Reducing TSH levels further would be harmful.
DEAR EDITOR - In their recent editorial on thyroid function tests and
hypothyroidism, Toft and Beckett discuss the target TSH (thyroid
stimulating hormone) concentration for patients receiving thyroxine
replacement therapy for primary hypothyroidism. They suggest that
patients with continuing non-specific symptoms (despite a TSH within the
laboratory reference range) are ‘under-replaced’. They conclude that
simply satisfying the recommendations of the American Thyroid Association
and restoring TSH concentrations to normal is inadequate. They state that
“some patients only achieve a sense of well-being if their TSH is low or
undetectable” and that “most patients feel well only with a low normal TSH
Primary care physicians in the UK provide sole continuing clinical
care for majority of patients (82%) with primary hypothyroidism. Before
considering changing their clinical practice, physicians should know that
almost no empirical evidence exists to support the assertion that
hypothyroid patients feel better with a TSH concentration that is ‘low
normal’, undetectable or suppressed. By comparison, two systematic
reviews with meta-analysis have found that reducing TSH levels with
thyroxine therapy increases the risk of osteoporosis - particularly in
post-menopausal women.[3,4] An issue of considerable clinical importance
as women over the age of 50 years comprise 84% of patients prescribed
thyroxine replacement therapy in primary care. TSH suppression also
increases the risk of atrial fibrillation.
Existing levels of TSH suppression in the community already pose a
threat to women’s health. Many hypothyroid patients are currently over-
replaced with thyroxine in the UK. The proportion of patients with
suppressed levels of TSH is over 20% [2,6] in primary care, whilst
undetectable TSH levels (on ultra-sensitive assay) are 12%. A change in
routine clinical practice which further reduces women’s TSH on thyroxine
replacement therapy is likely to increase both osteoporosis and atrial
fibrillation - without any good evidence that these women will feel any
Dr Mike Crilly
MRCGP, MFPHM, MPH.
Senior Lecturer in Clinical Epidemiology
& Public Health Medicine.
Aberdeen University Medical School, Department of Public Health, Polwarth Building at Foresterhill, Aberdeen AB25 2ZD
Conflicts of interest: None
 Toft AD, Beckett GH. Thyroid function tests and hypothyroidism
Measurement of serum TSH alone may not always reflect thyroid status. BMJ
2003;326:295-296 (8 February)
 Crilly,M. Thyroid adherence study. Impact of an educational
booklet on thyroxine adherence inpatients with primary hypothyroidism: a
randomised controlled clinical trial in primary care. [MD Thesis:
submitted University of Manchester UK, 2002]
 Faber J, Galloe AM. Changes in bone mass during prolonged
subclinical hyperthyroidism due to L-thyroxine treatment: a meta-analysis.
Eur J Endocrinol 1994;130(4):350-6.
 Uzzan B, Campos J, Cucherat M, Nony P, Boissel JP, Perret GY.
Effects on bone mass of long term treatment with thyroid hormones: a meta-
analysis. J Clin Endocrinol Metab 1996;81(12):4278-89.
 Sawin CT, Geller A, Wolf PA, Belanger AJ, Baker E, Bacharach P,
et al. Low serum thyrotropin concentrations as a risk factor for atrial
fibrillation in older persons. N Engl J Med 1994;331(19):1249-52.
 De Whalley P. Do abnormal thyroid stimulating hormone level
values result in treatment changes? A study of patients on thyroxine in
one general practice. Br J Gen Pract 1995;45(391):93-5
Competing interests: No competing interests