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Rebecca Abiog Castro, MD Pediatric 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 is no evidence of clinical xeropthalmia. WHO 1998


Major nutritional concern in poor societies, especially in developing countries Assessed by measuring the prevalence of deficiency in a population, represented by:
specific biochemical markers (low serum retinol) clinical indicators of status (xerophthalmia)



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


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



Vitamin A (called retinol in mammals) is a fat-soluble vitamin Beta-carotene is converted to vitamin A in the body: 6 mg of betacarotene = equivalent of 1 mg of vitamin A

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 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

Vitamin A: Functions
Vision Epithelial differentiation Growth Reproduction Pattern formation during embryogenesis Bone development Hematopoiesis Brain development Immune system function


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)

VITAMIN A: Absorption & Bioavailability

Within the enterocyte: precursors of vitamin A (carotenoids) are converted to active forms of the vitamin; Newly formed products & precursors packaged into chylomicrons and readied for transport throughout the body



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:
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 hepatic stellate (star-shaped) cells along with droplets of lipid (fatsoluble) Retinol returning to the liver is re-esterfied before storage

VITAMIN A: 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; Excess beta-carotene supplementation carotenemia

Vitamin A:


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 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):
Infancy Childhood Pregnancy Lactation

VITAMIN A Deficiency: Clinical Features

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 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 bronchial obstruction

Respiratory tract

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, blindness
poor overall growth, susceptibility to infections Anemia Apathy mental retardation

Bitot spot


Vitamin A Deficiency: Diagnosis

Clinical manifestations:
Night blindness Xeropthalmia (Bitots spot, keratomalacia)

Dark adaptation tests deficiency

assess early-stage vitamin A

Vitamin A levels (NV:2060 g/dL)


Sign of vitamin A deficiency Treatment:

< 6 months: 150,000 IU 6-12 months: 100,000 IU > 12 months: 200,000 IU X 3 = 450,000 IU x 3 = 300,000 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)

Green leafy vegetables Yellow fruits & vegetables Milk Egg Fortified foods



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 storage Low serum iron concentration Low transferrin No frank anemia 3. Iron deficiency anemia Low Hgb/Hct value

A significant body of causal evidence exists for: 1. Iron-deficiency anemia and work productivity 2. Severe anemia and child mortality 3. Severe anemia and maternal mortality 4. Iron-deficiency anemia and child development

Tissue effects of IDA: 1. GIT: anorexia, pica, atrophic glossitis, leaky-gut syndrome (exudative enteropathy) 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., sulfate, gluconate, fumarate) provides inexpensive and satisfactory therapy.

What can be done?

Therapeutic dose 46 mg/kg of elemental iron in 3 divided doses Ferrous sulfate - 20% elemental iron by weight.

Problems with oral iron tx


Unpleasant taste - can be camouflaged by mixing with flavored syrup

2. Older children and adolescents sometimes have GI complaints 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 to the 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. Complementary feeding of 4-6 tablespoons of porridge and 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.

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 buccal mucosa 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)
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; 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=24/hpf

Case: Laboratory Interpretation

Mild anemia microcytic (low MCV), hypochromic (low MCH) with low RBC count slightly 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?

Underweight Severe ( WFA: z= < -3) Stunted (LFA= < - 2) Wasting: WFL=

Vitamin A Deficiency
Bitots spot right eye

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 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 with blood indices determination Peripheral smear

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)

Vitamin A: 200,000 IU given for 3 doses on day 1, and 2 weeks after the first dose Adequate food intake with five basic groups eaten daily* 2

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

5) Outline the preventive measures on these problems.

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
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) laborers (Hard Labor, Manual Labor) Frequent Blood Donors

5. 6.

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