Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1997 Aug;42(2):214-8.
doi: 10.1203/00006450-199708000-00014.

The mechanisms of transient hypothyroxinemia in infants born to mothers with Graves' disease

Affiliations

The mechanisms of transient hypothyroxinemia in infants born to mothers with Graves' disease

N Matsuura et al. Pediatr Res. 1997 Aug.

Abstract

Transient hypothyroxinemia in infants born to mothers with Graves' disease is a unique disorder first reported by us in 1988. Most mothers of these infants have had no treatment, are diagnosed as having thyrotoxicosis during the last trimester, or were not well controlled during pregnancy. These infants are believed to have transient central hypothyroidism, the mechanisms of which have not been elucidated. We measured TSH-receptor antibody activities in maternal serum and blood thyroxine (T4) (free thyroxine, FT4) and TSH levels in blood dried on filter paper at 1, 3, and 5 d of age in 114 infants born to mothers with Graves' disease. The 114 infants were retrospectively divided into three groups according to the clinical course and thyroid function data: group G, neonatal thyrotoxicosis; group T, transient hypothyroxinemia; and group E, euthyroid. In group T, the dried blood T4 (FT4) level from cord blood and/or 1 d of age blood was 6.0 +/- 2.3 microg/dL (0.92 +/- 0.52 ng/dL), a value significantly higher than that at 5 d of age (3.6 +/- 1.0 microg/dL; 0.38 +/- 0.18 ng/dL) (p = 0.025 in T4, p = 0.042 in FT4). In contrast, these levels were significantly lower at birth relative to 5 d in group G (p = 0.0001 in T4) and not significantly changed in group E. The TSH level of cord blood and/or 1-d-old blood in group T was significantly lower than that of group E (p = 0.0006). Moreover, the TSH levels in response to thyrotropin-releasing hormone were blunted in most infants in group T. Bone maturation was not delayed in group T, compared with euthyroid infants. The higher blood T4 (FT4) levels at birth, relative to 5 d in group T, suggested that the fetal T4 level was higher than that of the newborn period. The fetal T4 level might have been elevated owing to transfer of T4 from mother to fetus during the last trimester when the mother's thyroid function was elevated and consequently the fetal pituitary-thyroid axis was suppressed. Although the serum T4 (FT4) levels were decreased after birth, TSH levels were not elevated, probably because the pituitary-thyroid axis was suppressed. This may be the reason for the transient hypothyroxinemia with a normal TSH level in infants born to mothers with poorly controlled Graves' disease. Weak maternal thyroid-stimulating antibody activities and differences in sensitivity of the thyroid gland to TSH-receptor antibodies may contribute to this unique disorder.

PubMed Disclaimer

Publication types