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Subclinical thyroid disease is defined by an abnormally high (subclinical hypothyroidism) or low (subclinical hyperthyroidism) serum thyrotropin (TSH) with peripheral thyroid hormone concentrations within the laboratory reference ranges. Such abnormalities in thyroid function tests are very common in the population and have been extensively dealt with in textbooks and reviews. Subclinical hypothyroidism is common especially in elderly women. There is no clear evidence to date that subclinical hypothyroidism causes clinical hearth disease. However, mild thyroid gland failure, evidenced solely by elevation of the serum TSH concentration, may be associated with increased morbidity, particularly for cardiovascular disease and subtly decreased myocardial contractility. In subclinical hypothyroidism both cardiac structures and function remain normal at rest, but impaired ventricular function as well as cardiovascular and respiratory adaptation to effort may became unmasked during exercise. These changes are reversible when euthyroidism is restored. Subclinical hypothyroidism does result in small increase in low density lipoprotein cholesterol and a decrease in high density lipoprotein, changes that enhance the risk for development of atherossclerosis and coronary artery disease. Because undetected subclinical hypothyroidism during pregnancy may adversely affect the neuropsychological development and survival of the fetus and be associated with hypertension and toxemia, screening pregnant women has been advocated. In addition, data suggesting that subclinical hypothyroidism is associated with ovulatory dysfunction and infertility may make screening worthwhile in this population as well. The combination of an undetectable serum thyrotropin concentration, as measured by an assay with a threshold of detection that is 0.1 mU per liter or less, and normal serum triiodothyronine and thyroxine concentrations (usually at the upper end of the normal range) is known as subclinical hyperthyroidism. This condition reflects the facts that before clinical features of thyrotoxicosis are apparent, the thyrotrophs usually respond to minor increments in thyroid hormone concentrations, which remain within the normal range, by switching off the production and secretion of thyrotropin. In the absence of clinical signs of thyroid disease, and even after additional investigations such as isotope uptake and imaging and measurement of the thyrotropin receptor antibody concentration, it may be difficult to decide whether the pattern seen on thyroid function tests is a consequence of nonthyroidal illness and concomitant medication, underlyling thyroid autonomous function or the initial phase of thyroiditis. Routine screening for thyroid disease with thyroid function tests is not recommended for asymptomatic children or adults. This recommendation does not mean that clinicians should not monitor thyroid function in patients with a previous history of thyroid disease. There is insufficient evidence to recommend for or against screening for thyroid disease with thyroid function tests in high-risk patients, including elderly persons, postpartum women, and persons with Down syndrome, but recommendations may be made on other grounds, such as the higher prevalence of disease and the increased likelihood that symptoms of thyroid disease will be overlooked in these patients. If screening is performed, the preferred test is measurement of thyroid-stimulating hormone (TSH) using a sensitive immunometric or similar assay, because of its superior sensitivity and specificity.