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Cardiovascular Consequences of Subclinical Thyroid Dysfunction: More Smoke but No Fire

Paul W. Ladenson, MD
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From The Johns Hopkins University School of Medicine, Baltimore, MD 21287-0003.

Potential Financial Conflicts of Interest: None disclosed.

Requests for Single Reprints: Paul W. Ladenson, MD, Division of Endocrinology and Metabolism, Department of Medicine, The Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, MD 21287-0003; e-mail, ladenson@jhmi.edu.

Ann Intern Med. 2008;148(11):880-881. doi:10.7326/0003-4819-148-11-200806030-00011
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Physicians delight in diagnosing and treating patients with overt thyroid dysfunction—those with a serum thyroxine level above or below the normal range—expecting that most or all of their symptoms will resolve and that serious, even life-threatening, complications will be avoided. At the same time, physicians recommend that individuals who have symptoms or such conditions as hypercholesterolemia, heart failure, atrial fibrillation and osteoporosis, but also normal free thyroxine and thyroid-stimulating hormone (TSH) levels, seek nonthyroidal causes and solutions for their clinical problems. Physicians remain uncertain, however, whether to treat patients who have pituitary thyrotropic cells that show that their thyroid hormone action is insufficient or excessive, even though their serum thyroid hormone concentrations remain within the population reference range.

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