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Letter
Tofacitinib for the treatment of antineutrophil cytoplasm antibody-associated vasculitis: a pilot study
  1. Yun Liu,
  2. Zongfei Ji,
  3. Wensu Yu,
  4. Sifan Wu,
  5. Huiyong Chen,
  6. Lili Ma,
  7. Zhenqi Ding,
  8. Lindi Jiang
  1. Department of Rheumatology, Zhongshan Hospital, Fudan University, Shanghai, China
  1. Correspondence to Dr Lindi Jiang, Department of Rheumatology, Zhongshan Hospital, Fudan University, Shanghai 200032, China; zsh-rheum{at}hotmail.com

https://doi.org/10.1136/annrheumdis-2021-220484

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    Antineutrophil cytoplasm antibody-associated vasculitis (AAV) is a group of necrotising vasculitis involving small vessels characterised by upper and lower respiratory tract, kidney, eye, ears–nose–throat, skin, gastrointestinal and neurological involvement. AAV includes granulomatosis with polyangiitis (GPA), microscopic polyangiitis (MPA), and eosinophilic granulomatosis with polyangiitis (EGPA).1 To date, maintenance therapy to prevent disease relapse remains the main therapeutic challenge for patients with AAV.

    Previous studies indicate that T cells and associated cytokine production (eg, interleukin (IL)-6, IL-10, IL-12, IL-23 and type l interferons) play an important role in the pathogenesis of AAV2–4 via activation of the Janus kinase (JAK)/signal transducer and activator of transcription pathway.5 Tofacitinib is a JAK1/3 inhibitor that functions by suppressing the activity of the JAK family of non-receptor tyrosine kinases (RTKs) and has been used successfully for the treatment of rheumatoid arthritis, psoriatic arthritis, Behçet’s disease and systemic lupus erythematosus6–9; however, the use of tofacitinib for the treatment of AAV has not been reported. Of particular interest, imatinib mesylate, an RTK inhibitor, has been reported to be an effective treatment for patients with EGPA.10 Therefore, we hypothesised that tofacitinib-mediated inhibition of JAK signalling …

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    Footnotes

    • Handling editor Josef S Smolen

    • Contributors YL participated in data collection and patient follow-up and wrote the manuscript. ZJ, WY and SW helped in patient data collection at baseline and follow-up. HC, LM and ZD helped with patient follow up. LJ contributed to the study design and manuscript revision.

    • Funding This work was supported by the National Natural Science Foundation of China (numbers 81800541, 81801598 and 81771730) and the Shanghai Shen Kang Hospital Development Centre Clinical Cultivation Project (SHDC12019X05).

    • Competing interests None declared.

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

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