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بسـم هللا الرحمن الر حیـم هوال 1 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 3 What is Iodine? 4 ● 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 6 What does iodine do? And Why do we need iodine? 7 Thyroid hormones synthesis requires: ◦ Normal thyroid gland ◦ Adequate secretion of T.S.H ◦ Availability of iodine 8 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. 9 Thyroid hormone synthesis 10 How much iodine should we get? 11 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 12 Where do we get iodine from? 13 Water Food Source of iodine 14 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. 15 Iodine sources Vegetables grown in iodine rich soil like kelp and onions Milk & milk product Salt water fish and seafood 16 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 18 What happens if we don’t get enough iodine? 19 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 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 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 23 Endemic goiter More than 5% of the preadolescent (6-12 years) school age children have enlarged thyroid glands. Simple (nontoxic goiter) 24 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 39 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) 26 Three women of the Himalayas with typical endemic goiters. 27 Huge Multinodular goiter 28 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 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) 31 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 34 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 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 37 Endemic Cretinism (Neurologic Form) 38 Endemic Cretinism (Myxedematous Form) Less sever degree of mental retardation Sever growth retardation Puffy features Myxedematous and dry skin Delayed sexual maturation No goiter 39 An adult male from the Congo, Myxedematous Cretinism with three women of the same age (17-20 years), all of whom are myxedematous cretins. 40 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. 41 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 Specific Etiologies of Goiter Congenital goiter ◦ Familial: genetics disorders of hormongenesis ◦ Sporadic: Intrauterine iodide deficiency Fetal exposure to goitrogen (Antithyroid drugs) 43 Cont’d Endemic goiter ◦ Iodine deficiency ◦ Dietary goitrogen Cabbage Turnip Kale Rape Cassava 44 Cont’d Sporadic goiter Iodine excess Wolff-chaikoff Jodbusedow ◦Goitrogenic drugs 45 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 46 and Thank You 47