Subclinical hyperthyroidism is defined as a patient having normal free thyroxine (FT4) and total triiodothyronine (T3) levels in conjunction with a thyrotropin (TSH) level persistently below the normal range in the absence of factors known to suppress TSH. Factors that may alter TSH value and thyroid function test results include medications such as corticosteroids and dopamine and clinical conditions to include hypothalamic or pituitary hypofunction and nonthyroid illness.1,2 Nonthyroid illness is a general term that applies to a wide variety of patients who have systemic illness that can result in altered thyroid function test results. In general, the diagnosis of subclinical hyperthyroidism is made in ambulatory outpatients who are not taking medications known to affect thyroid function. The incidence of subclinical hyperthyroidism is approximately 1%.3 The most common causes of endogenous subclinical hyperthyroidism include Graves disease (usually younger patients), multinodular goiter (typically older patients), and solitary autonomous nodules. The discrimination between endogenous hyperthyroidism from exogenous hyperthyroidism is important, since exogenous hyperthyroidism can usually be treated by modulation of the levothyroxine dose. Although the study by Collet et al4 focuses on cardiovascular effects, subclinical hyperthyroidism is also associated with an increased risk of osteopenia and/or osteoporosis, especially in older women, which may improve following treatment of the hyperthyroidism.5 It is controversial whether cognitive function is altered by the presence of subclinical hyperthyroidism.
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