Definition, Etiology, Pathogenesis Top
A toxic thyroid nodule is an adenoma (toxic adenoma) or a hyperplastic nodule observed on radionuclide scintigraphy that usually (but not always) causes hyperthyroidism. It develops most commonly as a result of a somatic mutation of the thyrotropin-stimulating hormone receptor or the alpha subunit of a stimulatory G-protein (Gs alpha). Unlike multinodular goiter, it is not related to iodine deficiency.
Clinical Features Top
Symptoms of hyperthyroidism are similar to those caused by toxic multinodular goiter, and the typical pattern of development is from a compensated autonomously functioning nodule to overt hyperthyroidism: Figure 5.6-9.
Diagnosis is based on radionuclide thyroid scintigraphy. Clinical examination and ultrasonography reveal a solitary nodule. TSH secretion can be decreased (but still within normal limits) or suppressed (subclinical or overt hyperthyroidism [see Thyrotoxicosis]).
The treatment of choice is radioiodine therapy (Table 5.6-6). Due to low serum TSH levels, iodine uptake of the thyroid parenchyma is inhibited (therefore, the risk of developing posttreatment hypothyroidism is low). Radioiodine therapy should be started after discontinuation of thionamides and when serum TSH levels are <0.1 mIU/L. In patients with indications for fine-needle biopsy (see Nontoxic Multinodular Goiter), the biopsy should not be performed within 1 to 2 weeks before the radioiodine therapy, as it may cause transient inhibition of iodine uptake by the nodule. Serum TSH levels should be monitored and follow-up ultrasonography performed to evaluate the size of the nodule every 6 to 12 months. In some centers, ethanol injections into the nodule are used with satisfactory outcomes.
The 6-year risk of developing overt hyperthyroidism in patients with a compensated or subtoxic nodule (ie, with subclinical thyrotoxicosis) is 2% to 5%. With an appropriately conducted radioiodine therapy, a complete resolution of hyperthyroidism may be achieved. The risk of malignancy is ~2%.