Subclinical hyperthyroidism and overt hyperthyroidism have the same causes, and, similarly to overt hyperthyroidism, subclinical hyperthyroidism can be persistent or transient.
Exogenous subclinical hyperthyroidism:
People on thyroid hormone replacement therapy are at risk for subclinical hyperthyroidism, whether intentional or unintentional. A good number of these patients have hypothyroidism, and in them subclinical hyperthyroidism is not the goal of thyroid hormone therapy. However, subclinical hyperthyroidism is the goal of thyroid hormone therapy in patients with thyroid cancer and in some patients with solitary thyroid nodules, multinodular or diffuse goiters, or a history of head and neck irradiation. In these patients, the benefits of TSH suppression are thought to outweigh the risks of subclinical hyperthyroidism.
Endogenous subclinical hyperthyroidism:
Thyroid adenomas and multinodular goiters that autosecrete thyroid hormones (without stimulation from high centers) are the most common causes of endogenous subclinical hyperthyroidism.
Subclinical hyperthyroidism also occurs in patients with thyroiditis. It may also be seen in patients with early Graves' disease prior to the onset of more overt hyperthyroidism. In addition, pregnant women (especially in the first trimester) and those with hyperemesis gravidarum (who vomit a lot during pregnancy), who have high serum chorionic gonadotropin concentrations, may have subclinical hyperthyroidism.
The diagnosis of subclinical hyperthyroidism is based upon the combination of a low serum TSH concentration and normal serum free T4 and T3 concentrations. It may occur in the presence or absence of mild symptoms of hyperthyroidism. Because the serum TSH concentration can be transiently reduced, a serum TSH measurement, along with a free T4 and T3, should be repeated after one to three months to confirm the diagnosis.
Other causes of low TSH concentrations should be excluded. There are three causes of the combination of low serum TSH and normal free T4 and T3 concentrations other than subclinical hyperthyroidism:
● Central hypothyroidism — Some patients with central (from high control centers on the brain) hypothyroidism have low serum TSH and normal (but usually low or low-normal) free T4 and T3 concentrations.
● Nonthyroidal illness — Euthyroid patients with nonthyroidal illness, especially those receiving high-dose glucocorticoids or dopamine, may have low serum TSH and low-normal free T4 and T3 concentrations.
● Recovery from hyperthyroidism — Serum TSH concentrations may remain low for up to several months after normalization of serum T4 and T3 concentrations in patients treated for hyperthyroidism or recovering from hyperthyroidism caused by thyroiditis.
When the diagnosis of subclinical hyperthyroidism is uncertain, measurement of 24-hour thyroid radioiodine uptake or thyroid radionuclide imaging may be helpful.