Transcript Vit D deficiency

Micronutrient
malnutrition
Vanessa Velazquez-Ruiz, MD
Emergency Medicine
Global Health Fellow
St. Luke’s-Roosevelt Hospital
Why talking about
micronutrient
malnutrition?
Micronutrients
 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”
Agenda
 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
Let’s begin our journey!!!!
Fasten your seatbelts and enjoy the ride…
Vitamin A
Overview
 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
 NEITHER HUMANS or ANIMALS
can synthesize or survive without
Vitamin A
Epidemiology
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
Epidemiology
 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
Sources of Vitamin A
 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
Vitamin A
 Essential in regulating numerous key biologic processes in the
body
 Morphogenesis
 Growth
 Nutrition
 Vision
 Reproduction
 Immunity
 Cellular differentiation and
proliferation
Vitamin A deficiency
disorders
VADDs
Main cause of deficiency:
 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)
Clinical features
Xerophthalmia
 Three clinical stages:
 Retinal dysfunction causing night blindness
 Conjunctiva and corneal xerosis
 Corneal ulceration and necrosis
Night blindness
 Earliest manifestation
 Most prevalent stage of xerophthalmia
 Failure in rod photoreceptors cells in the retina
 Responsive to Vitamin A supplementation
Ask about night blindness
 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
Conjuctival xerosis with
Bitot’s spots
 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
 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
Corneal Ulceration
 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
Corneal Necrosis
 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
Conjunctival xerosis and localized
corneal necrosis in a severely
malnourished 2-year-old Indonesian
boy.
Same eye 2 months after Vitamin A
therapy
Poor Growth
 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
Infection
 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
Treatment
 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
Replacement
 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
Prevention
 Dietary diversification
 Fortification
 Supplementation
Dietary diversification
 Increase intake from available and accessible foods
 Nutrition education
 Social marketing
 Community garden programs
 Measures to improve food security
Fortification
 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
Supplementation
 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
Nutritional Rickets
and Vitamin D
deficiency
Overview
 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
Definition
 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
Causes of Rickets
 Calciopenic rickets
 Phosphopenic rickets
 Primary defect of mineralization
* Nutritional Rickets is a form of calciopenic rickets and is classically associated
with Vitamin D deficiency
Effects of 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
Effects of Vitamin D
deficiency
 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
Effects of Vitamin D
deficiency
 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
Sources of Vitamin D
 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
Factors influencing Vitamin
D deficiency
 Decrease amount of UV-B reaching the earth
 Season of the year

time of the day
 pollution, clouds

distance form equator
Factors influencing Vitamin
D deficiency
 Human factors
 Amount of skin exposure (cloth coverage, social and
religious customs)
 Duration of exposure
 Sunscreens
 Degree of melanin concentration
Factors influencing Vit D
deficiency
 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
Clinical Features
 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
Age dependant
 Early
 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
Other clinical manifestations
 Hypotonia and myopathies resulting in delayed motor
milestones (muscle weakness)
 Hypocalcemia manifestations like apneic attacks and
convulsions in infants
Diagnosis
 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
Treatment
 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
Prevention
 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
Prevention
 Large doses of Vitamin D supplementation every 3
months???
 Add ground fish bones to pourish????
 Education about sunlight and animal food ingestion
To be Continued…
Stay tuned for more on micronutrient deficiencies next
week… same channel, same time
References