Osteoporose- und Frakturrisiko bei neurodegenerativen Erkrankungen

K. Abendroth

doi:10.1055/s-0038-1624234

Arthritis und Rheuma, Inhaltsverzeichnis

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

¹Regionaler Expertenkreis Osteoporose (REKO) Deutschland e. V., Gruppe Sachsen & Thüringen

²Praxis für Rheumatologie & Osteologie, Jena

› Institutsangaben

Abstract

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

Volltext

Referenzen

Literatur
1 Liu B, Fang F, Pedersen NL. et al. Vagotomy and Parkinson disease – A Swedish register–based matched-cohort study. Neurology 2017; 88: 1996-2002.
2 Recasens A, Dehay B. Alpha-synuclein spreading in Parkinson’s disease – Review. Frontiers in Neuroanatomy 2014; 08: 1-9.
3 van den Bos F, Speelman AD, Samson M. et al. Parkinson’s disease and osteoporosis. Age & Ageing 2013; 42: 156-162.
4 Torsney KM, Noyce AJ, Doherty KM. et al. Bone health in Parkinson’s disease: a systematic – review and meta-analysis. J Neurol Neurosurg Psychiatry 2014; 85: 1159-1166 doi:10.1136/jnnp-2013–307307.
5 Lyell V, Henderson E, Cevine M, Gregson C. Assessment and management of fracture risk in patients with Parkinson’s disease. Age and Ageing 2015; 44: 34-41.
6 Benzinger P, Rapp K, Maetzler W. et al. Risk for Femoral Fractures in Parkinson’s Disease Patients with and without Severe Functional Impairment. PLOS ONE 2014; 09: e97073.
7 Dennison EM, Compston JE, Flahive J. et al. Effect of co-morbidities on fracture risk: Findigs from Global Longitudinal Study of Osteoporosis in Women (GLOW). BONE 2012; 50: 1288-1293.
8 Bajayoa A, Bara A, Denesb A. et al. Skeletal parasympathetic innervation communicates central IL-1 signals regulating bone mass accrual. Proc Natl Acad Scie USA 2012; 109: 15455-15460.
9 Eimar H, Taminin I, Murshed M, Tamini F. Cholinergic regulation of bone. J Musculoskelet Neuronal Interact 2013; 13: 124-132.
10 Raglione LM, Sorbi S, Nacmias B. Osteoporosis and Parkinson’s disease – Mini-review. Clinical Cases in Mineral and Bone Metabolism 2011; 08: 16-18.
11 Newmark HL, Newmark J. Vitamin D and Parkinson’s disease—A hypothesis. Mov Disord 2007; 22: 461-468.
12 Evatt ML, Delong MR, Khazai N. et al. Prevalence of vitamin d insufficiency in patients with Parkinson disease and Alzheimer disease. Arch Neurol 2008; 65: 1348-1352.
13 Sato Y, Iwamoto J, Kanoko T, Satoh K. Homocysteine as a predictive factor for hip fracture in elderly women with Parkinson’s disease. Am J Med 2005; 118: 1250-1255.
14 Lee SH, Kim MJ, Kim BJ. et al. Hyperhomocysteinemia Due to Levodopa Treatment as a Risk Factor for Osteoporosis in Patients with Parkinson’s Disease. Calcified Tissue International 2010; 86: 132-141.
15 Arbouw MEL, Movig KLL, van Staa TP. et al. Dopaminergic drugs and the risk of hip or femur fracture: a population-based case-control study. Osteoporos Int 2011; 22: 2197-2204.
16 Vestergaard P, Rejnmark L, Mosekilde L. Fracture risk associated with Parkinsonism and anti-Parkinson drugs. Calcif Tissue Int 2007; 81: 153-161.
17 Invernizzi M, Carda S, Viscontini GS, Cisari C. Osteoporosis in Parkinson’s disease. Parkinsonism & Related Disorders 2009; 15: 339-346.
18 Stölting P. Knochengesundheit und Frakturrisiko bei Parkinson und MS. Ars Medici 2013; 21: 1080-1082.
19 Loskutova N, Honea RA, Vidoni ED. et al. Bone Density and Brain Atrophy in Early Alzheimer’s Disease. Journal of Alzheimer’s Disease 2009; 18: 777-785.
20 Loskutova N, Honea RA, Brooks WM, Burns JM. Reduced Limbic and Hypothalamic Volumes Correlate with Bone Density in Early Alzheimer’s Disease. J Alzheimers Dis 2010; 20: 313-322.
21 Zhou R, Zhou H, Rui L, Xu J. Bone Loss and Osteoporosis are Associated with Conversion from Mild Cognitive Impairment to Alzheimer’s Disease. Current Alzheimer Research 2014; 11: 706-713.
22 Zhao Y, Shen L, Ji H-J. Alzheimer’s Disease and Risk of Hip Fracture: A Meta-Analysis Study. Scientific World. 2012 doi:10.1100/2012/872173.
23 Baker NL, Cook MN, Arrighi HM, Bullock R. Hip fracture risk and subsequent mortality among Alzheimer’s disease patients in the United Kingdom, 1988–2007. Age & Ageing 2011; 40: 49-54.
24 Bohlken J, Jacob L, Schaum P. et al. Hip fracture risk in patients with dementia in German primary care practices. Dementia 2015; 00: 1-12 DOI:10.1177/1471301215621854.
25 Tsai CH, Chuang C-S, Hung C-H. et al. Fracture as an Independent Risk Factor of Dementia – A Nationwide Population-Based Cohort Study. Medicine 2014; 93: e188.
26 Guo X, Tang P, Liu P. et al. Dkk1: A promising molecule to connect Alzheimer’s disease and osteoporosis. Med Hypotheses 2016; 88: 30-32.
27 Annweiler C, Llewellyn DJ, Beauchet O. Low Serum vitamin D concentrations in Alzheimer’s disease: a systematic review and metaanalysis. J Alzheimers Dis 2013; 33: 659-674.
28 Mokry LE, Ross S, Morris JA. et al. Genetically decreased vitamin D and risk of Alzheimer disease. Neurology 2016; 87: 2567-2574.
29 Eyles DW, Smith S, Kinobe R. et al. Distribution of the vitamin D receptor and 1α-hydroxylase in human brain. J Chem Neuroanat 2005; 29: 21-30.
30 Kalueff AV, Tuohimaa P. Neurosteroid hormone vitamin D and is utility in clinical nutrition. Curr Opin Clin Nutr Metab Care 2007; 10: 12-19.
31 Annweiler C, Karras SN, Anagnostis P, Beauch O. Vitamin D supplements: a novel therapeutic approach for Alzheimer patients. Front Pharmacol 2014; 05: 1-4.
32 Tamimi I, Ojea T, Sanchez-Siles JM. et al. Acetylcholinesterase Inhibitors(AChEIs) and the Risk of Hip Fracture in Alzheimer’s Disease Patients: A Case-Control Study. Journal of Bone and Mineral Research 2012; 27: 1518-1527.
33 Eimar H, Perez ALara, Tamimi I. et al. Acetylcholinesterase inhibitors and healing of hip fracture in Alzheimer’s disease patients: a retrospective cohort study. J Musculoskelet Neuronal Interact 2013; 13: 454-463.
34 Sato Y, Iwamoto J, Kanoko T, Satoh K. Homocysteine as a predictive factor for hip fracture in elderly women with Parkinson’s disease. Am J Med 2005; 118: 1250-1255.