Urinary iodine concentrations thyroid hormones

Conceptually the whole field of iodine nutrition may be subdivided into two broad subdivisions, the process and the impact (or outcome) fields of iodine nutrition, each with its own assessment indicators. The impact side of the iodine nutrition field represents the response of the human body to the iodine delivered to and consumed by the consumer, and therefore follows the process phase sequentially. This response of the human body is usually assessed in terms of impact indicators, such as the median urinary iodine concentration, thyroid size, and blood constituents such as thyroid-stimulating hormone, thyroglobulin, or other thyroid hormones. The process side of iodine nutrition covers factors playing a role in the delivery of iodine to the consumer via iodized salt or via an alternative source, such as processed food, drinking (iodine-containing cleaning agents) used in the dairy industry water or iodophors. 

Urinary iodine concentration and palpation of goiter among schoolchildren is the most frequent method used by cross-sectional surveys to measure iodine deficiency. Because iodine is excreted by the kidneys, the urinary concentration of iodine is an indicator of iodine intake. Lower production of thyroxine leads to increased production of the thyroid-stimulating hormone, which results in thyroid hyperplasia known as goiter. The World Health Organization (2001) classifies iodine deficiency into mild, moderate and severe when urinary excretion is, respectively, 50—99, 20 9 and <20 p,g/l of urine. 

In KBD subjects, the evolution of thyroid function after correction of iodine was similar in selenium supplemented and nonsupplemented subjects. This finding corroborated previous studies, suggesting only a moderate effect of selenium deficiency on thyroid hormones in human (Calomme et al, 1995 St. Germain and Galton, 1997). In Tibet, the administration of an intramuscular injection of 475-mg of iodine to KBD subjects was sufficient to correct iodine deficiency for 16 months, because at this time serum T3 increased again to pre-iodine levels and mean iodine urinary concentrations had fallen... 

In iodine-deficient regions, free tetraiodothyronine (fT4) increases, especially in multinodular goiters, whereas thyroid-stimulating hormone (TSH) levels decrease significantly, especially in multinodular and diffuse goiters (Fassbender et al., 2001). The more contrast agent was used, the more urinary iodine excretion was measured. These observations are probably due to the fact that the thyroid transport mechanism for iodine is not saturated by high-iodine plasma concentrations (Fassbender et al., 2001). The concentration of total T3 remains constant (Fassbender et al., 2001). However, TSH levels decrease in... 

In the most simplistic physiological model, inadequate intake of iodine results in a reduction in thyroid hormone production, which stimulates increased TSH production. TSH acts directly on thyroid cells, and without the ability to increase hormone production, the gland becomes hyperplastic. In addition, iodine trapping becomes more efficient, as demonstrated by increased radioactive iodine uptake in deficient individuals. However, this simplistic model is complicated by complex adaptive mechanisms which vary depending on the age of the individual affected. In adults with mild deficiency, reduced intake causes a decrease in extrathyroidal iodine and reduced clearance, demonstrated by decreased urinary iodine excretion, but iodine concentration in the gland may remain within normal limits. With further reduction in intake, this adaptive mechanism is overwhelmed, and the iodine content of the thyroid decreases with alterations in iodination of thyroglobulin, in the ratio of DIT to MIT, and reduction in efficient thyroid hormone production. The ability to adapt appears to decrease with decreasing age, and in children the iodine pool in the thyroid is smaller, and the dynamics of iodine metabolism and peripheral use more rapid. In neonates, the effects of iodine deficiency are more directly reflected in increased TSH. Diminished thyroid iodine content and increased turnover make neonates the most vulnerable to the effects of iodine deficiency and decreased hormone production, even with mild deficiency. 

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