Iodide deficiency

Goiter due to iodide deficiency is best managed by prophylactic administration of iodide. The optimal daily iodide intake is 150-200 meg. Iodized salt and iodate used as preservatives in flour and bread are excellent sources of iodine in the diet. In areas where it is difficult to introduce iodized salt or iodate preservatives, a solution of iodized poppy-seed oil has been administered intramuscularly to provide a long-term source of inorganic iodine. 

Nontoxic goiter is a syndrome of thyroid enlargement without excessive thyroid hormone production. Enlargement of the thyroid gland is usually due to TSH stimulation from inadequate thyroid hormone synthesis. The most common cause of nontoxic goiter worldwide is iodide deficiency, but in the USA, it is Hashimoto s thyroiditis. Less common causes include dietary goitrogens, dyshormonogenesis, and neoplasms (see below). 

In individuals with iodide deficiency, which one of the following is... 

C. The patient exhibits symptoms of hypothyroidism including goiter, yet thyroid hormone levels are elevated. This pattern can only be explained by resistance of target cells to thyroid hormone, for example, a mutation of the receptor deaeasing its binding affinity for hormone. Iodide deficiency would lead to goiter but not increased hormone levels. 

Our research (e.g., Williams et al., 2004, 2005 Murphy et al., 2004 Hume et al., 2004 Richard et al., 1998 Ibrahim et al., 2003 Simpson et al., 2005) indicates that there are three potentially modifiable factors contributing to transient hypothyroxinemia infection and other illnesses of prematurity, certain drugs and iodine insufficiency of parenteral nutrition. Of the three factors, primary correction of iodide deficiency is essential to allow physiologically appropriate responses before correction of other modifiable factors. As universal T4 supplementation is detrimental in some groups (van Wassenaer et at, 1997b), it is not until the modifiable factors have been corrected or minimized that a trial of T4 supplementation is warranted in extreme preterms, and then only in those who are biochemically hypothyroxinemic. The necessary pilot work has been completed to allow a UK multicenter randomized controlled trial of iodide supplementation to take place safely. 

The thyroids of neonates and pregnant women are particularly sensitive to the effects of iodide deficiency. This is of special concern because adequate thyroid hormone is essential for normal brain development during early life. 

Iodine occurs to a minute extent (less than 0.001 %) in sea water, but is found in greater concentration, combined in organic form, in certain seaweeds, in oysters and in cod livers. Crude Chile saltpetre, or caliche contains small amounts of sodium iodate, NalOj. from which iodine can be obtained (see below). Some insoluble iodides, for example liiose of silver and mercury(II), occur in Mexico. Iodine is found in the human body in the compound thyroxin in the thyroid gland deficiency of iodine in diet causes enlargement of this gland (goitre). 

It is difficult to define the normal range of iodine intake in humans, and despite efforts to provide iodine supplementation in many geographic areas of the world, endemic iodine deficiency and attendant goiter remain a world health problem (147). Exposure to excess iodine may sometimes lead to the development of thyroid disease. This unusual type of iodide-induced goiter has been found, for example, in 10% of the population of a Japanese island where fishermen and their families consume large quantities of an iodine-rich seaweed and have an iodine intake as high as 200 mg/d (148). 

Iodized Salt. Iodized table salt has been used to provide supplemental iodine to the U.S. population since 1924, when producers, in cooperation with the Michigan State Medical Society (24), began a voluntary program of salt iodization in Michigan that ultimately led to the elimination of iodine deficiency in the United States. More than 50% of the table salt sold in the United States is iodized. Potassium iodide in table salt at levels of 0.006% to 0.01% KI is one of two sources of iodine for food-grade salt approved by the U.S. Food and Dmg Administration. The other, cuprous iodide, is not used by U.S. salt producers. Iodine may be added to a food so that the daily intake does not exceed 225 p.g for adults and children over four years of age. Potassium iodide is unstable under conditions of extreme moisture and temperature, particularly in an acid environment. Sodium carbonate or sodium bicarbonate is added to increase alkalinity, and sodium thiosulfate or dextrose is added to stabilize potassium iodide. Without a stabilizer, potassium iodide is oxidized to iodine and lost by volatilization from the product. Potassium iodate, far more stable than potassium iodide, is widely used in other parts of the world, but is not approved for use in the United States. 

USP XXII specifies that sodium iodide contains 99—101.5% Nal, calculated on an anhydrous basis (4). It is used iaterchangeably with potassium iodide as a therapeutic agent, except where sodium ion is contraindicated (see Potassium compounds). Intravenous sodium iodide formulations have been used for a variety of diseases, from thyroid deficiency to neuralgia (see Thyroid and antithyroid preparations). However, these solutions are no longer listed ia the XFXUII (4), iadicatiag that their therapeutic value has not been satisfactorily demonstrated. 

Seven procedures descnbe preparation of important synthesis intermediates A two-step procedure gives 2-(HYDROXYMETHYL)ALLYLTRIMETH-YLSILANE, a versatile bifunctional reagent As the acetate, it can be converted to a tnmethylenemethane-palladium complex (in situ) which undergoes [3 -(- 2] annulation reactions with electron-deficient alkenes A preparation of halide-free METHYLLITHIUM is included because the presence of lithium halide in the reagent sometimes complicates the analysis and use of methyllithium Commercial samples invariably contain a full molar equivalent of bromide or iodide AZLLENE IS a fundamental compound in organic chemistry, the preparation... 

Still another possibility of isomerization is illustrated by the easy interconversions between pentaphenylpentadienoie aeid chloride and 2-chloropentaphenyl-3-eyelopenten-l-one. Interestingly, 2,4,6-trimethylpjrrylium iodide maj be sublimed without decomposition in a vacuum, possibly as a covalent 6-iodo-4-methyl-3,5-heptadien-2-one or 2-iodo-2,4,6-trimethyl-2H-pyran valenee isomer. In a related case, chlorocyclopropenes are covalent and are converted into cyclo-propenium derivatives only by the action of Friedel-Crafts catalysts (electron-deficient metallic chlorides) (ef. also Section II,C, 2,c.)... 

An ANRORC mechanism has also been proposed (besides an inverse cycloaddition reaction) in the conversion of 1-methylpyrimidinium iodide into 3-ethoxycarbonyl-2-methylpyridine on treatment with ethyl -amino-crotonate (95RCB1272) (Scheme 23a). The reaction starts by addition of the -carbon of the crotonate at the electron-deficient 4-position of the... 

Potassium iodide is added as a nutrient to prevent goiter, a thyroid problem caused by lack of iodine, and to prevent a form of mental retardation associated with iodine deficiency. A project started by the Michigan State Medical Society in 1924 promoted the addition of iodine to table salt, and by the mid-1950s three-quarters of U.S. households used only iodized salt. Potassium iodide makes up 0.06 percent to 0.01 percent of table salt by weight. Sometimes cuprous iodide—iodide of copper—is used instead as the source of iodine. 

When iodine dissolves in organic solvents, it produces solutions having a variety of colors. These colors arise from the different interactions between the I2 molecules and the solvent (Fig. 15.21). The element is only slightly soluble in water, unless I ions are present, in which case the soluble, brown triiodide ion, I,, is formed. Iodine itself has few direct uses but dissolved in alcohol, it is familiar as a mild oxidizing antiseptic. Because it is an essential trace element for living systems but scarce in inland areas, iodides are added to table salt (sold as iodized salt ) in order to prevent an iodine deficiency. 

Figure 42-11. Model of iodide metabolism in the thyroid follicle. A follicular cell is shown facing the follicular lumen (top) and the extracellular space (at bottom). Iodide enters the thyroid primarily through a transporter (bottom left). Thyroid hormone synthesis occurs in the follicular space through a series of reactions, many of which are peroxidase-mediated. Thyroid hormones, stored in the colloid in the follicular space, are released from thyroglobulin by hydrolysis inside the thyroid cell. (Tgb, thyroglobulin MIT, monoiodotyrosine DIT, diiodotyro-sine Tj, triiodothyronine T4, tetraiodothyronine.) Asterisks indicate steps or processes that are inherited enzyme deficiencies which cause congenital goiter and often result in hypothyroidism.

Carbonic anhydrase (CA) exists in three known soluble forms in humans. All three isozymes (CA I, CA II, and CA III) are monomeric, zinc metalloenzymes with a molecular weight of approximately 29,000. The enzymes catalyze the reaction for the reversible hydration of C02. The CA I deficiency is known to cause renal tubular acidosis and nerve deafness. Deficiency of CA II produces osteopetrosis, renal tubular acidosis, and cerebral calcification. More than 40 CA II-defi-cient patients with a wide variety of ethnic origins have been reported. Both syndromes are autosomal recessive disorders. Enzymatic confirmation can be made by quantitating the CA I and CA II levels in red blood cells. Normally, CA I and CAII each contribute about 50% of the total activity, and the CAI activity is completely abolished by the addition of sodium iodide in the assay system (S22). The cDNA and genomic DNA for human CA I and II have been isolated and sequenced (B34, M33, V9). Structural gene mutations, such as missense mutation, nonsense... 

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