Thyroid hyperthyroidism

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. 

The selective uptake of iodide ion by the thyroid gland is the basis of radioiodine treatment in hyperthyroidism, mainly with although various other radioactive isotopes ate also used (40,41). With a half-life of eight days, the decay of this isotope produces high energy P-particles which cause selective destmction within a 2 mm sphere of their origin. The y-rays also emitted are not absorbed by the thyroid tissue and are employed for external scanning. 

Hyperthyroidism may be treated in several ways. One of these is interference with the synthesis of the thyroid hormones, possibly by removal of iodine. Thiourea and cyclic thioureas have this effect and of such cyclic compounds, thiouracil (1030 R = H), its 6-alkyl derivatives (1030 R = Me or Pr) and thiobarbital (1031) are effective thyroid drugs. Today only propylthiouracil (1030 R = Pr) is widely used, probably because it has fewer side effects than the others (71MI21302). The thiouracils are made by the Principal Synthesis from a /3-oxo ester (1032 R = H, Me, Pr, etc.) and thiourea (45JA2197) their fine structures are experimentally based (64AF1004). 

Hyperthyroidism, that is, the overproduction of thyroid hormones, is usually treated by surgical removal of the thyroid gland. Before such a procedure is undertaken, the hyperthyroidism is usually first brought under control by treatment with so-called antithyroid agents. 

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. 

The symptoms of hypothyroidism and hyperthyroidism are given in Table 51-1. A severe form of hyperthyroidism, called thyrotoxicosis or tiiyroid storm, is characterized by high fever, extreme tachycardia, and altered mental status. Thyroid hormones are used to treat hypothyroidism and antithyroid... 

Antithyroid drugp or thyroid antagonists are used to treat hyperthyroidism. In addition to the antithyroid drugs, hyperthyroidism may be treated by the administration of strong iodine solutions, use of radioactive iodine (131I), or by surgical removal of some or almost all of the tiiyroid gland (subtotal thyroidectomy). 

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. 

Thyroid function tests abnormal thyroid hormone levels may suggest hypo- or hyperthyroidism, either of which may be associated with constipation. 

Discuss the prevalence of thyroid disorders, including subclinical (mild) and overt (typical signs and/or symptoms present) hypothyroidism and hyperthyroidism. 

O In most patients with thyroid hormone disorders, the measurement of a serum thyroid-stimulating hormone (TSH) level is adequate for the diagnosis of hypothyroidism and hyperthyroidism. The target TSH for most patients being treated for thyroid disorders should be the mean normal value of 1.4 milliunits/L or 1.4 microunits/mL (target range 0.5-2.5 milliunits/L or 0.5-2.5 microunits/mL). 

The goals of treating hyperthyroidism are to relieve symptoms, to reduce thyroid hormone production to normal levels and achieve biochemical euthyroidism, and to prevent longterm adverse sequelae. 

Hyperthyroidism is much less common than hypothyroidism. In NHANES III,1 1.3% of the population was hyperthyroid (0.5% overt, 0.8% subclinical), with the highest incidences in women overall and in men and women in the 20 to 39 and over 80 years of age groups. The Colorado Thyroid Health Study2 showed a hyperthyroid incidence of 2.2% (2.1% subclinical). 

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. 

Iodine excess (including radiocontrast, amiodarone) Thyrotoxicosis without hyperthyroidism Subacute thyroiditis Silent (painless) thyroiditis... 

Some neonates born to mothers with Graves disease will be hyperthyroid at delivery. Antithyroid drug therapy (propylthiouracil 5-10 mg/kg per day or methimazole 0.5-1 mg/kg per day) may be required for up to 12 weeks. One drop per day of SSKI may be used in the first few days to rapidly reduce thyroid hormone synthesis and release. 

The growth and spread of thyroid carcinoma is stimulated hy TSH. An important component of thyroid carcinoma management is the use ofLT4 to suppress TSH secretion. Early in therapy, patients receive the lowest LT4 dose sufficient to fully suppress TSH to undetectable levels. Controlled trials show that suppressive LT4 therapy reduces tumor growth and improves survival. These patients are purposefully overtreated with LT4 and rendered subclinically hyperthyroid. Postmenopausal women should receive aggressive osteoporosis therapy to prevent LT4-induced bone loss. Other thyrotoxic complications, such as atrial fibrillation, should be monitored and managed appropriately. 

Interferon-a causes hypothyroidism in up to 39% of patients being treated for hepatitis C infection. Patients may develop a transient thyroiditis with hyperthyroidism prior to becoming hypothyroid. The hypothyroidism may be transient as well. Asians and patients with preexisting anti-TPOAbs are more likely to develop interferon-induced hypothyroidism. The mechanism of interferon-induced hypothyroidism is not known. If LT4 replacement is initiated, it should be stopped after 6 months to re-evaluate the need for replacement therapy. 

American Association of Clinical Endocrinologists Thyroid Task Force. Evaluation and Treatment of Hyperthyroidism and Hypothyroidism, 2002 www.aace.com/clin/guidelines/hypo hyper.pdf accessed October 30,2005. 

Hyperthyroidism State caused by excess production of thyroid hormone. 

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