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Mechanismen des Knochenmasseverlustes bei rheumatoider Arthritis

Darstellung anhand einer Kasuistik

The mechanism of bone loss in rheumatoid arthritis

Description based on a case report

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Zusammenfassung

Am Beispiel einer postmenopausalen Patientin mit einer hoch aktiven rheumatoiden Arthritis (RA) werden differente Einflussfaktoren auf den Knochenstoffwechsel und den Knochenmasseverlust bei RA beschrieben und diskutiert.

Dabei wird besonderes Augenmerk auf die Zusammenhänge zwischen entzündlicher Aktivität, Vitamin-D-Status, Parathormon und Kalziumstoffwechsel gelegt.

Wesentliche Aussagen dieser Fallbeschreibung sind, dass eine erhöhte Entzündungsaktivität mit erniedrigtem Vitamin-D- und besonders -1,25-D-Spiegeln assoziiert ist und auch Parathormon erniedrigt gefunden wird.

Trotz dieser Konstellation wird bei aktiver RA in der Regel nicht der Befund einer Osteomalazie erhoben.

Bemerkenswert ist der Tatbestand, dass eine therapiebedingte Normalisierung der Entzündungswerte auch die Mediatoren und Marker des Knochenstoffwechsels normalisiert. Letztlich legen die Daten nahe, dass Patienten mit aktiver RA bezüglich ihrer Auswirkungen auf den Knochenstoffwechsel frühzeitig kontrolliert und auch therapiert werden müssen.

Abstract

Various factors influencing bone turnover and bone loss in rheumatoid arthritis (RA) are illustrated using the example of a postmenopausal woman with a highly active RA.

In particular, the relationships between disease activity, vitamin D metabolism, parathyroid hormone (PTH) levels and calcium metabolism are described. High disease activity is associated with low levels of 25-hydroxycholecalciferol, and especially of 1.25-dihydroxycholecalciferol. Despite vitamin D deficiency, PTH levels were decreased and histomorphometric investigation of the iliac crest biopsy showed severe osteoporosis but no signs of osteomalacia. Suppression of the inflammatory disease activity of RA led to a normalisation of the serum levels of 1.25-dihydroxycholecalciferol and PTH. This was associated with a reduction in the initially increased levels of bone specific alkaline phosphatase to normal values.

This case report shows a close relationship between disease activity and bone turnover in RA and indicates that early investigation and therapy of disturbances of bone metabolism in RA are necessary.

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Authors and Affiliations

  1. Selbständiger Funktionsbereich Rheumatologie & Osteologie, Klinik für Innere Medizin III, Universitätsklinikum Jena, Erlanger Allee 101, 07740, Jena, Deutschland

    P. Oelzner & G. Hein

  2. Med. Klinik III, Charité-Universitätsmedizin Berlin, Campus Mitte, Berlin, Deutschland

    F. Buttgereit

  3. Mitglieder der Kommission Osteologie der DGRh, xxx, xxx

    F. Buttgereit, W. Demary, H. Franck, P. Kern & G. Hein

  4. Gemeinschaftspraxis Dr. von Hinüber/Dr. Demary, Hildesheim, Deutschland

    W. Demary

  5. Praxis für Rheumatologie/Endokrinologie, Bonn, Deutschland

    H. Franck

  6. Frank von Prümmer Klinik, Bad Brückenau, Deutschland

    P. Kern

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  1. P. Oelzner
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  2. F. Buttgereit
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  3. W. Demary
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  4. H. Franck
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  5. P. Kern
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  6. G. Hein
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Correspondence to P. Oelzner.

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Oelzner, P., Buttgereit, F., Demary, W. et al. Mechanismen des Knochenmasseverlustes bei rheumatoider Arthritis. Z. Rheumatol. 66, 337–340 (2007). https://doi.org/10.1007/s00393-007-0157-5

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  • DOI: https://doi.org/10.1007/s00393-007-0157-5

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