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Levothyroxine Therapy in Patients with Thyroid Disease

Susan J. Mandel, MD; Gregory A. Brent, MD; and P. Reed Larsen, MD
[+] Article and Author Information

From Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts. Requests for Reprints: P. Reed Larsen, MD, Thyroid Division, Brigham and Women's Hospital, 75 Francis Street, Boston MA 02115. Grant Support: In part by grants 5 T32 DK07529, 5 R01 DK 36256, and 1 R01 DK 43714 from the National Institutes of Health and by a grant from Daniels Pharmaceuticals.


Copyright 2004 by the American College of Physicians


Ann Intern Med. 1993;119(6):492-502. doi:10.7326/0003-4819-119-6-199309150-00009
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Purpose: To review the indications for and the proper monitoring of levothyroxine therapy in patients with thyroid disease.

Data Sources: Relevant English language articles published from 1966 to 1992 were identified through a MEDLINE search and manual searches of both identified articles and selected endocrinology texts.

Study Selection: Studies, case reports, and review articles that contained data on the pathophysiologic aspects of relevant thyroid disorders and on the pharmacologic aspects of, indications for, and administration of levothyroxine therapy.

Data Extraction: Data on the epidemiology, clinical manifestations, complications, and treatment of thyroid disorders were analyzed with respect to patient selection, methods, diagnostic criteria, and conclusions. These data were used to develop a rational approach to the management of such patients.

Results of Data Synthesis: Levothyroxine is a reliable and commonly prescribed drug to treat thyroid disease, but excessive dosage may have adverse effects. In patients with hypothyroidism, levothyroxine is used as replacement therapy. For most patients, therapy can be initiated with a full replacement dosage (1.6 g/kg body weight), which is usually 75 to 100 g/day for women and 100 to 150 g/d for men. The goal is to normalize the serum thyroid-stimulating hormone concentration. Levothyroxine is also used to suppress the serum thyroid-stimulating hormone concentration. A trial of thyroid-stimulating hormone suppressive therapy is indicated for most patients with benign solitary nonfunctioning thyroid nodules and for those with a history of thyroid cancer. Levothyroxine in nonthyroid-stimulating hormone-suppressive doses may also be indicated for patients with nontoxic multinodular goiter and for certain patients after lobectomy for benign thyroid nodules.

Conclusions: With proper patient monitoring, levothyroxine replacement therapy should be effective, inexpensive, and free of complications. Recommendations for thyroid-stimulating hormone suppression with levothyroxine are based on riskbenefit considerations of the biologic characteristics of the thyroid disorder and the individual patient.

Figures

Grahic Jump Location
Figure 1.
Role of thyroxine (T4) and 3,5,3 triiodothyronine (T3) in the feedback regulation of thyrotropin-releasing hormone (TRH) and thyroid-stimulating hormone (TSH) secretion.3

Thyroxine is secreted by the thyroid but must be deiodinated to T to produce its effects. This conversion may occur in the liver or kidney, catalyzed by the type I 5 deiodinase (5 DI), or intracellularly in the pituitary and central nervous system, catalyzed by the type II 5 deiodinase (5 DII). Somatostatin (SRIH) also inhibits TSH secretion. Reprinted with permission (Larsen PR, Ingbar SH. The thyroid. In: Wilson JE, Foster DW; eds. Williams Textbook of Endocrinology. 8th ed. Philadelphia: WB Saunders; 1991:357-487.).

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