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Division of Endocrinology, Sinai Hospital of Baltimore, and The Johns Hopkins University School of Medicine, Baltimore, Maryland 21215
Address all correspondence and requests for reprints to: David S. Cooper, M.D., Division of Endocrinology, Sinai Hospital of Baltimore, 2435 West Belvedere Avenue, Hoffberger Building, Suite 56, Baltimore, Maryland 21215. E-mail dcooper{at}lifebridgehealth.org.
Endogenous subclinical hyperthyroidism, defined by normal circulating levels of free T4 and T3 and low levels of TSH, is a common clinical entity and is typically caused by the same conditions that account for the majority of cases of overt hyperthyroidism: Graves disease, toxic multinodular goiter, and solitary autonomously functioning thyroid nodules. Subclinical hyperthyroidism has been associated with an increased risk of atrial fibrillation and mortality, decreased bone mineral density in postmenopausal women, and mild hyperthyroid symptoms. Treatment of subclinical hyperthyroidism remains controversial, given the lack of prospective randomized controlled trials showing clinical benefit with restoration of the euthyroid state. Nevertheless, it seems reasonable to treat older individuals whose serum TSH levels are less than 0.1 mU/liter and certain high-risk patients, even when the serum TSH is between 0.1 and the lower limit of the normal range.
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B. Biondi and D. S. Cooper The Clinical Significance of Subclinical Thyroid Dysfunction Endocr. Rev., February 1, 2008; 29(1): 76 - 131. [Abstract] [Full Text] [PDF] |
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