Goiter for Iodine Deficiency
Iodine is a trace element present in the human body in minute amounts. The function of iodine is to constitute an essential substrate for the synthesis of thyroid hormone, tetraiodothyronine (thyroxine or T4) and triiodothyronine (T3). The oceans are the primary stores and the sources of iodine in the world. Ocean water contains about 50 µg of iodine per liter.
The sun light to elemental iodine oxidizes iodide ions at the surface of the seas, which is volatile. Iodine returns to the earth by the rain and contains 1.8-8.5 µg per liter. The iodine contain of rain water diminishes as the distance from the coast increases. The rain enriches the superficial layer of the soil with iodine and contains 4-9mg/kg.
Heavy rain on the sloping ground may wash away the superficial iodine-rich layers, and iodine returns to the oceans by the rivers, the melting or the glaciers also leached away most of the iodine of the soil beneath. So, the areas of endemic goiter are those which have been subjected either to flooding, or to intense and prolonged glaciations, i.e. the highest mountains of the globe ( The Himalayas, the Andes, the Alps) or those which are remote from the sea (i.e. the central parts of Africa and European continents).
The main source of iodine for human consumption is food. The highest iodine content is found in sea foods, in which it can be as high as 3mg/kg. The other main dietary sources of iodine are milk, eggs, cereals, and meat.
The recommended daily allowance (RDA) endorsed by WHO are 90 µg for infants and children up to 6 years; 120 µg for children aged 7-10 years and 150 µg for adolescents. When the physiological requirements of iodine are not met in the children, a series of functional and developmental abnormalities occur which includes endemic goiter and cretinism, mental retardation, decreased fertility rate, increased prenatal death and infant mortality.
These disorders are grouped under the general heading of Iodine deficiency disorders, IDD. Additional consequences are the development of thyroid nodules, thyroid autonomy, and increased demand for thyroid surgery and radioiodine therapy and, in severe circumstances, neonatal hypothyroidism and neonatal goiter.
Severity of iodine deficiency :
Grade-I: Mean excretion of more than 50µg but less than lOOµg per 24 hour, per gm of creatinine or per liter of urine. At this level goiter will be rare.
Grade-II: Mean excretion between 25-50µg per 24 hours, per gm of creatinine, or per liter of urine. At this level goiter is frequent with nodular goiter and hypothyroidism of varying degrees.
Grade-Ill: Mean excretion below 25µg per 24 hours, per gm of creatinine or per liter of urine. Goiter will be frequent and cretinism is very common at this level.
The fundamental mechanism by which the thyroid gland adapts to an insufficient iodine supply is to increase the trapping of iodine. This result in the accumulation within the gland of a larger percentage of the ingested exogenous iodine. The increase of iodine trapping is the result of both TSH independent augmentation of membrane iodine trapping (thyroid autonomy.) and TSH stimulation of the iodine pump.
In addition, chronic TSH stimulation leads to an increase mass of thyroid tissue resulting in the development of goiter. Estimates of the iodine intake are usually derived from 24 hour urinary iodine excretion values or urinary iodine concentration expressed in relation to creatinine concentration.
The simplest, most efficient, and cheapest method for prevention of IDD is the iodization of salt at a level of 10 to 60 parts per million(ppm). The iodination should be calculated in such a way that salt should provide an additional 75-150 µg iodine per day. lodate is more stable than iodine and is recommended for tropical humid climates. Prolonged administration of iodine or thyroxine is very effective in reducing the size of the goiter.