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Der Nuklearmediziner 2019; 42(03): 241-244
DOI: 10.1055/a-0916-6728
Benigne Schilddrüsenknoten – Update 2019
© Georg Thieme Verlag KG Stuttgart · New York

Schilddrüse und Knochen

Thyroid and Bone
Onno Eilard Janßen
1   endokrinologikum Hamburg, Hamburg
,
Catharina Bullmann
2   amedes Hamburg, Hamburg
› Author Affiliations
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Publication History

Publication Date:
03 September 2019 (online)

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Zusammenfassung

In einer alternden Gesellschaft nimmt die Prävalenz der Osteoporose und die durch sie verursachte Morbidität und Mortalität eine zunehmende Rolle ein. Auch Schilddrüsenfunktionsstörungen sind im Alter häufiger, sodass sich ein fataler Synergismus in der Entstehung von osteoporotischen Frakturen ergibt. Im Erwachsenenalter geht eine Hyperthyreose mit Knochenverlust und erhöhtem Knochenumsatz einher, primär bedingt durch eine gesteigerte Knochenresorption durch Osteoklasten. Die manifeste Hyperthyreose gehört zu den gut etablierten Ursachen einer sekundären Osteoporose und von Fragilitätsfrakturen. Eine latente Hyperthyreose wirkt sich ebenfalls negativ auf die Knochenmineraldichte aus und ist mit Frakturen assoziiert. Bei den meisten Patienten mit manifester oder latenter Hyperthyreose führt die Wiederherstellung einer Euthyreose zu einer Normalisierung der Knochendichte und Reduktion des Frakturrisikos. Eine TSH-suppressive Substitutionstherapie nach Schilddrüsenoperation wegen eines differenzierten Schilddrüsenkarzinoms ist ebenfalls mit einem erhöhten osteoporotischen Frakturrisiko assoziiert, sodass eine zeitlich begrenzte und risikoadaptierte TSH-Suppression empfohlen wird und eine antiresorptive Behandlung indiziert sein kann. Eine Hypothyreose im Erwachsenenalter führt zu einem verlangsamten Knochenumsatz mit gesteigerter Mineralisierung. Die Assoziation mit einem erhöhten Frakturrisiko korreliert mit einer erhöhten Sturzneigung und nicht mit einer Veränderung des Knochenstoffwechsels. Bei Kindern und Jugendlichen ist eine normale Schilddrüsenfunktion zur Ausbildung einer adäquaten Knochenmasse und Knochenfestigkeit sowie zum Erreichen der vorgesehenen Körpergröße erforderlich. Sowohl Hyperthyreose als auch Hypothyreose führen im Kindes- und Jugendalter mit verschiedenen Mechanismen zu Minderwuchs und verminderter Knochenqualität.

Abstract

With increasing longevity, prevalence, morbidity and mortality of osteoporosis gains momentum. As thyroid dysfunction also becomes more prevalent with age, a fatal synergism causes an increase in osteoporotic fractures. In adults, hyperthyroidism leads to a loss of bone matrix and an increase in bone turnover, mostly due to an increased bone resorption by osteoclasts. Apparent hyperthyroidism has been well established as a cause of secondary osteoporosis and fragility fractures. Subclinical hyperthyroidism has a negative impact on bone mineral density, too and also causes an increase in fractures. In most patients with apparent or subclinical hyperthyroidism, restoration of euthyroidism normalizes bone density and reduces fracture risk. A TSH-suppressive thyroid hormone treatment after surgery for differentiated thyroid carcinoma has also been correlated with an increased risk for osteoporotic fractures. Thus, TSH-suppression should be temporary and stratified by risk. Also, concomittant antiresorptive treatment may be indicated. Hypothyroidism reduces bone turnover and increases its mineralization. Its association with an increased fracture risk correlates with postural instability and a tendency to fall rather than changes in bone metabolism. In children and adolescents, a normal thyroid function is essential for developing an adequate bone mass and stability, as well as obtaining the anticipated body length. Although by different mechanisms, both hyperthyroidism and hypothyroidism in childhood and adolescence cause growth retardation and a reduction of bone quality.

Schlüsselwörter

Hyperthyreose - Hypothyreose - Thyreoidektomie - Osteoporose - Knochenstoffwechselstörung - Frakturrisiko

Keywords

Hyperthyroidism - Hypothyroidism - Thyroidectomy - Osteoporosis - metabolic bone disease - fracture risk
 

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