VITAMIN A DEFICIENCY

&

IRON DEFICIENCY ANEMIA:

A GLOBAL HEALTH CONCERN

Rebecca Abiog Castro, MD

Pediatric Gastroenterology, Hepatology & NutritionPediatric Gastroenterology, Hepatology & Nutrition

UST Hospital

Vitamin A Deficiency (VAD):

Definition:

It is the tissue concentration of vitamin A low

enough to have adverse consequences even if there enough to have adverse consequences even if there

is no evidence of clinical xeropthalmia.

WHO 1998

VITAMIN A DEFICIENCY (VAD): A PUBLIC HEALTH PROBLEM

� Major nutritional concern in poor societies,

especially in developing countries

Assessed by measuring the prevalence of deficiency � Assessed by measuring the prevalence of deficiency

in a population, represented by:

� specific biochemical markers (low serum retinol)

� clinical indicators of status (xerophthalmia)

A GLOBAL HEALTH CONCERN

VITAMIN A DEFICIENCY (VAD): A PUBLIC HEALTH PROBLEM

Global prevalence of vitamin A deficiency in popula tions at risk 1995–2005WHO Global Database on Vitamin A Deficiency

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% of pregnant 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

PHILIPPINE DATA: VAD

� 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-

carotene = equivalent of 1 mg of vitamin A

VITAMIN A

carotene = equivalent of 1 mg of vitamin A

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

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

� Retinol Activity Equivalents based on age:

� infants 0–1 yr : 400–500 µg

� 3 yr : 300 µg

4–8 yr : 400 µg

VITAMIN A

� 4–8 yr : 400 µg

� 9–13 yr : 600 µg

� Boys 14–18 yr of age and men: 900 µg; Girls 14–18 of age and women: 700 µg

� During pregnancy: 750–770 µg

� during lactation: 1200–1300 µg

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

vitamin

Nelson Textbook of Pediatrics, 18th edition

Vitamin A: Functions

� Vision

� Epithelial differentiation

� Growth

� Reproduction

� Pattern formation during embryogenesis

� Bone development

� Hematopoiesis

� Brain development

� Immune system function

VITAMIN A: METABOLISM

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)

� 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

Transport

� After leaving the enterocytes, chylomicrons( carry retinyl esters,

carotenoids, and unesterfired retinol, triglycerides) are circulated

first through the lymphatic ����general circulation

� at extra-hepatic cells:

VITAMIN A:

� at extra-hepatic cells:

� 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.

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 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

� 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

of fat depots throughout the body;

VITAMIN A: Storage

of fat depots throughout the body;

� Excess beta-carotene supplementation ���� carotenemia

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.

� Main underlying cause of VAD: diet that is chronically

insufficient 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)

� Low vitamin A intake during nutritionally

demanding 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

� 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

� Beta-carotene is a form of pre-vitamin A����readily converted to

VITAMIN A Deficiency: Clinical Features

� Beta-carotene is a form of pre-vitamin A����readily converted to

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

Vitamin A deficiency: Clinical manifestations

� Associated with the requirement of this vitamin for the

maintenance of epithelial functions:

� GI tract ����diarrhea

� Respiratory tract ����bronchial obstruction

� Genito-urinary tract ����Squamous metaplasia of the renal pelvis,

ureters and vagina may lead to increased infections in,

hematuria and pyuria.

Vitamin A Deficiency: Clinical manifestations

� Skin ���� dry, scaly, hyperkeratotic patches, commonly on the

arms, legs, shoulders, and buttocks.

� Eye ���� night blindness, xerophthalmia, bitot spots

keratomalacia, corneal ulcers, blindnesskeratomalacia, corneal ulcers, blindness

� Others:

� poor overall growth,

� susceptibility to infections

� Anemia

� Apathy

� mental retardation

Bitot spot xerophthalmiaBitot spot xerophthalmia

Vitamin A Deficiency: Diagnosis

� Clinical manifestations:

�Night blindness

� Xeropthalmia (Bitot’s spot, keratomalacia)

� Dark adaptation tests ���� assess early-stage vitamin A

deficiency

� Vitamin A levels (NV:20–60 g/dL)

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� 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

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

IRON DEFICIENCY ANEMIA (IDA)

A PUBLIC HEALTH CONCERNA PUBLIC HEALTH CONCERN

For the period 1990 to 2001, the # of underweight pre-school children decreased 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.

In terms of geographical location, the Bicol Region appears to be the worst-off in underweight prevalence, followed by regions mostly in Mindanao island (Region 10, CARAGA, Regions 11, 9 and 12).

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%.

Stages of IDA

1. Iron depletion

Storage iron is absent or decreased

Normal serum iron conc and Hgb levels

2. Iron deficiency without anemia

Decreased or absent iron storageDecreased or absent iron storage

Low serum iron concentration

Low transferrin

No frank anemia

3. Iron deficiency anemia

Low Hgb/Hct value

IDA

A significant body of causal evidence exists for:

1. Iron-deficiency anemia and work

productivity

2. Severe anemia and child mortality 2. Severe anemia and child mortality

3. Severe anemia and maternal mortality

4. Iron-deficiency anemia and child

development

IDA

Tissue effects of IDA:

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

2. CNS: irritability, conduct disorder, ↓cognitive 2. CNS: irritability, conduct disorder, ↓cognitive function

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

What can be done?

Regular response to adequate amounts of iron is an important diagnostic and therapeutic feature.

Oral administration of simple ferrous salts (e.g., Oral administration of simple ferrous salts (e.g., sulfate, gluconate, fumarate) provides inexpensive and satisfactory therapy.

What can be done?

Therapeutic dose

4–6 mg/kg of elemental iron in 3 divided doses

Ferrous sulfate - 20% elemental iron by weight.

Problems with oral iron tx

1. Unpleasant taste - can be camouflaged by mixing with flavored syrup

2. Older children and adolescents sometimes have GI complaintscomplaints

Constipation can be minimized by ↑ water &

fiber intake

Abdominal discomfort can be minimized by

administering iron with food, but may

decrease iron absorption to some

extent.

Case: History

Samantha, an 18 month old female, was brought tothe out patient department due to cough and colds of 3days duration. She was also noted to have fast breathing.

Samantha is the youngest in the brood of 3. Shewas exclusively breastfed until 10 months old.Complementary feeding of 4-6 tablespoons of porridge andComplementary feeding of 4-6 tablespoons of porridge andnoodle soup, given once a day, was started at 12 monthsold.

Primary series of immunization except Measlesvaccine was given at the local health center.

She was given Vitamin C 0.5 mL daily only since 6months old.

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 buccalmucosamucosa

no significant adenopathies

symmetrical chest expansion, with intercostal retractions, fine crackles on both 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

Salient Features from the History

� 18 months old female

� Lower respiratory tract infection

� Exclusive breastfeeding until 10 months

� Late introduction of Complementary Foods (12 months)months)

� Inadequate CF

� Poor Quality of food intake (5 basic food groups not present)

� Delayed Measles vaccination

� Lack of iron supplements

Salient Features: Physical Findings

� Thin

� In respiratory distress

� Anthropometric measurements:

�Weight: z = < - 3; �Weight: z = < - 3;

� Length: z= < - 2;

� HC= 43 cm: z= -1.

� Whitish plaque right eye

� Pale soles and palms

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%; Platelet count=500 x 109/L

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

Case: Laboratory Interpretation

Mild anemia

microcytic (low MCV), hypochromic (low MCH)

with low RBC count

slightly elevated platelet countslightly elevated platelet count

normal WBC and differential count

Hypochromic cells and poikilocytes

Normal red blood cells

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

� PEM

� Underweight Severe ( WFA: z= < -3)

� Stunted (LFA= < - 2)

� Wasting: WFL=

� Vitamin A Deficiency

� Bitot’s spot right eye

� IDA:

� Pale soles and palms

� Mild anemia (hypochromic microcytic rbc)

Guide Questions:

2) Identify the risk factors for these nutritional

deficiencies?

� Still exclusively BF at 10 months� Still exclusively BF at 10 months

� Delayed introduction of CF

� Inadequate food intake:

� amount

� quality

� No iron supplements started at 6 months of age

3) What diagnostic tests will you request?

� PEM severe:

� Cbc

� TPAG� TPAG

� IDA:

� CBC with blood indices determination

� Peripheral smear

� VAD:

� Clinical manifestations

� Serum retinol if available

4) How do you manage these nutritional

deficiencies?

� PEM:� Nutritional rehabilitation ( Ten steps in the Mx of Severely

Malnourished children by WHO)

� VAD:� Vitamin A: 200,000 IU given for 3 doses on day 1, 2

and 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 prescr iption

5) Outline the preventive measures on these

problems.

� Exclusive BF until 6 months� Exclusive BF until 6 months

� Proper introduction of CF at 6 months

5) Outline the preventive measures on these problems

� Iron supplementation:

� 2 months for preterm infants

� 6 months for term 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

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