BMJ  2003;326:1086-1087 (17 May), doi:10.1136/bmj.326.7398.1086-b

Letter

Thyroid function tests and hypothyroidism

Restoring serum TSH to reference range should be goal of replacement

EDITOR—The article from Meier et al concludes that judicious initiation of thyroxine treatment in overt hypothyroidism should be guided by clinical and metabolic presentation and thyroid hormone concentrations and not by serum thyroid stimulating hormone concentrations.¹ This conclusion seems to contradict overwhelming evidence that serum thyroid stimulating hormone represents the most sensitive marker of primary hypothyroidism; furthermore, it is not supported by the findings of the study.

The cohort was a selected group of 49 patients with clinically significant hypothyroidism as evidenced by mean serum concentrations of thyroid stimulating hormone higher than 40 mU/l, and the study used a series of poorly specific and sensitive markers of thyroid status. Duration of hypothyroidism is an important factor determining the clinical symptoms and signs, which were not controlled for in this study.

Whether data from this study can be extrapolated to patients receiving thyroxine treatment is questionable. The accompanying editorial by Toft and Beckett says that some patients receiving thyroxine replacement continue to have symptoms despite restoration of normal concentrations of serum thyroid stimulating hormone and that exogenous subclinical hyperthyroidism is less harmful than endogenous subclinical hyperthyroidism. Few, if any, data support this view.

This statement conflicts with increasing evidence that excessive thyroxine replacement results in adverse symptoms and quality of life scores, increased bone loss, and adverse cardiovascular outcomes.^2–5 It is our belief that restoration of serum concentrations of thyroid stimulating hormone to within the reference range should be the goal of replacement. If symptoms persist despite adequate replacement then an alternative explanation should be sought.

Royal Free Hospital Trust, London NW3 2QG mark.vanderpump{at}royalfree.nhs.uk

Division of Medical Sciences, University of Birmingham, Queen Elizabeth Hospital, Birmingham B15 2TH, UK

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Competing interests: None declared.

References

1. Meier C, Trittibach P, Guglielmetti M, Staub JJ, Müller B. Serum thyroid stimulating hormone in assessment of severity of tissue hypothyroidism in patients with overt primary thyroid failure: cross sectional survey. BMJ 2003;326: 311-2. (8 February.)[Free Full Text]
2. Biondi B, Fazio S, Carella C, Sabatini D, Amato G, Cittadini A, Bellastella A, et al. Control of adrenergic overactivity by beta-blockade improves the quality of life in patients receiving long-term suppressive therapy with levothyroxine. J Clin Endocrinol Metab 1994;78: 1028-7.[Abstract]
3. Mercuro G, Panzutto MG, Bina A, et al. Cardiac function, physical exercise capacity, and quality of life during long-term thyrotropin-suppressive therapy with levothyroxine: effect of individual dose tailoring. J Clin Endocrinol Metab 2000;85: 159-64.[Abstract/Free Full Text]
4. 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: 4278-89.[Abstract]
5. 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: 1249-52.[Abstract/Free Full Text]

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Mark Oliver
bmj.com, 17 May 2003 [Full text]