Document Detail


The mechanisms of transient hypothyroxinemia in infants born to mothers with Graves' disease.
MedLine Citation:
PMID:  9262225     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
N Matsuura; S Harada; Y Ohyama; K Shibayama; M Fukushi; N Ishikawa; K Yuri; M Nakanishi; Y Yokota; K Kazahari; H Oguchi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Pediatric research     Volume:  42     ISSN:  0031-3998     ISO Abbreviation:  Pediatr. Res.     Publication Date:  1997 Aug 
Date Detail:
Created Date:  1997-10-02     Completed Date:  1997-10-02     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0100714     Medline TA:  Pediatr Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  214-8     Citation Subset:  IM    
Affiliation:
Department of Pediatrics, Kitasato University School of Medicine, Sagamihara, Japan.
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MeSH Terms
Descriptor/Qualifier:
Bone Development / physiology
Female
Follow-Up Studies
Graves Disease / complications*
Humans
Hypothyroidism / complications*
Infant, Newborn
Male
Pregnancy
Prenatal Exposure Delayed Effects*
Receptors, Thyrotropin / immunology
Retrospective Studies
Thyroid Function Tests
Thyroxine / blood*
Time Factors
Chemical
Reg. No./Substance:
0/Receptors, Thyrotropin; 7488-70-2/Thyroxine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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