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Goiters

Thirty isotopes are recognized. Only one stable isotope, 1271 is found in nature. The artificial radioisotope 1311, with a half-life of 8 days, has been used in treating the thyroid gland. The most common compounds are the iodides of sodium and potassium (KI) and the iodates (KIOs). Lack of iodine is the cause of goiter. [Pg.122]

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). [Pg.367]

Iodine. Of the 10—20 mg of iodine in the adult body, 70—80 wt % is in the thyroid gland (see Thyroid and antithyroid preparations). The essentiahty of iodine, present in all tissues, depends solely on utilisation by the thyroid gland to produce thyroxine [51-48-9] and related compounds. Well-known consequences of faulty thyroid function are hypothyroidism, hyperthyroidism, and goiter. Dietary iodine is obtained from eating seafoods and kelp and from using iodized salt. [Pg.386]

Myxedema and goiter are the main conditions for which thyroid preparations are indicated. The treatment of cretinism is difficult because it is recognized only at or after birth. Even if this disease could be diagnosed m utero, thyroid hormones do not readily cross the placental barrier. In addition, the fetus, as does a premature infant, rapidly deactivates the thyroid hormones. The halogen-free analogue DlMlT [26384-44-7] (3), which is resistant to fetal deiodinases, may prove useful for fetal hypothyroidism (cretinism). [Pg.47]

Lithium. In the lithium carbonate treatment of certain psychotic states, a low incidence (3.6%) of hypothyroidism and goiter production have been observed as side effects (6,36) (see Psychopharmacologicalagents). It has been proposed that the mechanism of this action is the inhibition of adenyl cyclase. Lithium salts have not found general acceptance in the treatment of hyperthyroidism (see Lithiumand lithium compounds). [Pg.53]

Several nonoccupational health problems have been traced to cobalt compounds. Cobalt compounds were used as foam stabilizers in many breweries throughout the world in the mid to late 1960s, and over 100 cases of cardiomyopathy, several followed by death, occurred in heavy beer drinkers (38,39). Those affected consumed as much as 6 L/d of beer (qv) and chronic alcoholism and poor diet may well have contributed to this disease. Some patients treated with cobalt(II) chloride for anemia have developed goiters and polycythemia (40). The impact of cobalt on the thyroid gland and blood has been observed (41). [Pg.379]

Graves disease Hot nodule and toxic multinodular goiter Etiology ... [Pg.192]

Fuhrer D, Krohn K, Paschke R (2005) Toxic Adenoma and toxic Multinodular Goiter. In Braverman, LE Utiger (Hrsg.) RD (eds) Lippincott Williams Wilkins, ISBN 0-7817-5047-4, The Thyroid, 508-518... [Pg.192]

Hyperthyroidism (thyrotoxicosis), defined as excessive thyroid activity, causes a state of thyroid hormone excess (thyrotoxicosis) characterized by an increased metabolic rate, increase in body temperature, sweating, tachycardia, tremor, nervousness, increased appetite and loss of weight. Common causes of hyperthyroidism are toxic multinodular goiter, toxic adenoma or diffuse toxic goitre ( Graves disease). Antithyroid diugs (methimazol, carbimazole, propylthiouracil) block thyroid hormone production and are hence suitable for the treatment of hyperthyroidism. [Pg.608]

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. [Pg.28]

Thyroid-associated ophthalmopathy (TAO) is present in 90% of patients with the classical triad of Graves disease (goiter, ophthalmopathy, dermopathy) but these features may follow independent courses and successful control of the hyperthyroidism improves TAO in less than 5% cases. Immunosuppression has been used since theories of the etiology of TAO include the presence of circulating antibodies to both thyroid and ocular muscle fibers, and of thyroglobulin-antithy-roglobulin complexes with high affinity for extraocular muscles. [Pg.338]

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. 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.
HYDOVITZ J D (1960) Occurrence of goiter in an infant soy diet. NEngl JMed. 262 351-3. [Pg.82]

SHEPHARD T H, PYNE G E, KiRSCHViNK J F, MCLEAN M (1960) Soybean goiter. NEngl JMed. 262 1099-1103. [Pg.85]

Isoflavones have been implicated in goiter induction. Soybean extracts inhibit reactions catalyzed by thyroid peroxidase (TPO), essential to the synthesis of thyroid hormones (Divi et al., 1997). Genistein and daidzein (at about 1-10 p,M of IC50) may act as alternative substrates for tyrosine iodination (Divi et al., 1997). Furthermore, genistein and daidzein have also been shown to cause the irreversible inactivation of TPO in the presence of hydrogen peroxide. Genistein also inhibits thyroxine synthesis in the presence of iodinated... [Pg.205]

Lithium is concentrated in the thyroid gland and can impair thyroid hormone synthesis. Although goiter is uncommon, as many as 30% of patients develop at least transiently elevated thyroid-stimulating hormone values. Lithium-induced hypothyroidism is not usually an indication to discontinue the drug. Patients can be supplemented with levothyroxine if continuation of lithium is desired.30... [Pg.597]

The common causes of thyrotoxicosis are shown in Table 41-6.29,30 Thyrotoxicosis can be related to the presence or absence of excess hormone production (hyperthyroidism). Graves disease is the most common cause of hyperthyroidism. Thyrotoxicosis in the elderly is more likely due to toxic thyroid nodules or multinodular goiter than to Graves disease. Excessive intake of thyroid hormone may be due to overtreatment with prescribed therapy. Surreptitious use of thyroid hormones also may occur, especially in health professionals or as a self-remedy for obesity. Thyroid hormones can be obtained easily without a prescription from health food stores or Internet sources. [Pg.676]

Primary hyperthyroidism Graves disease Toxic multinodular goiter... [Pg.676]

Subtotal thyroidectomy is indicated in patients with very large goiters and thyroid malignancies and those who do not respond or cannot tolerate other therapies. Patients must be euthyroid prior to surgery, and patients often are administered iodide preoperatively to reduce gland vascularity. The overall surgical complication rate is 2.7%. Postoperative hypothyroidism occurs in 10% of patients who undergo subtotal thyroidectomy. [Pg.680]

Goiter A nonmalignant enlargement of the thyroid gland, visible as a swelling at the front of the neck, that is often associated with iodine deficiency. [Pg.1567]


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Antithyroid drugs goiter

Colloid goiter

Diffuse toxic goiter

Endemic coast goiter

Endemic goiter

Euthyroid goiter, thyroid suppression

Exophthalmic goiter

Goiter amiodarone

Goiter and hyperthyroidism

Goiter assay

Goiter determination

Goiter diffuse

Goiter fetal

Goiter high iodine intake

Goiter hypothyroidism

Goiter lithium

Goiter mineral waters

Goiter multinodular

Goiter prevalence

Goiter prevalence rate

Goiter rate

Goiter sporadic

Goiter surveys

Goiter surveys technique

Goiter therapy

Goiter toxic

Goiter toxic multinodular

Goiter treatment

Goiter, congenital

Goiters iodine supplementation

Goiters surgery

Human diseases goiter

Hyperthyroidism diffuse toxic goiter

Hypothyroid goiter

Hypothyroid, goiter, from iodine

Hypothyroid, goiter, from iodine deficiency

India endemic goiter

Iodine goiter

Iodine induced goiter

Iodine-deficiency induced goiter

National Goiter Control Program

Neonatal goiter

Nodular goiter

Nonendemic goiter

Painful goiters

Physiological goiters

Thyroid gland goiter

Total goiter prevalence

Toxic and diffuse goiters, in iodine

Toxic and diffuse goiters, in iodine deficiency

Urinary iodine and goiter prevalence

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