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Aktuelle Rheumatologie 2001; 26(3): 95-100
DOI: 10.1055/s-2001-16300
GRUNDLAGEN
© Georg Thieme Verlag Stuttgart · New York

Pathophysiologie von medikamentös induzierten Osteoporosen und Osteoporose bei entzündlich rheumatischen Systemerkrankungen

Pathophysiology of Drug-Induced Osteoporosis and Osteoporosis in Inflammatory Systemic Rheumatic DiseasesD. Patschan, F. Buttgereit
  • Klinik für Rheumatologie und klinische Immunologie der Charité der Humboldt-Universität zu Berlin
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Publication History

Publication Date:
31 December 2001 (online)

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Zusammenfassung

Eine pathologische Abnahme der Gesamtkörperknochenmasse kann sowohl als Folge einer längerfristigen Behandlung mit bestimmten Medikamenten als auch im Rahmen verschiedener entzündlich-rheumatischer Erkrankungen auftreten. Hauptursache der sekundären Osteoporosen ist eine längerfristige Behandlung mit Glukokortikoiden. Steroide beeinflussen die Knochenbilanz vor allen Dingen über die Verminderung der proliferativen und metabolischen Aktivität von Osteoblasten negativ. Indirekte Glukokortikoidwirkungen auf den Knochenstoffwechsel resultieren sehr wahrscheinlich aus der Abnahme der intestinalen Kalziumresorption und der Zunahme der renalen Kalziumelimination. Auch Metothrexat, Cyclosporin A, bestimmte Antikonvulsiva und Antikoagulanzien können negative Effekte auf den Knochenstoffwechsel entfalten. Die dafür verantwortlichen molekularen Mechanismen sind noch weitgehend unbekannt. Innerhalb des Formenkreises der entzündlich-rheumatischen Krankheiten sind insbesondere die rheumatoide Arthritis (RA) und die ankylosierende Spondylitis (SPA) mit einem erhöhten Osteoporoserisiko vergesellschaftet. Dabei scheint insbesondere im Falle der rheumatoiden Arthritis die entzündliche Aktivität der Grundkrankheit „per se” den Knochenstoffwechsel negativ zu modifizieren. Zur Knochenmasseabnahme von RA-Patienten trägt darüber hinaus die Verminderung der individuellen Mobilität der Patienten maßgeblich bei.

Pathophysiology of Drug-Induced Osteoporosis and Osteoporosis in Inflammatory Systemic Rheumatic Diseases

Secondary osteoporosis is mainly caused by long-term glucocorticoid treatment. Glukokortikoids diminish the proliferative and metabolic activity of osteoblasts which results in changes in the balance between boneforming and bone-resorbing cells. Indirect glucocorticoid-mediated effects on bone metabolism occur probably from a decrease in intestinal calcium absorption and an increase in renal calcium elimination. Besides glucocorticoids, also methotrexate, cyclosporine A, some anticonvulsants and anticoagulants are discussed as diminishing bone mass. However, the exact molecular mechanisms involved are not known in detail. Furthermore, some rheumatic diseases per se seems to lead to osteoporosis. Especially patients with rheumatoid arthritis and ankylosing spondylitis often develop secondary bone loss. It is known of patients suffering from rheumatoid arthritis that the risk for osteoporosis increases with higher disease activity. Of particular importance in this regard are proinflammatory cytokines, which play a significant role in the pathogenesis of various inflammatory diseases. Besides the already mentioned effects of treatment, the reduction in the patient’s physical activity must also be taken into account.

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Dr. F. Buttgereit

Klinik für Rheumatologie und klinische Immunologie der
Charité der Humboldt-Universität zu Berlin

Schumannstraße 20/21
10117 Berlin

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