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Letter
Sequential interleukin-17/interleukin-23 inhibition in treatment-refractory psoriatic arthritis
  1. David Simon1,2,
  2. Filippo Fagni1,2,
  3. Georg Schett1,2
  1. 1 Department of Internal Medicine 3- Rheumatology and Immunology, Friedrich-Alexander-University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany, Erlangen, Germany
  2. 2 Deutsches Zentrum Immuntherapie, Friedrich-Alexander-University Erlangen-Nürnberg and Universitätsklinikum Erlangen, Erlangen, Germany
  1. Correspondence to Professor Georg Schett, Rheumatology, Friedrich-Alexander-Universitat Erlangen-Nurnberg, Erlangen, Bayern, Germany; georg.schett{at}uk-erlangen.de

https://doi.org/10.1136/annrheumdis-2022-222415

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    Treatment of psoriatic arthritis (PsA) has considerably improved by the introduction of biological disease modifying antirheumatic drugs.1 2 Monoclonal antibodies targeting tumour necrosis factor alpha (TNFa), interleukin-17 (IL-17) and IL-23 have shown efficacy in psoriatic joint and skin disease.3 While most of PsA patients respond to either one of these treatments, a subset of patients is highly resistant to all three cytokine blocking modalities and shows refractory active disease. This subset of patients represents a challenge that requires new therapeutic concepts.

    Combined cytokine inhibition might represent an attractive opportunity for such patients: Within the IL-17 family, this concept is followed by dual inhibition of IL-17A and IL-17F by bimekizumab,4 while evidence for inhibition across cytokine families is sparse to date. Dual inhibition of TNF and IL-17 has not shown additive efficacy over single TNF inhibition when used by PsA patients failing on methotrexate.5 In resistant PsA patients, combination of ustekinumab with TNF inhibitors has been used with success in two small case series,6 7 however, infection rate was high, suggesting that such treatment should be used with caution. These data indicate limitations of combined cytokine blockade with respect …

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    Footnotes

    • Handling editor Josef S Smolen

    • Contributors All authors identified the patients. DS and FF documented the patients. GS wrote the manuscript.

    • Funding GS is supported by the Deutsche Forschungsgemeinschaft (DFG-FOR2886 PANDORA and the CRC1181 Checkpoints for Resolution of Inflammation). Additional funding was received by the Bundesministerium für Bildung und Forschung (BMBF; project MASCARA; to GS) and the IMI funded project HIPPOCRATES (to GS and DS).

    • Competing interests None declared.

    • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

    • Provenance and peer review Not commissioned; externally peer reviewed.