Toxic adenoma, thyroid

Toxic adenoma Thyroid cancer Struma ovarii... 

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... 

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). 

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. 

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. 

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. 

Method Toxic adenoma goiter Toxic diffuse goiter Thyroiditis Graves disease... 

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). 

The ideal patient for application of radioactive iodine is therefore one who harbors a single toxic adenoma and shows a suppressed TSH (Table 81.3). Under these conditions, the surrounding healthy thyroid tissue is least affected and the patient leaves the therapy with a high chance of eliminating the overactive hyperfunctioning nodule and, at the same time, preserving the healthy tissue to resume normal thyroid function (Diedein et ai, 2004 Huysmans et aL, 1997 Reiners and Schneider, 2002 Sarkar, 2006). 

Rates of hypothyroidism posttreatment have been published to be low (10%) in toxic adenoma and much higher (20-60%) in toxic multinodular goiters, increasing with the amount of tissue exposed to radiation and the time of followup. Late occurrence of hypothyroidism has to be considered, cumulating to 60—80% after 10—20 years. The induction of autoimmune thyroid disease may contribute to this high rate. 

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. 

Before ultrasound-guided fine-needle aspiration came into use, scintigraphy was believed to be the most important test for the evaluation of nodules in the thyroid gland. Scintigraphy should, however, still be used when the patient with a nodule has low serum thyroid-stimulating hormone (TSH) value, to confirm the diagnosis of a toxic adenoma. 

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.

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). 

Toxicity 4-Aminophenyl ether is highly toxic to animals. It shows sufficient evidence as a carcinogen and has caused adenomas and carcinomas in the thyroid and liver of experimental rats.75,76... 

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