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Hashimoto Thyreoiditis, therapeutische Optionen und extrathyreoidale Assoziationen – ein aktueller Überblick

Hashimoto thyroiditis, therapeutic options and extrathyroidal options – an up-to-date overview

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Zusammenfassung

Die Hashimoto Thyreoiditis ist eine der häufigsten organspezifischen Autoimmunerkrankungen des Menschen mit konsekutiver Organdestruktion und folglich die häufigste Ursache einer primären Hypothyreose in ausreichend jodversorgten Gebieten. Immunpathogenetisch nehmen die CD4+ T‑Zellen und ihre Differenzierungen eine Schlüsselrolle ein. Ätiologisch Einfluss haben genetische, aber auch Umweltfaktoren, existentielle Faktoren (weibliches Geschlecht) und auch der Darm und die Darmflora. Zur Diagnosestellung benötigt werden eine ausführliche Anamnese, Sonographie und laborchemische Bestimmung der Schilddrüsenfunktion und Schilddrüsenantikörper. Bei laborchemischer Hypothyreose wird das fehlende Hormon durch synthetisch hergestelltes Levothyroxin ersetzt, mit besonderem Augenmerk auf Lebensphasen mit Mehrbedarf wie zum Beispiel Schwangerschaft. Ursache für eine persistierende Beschwerdesymptomatik trotz laborchemisch euthyreoter Funktionslage unter Substitution kann einerseits eine Fehlzuordnung der Beschwerden (Co-Morbiditäten wie z. B. Vorliegen weiterer Autoimmunerkrankungen, chronische Überlastung, psychiatrische Erkrankungen), Mangel an Vitamin- und Spurenelementen, aber auch pharmakokinetische und pharmakogenomische Eigenschaften der Levothyroxinmedikation sein. Andererseits werden Resistenzen, Transport- und Konversionsstörung von Schilddrüsenhormon auf molekularbiologischer Ebene durch endogene Störungen wie Insulinresistenz und Nebenniereninsuffizienz diskutiert. Auch die Einflüsse der Schilddrüse auf die Psyche und umgekehrt scheinen mannigfaltig und auf vielen Ebenen stattzufinden. Es bedarf noch vieler großer randomisierter Studien und biochemischer, molekularbiologischer, genetischer Untersuchungen und Forschung im Bereich des Neuroimaging, um die komplexen Zusammenhänge zu klären.

Summary

Hashimoto’s thyroiditis is one of the most common organspecific autoimune diseases and the most frequent cause of hypothyroidism in areas with sufficient iodine supply. Excessively stimulated T cells CD4+ and their differentiated cells are known to play a key role in the pathogenesis. It is currently accepted that on the one hand genetic susceptibility, environmental factors, existential factors (gender difference) play an important role, on the other hand gut and intestinal microbiota seem to contribute to its development too. Diagnosis requires a detailed medical history, sonography, and blood analysis of thyroid function and thyroid antibodies. In case of an overt or subclinical hypothyroidism long-term or lifelong levothyroxine replacement may be needed, with a special focus on phases with an additional demand like during pregnancy. There are multifactorial reasons for poor response to therapy despite normal TSH levels in blood sampling like co-morbidities (other organspecific autoimmune diseases, psychiatric diseases), lack of vitamin and trace elements. Pharmacogenomic and pharmacokinetic factors may impact on levothyroxine bioavailability, also thyroid hormone resistance and transport- or conversion disorder due to insulin resistance or adrenal insufficiency for example. The relations between thyroid function, mental status and psychiatric disorders seem to be complex and the mechanisms underlying the interactions remain to be clarified. Continuing research in biochemical, genetic and neuroimaging fields are needed.

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  1. Innere Medizin, Krankenhaus der Barmherzigen Brüder Graz, Standort Graz-Eggenberg, Bergstrasse 27, 8020, Graz, Austria

    Eva Petnehazy

  2. Institut für Schilddrüsendiagnostik und Nuklearmedizin Gleisdorf, Businesspark 2, 8200, Gleisdorf, Austria

    Eva Petnehazy &  Wolfgang Buchinger

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Correspondence to Eva Petnehazy.

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Petnehazy, E., Buchinger, W. Hashimoto Thyreoiditis, therapeutische Optionen und extrathyreoidale Assoziationen – ein aktueller Überblick. Wien Med Wochenschr 170, 26–34 (2020). https://doi.org/10.1007/s10354-019-0691-1

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