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The use of tocilizumab and tofacitinib in patients with resolved hepatitis B infection: a case series
  1. Naomi Serling-Boyd1,
  2. Amir M Mohareb2,
  3. Arthur Y Kim2,
  4. Emily P Hyle2,
  5. Zachary S Wallace1
  1. 1 Rheumatology Unit, Massachusetts General Hospital, Boston, Massachusetts, USA
  2. 2 Infectious Diseases, Massachusetts General Hospital, Boston, Massachusetts, USA
  1. Correspondence to Dr Zachary S Wallace, Rheumatology Unit, Massachusetts General Hospital, Boston, MA 02114, USA; zswallace{at}partners.org

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The use of immunosuppressive medications in people with hepatitis B virus (HBV) infection is associated with an increased risk of HBV reactivation, which can lead to liver failure and death. Tumour necrosis factor inhibitors, rituximab and other biologic treatments have been associated with HBV reactivation in up to 24% of people with resolved HBV (positive core antibody (HBcAb), negative surface antigen (HBsAg) and positive or negative surface antibody (HBsAb)) and 34% of people with chronic HBV (positive HBsAg); reactivation risk varies based on HBsAb status.1–3 Both tocilizumab (interleukin-6 (IL-6) receptor inhibitor) and tofacitinib (Janus kinase (JAK) inhibitor) interfere with IL-6 signalling, which moderates immune control of chronic HBV. Although HBV reactivation has been reported with tocilizumab and tofacitinib in Asia, limited data describe this risk in the USA.4

We performed a retrospective study of people who were prescribed tocilizumab or tofacitinib and had resolved or chronic HBV infection between 1995 and 2018 in the Partners Health Care System (PHS).5 We extracted relevant variables from the electronic health record and …

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Footnotes

  • Handling editor Josef S Smolen

  • Contributors NS-B and AM contributed to the acquisition and analysis of data. All authors contributed to the conception and design of the work as well as interpretation of data, drafting and critical revision of the manuscript, and all authors approve the final manuscript. All authors are accountable for all aspects of the work.

  • Funding NS-B is supported by the National Institutes of Health Ruth L. Kirschstein Institutional National Research Service Award (T32-AR-007258). AM is supported by the National Institutes of Health (T-32-AI-007433). AYK is part of a scientific advisory board with Biomarin. EH is supported by NIH/NIAID (K01HL123349). ZSW is funded by NIH/NIAMS (K23AR073334 and L30 AR070520).The National Institute of Health had no role in the design or authorship of this publication.

  • Disclaimer The article contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH.

  • 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.

  • Patient consent for publication Not required.

  • Ethics approval This study was considered to be exempt by the Partners HealthCare System (PHS) Institutional Review Board. The protocol number was 2019P000836. Informed consent from patients was not required given that the study was considered to be exempt.

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