Micronutrient deficiencies II
Download
Report
Transcript Micronutrient deficiencies II
Micronutrient
malnutrition II
Vanessa Velazquez-Ruiz, MD
Emergency Medicine
Global Health Fellow
St. Luke’s-Roosevelt Hospital
Today schedule….
Zinc Deficiency
Iodine deficiency
Lets begin the second part of our journey
Are you ready!!!!!!
Zinc Deficiency
Common but overlooked problem in developing
countries
Important role in biological processes
Gene expression
Cell development
Replication
Immune function
Growth and development
Overview
Intakes of zinc are commonly lower than recommended
Adaptation mechanisms preclude the development of
severe deficiencies
Many consequences to adaptation states to low zinc
levels
Overview
Probably affects a quarter or a third of pre school
children and their mothers
Lack of simple quantitative markers for zinc deficiency
Overall, 20.5% of the world population is at risk of zinc
deficiency
Estimated to be responsible for 800,000 deaths/year
from diarrhea, malaria, pneumonia in children under
five
One of the ten largest contributors to the burden of
disease in developing countries
Zn deficiency in world crops: major areas of reported problems (adapted
from Alloway, 2008a
Overview
Incidence and prevalence have not been defined
Lack of sensitive, practical, accepted indicators for zinc
deficiency
Population-based surveys have not been done
Marginal deficiency is not characterized as a specific
syndrome
Severe clinical deficiency is not seen owing to adaptation
or death
Risk factors for zinc
deficiency
Insufficient dietary intake
(low protein diet)
High phytate and/or fiber
intake (vegetarians)
Diarrheal disease
Malabsorption syndromes
Parasitosis
Hot, humid climate
Lactation
Rapid multiplicative cell
growth (pregnancy, infancy,
adolescence)
Genetic disease
(acrodermatitis
enteropatthica, Sickel cell
anemia)
Close geographical linkage between soil zinc deficiency and
human zinc deficiency
Zinc Metabolism
Zinc absorption
Absorbed at all levels of the small intestine
Intestine must recover zinc from both diet and
endogenous sources
Total body zinc content maintained with absorption of
5mg/day
Zinc Storage
No specific organ for storage
60% striated muscle
20% in bone
5% in blood and liver
3% in the skin and GI tract
Zinc excretion
Mostly in feces
Through urine
In tropical countries, sweat losses can be considerable
Turnover of skin, hair and nails
Menstrual blood and semen
Lactation (2-3mg per day in the first several weeks)
Sources of zinc
Animal products, seafood, cereals
Oysters and shellfish
Absorption impaired by phytates and fiber.
Protein acts as anti-phytate
Clinical presentation
Severe deficiency
Growth retardation
Impaired immune system
Skin lesions in extremities and perioral area
Hypogonadism
Anorexia
Cognitive dysfunction
Alopecia
Mild to moderate
Increases susceptibility to infection
Growth retardation
Failure to thrive
Impaired taste (hypogeusia)
During pregnancy
Birth defects
Spontaneous abortions
Fetal growth retardation
Low birth weight
Preterm delivery
Increase complications during delivery
Impairs estrogen-dependent gene expression in the
uterus (via zinc-finger protein)
Lack of estrogen impairs the conversion of uterus from
passive state to one capable of concerted contractions
with sufficient force to expel fetus
Zinc and diarrheal disease
Strong evidence that supplements improves the prognosis
(reduces severity and duration) of children treated for
diarrheal disease
Zinc supplement + oral rehydration treatments been
explored
UNICEF recommends packs of ten tablets of 20mg
Zinc/daily for tx of diarrhea
Zinc and respiratory
diseases
Regular zinc supplements have shown to prevent
respiratory diseases in children with lower birth weights
Pool analysis of randomized controlled trails showed
reduction of pneumonia by 41% in preschool children
supplemented with zinc
One trial in Bangladesh showed reduced duration of
severe pneumonia by 30% with zinc as adjunct therapy
Zinc and malaria
Gambia: 32% fewer clinic visits for malaria due to
Plasmodium falciparum in young children supplemented
with Zinc
69% reduction for malaria episodes accompanied by
high levels of parasitemia (>10,0000 parasites/μL)
Zinc and HIV
Low serum Zinc identifies in 29% of hospitalized AIDS
patients
Some studies showed that low zinc levels may reflect
HIV replication and the possibility that Zinc may
enhance viral replication, however,
Daily zinc supplementation for 30 days has proven to
reduce infectious disease morbidity in AIDS patients in
other studies
http://www.zincsaveskids.org/
http://www.youtube.com/watch?v=vN_qQPxPK3Q
Assessment
Plasma and Serum Zinc concentration
Circulating zinc less than 0.2% of total body
Cut-off values to assess risk of zinc deficiency
Below 10.71 μmol/L for fasting sample and less then
9.95μmol/L for non fasting
Dietary assessment
Food intake distributions of a population
Analysis of local staple foods
Recall of an individual for food consumed
Weighed food records by research assistants
24-hr dietary recall
Local food composition tables if available
Other
Hair zinc concentrations
Diminished taste acuity (hypogeusia)
Composite index for predicting the national risk of zinc
deficiency- uses a combination of stunting rates and
adequacy of zinc in the national supple
Replacement and
treatment
Table 1: Recommended Dietary
Allowances (RDAs) for Zinc
Age
Male
Female
Pregnancy Lactation
0–6 months
2 mg*
2 mg*
7–12 months 3 mg
3 mg
1–3 years
3 mg
3 mg
4–8 years
5 mg
5 mg
9–13 years
8 mg
8 mg
14–18 years
11 mg
9 mg
12 mg
13 mg
19+ years
11 mg
8 mg
11 mg
12 mg
* Adequate Intake (AI)
Recommended nutrient intakes (RNIs) for dietary zinc (mg/day) to meet the
normative storage requirements from diets differing in zinc bio-availability
Treatment
To combat zinc deficiency, five intervention strategies
can be used:
Supplementation using medicines
Food fortification through the incorporation of zinc
additives in food
Dietary modification/diversification
Genetic biofortification through plant breeding
Agronomic biofortification through zinc fertilization.
Iodine deficiency
Overview
Iodine is an essential constituent of the thyroid
hormones (T4, T3)
Deficiency can lead to Goiter or cretinism depending on
the severity
The ongoing global health effort to eliminate iodine
deficiency through iodization of salt presents one of the
largest public health efforts
By 1990, there were 1,572 million people worldwide
consuming inadequate amounts of iodine
Iodine deficiency is the leading cause of mental
retardation in the world
Problem is global, with mountainous regions and large
river deltas the most well-known areas of endemic
deficiencies
Epidemiology
Mountainous areas, high altitude and alluvial plains
Leaching of iodine form the soil due to erosion and
heavy rain, deforestation, overgrazing lead to loss of
iodine form soil and water
WHO Region
Proportion of population with UI
< 100 µg/L (%)
Africa
42.6
Americas
9.8
South East Asia
39.8
Europe
56.9
Eastern Mediterranean 54.1
Western Pacific
24
Total
35.2
Population with
UI < 100 µg/L
(millions)
260.3
75.1
624
435.5
228.5
365.3
1988.7
192 WHO Members States Based on population estimates for the year 2002 (United
Nations, Population Division, World Population Prospects: The 2002 Revision)
WHO 2003
Risk factors
Residency in an area where soil and water are poor in
iodine
Ingestion of substances known as “goitrogens”( found in
vegetables and fiber) that can interfere with metabolism
Cabbage, sweet potato, brussel sprouts, turnips
Cassava containing high concentration of thiocyanates
Role of iodine in biological
functions
Metabolism
Growth and development
Synthesis of growth hormone
Normal bone cell growth and development
Brain development
Early growth and differentiation of the brain and nervous
systems in the fetus
Immune function
Sources of Iodine
Seafood and seaweed
Crops grown on iodine rich soil
Iodized salt
Drinking water (less than 10%)
WHO recommended dietary
requirements
Spectrum of iodine deficiency
disorders
Fetus
Abortions
Stillbirths
Congenital anomalies
Increase perinatal mortality
Neurological cretinism: mental deficiency, deaf-mutism,
spastic diplegia, squint
Myxoedematous cretinism: dwarfism, mental deficiency
Spectrum of iodine deficiency
disorders
Neonate
Neonatal goiter
Neonatal hypothyroidism
Spectrum of iodine deficiency
disorders
Child and adolescent
Goiter
Juvenile hypothyroidism
Retarded physical development
Spectrum of iodine deficiency
disorders
Adult
Goiter
Hypothyroidism
Impaired mental function
Iodine-induce hyperthyroidism
Goiter
Enlargement of thyroid gland in response to insufficient
iodine intake
Low iodine -> decrease T4 -> increase production of
TSH -> stimulates hyperplasia of the thyroid -> increase
uptake of iodine -> Goiter
Definition by palpation: enlargement of the thyroid such
that lateral lobes are larger than the terminal phalanx of
the thumb of the person who is being examined
Goiter
Severity of goiter correlates with severity of the
deficiency
In areas of endemic goiter , the daily intake is less the
100 μg/day
Cretinism
Usually found where the prevalence of endemic goiter is
more than 30%
Characterized by mental retardation
Two extreme types of cretinism:
Neurological
Myxoedematouse
Myxoedematous cretinism (hypothyroid cretinism):
severe growth retardation, mental retardation not severe,
coarse, dry skin, husky voice.
Neurological cretinism: stature is normal, mental
retardation is severe, deaf-mutism, cerebral diplegia
Assessment of iodine
status
Urinary iodine
Most useful/reliable indicator I status
24hr or random (30 samples) urine collection
Related to recent dietary I intake
Adequate
100-200 μg/L
Mild deficiency
50-99μg/L
Moderate Deficiency
20-49μg/L
Severe Deficiency
Less than 20μ/L
Assessment of iodine
status
Thyroid size (goiter surveys)
Palpation
Ultrasound (more reliable)
“Total Goiter Rate”, schoolchildren
Classification for Goiter
Grade 0
No palpable or visible goiter
Grade 1
Palpable mass but not visible when neck in
normal position
Grade 2
Visible, palpable swelling of the neck
Goiter by palpation or by thyroid volume by US (>97% of percentile)
Mild
5-19.9
Moderate
20-30
Severe
>30
*School-children
TSH screening programs
For early detection of congenital hypothyroidism
Useful epidemiology information, not cost effective
The degree of iodine deficiency can be evaluated on the basis of
the frequency of neonatal blood TSH above the cutoff point of
3μU/ml
Mild deficiency
TSH 3-19.9
Moderate deficiency
TSH 20-40
Severe deficiency
TSH > 40
Prevention
Iodized salt: “Universal salt iodization” (150μg of I/day)
Oral iodide oil
Adult : 1ml (480mg)
0.5ml (240mg)
Iodized oil injections
Prevention
Other:
Iodization of drinking and irrigation water
Iodine saturated silicon matrices placed in wells and hand
pumps
Fortification of food
Conclusion
Iodine deficiency is the leading cause of preventable mental
retardation
Great progress in providing access to iodized salt
WHO/UNICEF/ICCIDD report in 1999, from 5 billion
people living in counties with iodine deficiencies, 68% now
have access to iodized salt.
From 130 counties, 104 have intersectoral coordination and
98 have legislations about iodized salt
Much work needs to be done…
To be Continued…
Stay tune for more on micronutrient deficiencies next
week… same channel, same time
Thanks
Any questions…
References
WHO website