Transcript Iodine deficiency is single most common cause of mental handicap

‫بسـم هللا الرحمن الر حیـم‬
‫هوال‬
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Overview of IDD
assessment and
indicators
H. Delshad M.D
Endocrinologist
Research Institute for Endocrine Sciences
IDD: Iodine Deficiency Disorders
The world’s most common endocrine
problem
 The most preventable cause of mental
retardation
 The easiest of the major nutritional
deficiencies to correct

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What is
Iodine?
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● Iodine is a chemical element
( as are Oxygen ,Hydrogen , Iron )
occurs in a variety of chemical forms
● Iodine is an essential trace element
for the human
● Iodine is an essential
part of the chemical
structure of thyroid
hormones
Total quantity present in body is (15-20 mg)
Mostly in thyroid gland
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What does iodine do?
And
Why do we need iodine?
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Thyroid hormones synthesis requires:
◦ Normal thyroid gland
◦ Adequate secretion of T.S.H
◦ Availability of iodine
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Iodine
The average adult body contains between
20-50 mg iodine.
 60% of total iodine is concentrated in
thyroid gland.
 Iodine is an essential component of the
thyroid hormones.
 Iodine contributes 65% of T4 and 59% of
T3 molecular weight.
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Thyroid hormone synthesis
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How much
iodine should
we get?
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Recommended daily intake of
iodine
Preschool children
90 g
Schoolchildren (6-12 y)
120 g
Adult (>12 y)
150 g
Pregnant
women
&
Lactating
250 g
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Where do we get
iodine from?
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Water
Food
Source of iodine
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Iodine sources
Most of the iodine ingested by humans
comes from food of animal and plant origin.
 This iodine in turn, is derived from the soil.
 Only a relatively small fraction is derived
from drinking water.
 Worldwide soil distribution of iodine is
extremely variable & food grown in areas of
low iodine does not contain enough of the
mineral to meet requirements.
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Iodine sources
 Vegetables
grown in iodine rich
soil like kelp and onions
 Milk & milk product
 Salt water fish and seafood
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Iodine deficiency – Disease of the soil
Gradual leaching of iodine from soil due to:
Floods
Melting of Glaciers
Rivers changing course
Iodine deficient areas

Large population who are living in an
environment where the soil has been
deprived of iodine are at risk of IDD.
◦
◦
◦
◦
Mountainous region of Europe
The northern Indian subcontinent
The extensive mountain ranges of china
The Andean region in South America
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What happens if
we don’t get
enough iodine?
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Mechanisms involved in the adaptation
to iodine deficiency

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
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
Increased thyroid clearance of plasma inorganic
iodine.
Hyperplasia of the thyroid and morphologic
abnormalities
Changes in iodine stores & TG synthesis
Modifications of the iodoamins acid content of the
gland.
Enrichment of thyroid secretion in T3
Enhanced peripheral conversion of T4 to T3
Increased T.S.H production
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The spectrum of IDD
Fetus
Abortions
Stillbirths
Congenital anomalies
Increased perinatal mortality
Neurologic creatinism
Psychomotor defects
Neonate
Neonatal goiter
Neonatal hypothyroidims
Child & adolescent
Goitrous juvenile hypothyroidism
Impaired mental function
Retarded physical development
Adult
Goiter with its complications
Hypothyroidism
Impaired mental function
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IDD : Spectrum of Disorders
From SIMPLE GOITER
Large MNG
Hypothyroidism
Severe myxedema
IQ
Psycho motor alteration
Deaf- Mutism
Diplegia
Retarded growth
.
.
To CRETINISM
Specific iodine deficiency disorders
Endemic
goiter
Endemic cretinism
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Endemic goiter
 More
than 5% of
the preadolescent
(6-12 years) school
age children have
enlarged thyroid glands.
Simple
(nontoxic goiter)
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World wide prevalence of goiter
WHO Region
Population
In millions
Population affected by
goitre
In millions
% of the
Region
122
20%
Africa
612
The Americas
788
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5%
South-East Asia
1477
172
12%
Europe
869
130
15%
Eastern Mediterranean
473
152
32%
Western Pacific
1639
124
8%
Total
5858
741
13%
Pathogenesis of goiter
Impaired hormone synthesis
• Iodine deficiency
• Goitrogen in the diet
• Dyshormogenesis
T.SH
Alter sensitivity
Thyroid follicular cell
Hyperplasia and hypertrophy
Thyroid enlargement
(GOITER)
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Three women of the Himalayas with typical endemic goiters.
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Huge Multinodular goiter
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Iodine deficiency in the fetus

Mental retardation:
◦ Is the result of iodine deficiency in the mother
◦ Insufficient supply of TH to the developing
brain may result in mental retardation.
◦ During the first and second trimesters of
pregnancy the supply of the TH to the
growing fetus is almost exclusively of maternal
origin.
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Importance of iodine in brain development

50,000 brain cells produced
per
Second in developing
fetal brain
90 % of human brain
development occurs
between 3rd month of
pregnancy & 3rd year of life
(Critical period)
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Importance of iodine in brain development

Deficiency of iodine during this critical period of
development results in permanent brain damage

This brain damage can primarily be prevented by
correcting iodine deficiency before & during
pregnancy

This makes it vital that all expectant & lactating
mothers get their daily requirement of iodine
Importance of iodine in brain development

Iodine deficiency is
single most common
cause of mental
handicap worldwide

It is totally preventable
Congenital Hypothyroidism
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Endemic Cretinism
Is now largely a disease in remote,
underdeveloped areas of the third world.
 It occurs when iodine intake is below a
critical level of 25 g/day
 It is an irreversible changes in mental
development of the fetus born in an area
of endemic goiter.
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Cretinism, Tip of the Iceberg
1% - 10%
Cretinism
5% - 30%
Some brain damage
30% - 70%
Loss of energy due to hypothyroidism
Endemic Cretinism
(Neurologic Form)
Sever mental deficiency
 Deaf mutism (Cochlear lesion)
 Motor spasticity (spastic diplegia)
proximal rigidity of both lower
and upper extremities and the trunk.
 Goiter
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Endemic Cretinism
(Neurologic Form)
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Endemic Cretinism
(Myxedematous Form)
Less sever degree of mental
retardation
 Sever growth retardation
 Puffy features
 Myxedematous and dry skin
 Delayed sexual maturation
 No goiter
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An adult male from the Congo,
Myxedematous Cretinism
with three women of the same
age (17-20 years),
all of whom are myxedematous cretins.
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Myxedematous Cretinism
Iodine deficiency is a prerequisite in the
etiology of the disorder.
 Three additional factors, acting alone or in
combination may be responsible for thyroid
atrophy.

◦ Thiocyanate overload resulting from the chronic
consumption of poorly detoxified cassava.
◦ Thiocyanate crosses the placenta and inhibits the
trapping of iodine by the placenta and fetal thyroid.
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Cont’d
◦ Selenium deficiency:
H2O2 is produced in excess in thyroid
cells hyperstimulated by T.S.H
H202 within the thyroid cells could
induce thyroid cell destruction.
Selenium detoxifies H202
◦ Blocking autoantibiotdies.
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Specific Etiologies of Goiter

Congenital goiter
◦ Familial: genetics disorders of hormongenesis
◦ Sporadic:
 Intrauterine iodide deficiency
 Fetal exposure to goitrogen (Antithyroid drugs)
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Cont’d

Endemic goiter
◦ Iodine deficiency
◦ Dietary goitrogen





Cabbage
Turnip
Kale
Rape
Cassava
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Cont’d
Sporadic
goiter
Iodine excess
Wolff-chaikoff
Jodbusedow
◦Goitrogenic drugs
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Drugs reported to cause goiter
Agent
Mechanisms
Iodide
Inhibition
synthesis
Thionamides
Aminoglutethimide
Inhibition of tyrosyl iodination and
coupling
Inhibition of iodide organization
Lithium
Amiodaron
Inhibition of iodide organization
Inhibition of TH synthesis
Fluoride
Exacerbation of effects of iodide
deficiency
Decreased iodide uptake and
inhibition of TH synthesis
Carbutamide
of
TH
release
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and
Thank
You
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