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DOI: 10.1055/s-0034-1387300
Schilddrüsenfunktionsstörungen in der Schwangerschaft
Thyroid dysfunction in pregnancyPublikationsverlauf
17. März 2014
07. August 2014
Publikationsdatum:
07. Oktober 2014 (online)
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Zusammenfassung
Schilddrüsenfunktionsstörungen können Fertilität, Schwangerschaftsverlauf und die kindliche Entwicklung ungünstig beeinflussen. Physiologische Veränderungen in der Schwangerschaft müssen von pathologischen Veränderungen der Schilddrüsenfunktion abgegrenzt werden.
Es handelt sich um eine Literaturrecherche (1990–2013) aus PubMed sowie um eine Auswertung der aktuellen Empfehlungen von Fachgesellschaften.
Es bestehen Trimenon-spezifische Unterschiede der Referenzwerte von TSH und T4 in der Schwangerschaft. Veränderungen der Schilddrüsenfunktion liegen in bis zu 15 % aller Schwangerschaften vor (0,4 % manifeste Hypothyreose, 0,1–0,4 % Hyperthyreose) und können zu vermeidbaren Komplikationen der Schwangerschaft und der Entwicklung des Kindes führen. Eine Hypothyreose erhöht das Risiko für Spontanabort, Früh- und Totgeburt, ferner für neurokognitive Defekte des Kindes, die auch bei einem gravierenden Jodmangel belegt sind.
In Ergänzung des Neugeborenenscreenings zur Früherkennung der angeborenen Hypothyreose (Inzidenz 0.03 %) sollte die Screening-Untersuchung auf Schilddrüsenfunktionsstörungen in der Schwangerschaft, insbesondere der Hypothyreose, fest in die Vorsorge nach den Mutterschaftsrichtlinien aufgenommen werden. Bei Nachweis einer manifesten Hypothyreose ist unverzüglich eine Schilddrüsenhormon-Substitution einzuleiten. Bei latenter Hypothyreose sollte eine Schilddrüsenhormon-Therapie ebenfalls in Erwägung gezogen werden. Eine Jodid-Supplementation ist bei allen Schwangeren und Stillenden zur Vermeidung einer fetalen bzw. neonatalen Hypothyreose und Struma zu empfehlen.
Abstract
Thyroid dysfunction may impair fertility, course of pregnancy and fetal development. Physiological alterations of thyroid function parameters, that occur during pregnancy need to be distinguished from pathophysiological states of hypo- and hyperthyroidism.
We performed a literature search (PubMed 1990-2013) and review relevant publications as well as consensus and practice guidelines of international thyroid/endocrine societies.
Interpretation of thyroid function values in pregnancy must be based on trimester-specific TSH and T4 ranges. Alterations in thyroid function are present in up to 15% of pregnancies (0.4% overt hypothyroidism, 0.1-0.4% hyperthyroidism) and may lead to preventable complications in the pregnant woman and the fetus. Hypothyroidism is associated with an increased risk for abortion, premature delivery and stillbirth, besides impairment of neurocognitive development. The latter has also been shown in situations of grave iodine deficiency.
In addition to new-born screening directed at early recognition of congenital hypothyroidism (incidence 0.03%), universal screening of all pregnant women should be implemented in health care guidelines. Newly diagnosed overt hypothyroidism in a pregnant woman requires immediate levothyroxine substitution at adequate doses. In subclinical hypothyroidism thyroid hormone replacement should be considered. Iodine supplementation is strongly recommended in all pregnant and breast-feeding women. Pregnancy causes a number of, that need to be 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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