Aktuelle Rheumatologie 2009; 34(4): 220-225
DOI: 10.1055/s-0029-1220678
Übersichtsarbeit

© Georg Thieme Verlag KG Stuttgart · New York

„Switch” nach TNF-alpha-Hemmer Versagen: Eine adäquate Strategie?

Switch after Anti-TNF-alpha Failure: Is it an Adequate Strategy?M. Pierer1 , U. Wagner1 , O. Malysheva2 , C. Baerwald3
  • 1Universitätsklinikum, Sektion Rheumatologie/Gerontologie, Leipzig
  • 2Universitätklinikum Leipzig, Rheumatologie, Leipzig
  • 3University Hospital, Rheumatology Unit, Leipzig
Weitere Informationen

Publikationsverlauf

Publikationsdatum:
15. April 2009 (online)

Zusammenfassung

Gegen Tumor-Nekrose-Faktor-Alpha (TNF-α) gerichtete Therapien haben die Behandlung der rheumatoiden Arthritis (RA) deutlich bereichert. Ein klinisches Problem ist derzeit, dass etwa ein Drittel der Patienten während einer Therapie mit einem TNF-α-Blocker keine messbare Symptombesserung erreicht. Weitere Probleme, die eine Therapieumstellung erfordern können, sind eine fehlende anhaltende Symptombesserung oder unerwünschte Wirkungen. Derzeit gibt es noch keine Leitlinien wie Patienten in dieser Situa-tion weiter behandelt werden sollten. Für einen Therapiewechsel gibt es mittlerweile mehrere gute Optionen, wobei sich in klinischen Studien und Kohorten zum Teil als praktikabel erwiesen hat, eine Umstellung („Switch”) auf einen zweiten TNF-α-Blocker vorzunehmen. Wie Studien und Kohorten zeigen, müssen jedoch Subgruppen von RA-Patienten definiert werden, die von einem Switch klinisch nicht profitieren. Das Konzept steht derzeit auf dem Prüfstand, zumal mit dem CD20-Antikörper Rituximab und dem T-Zell-Co-Stimulationsmodulator Abatacept alternative Therapiestrategien nach TNF-α-Blocker Versagen erhältlich sind. In dem Artikel beschreiben wir den Status quo der Studien zur Switch Situation und geben einen Ausblick auf mögliche Therapieoptionen.

Abstract

Therapies directed against tumour necrosis factor α (TNF-α) have revolutionised the management of patients with rheumatoid arthritis. However, it remains a clinical problem that approximately one-third of the patients do not respond adequately. Furthermore, it has become apparent that some patients gradually lose the effect over time or experience adverse effects with the TNFα antagonists. There are no clear guidelines on the therapy for these challenging patients. It might be useful to switch to another TNF-α antagonist that is supported by small studies and registries. However, cohort studies underline the necessity to identify patients who do not respond to such an anti-TNF switch. This is of particular interest since the T-cell co-stimulation antagonist Abatacept, as well as the B-cell depleting agent Rituximab, are also available for use in patients who have had an inadequate response or intolerance to the TNF-α antagonists. In this article, we review the current data and give an outlook on possible therapeutic strategies.

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Prof. Dr. med. Christoph Baerwald

University Hospital Rheumatology Unit

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