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Pilot study of baricitinib for active Sjogren’s syndrome
  1. Wei Bai1,2,
  2. Huilan Liu1,2,
  3. Lei Dou3,
  4. YunJiao Yang1,2,
  5. XiaoMei Leng1,2,
  6. Mengtao Li1,2,
  7. Wen Zhang1,2,
  8. Yan Zhao1,2,
  9. Xiaofeng Zeng1,2
  1. 1Department of Rheumatology and Clinical Immunology, Chinese Academy of Medical Sciences & Peking Union Medical College; National Clinical Research Center for Dermatologic and Immunologic Diseases (NCRC-DID), Ministry of Science & Technology, Dongcheng-qu, Beijing, China
  2. 2Department of Rheumatology and Clinical Immunology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital (PUMCH), Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education, Beijing, China
  3. 3Department of Rheumatology and Immunology, The Second People's Hospital of Wuhu, Wuhu, Anhui, China
  1. Correspondence to Dr XiaoMei Leng, Department of Rheumatology and Clinical Immunology, Department of Rheumatology and Clinical Immunology, Chinese Academy of Medical Sciences & Peking Union Medical College; National Clinical Research Center for Dermatologic and Immunologic Diseases (NCRC-DID), Ministry of Science & Technology; State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital (PUMCH); Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education, Dongcheng-qu, Beijing, China; lpumch{at}126.com; Dr Yan Zhao; zhaoyan_pumch2002{at}aliyun.com

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Sjogren’s syndrome (SS) is a systemic autoimmune disease involving not only the exocrine glands, but also multiple systems such as kidney, lung or nervous system. Janus kinase (JAK) plays a key role in many signal pathways of cytokines involving the pathogenesis of SS, including type I interferon (IFN) pathway, interleukin (IL)-6, IL-17, IL-12 and IL-23.1 Baricitinib, a selective JAK1 and JAK2 inhibitor, has reliable therapeutic benefit in patients with rheumatoid arthritis (RA).2 There were also some clinical trials and case reports of baricitinib in other autoimmune diseases, including systemic lupus erythematosus (SLE),3 dermatomyositis, polymyalgia rheumatica and giant cell arteritis.1 So far, only one basic study demonstrated baricitinib suppressed IFN-γ-induced CXCL10 expression in human salivary gland ductal cells and suggested its potential for the treatment of SS.4 There is no clinical evidence of baricitinib in SS.

In this pilot study, we explored the efficacy and safety of baricitinib in active SS patients. We enrolled 11 patients (table 1) fulfilling the criteria of the 2016 American College of Rheumatology/European League Against Rheumatism (EULAR) classification for primary SS,5 with moderate or high disease activity, which was defined as EULAR primary SS Disease Activity Index (ESSDAI) ≥5.6 The ESSDAI, EULAR primary SS Patient Reported Index (ESSPRI), Physician Global Assessment (PGA) scores, serological activity including erythrocyte sedimentation rate (ESR) and IgG level and remission of organ manifestations were evaluated. Response to treatment, or minimal clinically …

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Footnotes

  • Handling editor Josef S Smolen

  • Contributors WB, X-ML and YZ contributed to the conception and design of the study; WB, HL, LD, Y-JY and X-ML contributed to patient recruitment and follow-up; WB performed the literature review, literature screen, data collection and analysis; X-ML, ML, WZ, YZ and XZ helped data analysis and evaluation; WB drafted the manuscript; X-ML, YZ and XZ supervised the study and revised the manuscript.

  • Funding This study was supported by the Chinese National Key Technology R&D Programme, Ministry of Science and Technology (2017YFC0907601, 2017YFC0907605), CAMS Innovation Fund for Medical Sciences (CIFMS) (2019-I2M-2–008).

  • Competing interests None declared.

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

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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