Vit D deficiency

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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

Same eye 2 months after Vitamin A therapy

Conjunctival xerosis and localized corneal necrosis in a severely malnourished 2-year-old Indonesian boy.

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

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