Although l-T4 appears to be the main treatment for small to moderately enlarged nontoxic goiters, several complicating factors, in particular a large goiter and suspicion of thyroid malignancy, cause most clinicians to recommend surgery (Refs. Some years ago, the routine use of sonography was not recommended in the management of nodular goiters ( 126 , 130 ), but today this attitude is rapidly changing ( 6 - 9 ). Also, sonography has many favorable features, such as detection of nonpalpable nodules, estimation of nodule size/goiter volume (e.g., monitoring the effect of therapy), and guidance for FNAB ( Table 5 ). However, the high sensitivity can also lead to detection of clinically insignificant nodules and to unnecessary work-up and anxiety for the patient. Thus, in one large series of operated hyperthyroid patients, thyroid cancer was found in 1.6% of patients with a toxic multinodular goiter, contrasting with none among those with Graves' disease ( 102 ).

Blood tests measure the level of thyroid-stimulating hormone (TSH) present in the body to determine whether the goiter is being caused by hyperthyroidism or hypothyroidism. Treatments for goiters or enlarged thyroid will depend entirely on size, the associated signs and symptoms, and the underlying cause. A. The dosage of iodine recommended to treat goiter, which is an enlargement of the thyroid glands in the neck often caused by iodine deficiency, is approximately 0.3 micrograms per kilogram of body weight per day, although one source that I found recommended 2 to 4 milligrams per kilogram orally per day for two to three weeks, then once a week after that.

The two main causes of diffuse enlargement are goiter or swelling from thyroiditis (inflammation of thyroid gland). Removing all or part of your thyroid gland (total or partial thyroidectomy) is an option if you have a large goiter that is uncomfortable or causes difficulty breathing or swallowing, or in some cases, if you have a nodular goiter causing hyperthyroidism. According to legend, he was surprised when asked on his first day what research problem he would like to work on. He had noticed several dogs with large goiters in the neighborhood and replied without much reflection he would like to work on thyroid disease ( 21 ). Marine subsequently confirmed Baumann's finding that large goiters contained less total iodine than healthy glands ( 22 ). The American surgeon Halsted had reported when part of the thyroid was resected, the remaining tissue increased in size and called this compensatory hypertrophy” ( 23 ). Marine extended this observation and suggested goiter was a compensatory reaction to some deficiency” and it appeared …iodine is the most important single factor….” ( 22 ). That iodine deficiency was not the only potential dietary contributor to goiter was confirmed 15 y later when Marine published his work on the goitrogenic action of certain cyanides in animals ( 24 ).

In 1883, Semon suggested myxedema was due to a lack of activity of the thyroid ( 9 ) after reading a report by the Swiss surgeon Kocher describing myxedemic symptoms in patients after total thyroidectomy ( 10 ). British physicians began successfully treating myxedema with injections and/or oral doses of animal thyroid extracts; a 1893 review exclaimed it was one of the greatest therapeutic triumphs of the age” ( 11 ). The link between goiter, myxedema, and iodine was established when, in 1896, Baumann and Roos, working in Freiburg, Germany, digested animal thyroid glands and were surprised to isolate a residual insoluble fraction that was ∼10% iodine ( 12 ). They found this substance, termed thyroiodine, to be effective in the treatment of both myxedema and goiter. In some patients, the clinical question is Graves disease versus toxic multinodular goiter and in others Graves disease versus subacute thyroiditis. Similar to solitary toxic thyroid adenomas, somatic mutations in the TSH receptor have also been detected in hot nodules of toxic multinodular goiters (see Fig.