Letters to the Editor
Assessment of thyroid function in pregnancy
- Aust Prescr 2006;29:3-5
- 1 February 2006
- DOI: 10.18773/austprescr.2006.002
The Editorial Executive Committee welcomes letters, which should be less than 250 words. Before a decision to publish is made, letters which refer to a published article may be sent to the author for a response. Any letter may be sent to an expert for comment. When letters are published, they are usually accompanied in the same issue by their responses or comments. The Committee screens out discourteous, inaccurate or libellous statements. The letters are sub-edited before publication. Authors are required to declare any conflicts of interest. The Committee's decision on publication is final.
Editor, – Some further points on testing thyroid function need to be added to the useful information in Associate Professor Tran's review, 'Biochemical tests in pregnancy' (Aust Prescr 2005;28:98-101). First, a small but significant decrease in the concentration of serum free T4, most marked in the third trimester, has been clearly documented.12 In addition, albumin-dependent methods of free T4 estimation show marked negative bias, relative to the non-pregnant reference interval; in the late third trimester, such methods may give subnormal free T4 estimates in up to 50% of samples.3
These methods are unsuitable for assessing thyroid status during pregnancy4, unless results are evaluated in relation to reference intervals that reflect method-specific bias at various stages of pregnancy. Clinical chemists need to be aware of this issue when choosing an appropriate free T4 method for obstetric practice and by indicating appropriate reference intervals.
Professor Tran's counsel that 'Graves' disease needs to be rigorously controlled' in pregnancy goes beyond interpretation of test results. This advice must be tempered by the fact that any degree of maternal hypothyroidism in the first trimester can have an adverse effect on fetal brain development56, and that over treatment in the third trimester can be associated with fetal goitre.6 As thyrotoxicosis of immune origin often becomes less severe during pregnancy, it is often advisable to decrease the dose of antithyroid drug to minimise the chance of these adverse effects.6 As pointed out by Professor Tran, the exact cause of newly-diagnosed thyrotoxicosis can be difficult to establish in early pregnancy. When the disorder is mild, as judged by clinical rather than laboratory criteria, it may be best followed without treatment for several months until there is a clear indication for active treatment.6
Jim R. Stockigt
Epworth and Alfred Hospitals
Professor of Medicine, Monash University
Associate Professor H.A. Tran, author of the article, comments:
Professor Stockigt's comments are appreciated. As usual, they are incisive and informative. The small but significant decrease in serum free tetra-iodothyronine (fT4) can, in part, be explained by the peak of thyroid binding globulin concentrations in the third trimester, although these remain within the reference range in most cases.7
Selecting a special method for the obstetric population serviced by the relevant laboratory would always be a challenging task given the large scope of services imposed upon large laboratories by the current practice of pathology. The nuances of such a task are probably best reserved within the realm of clinical biochemists' practice.
As emphasised, the management of thyrotoxicosis in pregnancy is not a simple task. It should not be simply a matter of medication adjustment according to biochemical results, which are never error proof. The literature is littered with, sometimes fatal, adverse reactions8where laboratory results as given, are acted upon, when instead a considered and competent clinical assessment is warranted. As inferred by Professor Stockigt, it is best to first do no harm; a caveat that is not applicable to pregnancy alone.