| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on January 17, 2006
Accepted on April 21, 2006
Departments of Endocrinology and Diabetes (JPW, LW, BGAS, DH, MG) and Psychiatry and Behavioural Science (LS), Sir Charles Gairdner Hospital; School of Medicine and Pharmacology, University of Western Australia (JPW, VB, BGAS) and PathWest Laboratory Medicine WA (RG, CIB, MT), Nedlands, Western Australia 6009
* To whom correspondence should be addressed. E-mail: john.walsh{at}health.wa.gov.au.
Context: In patients with primary hypothyroidism, anecdotal evidence suggests that well-being is optimized by fine adjustment of thyroxine dosage, aiming for a serum TSH concentration in the lower reference range. This has not been tested in a clinical trial.
Objective: To test whether adjustment of thyroxine dosage aiming for a serum TSH concentration < 2 mU/L improves well-being compared with a serum TSH concentration in the upper reference range.
Design: Double blind, randomized clinical trial with a crossover design.
Participants: Fifty-six subjects (52 females) with primary hypothyroidism taking thyroxine (
100 µg/day) with baseline serum TSH 0.1-4.8 mU/L.
Interventions: Each subject received three thyroxine doses (low, middle, high; 25 µg increments) in random order.
Outcome measures: Visual analog scales assessing well-being (the primary endpoint) and hypothyroid symptoms, quality of life instruments (General Health Questionnaire 28, SF-36 and Thyroid Symptom Questionnaire), cognitive function tests and treatment preference.
Results: Mean (± SEM) serum TSH concentrations were 2.8 ± 0.4, 1.0 ± 0.2 and 0.3 ± 0.1 mU/L for the three treatments. There were no significant treatment effects on any of the instruments assessing well-being, symptoms, quality of life or cognitive function, and no significant treatment preference.
Conclusions: Small changes in thyroxine dosage do not produce measurable changes in hypothyroid symptoms, well-being or quality of life, despite the expected changes in serum TSH and markers of thyroid hormone action. These data do not support the suggestion that the target TSH range for the treatment of primary hypothyroidism should differ from the general laboratory range.
This article has been cited by other articles:
 |
|
 |
|
  M. H. Samuels, K. G. Schuff, N. E. Carlson, P. Carello, and J. S. Janowsky Health Status, Mood, and Cognition in Experimentally Induced Subclinical Thyrotoxicosis J. Clin. Endocrinol. Metab., May 1, 2008; 93(5): 1730 - 1736. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Schlechte Update in Endocrinology Ann Intern Med, October 16, 2007; 147(8): 563 - 572. [Full Text] [PDF]
|
|
|
|
|
|
M. H. Samuels, K. G. Schuff, N. E. Carlson, P. Carello, and J. S. Janowsky Health Status, Mood, and Cognition in Experimentally Induced Subclinical Hypothyroidism J. Clin. Endocrinol. Metab., July 1, 2007; 92(7): 2545 - 2551. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 What Thyroxine Dose Is Optimal for Patients with Hypothyroidism? Journal Watch (General), August 3, 2006; 2006(803): 1 - 1. [Full Text]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
