 = 300,000 IU

    > 12 months: 200,000 IU x 3 = 600,000 IU

    Given on day 1, day 2 and 2 weeks from first dose

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    Preventive Measures

    NO sign of vitamin A deficiency: Prophylaxis

    50,000 IU single dose (< 6month) 100,000 IU single dose (6-12 month)

    200,000 IU single dose (>12 month)

    Diet:

    Green leafy vegetables

    Yellow fruits & vegetables

    Milk

    Egg

    Fortified foods

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    IRON DEFICIENCY ANEMIA (IDA)

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    For the period 1990 to 2001, the # of underweight pre-school childrendecreased by a mere 3.9 percentage points from 34.50% in 1990 to 30.60% in 2001. In terms of pop., this translates into an estimated 3.67 million

    underweight preschool children in 2001.

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    In terms of geographical location, the Bicol Region appears to

    be the worst-off in underweight prevalence, followed byregions mostly in Mindanao island (Region 10, CARAGA,

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    The prevalence of anemia among 6 months to < 1 year has

    remained unabated since 1993, and increased from 49.2%to an alarming rate of 66 %.

    Anemia among 1-5 y/o remained at 29.1%.

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    Stages of IDA1. Iron depletion

    Storage iron is absent or decreased

    Normal serum iron conc and Hgb levels

    2. Iron deficiency without anemia

    Decreased or absent iron storage

    Low serum iron concentration

    Low transferrin

    No frank anemia

    3. Iron deficiency anemia

    Low Hgb/Hct value

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    IDAA significant body of causal evidence exists for:

    1. Iron-deficiency anemia and workproductivity

    . evere anem a an c mor a y

    3. Severe anemia and maternal mortality

    4. Iron-deficiency anemia and child

    development

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    IDATissue effects of IDA:

    1. GIT: anorexia, pica, atrophic glossitis, leaky-gutsyndrome (exudative enteropathy)

    . , ,

    function

    3. CVS: HR & CO, cardiac hypertrophy, plasma

    volume

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    What can be done?

    Regular response to adequate amounts of iron is an

    important diagnostic and therapeutic feature.

    . .,

    sulfate, gluconate, fumarate) provides inexpensiveand satisfactory therapy.

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    What can be done?

    Therapeutic dose

    46 mg/kg of elemental iron in 3 divided doses

    Ferrous sulfate - 20% elemental iron by weight.

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    Problems with oral iron tx

    1. Unpleasant taste - can be camouflaged by mixingwith flavored syrup

    2. Older children and adolescents sometimes have GIcom laints

    Constipation can be minimized by water &fiber intake

    Abdominal discomfort can be minimized by

    administering iron with food, but maydecrease iron absorption to some

    extent.

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    Case: History

    Samantha, an 18 month old female, was brought tothe out patient department due to cough and colds of 3

    days duration. She was also noted to have fast breathing.Samantha is the youngest in the brood of 3. She

    was exclusively breastfed until 10 months old.omp ementary ee ng o 4-6 ta espoons o porr ge an

    noodle soup, given once a day, was started at 12 months

    old.

    Primary series of immunization except Measles

    vaccine was given at the local health center.She was given Vitamin C 0.5 mL daily only since 6

    months old.

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    Case:Physical Examination

    PPE:

    irritable, in respiratory distress, not dehydrated, thin, not ill looking

    Wt=7.8kg (Z=< -3) Lt= 74.0cm (z=< -2) HC = 43.0cm (z= -1)CR= 135/min RR= 55/min T=380C

    sunken eyeballs, whitish plaque on right medial conjunctivae, dry buccalmucosa

    no significant adenopathiessymmetrical chest expansion, with intercostal retractions, fine crackles onboth lower lung fields

    adynamic precordium, apex beat at 4th LICS MCL, no murmurs

    abdomen slightly globular, soft, non-tender, normoactive bowel sounds,liver 2 cm below RCM, spleen not palpable

    Full pulses, slightly pale palms and soles

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    Salient Features from the History

    18 months old female

    Lower respiratory tract infection Exclusive breastfeeding until 10 months

    Late introduction of Complementary Foods (12months)

    Inadequate CF

    Poor Quality of food intake (5 basic food groups notpresent)

    Delayed Measles vaccination

    Lack of iron supplements

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    Salient Features: Physical Findings

    Thin

    In respiratory distress Anthropometric measurements:

    -

    Length: z= < - 2;

    HC= 43 cm: z= -1.

    Whitish plaque right eye

    Pale soles and palms

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    Case: Laboratory Results

    Lab results:

    CBC: Hgb=9.5g/dL; Hct=30 vol%;

    RBC=3.5M/mm3; MCV=68fL; MCH=21pg/cell;WBC=12 x 109/L, neutros=40%, lymphos=60%; Plateletcount=500 x 109/L

    Urinalysis: yellow, clear, pH=6.5, SG=1.010, RBC= 0-3/hpf, WBC=2-4/hpf

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    Case: Laboratory Interpretation

    Mild anemia

    microcytic (low MCV), hypochromic (low MCH)with low RBC count

    s g y e eva e p a e e coun

    normal WBC and differential count

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    Hypochromic cells and poikilocytes

    Normal red blood cells

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    1) What are the nutritional deficiencies present in this patient?

    PEM

    Underweight Severe ( WFA: z= < -3)

    Stunted (LFA= < - 2)

    Wasting: WFL=

    Vitamin A Deficiency

    Bitots spot right eye

    IDA:

    Pale soles and palms

    Mild anemia (hypochromic microcytic rbc)

    Guide Questions:

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    Guide Questions:

    2) Identify the risk factors for these nutritionaldeficiencies?

    Delayed introduction of CF

    Inadequate food intake:

    amount

    quality

    No iron supplements started at 6 months of age

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    3) What diagnostic tests will you request?

    PEM severe: Cbc

    TPAG

    IDA: CBC with blood indices determination

    Peripheral smear

    VAD:

    Clinical manifestations

    Serum retinol if available

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    4) How do you manage these nutritional

    deficiencies?

    PEM:

    Nutritional rehabilitation ( Ten steps in the Mx of Severely

    Malnourished children by WHO)

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    VAD:

    Vitamin A: 200,000 IU given for 3 doses on day 1, 2and 2 weeks after the first dose

    Adequate food intake with five basic groups eaten daily*

    IDA:

    3-6 mg / kg /day for 3 months

    Adequate food intake with five basic food groups eaten daily*

    * Use the PSPGN Food Guide Pyramid & Dietary prescription

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    5) Outline the preventive measures on these

    problems.

    Proper introduction of CF at 6 months

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    5) Outline the preventive measures on these problems

    Iron supplementation: 2 months for preterm infants

    6 months for term infants

    High risk groups Neonates: Prematurity, LBW, Blood loss

    Infants/toddlers and adolescentsid growth, Inadequate

    Women from menarche to menopause:

    Vegetarians esp vegans (no eggs, meat, butter, cheese)

    5. laborers (Hard Labor, Manual Labor)

    6. Frequent Blood Donors

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    5) Outline the preventive measures on these problems.

    Balanced diet: adequate intake of 5 basic food groups

    Regular growth monitoring with the use of growth charts Monthly 1st 12 months

    Quarterly > 12 months

    Annually > 5 years

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