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1 بسـم الله الرحمن الر حیـم هوال طیف. Overview of IDD assessment and indicators H. Delshad M.D Endocrinologist Research Institute for Endocrine Sciences.

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Presentation on theme: "1 بسـم الله الرحمن الر حیـم هوال طیف. Overview of IDD assessment and indicators H. Delshad M.D Endocrinologist Research Institute for Endocrine Sciences."— Presentation transcript:

1 1 بسـم الله الرحمن الر حیـم هوال طیف

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

3 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 3

4 W hat is Iodine ? W hat is Iodine ? 4

5 ● 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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7 What does iodine do? And Why do we need iodine? 7

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

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 T 4 and 59% of T 3 molecular weight. 9

10 10 Thyroid hormone synthesis

11 How much iodine should we get? 11

12 Recommended daily intake of iodine Preschool children 90  g Schoolchildren (6-12 y) 120  g Adult (>12 y) 150  g Pregnant & Lactating women 250  g 12

13 Where do we get iodine from? 13

14 14 Source of iodine Water Food

15 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. 15 Iodine sources Iodine sources

16 Iodine sources Vegetables grown in iodine rich soil like kelp and onions Milk & milk product Salt water fish and seafood 16

17 Iodine deficiency – Disease of the soil Melting of Glaciers Floods Rivers changing course Gradual leaching of iodine from soil due to:

18 Iodine deficient areas 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 18

19 What happens if we don’t get enough iodine? 19

20 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 20

21 The spectrum of IDD 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 21

22 IDD : Spectrum of Disorders From SIMPLE GOITER Large MNG Hypothyroidism Severe myxedema IQ Psycho motor alteration Deaf- Mutism Diplegia Retarded growth. To CRETINISM

23 Specific iodine deficiency disorders Endemic goiter Endemic cretinism 23

24 Endemic goiter More than 5% of the preadolescent (6-12 years) school age children have enlarged thyroid glands. 24 Simple (nontoxic goiter)

25 World wide prevalence of goiter

26 Pathogenesis of goiter Pathogenesis of goiter 26 Impaired hormone synthesis Iodine deficiency Goitrogen in the diet Dyshormogenesis  T.SH Alter sensitivity Thyroid follicular cell Hyperplasia and hypertrophy Thyroid enlargement (GOITER)

27 27 T hree women of the Himalayas with typical endemic goiters.

28 28 Huge Multinodular goiter

29 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. 29

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 3 rd month of pregnancy & 3 rd year of life (Critical period)

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

34 34 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. 35

36 Cretinism, Tip of the Iceberg

37 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 37

38 38 Endemic Cretinism (Neurologic Form)

39 Endemic Cretinism (Myxedematous Form) 39 Less sever degree of mental retardation Sever growth retardation Puffy features Myxedematous and dry skin Delayed sexual maturation No goiter

40 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

41 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. 41

42 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. 42

43 Specific Etiologies of Goiter Congenital goiter ◦ Familial: genetics disorders of hormongenesis ◦ Sporadic:  Intrauterine iodide deficiency  Fetal exposure to goitrogen (Antithyroid drugs) 43

44 Cont’d Endemic goiter ◦ Iodine deficiency ◦ Dietary goitrogen  Cabbage  Turnip  Kale  Rape  Cassava 44

45 Cont’d Sporadic goiter Iodine excess Wolff-chaikoff Jodbusedow ◦ Goitrogenic drugs 45

46 Drugs reported to cause goiter AgentMechanisms IodideInhibition of TH release and synthesis ThionamidesInhibition of tyrosyl iodination and coupling AminoglutethimideInhibition of iodide organization LithiumInhibition of iodide organization AmiodaronInhibition of TH synthesis FluorideExacerbation of effects of iodide deficiency CarbutamideDecreased iodide uptake and inhibition of TH synthesis 46

47 47 Thank You


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