Iodine in the thyroid

This drug has a pronounced thyrostatic effect and canses reduced thyroxine synthesis in the thyroid gland. It inhibits the process of iodination of thyroglobnUn, reduces formation of the active form of iodine in the thyroid gland, and blocks the peroxidase system. Propylthionracil is nsed for hyperthyrosis, thyrotoxic crises, and on thyrodectomia. Synonyms of this dmg are propycil and tireostat. 

Mecfianism of Action A thiourea derivative that blocks oxidation of iodine in the thyroid gland and blocks synthesis of thyroxine and triiodothyronine. Therapeutic Effect Inhibits synthesis of thyroid hormone. 

Oral contraceptives can cause an increase in total thyroxine (163) and a fall in the percentage of free thyroxine (164). The uptake of radioactive iodine in the thyroid is usually normal total uptake of radioactive iodine may be reduced (164). The effect of progestogens on thyroxinebinding globulin may possibly counteract the estrogenic action. The net result will be a rise in protein-bound iodine and a fall in resin triiodothyronine uptake (165). It has been suggested that oral contraceptives may actually have some protective effect against thyroid disease. 

Patients with beta-thalassemia major have an increased risk of primary hypothyroidism. In 23 patients with beta-thalassemia amiodarone was associated with a high risk of overt hypothyroidism (33 versus 3% in controls) (43). This occurred at up to 3 months after starting amiodarone. The risk of subclinical hypothyroidism was similar in the two groups. In one case overt hypothyroidism resolved spontaneously after withdrawal, but the other patients were given thyroxine. After 21-47 months of treatment three patients developed thyrotoxicosis, with remission after withdrawal. There were no cases of hyperthyroidism in the controls. The authors proposed that patients with beta-thalassemia may be more susceptible to iodine-induced hypothyroidism, related to an underlying defect in iodine in the thyroid, perhaps associated with an effect of iron overload. 

Hypothyroidism, known as myxedema in adults, when severe, is the most common disorder of the thyroid gland. Worldwide, hypothyroidism is most often the result of endemic iodine deficiency. In nonendemic areas, where iodine is sufficient in the diet, chronic autoimmune thyroiditis (Hashimoto s thyroiditis) accounts for the majority of cases. This disorder is primarily characterized by high levels of circulating antibodies against a key enzyme (thyroid peroxidase) in the processing of iodine in the thyroid gland. Blocking antibodies directed at the TSH receptor may also be present. Thyroid destruction may also occur via apoptotic cell death. 

Radioactive isotopes have the same chemical properties as the nonradioactive isotopes of the same element. Because they undergo the same chemical reactions, radioactive atoms are often used as tracers to determine what ordinary atoms are doing. For example, to detect problems in the human thyroid gland, physicians often presCTibe iodine that includes a tiny fraction of 53 , a radioactive isotope of iodine. The body should utilize all the iodine in the thyroid gland. With a Geiger counter, the physician can follow the path of the radioactive isotope. If the radioactive iodine is not absorbed by the thyroid, then the regular iodine has not been absorbed either, and the physician has confirmed that a certain problem exists. 

Selective distribution within the body occurs because of special affinity between particular drugs and particular body constituents. Many drugs bind to proteins in the plasma phenothiazines and chloro-quine bind to melanin-containing tissues, including the retina, which may explain the occurrence of retinopathy. Drugs may also concentrate selectively in a particular tissue because of specialised transport mechanisms, e.g. iodine in the thyroid. 

The antithyroid compounds currently used in the United States are propylthiouracil (6- -propylthiouracil) and methimazole (/-methyl-2-mercaptoimidazole Tapazole). In Great Britain and Europe, carbimazole (Neo-mercazole), a carbethoxy derivative of methimazole, is available, and its antithyroid action is due to its conversion to methimazole after absorption. Measurements of the course of organification of radioactive iodine by the thyroid show that absorption of effective amounts of propylthiouracil follows within 20 to 30 minutes of an oral dose, and that the duration of action of the compounds used clinically is brief. The effect of a dose of 100 mg of propylthiouracil begins to wane in 2 to 3 hours, and even a 500-mg dose is completely inhibitory for only 6 to 8 hours. As little as 0.5 mg of methimazole similarly decreases the organification of radioactive iodine in the thyroid gland, but a single dose of 10 to 25 mg is needed to extend the inhibition to 24 hours. 

The availabihty of iodine varies geographically, and therefore, the size of the total iodine pool, as well as the concentration of iodine in the thyroid gland, can vary significantly depending on the access to iodine and on the thyroid size. Factors such as sex, age, and diet (that may... 

XRF is not a new method since the first measurements of stable iodine in the thyroid by Hoffer et al. (1968), the use of XRF has spread to include several other elements in medical apphcations, as well as applications in occupational and environmental surveillance. Today, XRF is primarily used as a nondestructive method for investigation of metals, minerals, environmental samples, food constituents, and body fluids. Examples of in vivo XRF elemental analysis are measurements of lead in bone (Ahlgren and Mattsson, 1979 Somervaille et al., 1985 Todd and Chettle, 1994) and studies on cadmium, mercury, gold, and platinum (Ahlgren and Mattsson, 1981 Borjesson et al, 1993, 1995), but the method is not, to our knowledge, used clinically as a tool in the routine assessment of thyroid function. Some in vivo applications of the method are listed in Table 3.1. 

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. 

In vitro models ofTPO activity and which use thiourey-lene compounds, as well as iodine (Taurog, 1996) and H2O2, and similar models of lactoperoxidase activity (Edelhoch et al., 1979) demonstrate that other substrates are often oxidized in preference to iodide. The peroxidase catalyzes the formation of disulfide compounds. These are subsequently oxidized and excreted, but only in the presence of iodine. Absolute iodine deficiency or relative deficiency in the presence of high concentrations of thioureylene compounds results in recovery of the thioureylene from the disulfide and irreversible inhibition of peroxidase (Taurog, 1996). In the sow and cow experiments inactivation of thioureylenes by TPO at the expense of iodide oxidation, and therefore storage of elemental-iodine in the thyroid, resulted in increased iodine (and presumably iodide) concentrations in urine and feces, respectively. 

The overall iodine content of the human body is of interest to students of the thyroid, but has eluded precise measurement. Iodine in the thyroid gland can now be measured with confidence using fluorescent scanning, its normal value ranging from 5 to 15 mg (Cavalieri and McDougall, 1996). However, the amount of iodine in the extrathy-roidal spaces has been much more difficult to determine. Published estimates of total human iodine content are listed in Table 19.1. 

Iodine is an essential element to humans and presents in the human body in minute amounts (15-20mg in adults), of which more than 80% exists in the thyroid gland. Iodine in the human body mainly comes from food intake and inhalation of atmospheric iodine. In the thyroid, iodine is added to the essential amino acid thyroxine residue on thyroglobulin. 

An X-ray fluorescence method has been developed for in vivo determination of iodine in thyroid (Aubert et al., 1981 Jonckheer and Deconinck, 1982). This method is based on the irradiation of iodine in the thyroid by o(-rays provided by a -source, such as Am. The excited iodine atoms emit a characteristic X-ray fluorescence radiation, which is proportional to the amount of iodine present in the gland. The reported detection fimit reaches 0.01 mg/ml thyroid, this value is much lower than the iodine concentration in thyroid. The reported radiation dose equivalent is only 60mSv per measurement. This method has been successfully used for the clinical determination of in thyroid (Milakovic et al., 2006 Reiners et al., 1996, 2006 Briancon et al., 1992). An indirect method was also reported to determine of thyroid iodine in vivo (Imanishi et al., 1991), which is based on the relationship of CT attenuation values with iodine concentration in the thyroid. It was reported that the CT value correlated finearly with iodine concentration in thyroid nodules when iodine concentration was higher than 0.02 mg/g. 

NAA and X-ray fluorescence are used for in vivo determination of stable iodine in the thyroid the most frequently used method for iodine in urine is colorimetry of the Sandell—Koltoff reaction, while ICP-MS is a more accurate and simple method compared to others. 

Very high bromide intake in the animal (>160 mg bro-mide/day) significantly shortens the biological half fife of iodine in the thyroid (from about 100 to 30 h). 

The uptake of iodine in the thyroid gland (21% in 24 h) is lower than in a Swedish population studied 45 years earfier (38%), showing the long-term adaptation to an environment higher in iodine. These figures correspond to an intake of iodine of about 260 pg/day in 2000 compared to 100 j,g/day in 1955. 

Suppression of the organification of iodine in the thyroid gland by high doses of iodine was originally described by Wofif and Chaikoff (1948), and is known as the acute... 

Wolfi ChaikofF effect. Raben (1949) showed that this effect was dependent on the amount of iodine in the thyroid gland and not on the plasma concentration of iodine. The acute inhibitory effect of iodine overload is usually transient. Intrathyroidal iodine decreases within a few days despite a high plasma iodine concentration and thyroid hormone synthesis then returns to the previous level. This resumption of the organification of iodine is known as the escape phenomenon (Wolff, 1969), and it means that hypothyroidism will not develop in most individuals despite excessive iodine intake. 

Fig. 19.1 Half a century ago, measurement of radioactive Iodine In the thyroid gland with a Geiger-Mueller counter placed at different points indicated...

Normally the human body concentrates iodine in the thyroid gland. The purpose of the large doses of K1 is to displace radioactive iodine from the thyroid and allow its excretion from the body. 

Iodine has as many as 37 isotopes, many of which happen to be radioactive. Further to this, many of these isotopes form in the event of a nuclear explosion, and should they be released into the atmosphere it s advisable to take iodine supplements to prevent the natural iodine in the thyroid gland from being replaced by a radioactive type. This helps mitigate the risk of cancer forming in the thyroid gland. 

Some antagonists of the formation or secretion of hormones are known. For example, the thiocyanate ion (absorbed from excess intake of cabbage) inhibits the concentration of iodine in the thyroid gland. The thiourea-derived drugs, such as propylthiouracil and carbimazole (3.44), prevent the iodination of tyrosine in thyroglobulin, and are much used in treating hyperthyroidism. 

Concentration of Protein-Bound Iodine in the Thyroid Gland of a Teleost Fish (Scarus guacamaia) in Relation to Body Weight (Aqe) ... 

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