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© Research
Publication : Arthritis care & research

Kinetic profiles and management of hepatitis B virus reactivation in patients with immune-mediated inflammatory diseases

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Arthritis care & research - 01 Sep 2013

Droz N, Gilardin L, Cacoub P, Berenbaum F, Wendling D, Godeau B, Piette AM, Dernis E, Ebbo M, Fautrel B, Le Guenno G, Mekinian A, Bernard-Chabert B, Costedoat-Chalumeau N, Descloux E, Michot JM, Radenne S, Rigolet A, Rivière S, Yvin JL, Thibault V, Thabut D, Pol S, Guillevin L, Mouthon L, Terrier B

Link to Pubmed [PMID] – 23436730

Arthritis Care Res (Hoboken) 2013 Sep;65(9):1504-14

OBJECTIVE: Immunosuppressive therapy may trigger hepatitis B virus (HBV) reactivation for increased morbidity and mortality. We aimed to describe HBV reactivation in patients receiving treatment for immune-mediated inflammatory diseases (IMIDs) and to evaluate a predefined algorithm for its prevention.

METHODS: Physicians submitted data for patients receiving treatment for IMIDs and exhibiting HBV reactivation, defined as an increase of >1 log10 IU/ml of HBV DNA levels or DNA reappearance. We systematically reviewed cases in the literature.

RESULTS: The 35 physician-collected patients had rheumatoid arthritis (n = 14), connective tissue disease (n = 7), vasculitis (n = 5), and other diseases (n = 9). At baseline, 65.7% of patients were positive for hepatitis B surface antigen (HBsAg), 31.4% had a history of HBV infection, and 2.9% had occult HBV infection. Reactivation occurred a median of 35 weeks (range 2-397 weeks) after the start of corticosteroid and/or immunosuppressive therapy. In all, 88.6% of patients were clinically asymptomatic, but 25.7% had severe hepatitis; none had fulminant hepatitis. Management was antiviral therapy for 91.4%, with discontinuation or decrease of immunosuppressive therapy for 45.7%. In pooling these 35 cases and 103 patients from the literature, 73.9% of patients were clinically asymptomatic, 33.3% had severe hepatitis, and 12.3% died and/or had fulminant hepatitis. Reactivation occurred early with rituximab or cyclophosphamide therapy and in HBsAg-positive/HBV DNA-positive patients. Using the predefined algorithm, 78% of patients with reactivation would have received preemptive antiviral therapy.

CONCLUSION: We provide new insights into HBV reactivation in patients receiving treatment for IMIDs. A predefined algorithm may be effective in reducing the risk of HBV reactivation in this population.

https://www.ncbi.nlm.nih.gov/pubmed/23436730