Anti-TNF therapy in patients with HBV infection—analysis of 87 patients with inflammatory arthritis

Ye, Hua; Zhang, Xuewu; Mu, Rong; Fang, Lin; Gu, Jun; Lin, Jin; Du, Jinfeng; Chen, Jinwei; Chen, Yi-jia; Wu, Lijun; Xuefeng, Pang; Li, Zhanguo

doi:10.1007/s10067-013-2385-1

Cited by 46 publications

(42 citation statements)

References 10 publications

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“…24,25 A recent study analyzing patients with inflammatory arthritis also revealed an increased risk of HBV reactivation associated with anti-TNF therapy in patients with chronic HBV infection. 41 However, due to limited wellcontrolled studies, the association between TNF-a blockage and HBV reactivation remains uncertain. In this study, we further addressed the dynamic change of HBV viral load in blockage of TNF-a.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-alpha blockage therapy impairs hepatitis B viral clearance and enhances T-cell exhaustion in a mouse model

Chyuan

Tsai²,

Tzeng

et al. 2015

Cell Mol Immunol

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Hepatitis B virus (HBV) reactivation and recurrence are common in patients undergoing immunosuppression therapy. Tumor necrosis factor (TNF) blockage therapy is effective for the treatment of many autoimmune inflammatory diseases. However, the role of TNF-a blockage therapy in the innate and adaptive immune responses against HBV is still not clear. A detailed analysis of HBV infection under TNF-a blockage therapy is essential for the prophylaxis and therapy for HBV reactivation and recurrence. In this study, HBV clearance and T-cell responses were analyzed in a HBV-transfected mouse model under anti-TNF blockage therapy. Our results demonstrated that under TNF-a blockage therapy, HBV viral clearance was impaired with persistent elevated HBV viral load in a dose-and temporal-dependent manner. The impairment of HBV clearance under anti-TNF-a blockage therapy occurred at early time points after HBV infection. In addition, TNF-a blockade maintained a higher serum HBV viral load and increased the number of intrahepatic programmed cell death (PD)-1 high CD127 low exhausted T cells. Furthermore, TNF-a blockade abolished Toll-like receptor 9 (TLR9) ligand-induced facilitation of HBV viral clearance. Taken together, TNF-a blockade impairs HBV clearance and enhances viral load, and these effects depend on early administration after HBV infection. Our results here demonstrate that early TNF-a blockade reduces viral clearance and persistently maintains elevated HBV viral load in a mouse model, suggesting that HBV may reactivate during therapy with TNF-a-blocking agents.

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Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-alpha blockage therapy impairs hepatitis B viral clearance and enhances T-cell exhaustion in a mouse model

Chyuan

Tsai²,

Tzeng

et al. 2015

Cell Mol Immunol

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“…The available data reported in literature do not provide clear indications on the anti-TNF-α agents of choice with regard to the safety in patients exposed to HBV. In older reports, INF was associated to higher risk of HBV reactivation, mainly due to its pharmacological characteristics [84], but several case reports [59,64,69,[85][86][87][88][89][90][91] and studies [53,57] highlighted reactivations during treatment with ETA; similar results can be found with ADA [49,63,66].…”

Section: Resultsmentioning

confidence: 79%

“…The second prospective study reported by Ye H et al [57] was conducted from January 2008 to January 2011 in six centers in China. 87 patients enrolled with HBV and inflammatory arthritis (RA, SpA, and PA) were followed up every 1-3 months until January 2012.…”

Section: Citationmentioning

confidence: 99%

Reactivation of Hepatitis B Virus Infection Associated with Anti-Tumor Necrosis Factor-α Therapy

Albani¹

2014

J Antivir Antiretrovir

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The use of TNF-α inhibitors, nowadays widely employed as first choice drugs for the therapy of chronic inflammatory diseases such as Rheumatoid Arthritis (RA), Psoriatic Arthritis (PA), and Inflammatory Bowel Diseases (IBD), may be associated to reactivation of HBV infection. In this review we summarized the case reports/series and prospective/retrospective studies focusing on this topic, and analyzed the guidelines of the major scientific societies dealing with this problem. Reactivation may occur mainly in HBV inactive carriers positive for HBsAg; the likelihood of reactivation is lower in HBsAg positive subjects with low DNA level (<2000 UI/L) and rare in HBsAg negative patients. Anti-TNF-α candidate patients should be screened for HBV serum markers. On the basis of HBV serology, it is possible to suggest different therapeutic strategies. In patients with chronic hepatitis B infection it is necessary to start an appropriated antiviral therapy and adequate follow-up. Inactive HBsAg carriers must be treated with HBV prophylactic agents. Patients with resolved hepatitis B should be tightly monitored for elevation of liver enzymes and HBV DNA levels. All HBV negative patients should receive vaccination before starting anti-TNF-α treatment.

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“…However, Lee et al [49] reported that HBV reactivation occurred in 1.7% among 468 rheumatic patients with resolved HBV infection during anti-TNF therapy. Ye et al [58] reported that HBV reactivation was not found in the 50 patients with resolved HBV infection. Recent prospective study also demonstrated that none of 146 rheumatic patients with resolved HBV infection who received anti-TNF developed HBV reactivation during 56 months follow-up periods.…”

Section: Incidence and Clinical Outcomes Of Hbv Reactivation In Patiementioning

confidence: 99%

“…All 5 patients recovered after treatment of lamivudine. A recent prospective study [58] investigated the incidence of HBV reactivation in inflammatory arthritis patients with HBV infection using anti-TNF therapy and evaluated the efficacy of antiviral therapy. Among the 6 chronic hepatitis B patients (defined by HBV DNA ＞ 2×10 4 IU/mL, elevated ALT), HBV reactivation occurred in two patients (33.3%) without antiviral prophylaxis and no HBV reactivation was observed in the other 4 patients with antiviral prophylaxis.…”

Section: Incidence and Clinical Outcomes Of Hbv Reactivation In Patiementioning

confidence: 99%

Reactivation of Hepatitis B Virus and Its Prevention in Patients with Rheumatic Diseases Receiving Immunosuppressive Therapy

2017

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Introduction of biologic agents to treat patients with rheumatic diseases and cancer has improved clinical outcomes. However, this advance increases the risk of hepatitis B virus (HBV) reactivation in hepatitis B surface antigen carrier and even in resolved HBV infection, which can lead to liver failure and even death. In particular, the risk of HBV reactivation is heightened by the use of B-cell depleting agents such as rituximab, high dose corticosteroid, and anti-tumor necrosis factor-α. Therefore, identification of individuals at risk, and understanding the mechanism of HBV reactivation are essential to preventing HBV reactivation before initiating immunosuppressive therapy. Here, we review the mechanism, incidence, and prevention of HBV reactivation in the setting of immunosuppression. (J Rheum Dis 2017;24:261-270)

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Anti-TNF therapy in patients with HBV infection—analysis of 87 patients with inflammatory arthritis

Cited by 46 publications

References 10 publications

Tumor necrosis factor-alpha blockage therapy impairs hepatitis B viral clearance and enhances T-cell exhaustion in a mouse model

Tumor necrosis factor-alpha blockage therapy impairs hepatitis B viral clearance and enhances T-cell exhaustion in a mouse model

Reactivation of Hepatitis B Virus Infection Associated with Anti-Tumor Necrosis Factor-α Therapy

Reactivation of Hepatitis B Virus and Its Prevention in Patients with Rheumatic Diseases Receiving Immunosuppressive Therapy

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