Iodine deficiency

Iodine deficiency goiter is rare in the United States but still might be encountered by a physician. Iodine deficiency leads to an increase in RAIU. In mild or moderate iodine deficiency there is said to be a decrease in T4 and THBR values, but values usually remain within their reference range. Often T3-RIA is increased. Assay levels of TSH are usually normal. In severe iodine deficiency, T4 and THBR values often decrease and T3-RIA increases. The TSH level may be elevated but only to a mild or moderate degree. Thus, iodine deficiency may simulate thyrotoxicosis (goiter and RAIU increases), T3 toxicosis (goiter with normal or decreased T4 levels and elevated T3-RIA) or even hypothyroidism (decreased T4 level).

Iodine excess

As noted previously, excess iodine usually results from inorganic iodide, most commonly found in respiratory tract medications such as SSKI, or from organic iodine present in x-ray contrast media and in certain medications such as the antiarrhythmic drug amiodarone. With long-term SSKI therapy, when the medication is initially administered, there is a decrease in T4 values of varying degree accompanied by an increase in TSH values, followed by a return of the T4 and TSH values toward baseline levels in days or weeks. However, some of those whose T4 level stabilizes within reference range have persisting mildly elevated TSH level. A minority of patients have persistently decreased T4 and increased TSH values, which tend to be more frequent in patients with preexisting thyroid diseases such as Hashimoto’s thyroiditis, therapy with lithium carbonate, previous iodine deficiency, and patients with treated Graves’ disease or toxic nodules. On the other hand, inorganic iodide can occasionally induce thyrotoxicosis (Jod-Basedow disease), most commonly when administered to persons who are iodine deficient. As noted previously, certain x-ray contrast media (ipodate and iopanoic acid) may temporarily increase T4 levels (due to inhibition of T4 to T3 conversion) but usually only to a mild degree (20%-40% over baseline). This may or may not be accompanied by a mild increase in TSH values. Marked T4 elevation suggests Jod-Basedow disease. If this occurs, it is usually associated with a decreased RAIU value. Amiodarone is an antiarrythmia drug that contains a considerable amount of inorganic iodide. It produces more frequent and substantial thyroid test abnormalities than does x-ray contrast media. In some patients it may cause iodine-induced thyrotoxicosis (Jod-Basedow disease; more common in patients with preexisting iodine deficiency). In others, it may lead to iodine suppression of the thyroid (similar to SSKI therapy), producing decreased T4 and elevated TSH values. A third effect is inhibition of peripheral tissue conversion of T4 to T3; the patients remain euthyroid, but there is elevation of T4 and TSH in some patients, while T3-RIA is relatively normal. Overall, in patients on amiodarone therapy the T4 level is elevated over reference range upper limit in 20%-30% (range, 10%-40%) of patients; there are no clinical signs of hyperthyroidism, and the elevated T4 level is accompanied by increased reverse T3 and normal T3-RIA, THBR, and TSH values. The RAIU value can be decreased or normal. In those patients who develop iodine-induced clinically evident thyrotoxicosis, the T4, FT4, FT4 I, THBR, and T3-RIA values are elevated, whereas the TSH value is low. On the other hand, decreased T4 and elevated TSH values with clinical hypothyroidism occurs in 15%-20% of patients. In almost all patients with thyroid test abnormalities, the test results usually return to normal in 3-7 months after the end of amiodarone therapy.