Related Content and previous articles on similar topics:
Reasons Why Thyroid Testing Can Be Unreliable by Jeffrey Dach MD
http://jeffreydach.com/2007/12/16/reasons-why-thyroid-testing-can-be-unreliable-by-jeffrey-dach-md.aspx
Hunt Study Shows Thyroid Prevents Heart Attacks by Jeffrey Dach MD
http://jeffreydach.com/2008/10/12/hunt-study-shows-thyroid-prevents-heart-attacks-by-jeffrey-dach-md.aspx
Links and References
http://www.amazon.com/review/RSKEFGC2G8IZO
Barry Durrant Peatfield, "Your Thyroid and How to Keep It Healthy".
http://www.altsupportthyroid.org/tsh/tshmedrefs5.php
http://www.altsupportthyroid.org/tsh/tshmedrefs5.php
Suppressed TSH Levels: Medical Journals
http://www.altsupportthyroid.org/tsh/tshexp1pr.php
TSH and Patients' Experiences: Suppressed to 0.5
http://ccpd.ucsf.edu/hypothyroidism.shtml
Hypothyroidism (Thyroid Hormone Deficiency) UCSF Pituitary Disorders
TSH is often an unreliable measure of secondary hypothyroidism and should not be used to assess the adequacy of thyroid replacement in these patients. The inappropriate use of TSH levels to determine hormone replacement is one of the more common mistakes that we see in the patients we follow, and patients should be cautious if another physician discusses changing their thyroid hormone dose. Many patients have returned for their one-year follow-up visits having had their doses lowered in response to "low TSH levels." Most of them feel poorly, but improve after we increase or restart their medication.
http://www.bmj.com/cgi/content/full/326/7398/1087
BMJ 2003;326:1087 (17 May), doi:10.1136/bmj.326.7398.1087
Letter- Thyroid function tests and hypothyroidism
In the Framingham study a low serum thyroid stimulating hormone concentration was shown to be a risk factor for the development of atrial fibrillation,1 but the patients in question were a heterogeneous group, the minority of whom were taking thyroxine. A similarly misleading conclusion has been drawn from the recent Birmingham study in which a low serum thyroid stimulating hormone (< 0.5 mU/l) was associated with an increase in cardiovascular mortality.2
This finding has been used to argue that a suppressed serum concentration of thyroid stimulating hormone should be avoided in patients taking thyroxine replacement,3 although thyroxine treatment was one of the exclusion criteria. The weakness of the meta-analysis, showing that thyroxine induced suppression of thyroid stimulating hormone led to reduced bone mineral density, was recognised by the authors themselves, who said that their design (cross sectional studies) was not appropriate because the many risk factors for bone loss do not allow correct matching of controls with cases.4 This realistic assessment accords with the earlier views of Franklyn et al that thyroxine treatment alone does not represent a significant risk factor for loss of bone mineral density.5
We have long taken the view that most hypothyroid patients are content with a dose of thyroxine that restores serum concentrations of thyroid stimulating hormone to the low normal range. However, some achieve a sense of wellbeing only when serum thyroid stimulating hormone is suppressed, when we take care to ensure that serum tri-iodothyronine is unequivocally normal.
Until valid evidence shows that such a policy is detrimental we will continue to treat patients holistically rather than insist on adherence to a biochemical definition of adequacy of thyroxine replacement. The issue of whether a little too much thyroxine is dangerous is likely to evaporate when appropriate preparations become available to allow treatment of hypothyroidism with both tri-iodothyronine and thyroxine.
A D Toft, consultant physician - Endocrine Department Royal Infirmary of Edinburgh, Edinburgh EH3 9YW G J Beckett, reader University Department of Clinical Biochemistry Royal Infirmary of Edinburgh, Edinburgh EH3 9YW
