Vanessa Velazquez-Ruiz, MD
Emergency Medicine
Global Health Fellow
St. Luke’s-Roosevelt Hospital
Affect a variety of health and disease outcomes:
Child growth and development
Maternal health
Malnutrition and vulnerability to infectious diseases
Estimates of micronutrient malnutrition vary from 20% of the world population (or more than one billion persons)
Dietary deficiencies represents an enormous problem of
“hidden hunger”
Series of lectures
Week #1: Vitamin A and D
Week #2: Iron, Iodine and Zinc deficiencies
Week #3: Obesity and the other spectrum of malnutrition
Fasten your seatbelts and enjoy the ride…
Third most common deficiency in the world
Affects an estimated
125-130 million preschool age children
And 7 million pregnant women in low-income countries
Prevalent cases of pre school xerophthalmia are believed to number about 5 million
10% can be considered potentially blinding
Leading cause of preventable pediatric blindness in developing world
Underlying cause of at least 650,000 early childhood deaths due to diarrhea, measles, malaria and other infectious disease
Maternal deficiency may increase risk of maternal morbidity and mortality
Public Health problem in approx 78 countries
Most widespread across South and Southeast Asia and
Sahelian and Sub-Saharan Africa (where food supplies lack preformed vitamin A)
Clusters within counties due to common exposures to poor diet and inadequate care, malnutrition
Age
Corneal xerophthalmia- 2-3y/o
Acute onset of corneal disease may follow recent weaning from breast milk, or s/p illnesses
Gender
Male > Girls
Socioeconomics
Inversely correlates with Vit A deficiency
Retinol (preformed Vit A): animal products, liver
Beta-carotenes : Provitamin A (converted to Vit A in intestines)
Plant source of retinol from which mammals make 2/3 of their Vit A
Carotenoids: yellow, red fruits/vegetables
Essential in regulating numerous key biologic processes in the body
Morphogenesis
Growth
Nutrition
Vision
Reproduction
Immunity
Cellular differentiation and proliferation
Insufficient intake
Increase requirements during growth, pregnancy and lactation, infection
Change from breast feeding to inadequate complimentary feeding
Socio-cultural and economics factors (intra household distribution and gender preferences)
Three clinical stages:
Retinal dysfunction causing night blindness
Conjunctiva and corneal xerosis
Corneal ulceration and necrosis
Earliest manifestation
Most prevalent stage of xerophthalmia
Failure in rod photoreceptors cells in the retina
Responsive to Vitamin A supplementation
A positive history of night blindness is associated with low-to-deficient serum retinol concentrations in preschool aged children and pregnant women
Can serve as an indicator of individual and community risk of Vitamin A deficiency
Xerosis of the conjunctiva
Appears as dry, non-wettable, rough or granular surface
(best seen on oblique illumination with hand light)
Histological: transformation of normal columnar epithelium with abundant goblet cells to stratified, squamous epithelium that lacks goblet cells.
Bitot’s spots: gray-yellow patches of keratinized cells and saprophytic bacilli that aggregate on temporal limbus (lesions are bubbly, foamy or cheesy like)
Corneal xerosis (“drying”) presents as superficial punctuate erosions that lend a hazy, non-wettable, irregular appearance to the cornea
Usually both eyes
Severe xerosis, cornea becomes edematous with dry granular appearance (“peel of an orange”)
Vitamin A successfully treats corneal xerosis
Appearance: Round or oval, shallow or deep, sharply demarcated and often peripheral to the visual axis
Only one eye
Vit A will heal lesion leaving a stromal scar or leukoma
Keratomalacia (“corneal melting or softening”)
Initially opaque localized lesions that can cover and blind the cornea
Treatment with Vit A leaves a densely scarred cornea
Same eye 2 months after Vitamin A therapy
Conjunctival xerosis and localized corneal necrosis in a severely malnourished 2-year-old Indonesian boy.
Experimental Vitamin A depletion in animals causes a deceleration in weight gain to a “plateau” as hepatic retinol reserves becomes exhausted
Corneal xerophthalmia is associated with severe linear growth stunting and acute wasting malnutrition
Recovery from xerophthalmia has been associated with gain in weight
Predisposes individuals to severe infection
Higher mortality rates in children and pregnant women
Vit A maintains epithelial barrier function and regulates cellular and antibody-mediated immunity
Children with any stages of xerophthalmia
High potency Vit A at presentation, the next day and 1-4 weeks later (WHO recommendations)
Children at high risk Vit A deficiency: measles, diarrhea, respiratory diseases, severe malnutrition
High dose supplementation: single dose if no supplement in
1-4 mo
q4-6 months
Infants 50K IU PO
Infants 6-12mo: 100K IU PO
Mothers: 200K IU PO w/in 8 wks delivery (WHO recommendation)
Pregnant or women of reproductive age: small doses 10K IU/d or 25K IU wkly
Dietary diversification
Fortification
Supplementation
Increase intake from available and accessible foods
Nutrition education
Social marketing
Community garden programs
Measures to improve food security
Taking advantages of existing consumption patterns of fortifiable foods to carry Vitamin A into the diets
Examples:
Vitamin A fortification of sugar in Guatemala
Vitamin A fortified monosodium glutamate in Southeast
Asia
Encompassing community based efforts to provide Vit A supplements to high-risk groups
Preschool-aged children
Mothers within 6-8weeks after childbirth
UNICEF procures and distributes over 400 million Vit A supplements to nearly 80 countries
Integrating vitamin A delivery with immunization services during each of three routine contacts in the first 6 months of life
Resurgence in the prevalence of Rickets
In developing countries, not only associated with effects on bone growth and mineral homeostasis but also with infant and child mortality when accompanying lowerrespiratory tract infections
Disease of the growing bones from a failure or delay in the calcification of newly formed cartilage at the growth plates of long bones and failure of mineralization of newly formed osteoid (osteomalacia)
Bones no longer able to maintain normal shapes
Calciopenic rickets
Phosphopenic rickets
Primary defect of mineralization
*
Nutritional Rickets is a form of calciopenic rickets and is classically associated with Vitamin D deficiency
Active Rickets
Impaired Calcium homeostasis
Consequent to impaired dietary calcium absorption or inadequate intake
Vit D (or more specifically 1,25-(OH)2D) controls the absorption of Calcium
↓ serum Ca → induce ↑ PTH secretion → osteoclasts ↑ resorb bone → demineralization of bone & cartilage at sites of rapid growth & remodeling
Predisposition to lower respiratory tract infections by
Effects on immune system
Muscle weakness and hypotonia
Effects of rickets and osteomalacia on rigidity and support provided by the ribs during respiration
During pregnancy and early infancy
Poor maternal weight gain
Higher incidence of maternal hypocalcaemia, poor neonatal bone mineralization and fractures, and reduced longitudinal growth
Increase risk of DM type 1, multiple sclerosis and bipolar disorder
Diet
Fortified food products
Fish oils, egg yolks, mushrooms
Animal products (fatty parts, liver)
Vit D in diet: cholecalciferol or ergocalficerol
Via skin synthesis under the influence of UV-B radiation
Decrease amount of UV-B reaching the earth
Season of the year
time of the day
pollution, clouds
distance form equator
Human factors
Amount of skin exposure (cloth coverage, social and religious customs)
Duration of exposure
Sunscreens
Degree of melanin concentration
In young children
Before children start to walk- decrease sun exposure
Breast-fed – very little Vit D in breast milk
Low dietary Calcium intake (ex. Consumption of polish rice)
Genetic causes
Malabsorption (repeated GI infections)
Chronic renal, liver disease
Results of the widening and splaying of the growth plates and resultant deformities of the metaphyses of the long bones
Widening of wrist, knees and ankles
Palpable and enlarged costochondral junctions (rickety rosary)
Deformities of the long bones
Craniotabes, head asymmetry, frontal bossing, delayed closing anterior fontanelle
Delayed tooth eruption, abnormal formation enamel, cavities
Rachitic rosary
Late
Pigeon chest irregularity, Harrison groove
Classic limb abnormalities
Genu varum, genu valgum
Fraying, widening, cupping metaphysis long bones, fxs
Lordosis, kyphosis, scoliosis
Narrow pelvis: obstructed labor
Hypotonia and myopathies resulting in delayed motor milestones (muscle weakness)
Hypocalcemia manifestations like apneic attacks and convulsions in infants
Clinically: presence of bony deformities
Radiological examination of growth plates
Biochemically
hypocalcemia
hypophosphatemia
elevated alkaline phosphatase
elevated PTH
Confirmation of low 25(OH)D concentrations
Vitamin D supplements (Oral Vitamin D2 or D3)
5,000 to 15,000 IU/day for 4-8 weeks
Single large dose when compliance problematic??
Adequate UV radiation
Vitamin D + Calcium supplementation (50mg/kg for several months)
Calcium supplementation alone
In US and Canada- fortification of all dairy milk formulas with Vit D (400
IU/quart)
American Academy of Pediatrics recommends supplementation with
200 IU/day to all breast-fed and children not drinking at least 500ml of cow’s milk
Large doses of Vitamin D supplementation every 3 months???
Add ground fish bones to pourish????
Education about sunlight and animal food ingestion
Stay tuned for more on micronutrient deficiencies next week… same channel, same time