Kinetic Profiles and Management of Hepatitis B Virus Reactivation in Patients With Immune‐Mediated Inflammatory Diseases. Issue 9 (26th August 2013)

• Record Type: Journal Article
• Authors: Droz, Nina; Gilardin, Laurent; Cacoub, Patrice; Berenbaum, Francis; Wendling, Daniel; Godeau, Bertrand; Piette, Anne‐Marie; Dernis, Emmanuelle; Ebbo, Mikael; Fautrel, Bruno; Le Guenno, Guillaume; Mekinian, Arsène; Bernard‐Chabert, Brigitte; Costedoat‐Chalumeau, Nathalie; Descloux, Elodie; Michot, Jean‐Marie; Radenne, Sylvie; Rigolet, Aude; Rivière, Sophie; Yvin, Jean‐Luc; Thibault, Vincent; Thabut, Dominique; Pol, Stanislas; Guillevin, Loïc; Mouthon, Luc; Terrier, Benjamin
• Is Part Of: Arthritis care & research. Volume 65:Issue 9(2013:Sep.)
• Page Start: 1504
• Page End: 1514
• Publication Date: 2013-08-26
• Subjects: Arthritis -- Periodicals; Rheumatism -- Periodicals; 616.72
• DOI: 10.1002/acr.21990
• Languages: English
• ISSNs: 2151-464X

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="acr21990-sec-0001" sec-type="section"> <title>Objective</title> <p>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.</p> </sec> <sec id="acr21990-sec-0002" sec-type="section"> <title>Methods</title> <p>Physicians submitted data for patients receiving treatment for IMIDs and exhibiting HBV reactivation, defined as an increase of >1 log<sub>10</sub> IU/ml of HBV DNA levels or DNA reappearance. We systematically reviewed cases in the literature.</p> </sec> <sec id="acr21990-sec-0003" sec-type="section"> <title>Results</title> <p>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.</p> </sec> <sec id="acr21990-sec-0004" sec-type="section"> <title>Conclusion</title> <p>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.</p> </sec> </abstract>