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Treatment of the autonomous thyroid nodule: a review

Pathophysiological and clinical aspects of the autonomous thyroid nodule have been reviewed previously (1, 2). Interest in this disease has been renewed in recent years by exciting molecular studies showing that somatic mutations activating the TSH receptor are the main cause of autonomous adenoma (3–6). For the purposes of the present discussion on the treatment of this disease, it is sufficient to recall that it may present at one of three clinical stages (1, 2, 7–9):

1. "compensated" nodule, i.e. a nodule that is hot or warm at scintigraphy performed with a radioisotope of iodine (to exclude the possibility of a nodule of the trapping-only type (10)) but that fails to inhibit completely or substantially the radionuclide uptake by the extranodular tissue; patients with compensated nodules have detectable and usually normal serum TSH, as well as normal free (F) thyroid hormone levels (FT3 and FT4);
   
2. non-toxic or "pretoxic" nodule,
   

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