Role of Hepatitis B Surface Antibodies in Risk for Hepatitis B Virus Reactivation During Anti–Tumor Necrosis Factor Therapy

Poola, Shiva; Kratzer, MaryKate; Sanaka, Sirish; Sewell, Kerry; Tillmann, Hans L.

doi:10.1016/j.cgh.2022.02.027

Cited by 5 publications

(5 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A meta‐analysis of HBsAg−/HBcAb+ patients with non‐haematological diseases indicated that those with positive anti‐HBs exhibited a lower incidence of HBV reactivation compared to their negative anti‐HBs counterparts (2.5% vs. 10.7%; relative risk: 0.28) 11 . A meta‐analysis has explored HBV reactivation in HBsAg−/HBcAb+ patients on anti‐TNF therapy 31 . It revealed a heightened risk of HBV reactivation in anti‐HBs negative patients compared to anti‐HBs positive patients (1.98% [6/303] vs. 0.56% [6/1072]).…”

Section: Discussionmentioning

confidence: 99%

“…11 A meta-analysis has explored HBV reactivation in HBsAg−/ HBcAb+ patients on anti-TNF therapy. 31 Another research from Taiwan identified a high baseline anti-HBs level (>100 mIU/mL) as protective against HBsAg seroreversion in resolved HBV infections. 18 There's an inverse relationship between HBsAg seroreversion risk and anti-HBs levels during bDMARDs use.…”

Section: Status a N = 27mentioning

confidence: 99%

See 1 more Smart Citation

HBV reactivation in HBsAg−/HBcAb+ rheumatoid arthritis patients receiving biologic/targeted synthetic DMARDs

Kuo,

Tseng,

et al. 2023

Liver International

View full text Add to dashboard Cite

BackgroundRheumatoid arthritis (RA) patients seropositive for hepatitis B core antibody (HBcAb) and negative for hepatitis B surface antigen (HBsAg) are at risk of hepatitis B virus (HBV) reactivation when treated with biologic or targeted synthetic (b/ts) disease‐modifying antirheumatic drugs (DMARDs). The study aims to investigate the risk in this population.MethodsFrom January 2004 through December 2020, 1068 RA patients undergoing b/tsDMARDs therapy and 416 patients with HBsAg−/HBcAb+ were enrolled. Factors associated with HBV reactivation were analysed.ResultsDuring 2845 person‐years of follow‐up, 27 of 416 (6.5%,9.5 per 1000 person‐years) patients developed HBV reactivation, with a cumulative rate of HBV reactivation of 3.5% at 5 years, 6.1% at 10 years and 24.2% at 17 years. The median interval from beginning b/tsDMARDs to HBV reactivation was 85 months (range: 9–186 months). The risk of HBV reactivation varied by type of b/tsDMARD, with rituximab having the highest risk (incidence rate: 48.3 per 1000 person‐years), followed by abatacept (incidence rate: 24.0 per 1000 person‐years). In multivariate analysis, rituximab (adjusted hazard ratio [aHR]: 15.77, 95% confidence interval [CI]: 4.12–60.32, p = .001), abatacept (aHR: 9.30, 1.83–47.19, p = .007), adalimumab (aHR: 3.86, 1.05–14.26, p = .04) and negative baseline HBV surface antibody (anti‐HBs, <10 mIU/mL) (aHR: 3.89, 1.70–8.92, p < .001) were independent risk factors for HBV reactivation.ConclusionHBsAg−/HBcAb+ RA patients are susceptible to HBV reactivation during b/tsDMARD therapy. Those with negative baseline anti‐HBs and those on certain b/tsDMARDs, such as rituximab, abatacept and adalimumab, have high reactivation risks. Risk stratification and management should be based on the patient's baseline anti‐HBs titre and type of therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Status a N = 27mentioning

confidence: 99%

HBV reactivation in HBsAg−/HBcAb+ rheumatoid arthritis patients receiving biologic/targeted synthetic DMARDs

Kuo,

Tseng,

et al. 2023

Liver International

View full text Add to dashboard Cite

show abstract

“…In functionally cured patients, our analysis found that HBsAb titers ≥100 mIU/ml decrease HBsAg seroreversion after ceasing PEG-IFN therapy, with an OR of 0.11 versus those with negative HBsAb According to previous studies, the acquisition of higher peak HBsAb titres is also desirable to maintain the protective HBsAb titers in HBV vaccination and in patients undergoing chemotherapy. 13,14 High titres of HBsAb can further decrease the risk of HBV reactivation under anti-tumour necrosis factor therapy in occult hepatitis B infection (OBI) or direct-acting antiviral therapy in hepatitis C. 15,16 Recent studies have shown that HBsAb levels are related to the recovery of HBV-specific CD8 + T and B cells in functionally cured patients, indicating that HBsAb can be a biological marker for the restoration of host immunity to HBV. 11 Furthermore, children with HBsAg loss and negative HBsAb serostatus do not respond well to HBV vaccination, which indicates that host immunity might not be well restored in these patients.…”

Section: Discussionmentioning

confidence: 99%

“…According to previous studies, the acquisition of higher peak HBsAb titres is also desirable to maintain the protective HBsAb titers in HBV vaccination and in patients undergoing chemotherapy 13,14 . High titres of HBsAb can further decrease the risk of HBV reactivation under anti‐tumour necrosis factor therapy in occult hepatitis B infection (OBI) or direct‐acting antiviral therapy in hepatitis C 15,16 …”

Section: Discussionmentioning

confidence: 99%

Role of hepatitis B surface antibody in seroreversion of hepatitis B surface antigen in patients achieving hepatitis B surface antigen loss with pegylated interferon‐based therapy

Gao

Zhang

et al. 2022

Journal of Viral Hepatitis

View full text Add to dashboard Cite

It is unclear whether hepatitis B surface antibody (HBsAb) confers clinical benefits after HBsAg seroclearance, especially in hepatitis B surface antigen (HBsAg) seroreversion and maintenance of HBsAb. We evaluated this in patients (n = 222) with HBsAg loss following treatment with pegylated interferon (PEG‐IFN)‐based therapy who completed a 48‐week follow‐up period. Serum hepatitis B virus (HBV) markers and biochemical indicators were evaluated every 3 months. The primary endpoint was HBsAg seroreversion. Factors associated with HBsAg seroreversion were also investigated. HBsAb ≥100 mIU/ml resulted in a lower HBsAg seroreversion rate than an HBsAb‐negative status (5.5% vs. 29.5%, p < .001); however, the seroreversion rate was not significantly different between patients with HBsAb 10–100 mIU/ml and those in the HBsAb‐negative group. Patients with HBsAb ≥100 mIU/ml had a lower HBsAb loss rate than those with HBsAb 10–100 mIU/ml (7.3% vs. 21.7%, p = .005). The final HBsAg seroreversion and HBV DNA relapse rates were 13.5% and 1.8%, respectively. HBsAb ≥100 mIU/ml at the off‐treatment time (odds ratio [OR] 0.110, 95% confidence interval [CI]: 0.034–0.353, p < .001) and treatment time to attain HBsAg loss >28 weeks (OR 2.508, 95% CI: 1.068–5.890, p = .035) were predictors of HBsAg seroreversion. Consolidation therapy for 12–24 weeks resulted in higher HBsAb titres than consolidation therapy for ≤12 weeks in HBsAb‐negative patients at the off‐treatment time (p < .001). HBsAg seroconversion with HBsAb ≥100 mIU/ml decreases HBsAg seroreversion and provides an efficient maintenance rate of HBsAb. HBsAg seroconversion with high HBsAb titres may be clinically beneficial for chronic hepatitis B treated with PEG‐IFN‐based therapy.

show abstract

“…10 HBVr associated with rh TNFR:Fc treatment is rare; and HBVr mostly occurs either when the recommended HBV testing is performed without adhering to the recommended monitoring guidelines (such as monitoring anti-hepatitis B surface antigen antibody [anti-HBs] levels or HBV DNA) or when no testing is performed at all. 11,12 Herein, this current report describes a case of acute-on-chronic liver failure induced by rh TNFR:Fc therapy-induced occult HBV reactivation and provides a medical reference for subsequent use of drugs in patients with similar diseases.…”

Section: Introductionmentioning

confidence: 99%

Case report: Recombinant human type II tumour necrosis factor receptor-antibody fusion protein induced occult hepatitis B virus reactivation leading to liver failure

Qin,

Zhou,

Zhou

et al. 2024

J Int Med Res

View full text Add to dashboard Cite

Recombinant human type II tumour necrosis factor receptor-antibody fusion protein (rh TNFR:Fc) is an immunosuppressant approved for treating rheumatoid arthritis (RA). This case report describes a case of hepatitis B reactivation in a patient with drug-induced acute-on-chronic liver failure. A 58-year-old woman with a history of RA was treated with rh TNFR:Fc; and then subsequently received 25 mg rh TNFR:Fc, twice a week, as maintenance therapy. No anti-hepatitis B virus (HBV) preventive treatment was administered. Six months later, she was hospitalized with acute jaundice. HBV reactivation was observed, leading to acute-on-chronic liver failure. After active treatment, the patient’s condition improved and she recovered well. Following careful diagnosis and treatment protocols are essential when treating RA with rh TNFR:Fc, especially in anti-hepatitis B core antigen antibody-positive patients, even when the HBV surface antigen and the HBV DNA are negative. In the case of HBV reactivation, liver function parameters, HBV surface antigen and HBV DNA should be closely monitored during treatment, and antiviral drugs should be used prophylactically when necessary, as fatal hepatitis B reactivation may occur in rare cases. A comprehensive evaluation and medication should be administered in a timely manner after evaluating the patient’s physical condition and closely monitoring the patient.

show abstract

Role of Hepatitis B Surface Antibodies in Risk for Hepatitis B Virus Reactivation During Anti–Tumor Necrosis Factor Therapy

Cited by 5 publications

References 7 publications

HBV reactivation in HBsAg−/HBcAb+ rheumatoid arthritis patients receiving biologic/targeted synthetic DMARDs

HBV reactivation in HBsAg−/HBcAb+ rheumatoid arthritis patients receiving biologic/targeted synthetic DMARDs

Role of hepatitis B surface antibody in seroreversion of hepatitis B surface antigen in patients achieving hepatitis B surface antigen loss with pegylated interferon‐based therapy

Case report: Recombinant human type II tumour necrosis factor receptor-antibody fusion protein induced occult hepatitis B virus reactivation leading to liver failure

Contact Info

Product

Resources

About