scholarly journals Highly sensitive HBsAg, anti-HBc and anti HBsAg titres in Early Diagnosis of HBV Reactivation in Anti-HBc-Positive onco-haematological Patients.

2021 ◽  
Author(s):  
Carlotta Cerva ◽  
Romina Salpini ◽  
Mohammad Alkhatib ◽  
Vincenzo Malagnino ◽  
Lorenzo Piermatteo ◽  
...  
Keyword(s):  
Hbv Dna ◽  
Hbv Reactivation ◽  
Virus Reactivation ◽  
Hepatitis B Virus Reactivation ◽  
Upper Limit ◽  
Early Markers ◽  
Highly Sensitive ◽  
B Virus ◽  
Haematological Patients

Abstract The role of novel HBV markers in predicting Hepatitis B virus reactivation (HBV-R) in HBsAg-negative/anti-HBc-positive oncohaematological patients was examined. One hundred and seven HBsAg-negative/anti-HBc-positive oncohaematological patients, receiving anti-HBV prophylaxis for > 18 months were included. At baseline, all patients had undetectable HBV DNA, and 67.3% were anti-HBs positive. HBV-R occurred in 17 (15.9%) patients: 6 during and 11 after the prophylaxis period. At HBV-R, the median (IQR) HBV-DNA was 44 (27–40509) IU/ml, and the alanine aminotransferase upper limit of normal (ULN) was 44% (median [IQR]: 81[49–541] U/L). An anti-HBc>3 cut-off index (COI) plus anti-HBs persistently/declining to <50 mIU/ml was predictive for HBV-R (OR [95% CI]: 9.1 [2.7–30.2]; 63% of patients with vs. 15% without this combination experienced HBV-R, P<0.001). The detection of highly sensitive (HS) HBsAg and/or HBV-DNA confirmed at > 2 time points, also predicts HBV-R (OR [95% CI ]: 13.8 [3.6–52.6]; 50% of positive vs. 7% of negative patients to these markers experienced HBV-R, P=0.001).HS-HBs and anti-HBc titration proved useful early markers of HBV-R.The use of these markers demonstrated that HBV-R frequently occurs in oncohaematological patients with signs of resolved HBV infection, raising issues of proper HBV-R monitoring.

High Risk of Hepatitis B Virus Reactivation in Isolated Anti-Hbc Positive Patients with B-Cell Lymphoma Receiving Rituximab Containing Chemotherapy.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 1944-1944
Author(s):  
Hideaki Fujiwara ◽  
Kosei Matsue
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Hbv Dna ◽  
Hbv Reactivation ◽  
Virus Reactivation ◽  
Hepatitis B Virus Reactivation ◽  
B Virus

Abstract Abstract 1944 Poster Board I-967 Reactivation of hepatitis B virus (HBV) infection in patients receiving chemotherapy, immunosuppressive therapy, and organ transplantation is well-recognized complication in patients with HBsAg positive patients. Although, prophylaxis with anti-viral drug is proposed for HBV surface antigen (HBsAg) positive patients and is considered as a standard managements, the risk of developing HBV reactivation and optimal therapy in HBsAg negative but anti-HBV core antigen (anti-HBc) positive patients remained to be elucidated. In addition the use of rituximab has been reported to cause even fatal HBV related hepatic failure in these patients. We retrospectively investigated the occurrence of HBV reactivation after rituximab containing chemotherapy in HBsAg negative 261 consecutive patients with CD20 positive B-cell lymphoma who admitted Kameda General Hospital over past 5 years. Prior to September 2006, anti-HBc and antibody to HBsAg (anti-HBs) were performed at the discretion of the treating physician. After October 2006, anti-HBc and anti-HBs tests were performed for all patients. HBV reactivation was defined by the seroconversion from HBsAg negative to positive with or without an increase of HBV-DNA from base line levels (>2.6 log copies/ml). Hepatitis attributable to reactivation was defined as a serum alanine aminotransferase (ALT) level greater than 3 folds above the normal upper limit of 2 consecutive determinations more than 5 days apart without feature of hepatitis A, hepatitis C or other causes. Lymphoma subtypes were diffuse large B cell lymphoma (DLBCL; 162 cases, 61%), follicular lymphoma (FL; 58 cases, 22%), mantle cell lymphoma (MCL; 11 cases, 4%), Burkitt lymphoma (BL; 6 cases, 2%), chronic lymphocytic leukemia (CLL; 6 cases, 2%), and other B cell lymphomas (18 cases, 7%) and various courses and treatments containing rituximab were performed such as CHOP, ESHAP, hyper-CVAD etc. Among the 261 patients, the prevalence of HBsAg positive is 9 (3.4%) and all of them were successfully treated by rituximab containing regimens and concurrent use of antiviral agents without development of severe hepatitis. Twenty-two patients were not tested both anti-HBc and anti-HBs before rituximab administration. Therefore, 230 patients were tested both HBsAg and anti-HBc before treatment. Fifty-six of 230 patients (24.3%) were isolated anti-HBc positive and the rest of 174 patients were anti-HBc negative. Anti-HBc IgM was tested in 29 of 56 anti-HBc positive patients and all of the 29 patients were negative for anti-HBc IgM. Anti-HBs was positive in 5/174 patients (2.8%) and 36/56 patients (65.4%) in anti-HBc negative patients and positive patients, respectively. Among 56 patients with positive anti-HBc, 5 patients (13.9%) became HBsAg positive after rituximab containing therapy, while none of 174 patients with negative anti-HBc became positive for HBsAg with median follow up of 24 months. Among 5 patients with HBV reactivation, 4 patients were isolated anti-HBc and one patient who received allogeneic stem cell transplantation was both anti-HBs and anti-HBc positive before the start of rituximab, although his anti-HBs decline and disappeared after transplantation with the use of prednisone for chronic GVHD. All of the 5 patients received entecavir on detection of HBsAg and showed prompt decrease of HBV-DNA, however, 4 of 5 patients exhibited mild to moderate elevation of ALT. None of them developed fulminant hepatic failure. We conclude that patients with isolated anti-HBc are at high risk for HBV reactivation (p=0.011, by Fisher's exact test) and should be monitored closely for HBsAg, anti-HBs, HBV-DNA, transaminase levels during and after rituximab containing treatment. Although preemptive use of entecavir from detection of HBsAg or HBV-DNA enabled us to manage hepatitis B virus reactivation and liver injury successfully, mild to moderate hepatic flare could not prevented in our patients. Therefore, these approaches should be further evaluated in the context of clinical usefulness, safety, cost-effectiveness. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Potential risk factors for the reactivation of the replication of hepatitis B viruses after transcatheter arterial chemoembolization of hepatocellular carcinoma: a retrospective analysis

2020 ◽  
Author(s):  
Xiaoguang Wang ◽  
Xiaodan Yang ◽  
Haitao Yu ◽  
Zhengwei Song ◽  
Fei Chen ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Survival Rates ◽  
Hbv Dna ◽  
Hbv Reactivation ◽  
Virus Reactivation ◽  
Hepatitis B Virus Reactivation ◽  
B Virus ◽  
The Relationship

Abstract Objective: To investigate the clinical features of hepatitis B virus(HBV) reactivation after transcatheter arteriaI chemoembolization (TACE) treatment in patients with hepatocellular carcinoma (HCC), and analyze the relationship between hepatitis B virus reactivation and clinicopathological factors and prognosis. Methods: Clinical data of 108 patients with HCC treated by TACE from January 2006 to January 2014 were retrospectively studied. The relationship between the clinical data and HBV reactivation were analyzed and the differences in survival rates between the reactivation group and the non-reactivation group were also compared. Results: 42 (38.9%) patients developed HBV reactivation. The reactivation rate in patients with HBV DNA ≥ 104 was 65.8% (25/38), and was much higher than that of the patients with HBV DNA < 104 (24.3%, 17/70). The cellular immune function of reactivation group was significantly lower than that of non-reactivation group(P < 0.01). There was a significant difference (P=0.03) in 2-year survival rate between the activated and non-activated groups, and their survival rates were 35.9% and 53.3%, respectively. Conclusion: Some patients with primary hepatocellular carcinoma may have hepatitis B virus reactivation after receiving TACE treatment, and positive HBV DNA, immunosuppression were the risk factors for the development of HBV reactivation. Patients with hepatitis B virus reactivation after TACE have poor prognosis. The study suggests that antiviral therapy and immunoenhancer were necessary to improve curative effect and survival rate in HCC patients who underwent TACE.

scholarly journals Hematological Malignancies and HBV Reactivation: Suggestions for Clinical Management

2019 ◽  
Author(s):  
Alessandra Zannella ◽  
Massimo Marignani ◽  
Paola Begini
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hematological Malignancies ◽  
Immunosuppressive Drugs ◽  
Viral Reactivation ◽  
Hbv Reactivation ◽  
Virus Reactivation ◽  
Hepatitis B Virus Reactivation ◽  
B Virus ◽  
Clinical Consequences

It is well known that the event of hepatitis B virus reactivation can occur among patients undergoing treatment for hematological malignancies. In this paper we will present the available data regarding the risk of hepatitis B virus reactivation in this special population of immunosuppressed patients and explore the relevance of an accurate prevention and management of this condition. A computerized literature search was performed using appropriate terms arrangement, including English-written literature only or additional relevant articles. The evaluation of hepatitis B reactivation risk is a multidimensional process, which includes conducting an accurate clinical and physical history, considering the virological categories, the knowledge of the medication chosen to treat these hematological malignancies and the induced grade of immunosuppression. Adopting adequate preventive strategies and surveillance according to the current international recommendations is crucial to prevent HBVr and its dire clinical consequences (hepatitis, liver failure, interruption of lifesaving anti-neoplastic treatments). Universal HBV screening of patients scheduled to undergo treatment for hematological malignancies should be the chosen policy, and clinicians should be aware of the inherent risk of viral reactivation among the different virological categories and the classes of immunosuppressive drugs.

scholarly journals Rituximab Biosimilar Combined with Pegylated Interferon α-2b in Patients with Untreated Advanced Indolent B-Cell Non-Hodgkin's Lymphoma: Preliminary Results from a Multicenter, Single-Arm, Phase II Study

Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 1359-1359
Author(s):  
Gao Yan ◽  
Jianqiu Wu ◽  
Yunhong Huang ◽  
Hui Zhou ◽  
Ru Feng ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Pegylated Interferon ◽  
Hbv Dna ◽  
Interferon Α ◽  
Newly Diagnosed ◽  
Virus Reactivation ◽  
Hepatitis B Virus Reactivation ◽  
B Virus ◽  
Common Grade

Abstract Background: Indolent B-cell lymphoma (iBCL) are clinically heterogeneous and accounts for 10-15% of all kind of subtypes in NHL in China. Although iBCL have a relatively good survival, majority of these lymphomas is considered incurable. The favorable activity and safety profile of rituximab monotherapy in the initial treatment of iBCL has been proven. Interferon alpha (IFN-α) has been proven to be effective in modulating immune responses and may enhance the clinical responses to rituximab in vitro and in vivo studies. Clinical combination of rituximab and IFN-α was associated with fewer early treatment failures compared to single agent rituximab. Peginterferon-α-2(peg-IFN-α2) has a longer half-life with less toxicity. It also is one of the options for the treatment of chronic hepatitis B virus (CHB) infection. Therefore, we hypothesized that peg-IFN-α2 may synergize with rituximab and would minimize or eliminate minimal residual disease (MRD). The purpose of this study is to evaluate the efficacy and safety for this combination in pts(pts) with treatment-naive iBCL. Methods: This trial enrolled eligible pts aged 18-80 years with newly diagnosed iBCL including FL(grade 1-2,3a) and MZL. Pts were eligible if they had ECOG ≤ 2, adequate organ function and bone marrow function, and at least one measurable or evaluable lesion. Further eligibility criteria were HBsAg positivity with HBV DNA load &lt;3000 IU/mL prior to study; serum ALT level of &lt;5 times the upper limit of normal. During induction phase, pts received rituximab biosimilar (Henliritux ® Shanghai Henlius Biotech) 375 mg/m 2 intravenous infusion on d1. Peg-IFN-α2b (Pegberon ®, Xiamen Amoytop Biotech) was given at a dose of 135ug, subcutaneously, on d1,8. The combination repeated every 21 days for 6 cycles. Responded pts receive rituximab (every 2 months) plus peg-IFN-α2b (every month) maintenance at the dose described above, for up to 2 years until disease progression and intolerance. Simultaneously, CHB pts orally treated with entecavir continuously. The primary endpoint is ORR assessed by investigators per Lugano 2014 criteria. Key secondary endpoints included TTR, DOR, PFS, OS, HBV DNA load clearance, and safety. Adverse events (AEs) were summarized according to NCI CTCAE v5.0. All pts' blood samples were collected for circulating tumor DNA (ctDNA) assessment before treatment in each of cycles. ctDNA samples were analyzed by capture-based NGS targeting 475 lymphoma- and cancer- relevant genes. This trial was registered at ClinicalTrials.gov (NCT04246359). Results: From January 2020 to July 2021, 52 eligible pts with median age of 54 (range, 29-75) years were enrolled from 6 institutions in China. Thirty (54.5%) are female, 20(36.4%) pts were symptomatic and 22(40.7%) pts with FLIPI score≥3, 6(10.9%) pts suffer from hepatitis B with HBV DNA load &lt;3000 IU/mL at study entry. At cutoff date, there were 25(46.3%) FL (grade 1-2), 19(35.2%) MALT, 8(14.8%) FL (grade 3a) pts enrolled. Of 50 response evaluable pts, 31(62.0%) pts achieved an objective response including 19(38.0%) pts with CR based on investigators. ORR were 58.3% (14/24), 75.0% (6/8), 61.1% (11/18) and the CR rates were 29.2% (7/24), 62.5% (5/8), 38.9% (7/18), 0,0 for FL (grade 1-2), FL (grade3a), MALT respectively. Median HBV DNA load clearance time was 1.8 months (1.3-2.1months), no hepatitis B virus reactivation reported. With median follow-up time was 6.2 months (range: 1.4-18.3 months), median OS, PFS and DoR was not reached; 6-month OS and PFS rate of whole cohort was 96.7±3.3%, 85.3±6.1%, respectively. Median TTR was 3.0months (1.5-5.2months). Dynamics ctDNA assay is in progress, data in detail will be reported at the ASH conference. The most common treatment-emergent adverse events (TEAEs) were hematological relevance toxicities. The most common grade hematological TEAEs (&gt;30%) were neutropenia 63.5%, anemia 34.6%, thrombocytopenia 28.8%. Non-hematological TEAEs (&gt;10%) were fever (28.8%), transaminase elevated (28.8%), fatigue (26.9%), infusion reaction (17.4%). Most common grade 3-4 TEAEs (&gt;5%) were neutropenia（17.3%）, anemia (7.7%). No treatment-related death occurred. Conclusion: Rituximab biosimilar plus pegylated interferon α-2b provided favorable response in newly diagnosed advanced iBCL and was well tolerated. No hepatitis B virus reactivation was observed. Further investigation is warranted. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.

Risk of Hepatitis B Virus (HBV) Reactivation and the Role of Anti-Viral Prophylaxis in Multiple Myeloma Patients with HBV Infection in the Era of Novel Therapies.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3882-3882
Author(s):  
Dawn Mya ◽  
Shuting Han ◽  
Yeow Tee Goh ◽  
Daryl Tan
Keyword(s):  
Multiple Myeloma ◽  
Viral Load ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hbv Dna ◽  
Hbv Infection ◽  
Hbv Reactivation ◽  
B Virus ◽  
Lamivudine Prophylaxis

Abstract Abstract 3882 Poster Board III-818 Introduction Patients with hepatitis B virus (HBV) infection, defined by the presence of HBV surface antigen (HBsAg), have an increased risk of HBV reactivation when they are on immunosuppressive treatment for multiple myeloma (MM). Although there is no guideline for MM patients with HBV infection, current lymphoma guidelines do recommend that these patients should receive antiviral prophylaxis during and after chemotherapy. Of late, the advent of bortezomib in the management of MM has resulted in a high reported incidence of variecella-zoster reactivation. The risk of HBV reactivation in MM patients with HBV infection undergoing treatment has not been previously studied. As HBV infection is endemic in Asia, we sought to evaluate the prevalence of HBV infection in our patients, the incidence of its reactivation especially in patients receiving bortezomib and the role of anti-viral prophylaxis. Methods Previously untreated MM patients diagnosed from 2000-2008 who were tested for HBsAg in our institution were included. Hepatitis attributable to HBV reactivation was defined as an increase in HBV DNA levels of tenfold, or an absolute increase greater than105 copies/ml in the HBV DNA level. HBV infected patients were prospectively followed. 33% of all patients have been exposed to bortezomib, while 26% received high dose therapy with autologous stem cell transplantation (HDT/ASCT). Results 243 untreated MM patients were identified. The prevalence of HBV infection is 5.8% (14/243). 6 (43%) HBV infected patients had detectable HBV DNA viral load (>3 log) at baseline. All 6 patients had normal baseline liver function tests and received lamivudine prophylaxis. All 14 HBV infected patients went on to receive systemic therapy for MM, with continual monitoring of HBV DNA viral load and liver enzymes for viral reactivation. 4 patients with undetectable HBV DNA load did not receive anti-viral prophylaxis. Of these 14 patients, 3 (21%) who had been on lamivudine prophylaxis had reactivation of the virus, with 1 dying from it, and 1 having emergence of a mutant viral strain. Two of them had no detectable viral load at presentation. Two patients reactivated 3 and 5 months after HDT/ASCT, while 1 reactivated immediately after a bortezomib/ doxil salvage regimen. Conclusion The risk of HBV reactivation appeared to be commonest during the immune reconstitution phase after HDT/ASCT. Although the majority of patients with HBV infection and not receiving HDT/ASCT do not reactivate, the risk may not negligible when bortezomib is used (7%). Undetectable HBV DNA and the use of anti-viral prophylaxis do not appear to preclude reactivation. The optimal use of anti-viral prophylaxis, particularly if bortezomib is given, should be further evaluated. This is particularly relevant in the current era where bortezomib plays a dominant role in the treatment of MM, and especially in endemic regions where the incidence of HBV infection is high. Disclosures: No relevant conflicts of interest to declare.

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