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Arthritis und Rheuma 2017; 37(06): 386-394
DOI: 10.1055/s-0038-1624234
Osteologie aktuell
Schattauer GmbH

Osteoporose- und Frakturrisiko bei neurodegenerativen Erkrankungen

Morbus Parkinson und Morbus Alzheimer/DemenzOsteoporosis and fracture risk in neurodegenerative diseasesParkinson's disease/Alzheimer's disease/dementia
K. Abendroth
1   Regionaler Expertenkreis Osteoporose (REKO) Deutschland e. V., Gruppe Sachsen & Thüringen
2   Praxis für Rheumatologie & Osteologie, Jena
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Further Information

Publication History

Publication Date:
10 January 2018 (online)

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Zusammenfassung

Ein erhöhtes Osteoporose- und Frakturrisiko besteht beim Morbus Parkinson (PD) und beim Morbus Alzheimer (AD). Bei der PD ist eine Osteopenie meist schon im Anfangsstadium nachweisbar und steigert sich mit zunehmender Krankheitsdauer durch Muskelfunktionsstörungen bis hin zur Inaktivität. Bei der AD geht die Osteoporose-Entwicklung parallel mit der progredienten Hirnatrophie. Dabei spielen auch Störungen der zentralnervös-endokrinen Steuerung des Bone Remodeling eine Rolle. Das Frakturrisiko wird durch einen latenten bis manifesten Prohormon-D [25OHD3]-Mangel und eine Hyper-Homozysteinämie gesteigert. In die Betreuung und Behandlung der Parkinson- und Alzheimer-Patienten sollte möglichst zeitig osteologische Kompetenz eingebunden werden. Dabei spielen neben der OsteoporoseDiagnostik und Therapie die gegebenenfalls notwendige Folsäure- und Vitamin-B12-Supplementierung und der Ausgleich des Pro-Hormon-D[25OHD3]-Mangels eine Rolle. Bei der PD ist die Erhöhung des Homozysteinspiegels und damit des Hüftfrakturrisikos als Folge der therapeutischen Dopamin-Substitution zu bedenken. Bei der AD reduziert sich mit einer Cholin-Acetyl-Transferase-InhibitorTherapie das Hüftfrakturrisiko, eine frische Hüftfraktur heilt darunter schneller.

Summary

Patients with Parkinson’s disease (PD) and Alzheimer’s disease (AD) have a lower bone mineral density (BMD) than age-matched controls. BMD is reduced in the earliest clinical stages of AD and associated with brain atrophy and memory decline, suggesting that central mechanisms may contribute to bone loss in early AD. Bone loss in both diseases is multifactorial, resulting from immobility, decreased muscle strength, postural instability as well as low body weight and they are associated with substantially increased fracture risk, in particular hip fracture, which can occur relatively early in the course of PD. Prohormone-D [=25OHD3] deficiency is also important, not only because it reduces BMD, but also because cell function in the different regions of the central nervous system (CNS) depends on D-hormone. Recently many observations indicated that this D-Hormone [=1,25(OH)2D3] is synthesized directly by the CNS with controlling and neuro-protective effects. Hyperhomocysteinaemia, an independent risk factor for osteoporosis, is common in PD, due to levodopa use, as well as vitamin B12 and folic acid deficiency.

Schlüsselwörter

Morbus Parkinson - Morbus Alzheimer - Osteoporose - Frakturrisiko

Keywords

Parkinson´s disease - Alzheimer´s disease - osteoporosis - fracture risk
 

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