Micronutrient malnutrition

Vanessa Velazquez-Ruiz, MDEmergency 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 disordersVADDs

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 withBitot’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 Ricketsand 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 lower-respiratory 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