Maternal-fetal T4transfer does not suffice to prevent the effects of in utero hypothyroidism

Joseph Sack, Igor Kaiserman, Ran Siebner

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


IT has been suggested recently that in congenitally hypothyroid infants with organification defect there is a maternal-fetal transfer of thyroxine (T4). The present study was conducted to evaluate how effective the maternal-fetal transfer is and whether the maternal T4 can prevent intrauterine hypothyroidism. The clinical, laboratory and radiological data on 271 full-term infants with persistent primary congenital hypothyroidism, detected by the national screening program, were used to assess the degree of in utero hypothyroidism. For 6 out of 50 athyroid infants, two pretreatment blood samples spotted on filter paper were available for calculating the T4 disappearance rate. Most infants with agenesis of the thyroid had very low T4 and very high levels of thyroid-stimulating hormone compared to infants with ectopic thyroid. In the athyroid infants the initial T4 declined to low and undetectable levels. Bone maturation was significantly delayed while the clinical symptomatology was more prominent in the athyroid congenital hypothyroid infants, as compared with the ectopic thyroid infants. In conclusion, there is some maternal-fetal transfer of T4. However, this transfer is insufficient to suppress the fetal levels of thyroid-stimulating hormone and prevent intrauterine hypothyroidism.

Original languageEnglish
Pages (from-to)1-7
Number of pages7
JournalHormone Research in Paediatrics
Issue number1-2
StatePublished - 1 Jan 1993
Externally publishedYes


  • Bone age
  • In utero hypothyroidism
  • Neonatal screening
  • Primary congenital hypothyrodism

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Endocrinology, Diabetes and Metabolism
  • Endocrinology


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