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Treatment of toxic adenoma and toxic multinodular goiter

INTRODUCTION

Toxic adenoma and toxic multinodular goiter (MNG) are common causes of hyperthyroidism, second in prevalence only to Graves' disease. The prevalence of toxic nodular goiter increases with age and in the presence of iodine deficiency, and may therefore be more common than Graves’ disease in older populations in regions of iodine deficiency. Toxic adenoma and MNG are the result of focal and/or diffuse hyperplasia of thyroid follicular cells whose functional capacity is independent of regulation by TSH. Twenty to 80 percent of toxic adenomas and some nodules of multinodular goiters have somatic mutations of the thyrotropin (TSH) receptor gene that confers autonomous hyperactivity [1,2].

Following a brief discussion of the diagnosis and evaluation of toxic adenoma and MNG, the treatment of these disorders will be presented here. Other disorders that cause hyperthyroidism, the clinical manifestations and diagnosis of hyperthyroidism, and treatment of Graves’ hyperthyroidism are reviewed separately. (See "Disorders that cause hyperthyroidism" and "Overview of the clinical manifestations of hyperthyroidism in adults" and "Hyperthyroidism during pregnancy: Clinical manifestations, diagnosis, and causes" and "Diagnosis of hyperthyroidism" and "Hyperthyroidism during pregnancy: Treatment" and "Treatment of Graves' hyperthyroidism in adults".)

DIAGNOSIS AND EVALUATION

Because the treatment of hyperthyroidism differs according to the etiology, the correct diagnosis must be made before therapy is instituted. (See "Diagnosis of hyperthyroidism".) The diagnosis of hyperthyroidism is usually evident in patients with unequivocal clinical and biochemical manifestations of the disease. Other patients have fewer and less obvious clinical signs, but definite biochemical hyperthyroidism (low serum TSH and high free T4 and/or T3 concentrations). Still others have low serum TSH concentrations (<0.5 mU/mL) but normal serum free thyroxine (T4) and triiodothyronine (T3) concentrations, a constellation of biochemical findings defined as subclinical hyperthyroidism. (See "Subclinical hyperthyroidism".)

Thyroid scintigraphy — Once the diagnosis of hyperthyroidism has been established, the cause of the hyperthyroidism should be distinguished by the findings on the 24-hour radioiodine uptake and scan. Women of childbearing age should have a negative pregnancy test prior to undergoing radioactive iodine scanning.

A classic clinical presentation for toxic adenoma is a hyperthyroid patient with a palpable thyroid nodule that corresponds to an area of increased radioiodine concentration on thyroid scintigraphy; there should also be suppression of radioiodine uptake in surrounding and contralateral tissue (picture 1).

                  

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Literature review current through: Jul 2014. | This topic last updated: Jul 26, 2013.
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