Etiology
	The causes of subclinical hyperthyroidism are similar to those that cause overt thyrotoxicosis 2 . (Table 1). In iodine-sufficient regions such as the United States, overt hyperthyroidism in women of all ages is most commonly due to Graves’ disease, and early Graves’ disease may present as subclinical hyperthyroidism. Multinodular or uninodular toxic goiter is another major cause of subclinical hyperthyroidism, especially in areas of marginal iodine intake. The natural history of multinodular goiter (Plummers’s disease) appears to be the gradual development of autonomy, leading first to subclinical and then to overt hyperthyroidism 3 . The prevalence of thyroid nodularity generally increases with age, especially in women. In one English post-mortem study 23 % of women over age 60 had nodular glands 4 . A German post-Merck mortem study (in an area of moderate iodine deficiency) found nodules in 88 % of elderly women 5 . Subclinical thyrotoxicosis is frequently iatrogenic, the result of overzealous thyroid hormone replacement therapy for hypothyroidism, or of TSH suppressive therapy for thyroid cancer. In older patients with autonomous nodules, hyperthyroidism may be precipitated by an exogenous iodine load due to radiocontrast agents, amiodarone, and other iodine-containing medications, including all forms of kelp. Subclinical hyperthyroidism must be differentiated from other causes of low serum TSH values including non-thyroidal illness, pregnancy, pituitary or hypothalamic insufficiency, and the use of medications including glucocorticoids, dopamine, aspirin, furosemide, and fenclofenac 6 . A suppressed TSH may be a transient finding. For example, in the Framingham Heart Study, 88 % of those who had subclinical hyperthyroidism at baseline had serum TSH values > 0.1 on repeat testing four years later 7 .