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Beschleunigte Arteriosklerose bei rheumatischen Systemerkrankungen am Beispiel des systemischen Lupus erythematodes—was ist die Konsequenz?

Considering systemic lupus erythematosus as example for accelerated atherosclerosis in rheumatic diseases—what is the consequence?

  • BEITRAG ZUM SCHWERPUNKTTHEMA
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Zusammenfassung

In den letzten Jahren wurde ein deutlicher Anstieg der Mortalität aufgrund vorzeitiger Arteriosklerose mit koronarer Herzerkrankung und zerebralem Insult bei Patienten mit Kollagenosen, insbesondere systemischem Lupus erythematodes, beschrieben. Studien fanden ein 5- bis 7fach erhöhtes Risiko für Myokardinfarkte bei SLE-Betroffenen. Traditionelle epidemiologische Risikofaktoren können die akzelerierte Arteriosklerose bei SLE nicht vollständig erklären, zusätzliche Einflussgrössen scheinen beispielsweise die kumulative Steroidtherapie und die Krankheitsdauer zu sein. Die Erkrankung selbst stellt per se einen unabhängigen Risikofaktor dar. Die Arteriosklerose wird aktuell als chronische, inflammatorisch-fibroproliferative Erkrankung der Gefäßwand als Resultat unterschiedlicher Schädigungen gedeutet. Autoantikörper und Immunkomplexe (die Antikörper gegen Phospholipide, oxidierte LDL und Endothelzellen beeinhalten), CD40/CD-40-Ligand Interaktionen und Infektionen, die eine Immunantwort induzieren, sind dabei möglicherweise involviert. Das Erfassen von klassischen und neuen Risikofaktoren, zusammen mit z. B. dem Einsatz von Karotis- Duplexsonographie sind methodisch geeignet, frühe arteriosklerotische Veränderungen zu erfassen. Therapeutische Strategien mit früher Risikofaktor-Intervention und effektiver Kontrolle von Krankheitsaktivität sind für die Reduktion von Morbidität und Mortalität entscheidend und sollten in der Betreuung von Patienten mit Kollagenosen eingesetzt werden.

Summary

Large increases in mortality related to premature atherosclerosis with coronary artery disease and stroke have been reported during the last few years in patients with systemic lupus erythematosus (SLE). Studies found relative risks of 5 to 7 for myocardial infarction in SLE patients. The traditional risk factors fail to fully account for accelerated atherosclerosis in SLE and APS, in addition prolonged glucocorticoid therapy and long duration of SLE seem to be of importance. The disease SLE per se is an independent risk factor. The current pathogenic hypothesis for atherosclerosis involves an inflammatory response, autoantibodies, immune complexes (containing antibodies to phospholipids, to oxidized LDLs, and to endothelial cells), CD 40/CD40 ligand interactions, and bacterial or viral infections responsible for an immune response. The determination of classic and new risk factors, together with specific autoantibody titers and the use of Doppler carotid ultrasound, are useful methods to detect early atherosclerosis. Therapeutic strategies, including early risk factor intervention and effective control of inflammation, are essential to reduce morbidity and mortality and should be incorporated into the management of connective tissue disease with the goal of protecting patients against atherosclerosis.

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  1. Rheumazentrum Düsseldorf, Heinrich-Heine-Universität, Moorenstraße 5, 40225, Düsseldorf, Germany

    R. Fischer-Betz, S. Beer &  M. Schneider

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  2. S. Beer
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  3. M. Schneider
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Fischer-Betz, R., Beer, S. & Schneider, M. Beschleunigte Arteriosklerose bei rheumatischen Systemerkrankungen am Beispiel des systemischen Lupus erythematodes—was ist die Konsequenz?. Z. Rheumatol. 64, 229–238 (2005). https://doi.org/10.1007/s00393-005-0733-5

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  • DOI: https://doi.org/10.1007/s00393-005-0733-5

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