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Letters |
1 St. Thomas’ Hospital, Department of Chemical Pathology, London SE1 7EH, United Kingdom
To the Editor:
Fantz et al (1) describe a case of hyperthyroidism of hyperemesis gravidarum. They discuss the changes in thyroid function during pregnancy and the causes and investigations of hyper- and hypothyroidism during pregnancy. One of the important differential diagnoses is to determine whether the hyperthyroidism is likely to be transient (as in hyperemesis gravidarum) or related to underlying thyroid disease such as Graves disease.
Red cell zinc or red cell carbonic anhydrase (CA1) is useful in this differentiation. The zinc-containing CA1 is inhibited by thyroid hormones, and in hyperthyroidism red cell zinc and CA1 are low (2)(3). Because the inhibition of this enzyme takes place in developing red cells, changes in red cell zinc or CA1 require several weeks. Thus, it is a useful test to differentiate between transient hyperthyroidism and Graves disease (4)(5).
With regard to the etiology of the hyperthyroidism in hyperemesis, not all studies show a difference in serum human chorionic gonadotropin (hCG) concentration between those hyperemetic subjects with hyperthyroidism and those without (6). Several studies have suggested that there may be subtle differences in the hCG molecule, such as acidic isoforms with increased thyrotropic activity (7)(8).
Frantz et al. (1) also fail to mention that hyperemesis is more common in certain racial/ethnic groups (9)(10).
References
2
Department of Pathology, and,
3
Division of Endocrinology, Department of Medicine, Washington University, School of Medicine, Saint Louis, MO 63110
a Address correspondence to this author at: Department of Pathology, Washington University School of Medicine, Box 8118, Saint Louis, MO 63110. Fax 314-362-1461; e-mail gronowski{at}pathology.wustl.edu
To the Editor:
We thank Drs. Amino and Swaminathan for their comments on our review of thyroid function during pregnancy (1).
In response to Dr. Amino, the low but measurable serum thyroid-stimulating hormone (TSH) concentration observed in our patient is atypical. The TSH and thyroxine (T4) were obtained on the same date, and it is unlikely that the TSH represents cross-reactivity with human chorionic gonadotropin (hCG) in the patient’s serum because the assay used (IMx; Abbott Laboratories, Abbott Park, IL) shows no detectable interference up to 200 000 IU/L hCG. It would have been informative to follow this patient over time because these values may reflect changing titers, but this was not possible in this patient.
The information on serum thyroglobulin concentrations in pregnancy is appreciated.
The comments regarding various terminologies for TSH receptor antibodies are noteworthy from a historical perspective. However, we feel that the terminology as used in our review is commonly accepted (2)(3)(4)(5).
In response to Dr. Swaminathan, we agree, and in fact discuss in our review, that the etiology of hyperthyroidism in hyperemesis is unclear.
The information on hyperemesis in different racial groups is very useful.
Although red cell zinc and red cell carbonic anhydrase have been proposed as markers of long-standing thyroid disease, they are not widely used, nor are they readily available. For this reason, they were not included in our review.
References
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