Thyroid adenoma hyperthyroidism

Toxic adenomas may result in hyperthyroidism with larger nodules. Because there may be isolated elevation of serum T3 with autonomously functioning nodules, a T3 level must be measured to rule out T3 toxicosis if the T4 level is normal. After a radioiodine scan demonstrates that the toxic thyroid adenoma collects more radioiodine than the surrounding tissue, independent function is documented by failure of the autonomous nodule to decrease its iodine uptake during exogenous T3 administration. 

Hyperthyroidism, for example, can result from activating germline mutations that are located in the TSHR TM domains. By contrast, thyroid adenomas and multin-odal goiter (25-31) result from a variety of somatic mutations in other regions of the TSHR. For example, a rare constitutively active TSHR mutation in the first TM domain results from a Gly substitution at the conserved Ser position (28). 

Mutations with similar outcomes have been identified in nonautoimmune autosomal dominant hyperthyroidism (toxic thyroid hyperplasia) (25,26,28,32,33). These variants are located in the third TM (Val509Ala), the seventh TM (Cys672Tyr), and the carboxyl tail (Asp727Glu) regions (34). These variants result in a form of congenital hyperthyroidism that is the germline counterpart of a hyperfunctioning thyroid adenoma, with similar functional characteristics (25,33). 

Primary hyperthyroidism Graves disease Thyroid adenoma/carcinoma Secondary hyperthyroidism... 

These germ-line variants, resulting in a form of congenital hyperthyroidism, share similar functional characteristics somatic mutations present in hyperfunctioning thyroid adenoma [24, 32],... 

Mutations of the TSH receptor result in clinical thyroid dysfunction. Germline mutations can present as autosomal dominant toxic thyroid hyperplasia (gain-of-frmction mutations) or as gestational hyperthyroidism due to receptor hypersensitivity to hCG. Somatic mutations that result in constitutive activation of the receptor are associated with hyperfrmctioning thyroid adenomas. 

Figure 47.3 Nosological types of hyperthyroidism with different iodine intake levels. Relative frequency of the four most common nosological types of hyperthyroidism in Iceland, with relatively high iodine intake from consumption of fish and high iodine content of dairy products, and from East Jutland, Denmark, with mild-to-moderate iodine deficiency. MNTG, multinodular toxic goiter GD, Graves disease STA, solitary toxic thyroid adenoma SAT, subacute thyroiditis. Data from Laurberg et al., (1991).

However, these same characteristics make lithium a useful adjunct in the treatment of hyperthyroidism with i l. A 39-year-old woman with Graves disease who may have developed thyrotoxicosis secondary to treatment with amiodarone, an iodine-rich medication [92 ]. She was administered lithium 900mg/day for 12 days to increase uptake. When this was combined with two doses of 0.9 mg of recombinant human thyroid stimulating hormone (rhTSH), there was a fivefold increase in uptake [92 ]. In a retrospective study of 204 hyperthyroid patients (n = 163 Graves disease, n = 26 toxic multinodular goiter, and n=15 solitary toxic thyroid adenoma), 103 patients received alone (median dose 558 MBq) and 101 received 1 with lithium (median... 

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. 

An autonomous thyroid nodule (toxic adenoma) is a discrete thyroid mass whose function is independent of pituitary control. Hyperthyroidism usually occurs with larger nodules (i.e., those greater than 3 cm in diameter). 

The manifestations of hyperthyroidism depend on the severity of the disease, the age of the patient, the presence or absence of extrathyroidal manifestations, and the specific disorder producing the thyrotoxicosis. Of the various types of hyperthyroidism, only two are common Graves disease and toxic multinodular goiter. Less common causes include toxic adenoma and postpartum thyroiditis, among others. 

Extensive iodine absorption from povidone-iodine can cause transient hypothyroidism or in patients with latent hypothyroidism the risk of destabilization and thyrotoxic crisis (SEDA-20, 226 SEDA-22, 263). Especially at risk are patients with an autonomous adenoma, localized diffuse autonomy of the thyroid gland, nodular goiter, latent hyperthyroidism of autoimmune origin, or endemic iodine deficiency (51). 

The treatment of hyperthyroidism due to Graves disease is either 12 months treatment with carbimazole or propylthiouracil or a single diagnosis of 1.These drugs do not have a place in the 5 10% of patients in whom thyrotoyicosis is due to a toyic adenoma or to subacute thyroiditis. 

Thyroid disorders. Disturbances in thyroid metabolism can occur at any level of the hypothalams-pituitary-thyroid-peripheral tissue axis. Several of these disorders have been discussed previously. Hyperthyroidism is more prevalent in women than men. The three most common causes of hyperthyroidism are Graves hyperthyroidism, toxic multinodular goiter, and toxic adenoma. The clinical features of hyperthyroidism include hyperkinesis, weight loss, cardiac anomalies (e.g., atrial fibrillation), fatigue, weakness, sweating, palpitations, and nervousness. The typical biochemical laboratory parameters are increased serum free T4 and decreased serum TSH. 

Functionally, the state may be compensated up to a certain degree of iodine deficiency and for a considerable period of time, described in clinical terms as euthyroid diffuse or nodular goiter. Functional failure follows only in the presence of severe iodine deficiency, and hypothyroidism may then develop. Much more frequently and somewhat paradoxically, hyperthyroidism ensues after many years of iodine depletion. Rarely, hyperthyroidism may be found in cases of diffuse goiter, which are then termed as diffuse thyroid autonomy. Fiowever, hyperthyroidism frequendy occurs in conjunction with uninodular (toxic adenoma) and multinodular goiters (toxic multinodular goiter). 

From a functional point of view, euthyroid diffuse goiter and hypofunctional thyroid nodules have to be discerned from hyperthyroid conditions, mainly toxic adenoma and toxic multinodular goiter. 

Fig. 1. Relative contribution of different types of thyroid disease to the incidence of hyperthyroidism in East-Jutland, Denmark, and in Iceland. Onfy the contr ution of the four major forms is shown. GD = Graves disease, MNG = multinodular toxic goitre, STA = solitary toxic adenoma, SAT = subacute and painless thyroiditis. The numbers represent the percentage of all cases.

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