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Overview of IDD assessment and indicators

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Title: Overview of IDD assessment and indicators


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Overview of IDD assessment and indicators
  • H. Delshad M.D
  • Endocrinologist
  • Research Institute for Endocrine Sciences

3
IDD Iodine Deficiency Disorders
  • The worlds 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?

8
  • Thyroid hormones synthesis requires
  • Normal thyroid gland
  • Adequate secretion of T.S.H
  • Availability of iodine

9
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 (gt12 y) 150 ?g
Pregnant Lactating women 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
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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 dont get
  • enough iodine?

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Mechanisms involved in the adaptation to iodine
deficiency
  • 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

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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
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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)

27
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.

30
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

33
Importance of iodine in brain development
  • Iodine deficiency is single most common cause of
    mental handicap worldwide
  • It is totally preventable

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Congenital Hypothyroidism
35
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
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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

40
An adult male from the Congo, with three women
of the same age (17-20 years), all of whom are
myxedematous cretins.
Myxedematous Cretinism
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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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Contd
  • 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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Contd
  • Endemic goiter
  • Iodine deficiency
  • Dietary goitrogen
  • Cabbage
  • Turnip
  • Kale
  • Rape
  • Cassava

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Contd
  • Sporadic goiter
  • Iodine excess
  • Wolff-chaikoff
  • Jodbusedow
  • Goitrogenic drugs

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Drugs reported to cause goiter
Agent Mechanisms
Iodide Inhibition of TH release and synthesis
Thionamides Inhibition of tyrosyl iodination and coupling
Aminoglutethimide Inhibition of iodide organization
Lithium Inhibition of iodide organization
Amiodaron Inhibition of TH synthesis
Fluoride Exacerbation of effects of iodide deficiency
Carbutamide Decreased iodide uptake and inhibition of TH synthesis
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