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Letters |
1
Department of Laboratory Medicine, Osaka University, Graduate School of Medicine D2, 2-2 Yamadaoka Suita, Osaka 565-0871, Japan
a Author for correspondence. Fax 81-6-6879-3239; e-mail namino{at}labo.med.osaka-u.ac.jp
To the Editor:
We read with interest the case conference by Fantz et al. (1) on thyroid function during pregnancy. The presented case is typical of gestational thyrotoxicosis (2), and the authors reviewed beautifully the related problems of interpretation of thyroid function tests in pregnancy.
We had proposed a new clinical entity, "gestational thyrotoxicosis", defined by clinical features as follows (3): (a) thyrotoxic symptoms, such as palpitation, increased sweating, and weight loss in early pregnancy; (b) marked increase in free thyroxine (T4; more than twice the upper limit of the reference range) and free triiodothyronine (T3); (c) complication with hyperemesis gravidarum; (d) spontaneous recovery in the later half of pregnancy; (e) negative for antithyroid microsomal or thyroid peroxidase antibodies; (f) negative for anti-thyroid-stimulating hormone (TSH) receptor antibodies; (g) no goiter; and (h) circulating human chorionic gonadotropin (hCG) with high biological activity.
We examined the case of Fantz et al. (1) in light of our experience. They did not examine the anti-thyroid antibodies in their case, although the importance of antibody measurement was described in the discussion.
Their laboratory data on thyroid function are curious. The free
T4 index was more than fourfold higher than the
upper reference value of nonpregnant healthy subjects, but the TSH was
0.8 mIU/L (1). The negative feedback regulation in
the pituitary-thyroid axis is well preserved even during pregnancy
(4); thus, TSH should completely be suppressed. The TSH
value of 0.8 mIU/L might be obtained if high hCG 
-submit interfered
in the assay or if the sample was obtained at a different date than the
free T4 sample.
The increase of serum thyroglobulin concentration in normal pregnancy may not be correct. Earlier reports on thyroid function tests in pregnancy from European countries mainly observed the effect of relative iodine deficiency rather than physiological gestational changes because iodine intake is relatively low in these countries and iodine requirements are increased during pregnancy. Iodine supplementation during pregnancy decreases, rather than increases, thyroglobulin (5). Decreased serum thyroglobulin in pregnancy is compatible with a previous report from Japan where iodine intake is sufficient (6). A recent study in the United States also clarified that there was no significant change in thyroglobulin concentration during and after normal pregnancy (7). Gestational thyrotoxicosis is induced mainly by the overstimulation of asialo-hCG, which has strong thyroid stimulation bioactivity (2). The conventional immunoassay for hCG cannot specifically detect asialo-hCG, and thus, the serum concentrations of hCG in gestational thyrotoxicosis did not differ significantly from those in euthyroid normal pregnant subjects (2).
In the cases of Graves thyrotoxicosis, measurement of anti-TSH receptor antibodies (TRAbs) is important for diagnosis, as the authors discussed. The radioreceptor assay for TRAbs was developed first by Smith et al. (8) in the United Kingdom, and they used the term "TSI". Therefore, TSI indicates TRAbs measured by radioreceptor assay and does not express biological activity. At present, the term TSH receptor-binding inhibitory immunoglobulin (TBII) is widely used (9). Instead of TSI, thyroid-stimulating antibody (TSAb) is commonly used for the expression of biological stimulating activity. Thyroid growth-stimulating immunoglobulin (TGI) is somewhat difficult to assay for a routine test, and there is still debate whether TGI is the same as TSAb.
Fantz et al. (1) are thoughtful to discuss postpartum thyroid dysfunction because this problem is far more common than gestational thyrotoxicosis. Our recent review provides further discussion of the clinical importance of postpartum thyroid dysfunction (10).
References
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