Abstract
Congenital hypothyroidism due to a malformation of the thyroid gland is a disease which has been well known since the 17th century (Cranefield 1962). The pathophysiological mechanisms leading to these malformations are still unknown today in the majority of cases. The frequency of congenital hypothyroidism, as assessed by neonatal screening programs, is 1 in 3000 newborns in most of the countries (Toublanc 1990). Only 25% of the newborns have a gland of a normal size and in the normal position, and in these patients hypothyroidism is most probably caused by an inherited defect of thyroid hormone synthesis. 75% of the patients with congenital hypothyroidism have a malformed thyroid gland. In 40% the thyroid cannot be detected by radionuclear imaging studies, but modern ultrasound techniques demonstrated small remnants of thyroid tissue in those athyrotic patients (Hassan et al. 1989). In the remaining 35% of the patients, the glands are hypoplastic or located in an ectopic position. As pathogenic mechanisms for the defective migration infectious or genetic causes were discussed (Aagaard and Melchior 1959; Mihai et al. 1979).
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© 1992 Springer-Verlag Berlin Heidelberg
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Grüters, A., Bogner, U., Schumm-Draeger, P., Helge, H. (1992). Maternal Thyroid Autoantibodies and Fetal Thyroid Growth. In: Neubert, D., Kavlock, R.J., Merker, HJ., Klein, J. (eds) Risk Assessment of Prenatally-Induced Adverse Health Effects. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-77753-0_34
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DOI: https://doi.org/10.1007/978-3-642-77753-0_34
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