• D Führer.
• Zentrum für Innere Medizin, Klinik für Endokrinologie, Bereich Forschung und Lehre des Zentrallabors, Universitätsklinikum Essen, Hufelandstraße 55, 45122, Essen, Deutschland. dagmar.fuehrer@uk-essen.de
• Internist (Berl). 2011 Oct 1; 52 (10): 1158-66.

AbstractPregnancy causes a number of physiological alterations in thyroid hormone metabolism that need to be distinguished from the pathophysiological states of thyroid dysfunction. Both hypothyroidism and thyrotoxicosis may impair the course of pregnancy and may negatively affect the fetus. In particular, maternal hypothyroidism may lead to irreparable and detrimental deficits in the neurocognitive development of the fetus. Autoimmune thyroid disease is the most common cause of thyroid dysfunction in pregnancy. Hashimoto's thyroiditis is associated with impaired fertility and miscarriage, and may first manifest in pregnancy due to the increased thyroid hormone requirement. Graves' disease often shows a characteristic course in pregnancy with amelioration of thyrotoxicosis in the second half of pregnancy and exacerbation after delivery. In addition transplacental passage of maternal TSH receptor antibodies may lead to thyrotoxicosis in the fetus and/or newborn.

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