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Iodine deficiency symptoms

Iodine deficiency symptoms will disappear. The determination of protein-bound... [Pg.1478]

Absorption, Metabolism, Excretion Functions of Iodine Deficiency Symptoms Interrelationships... [Pg.591]

Worldwide, the most common thyroid disorder is hypothyroidism resulting from dietary iodine deficiency. In iodine-replete areas of the world, most thyroid disorders are the result of autoimmune disease. The symptoms manifested in hypothyroid and hyperthyroid states are largely independent of any underlying disorder of the thyroid gland itself they are a function of the degree of hormone deficiency or excess. [Pg.742]

Juvenile or adult patients with primary hypothyroidism (as indicated by low serum free T4 and high serum TSH concentrations) are usually treated with thyroxine with the aim of relieving symptoms and reducing the serum TSH concentration into the normal reference range. If the primary hypothyroidism is the result of iodine deficiency, then gradually increasing dietary iodine supplementation may also be instituted in addition to the thyroxine replacement therapy. Iodine supplementation alone may lead to the development of acute hyperthyroidism. [Pg.747]

The toxicological hazard of perchlorate salts may depend on the cation in the compound. In general, the salts should be considered as skin irritants and treated as such. Perchlorate ion, C104, may compete physiologically with iodide ion, U. This can occur in the uptake of iodide by the thyroid, leading to the biosynthesis of thyroid hormones. As a consequence, perchlorate can cause symptoms of iodine deficiency. [Pg.258]

Iodine deficiency has its most devastating effects on babies while they are in the womb and during their first three months oflife. These are the critical periods of brain development and lack of iodine leads to irreversible effects and permanent mental retardation and on average such children have an IQ of around 85 compared to the IQ of 100 of children who develop normally. Many exhibit the symptoms of brain damage due to lack of iodine, and this condition affects as many... [Pg.106]

The systemic toxicity of perchlorate appears to be directly related to its action as a competitive inhibitor of iodide, and the symptoms tend to be similar to those of iodine deficiency. [Pg.106]

Hypothyroidism (thyroid hormone deficiency) may result from autoimmune disease (Hashimoto s disease) or from deficient synthesis of TSH or TRH (thyroid-stimulating hormone-releasing factor). Because adequate ingestion of iodine is a prerequisite for thyroid hormone synthesis, iodine deficiency also causes hypothyroidism. In children, thyroid hormone deficiency (called cretinism) causes depressed growth and mental retardation. Severe hypothyroidism in adults (myxedema) results in symptoms such as edema (abnormal fluid accumulation) and goiter. Hypothyroidism is usually treated with hormone replacement therapy. [Pg.551]

Sheep and cattle developed the same symptoms of iodine deficiency. Abortion rate, length of pregnancy (4 days longer) and mortality of the lambs were significantly increased (Groppel 1986, Groppel and Korber 1982, Groppel etal. 1983). Cows with an iodine intake of 70 pg kg feed DM produced 19% less milk than con-... [Pg.1477]

Early animal studies focused on preventing marked symptoms of iodine deficiency diseases (e.g., goiter) and reduction of yield, mainly in growing animals. More recent dose—response studies in animals have investigated levels of iodine in the thyroid gland, serum concentrations of iodine and thyroid hormones, the milk iodine concentration of dairy cows, lactating ewes, goats, or sows, and the iodine content of excrements. [Pg.153]

Although trace amounts of supplemental iodine (50-100 rg/kg feed dry matter) effectively prevent goiter, they are currently difficult to detect and measure accurately. More sensitive methods to determine the iodine content of feed, including matrix disintegration, are required. Methods with the potential to reliably detect < 20 ig iodine/kg should be critically evaluated. The reliability of the reported feed iodine content should be questioned in animal studies if goiter or other symptoms of iodine deficiency are reported, despite the use of diets thought to contain more than 100 xg detected iodine/kg... [Pg.155]

A twelve-month selenium-supplementation trial in children with KBD in Tibet did not show any effect on the main symptoms and signs of the disease (Moreno-Reyes et al., 2003). But, in the same study, correction of iodine deficiency before the administration of selenium supplements induced partial recovery of growth retardation. Selenium had no additional effect on either growth or thyroid function, despite the normalization of serum-selenium levels. [Pg.695]

The objective of this study is to gain better insight into the effects of severe, chronic iodine deficiency on various aspects of the mental and psychomotor development of that part of a population, that does not have the manifest symptoms of endemic cretinism. [Pg.272]

Deficiency of T. e. can lead to characteristic deficiency symptoms or diseases, thus indicating the essential nature of these nutritional factors, e g. iodine is a component of the thyroid hormones and essential for thyroid function. Iodine deficiency is responsible for endemic goiter, and certain types of cretinism it can be avoided by addition of iodides to drinking water. Other T. e. are chromium, copper, fluoride, magnesium, manganese, nickel, vanadium, silicon, tin, selenium, zinc (see individual entries). [Pg.677]

Proof that the deficiency produced by the inclusion of mineral oil in the diet is a fat deficiency was based not only upon the typical symptoms which developed but also upon the fact that the inclusion of 50 mg. of linoleate per day in the diet prevented them. Moreover, there was an increased excretion of fatty acids in the feces of mineral oil-fed rats in addition, the fecal fatty acids were found to have an increased iodine value after the ingestion of mineral oil. However, it is believed that this effect cannot be ascribed solely to the solvent action of the hydrocarbon on EFA, since the deficiency symptoms were prevented by the administration of linoleate either orally or intraperitoneally. [Pg.48]


See other pages where Iodine deficiency symptoms is mentioned: [Pg.1483]    [Pg.1483]    [Pg.669]    [Pg.682]    [Pg.319]    [Pg.43]    [Pg.106]    [Pg.173]    [Pg.1898]    [Pg.1376]    [Pg.1378]    [Pg.411]    [Pg.277]    [Pg.1481]    [Pg.1483]    [Pg.65]    [Pg.154]    [Pg.158]    [Pg.250]    [Pg.323]    [Pg.418]    [Pg.627]    [Pg.675]    [Pg.789]    [Pg.794]    [Pg.960]    [Pg.1049]    [Pg.1061]    [Pg.1088]    [Pg.1113]    [Pg.1169]    [Pg.270]    [Pg.270]    [Pg.131]    [Pg.933]    [Pg.427]   


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Deficiency symptoms

Iodine deficiency

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