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.

scholarly journals Low Risk of Hepatitis B Virus Reactivation in HBsAg-negative/Anti-HBc–positive Carriers Receiving Rituximab for Rheumatoid Arthritis: A Retrospective Multicenter Italian Study

2016 ◽  
Vol 43 (5) ◽  
pp. 869-874 ◽  
Author(s):  
Valentina Varisco ◽  
Mauro Viganò ◽  
Alberto Batticciotto ◽  
Pietro Lampertico ◽  
Antonio Marchesoni ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Hepatitis B Surface Antigen ◽  
Hbv Dna ◽  
Hbv Infection ◽  
Core Antigen ◽  
Hbv Reactivation ◽  
Serum Hbsag ◽  
B Virus

Objective.Patients with resolved hepatitis B virus (HBV) infection, i.e., hepatitis B surface antigen (HBsAg)-negative/antihepatitis B core antigen (anti-HBc)-positive, undergoing rituximab (RTX)-based chemotherapy for hematological malignancies without anti-HBV prophylaxis are at risk of HBV reactivation, but the risk in such patients receiving RTX for rheumatological disorders is not clear. We evaluated this risk in HBsAg-negative/anti-HBc–positive patients with rheumatoid arthritis (RA) undergoing RTX without prophylaxis.Methods.Thirty-three HBsAg-negative/anti-HBc–positive outpatients with RA with undetectable HBV DNA by sensitive PCR assay [73% women, median age 60 years, 85% with HBsAg antibodies (anti-HBs), 37% with antihepatitis B envelope antigen] received a median of 3 cycles of RTX (range 1–8) over 34 months (range 0–80) combined with disease-modifying antirheumatic drugs (DMARD) without prophylaxis. All underwent clinical and laboratory monitoring during and after RTX administration, including serum HBsAg and HBV DNA measurements every 6 months or whenever clinically indicated.Results.None of the patients seroreverted to HBsAg during RTX treatment, but 6/28 (21%) showed a > 50% decrease in protective anti-HBs levels, including 2 who became anti-HBs–negative. One patient (3%) who became HBV DNA-positive (44 IU/ml) after 6 months of RTX treatment was effectively rescued with lamivudine before any hepatitis flare occurred. Among the 14 patients monitored for 18 months (range 0–70) after RTX discontinuation, no HBV reactivation was observed.Conclusion.The administration of RTX + DMARD in patients with RA with resolved HBV infection leads to a negligible risk of HBV reactivation, thus suggesting that serum HBsAg and/or HBV DNA monitoring but not universal anti-HBV prophylaxis is justified.

Lamivudine therapy for prevention of immunosuppressive-induced hepatitis B virus reactivation in hepatitis B surface antigen carriers

Blood ◽  
2002 ◽  
Vol 100 (2) ◽  
pp. 391-396 ◽  
Author(s):  
Oren Shibolet ◽  
Yaron Ilan ◽  
Shmuel Gillis ◽  
Ayala Hubert ◽  
Daniel Shouval ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Immunosuppressive Therapy ◽  
Hepatitis B Surface Antigen ◽  
Hbv Dna ◽  
Hbv Reactivation ◽  
Hbsag Carriers ◽  
B Virus ◽  
Lamivudine Prophylaxis

Abstract Viral reactivation in hepatitis B surface antigen (HBsAg) carriers undergoing immunosuppressive therapy is well documented. To evaluate the role of lamivudine prophylaxis in Hepatitis B virus (HBV) carriers treated with immunosuppression for nonhepatic disorders, we reviewed our experience between 1997 and 2000 at Hadassah University Hospital (Jerusalem, Israel). Controls were patients who were HBV carriers and who, between 1990 and 1995, were treated for hematological malignancies but were not treated with lamivudine. Eighteen HBsAg-positive patients were treated with immunosuppression. Fourteen were males, with a mean age of 48 years. Eleven patients had lymphoma; 2 had colonic adenocarcinoma; and 5 had cryoglobulinemia, enophthalmitis, vasculitis, malignant histocytosis, or ulcerative colitis. Fourteen patients were treated with chemotherapy, and 4 with prolonged high-dose corticosteroids. All patients were HBsAg-positive; 4 had hepatitis B e antigen, and 10 had HBV DNA by polymerase chain reaction. Lamivudine was administered to 13 patients in the treatment group 1 to 60 days (mean, 15 days) before immunosuppressive treatment and continued 0.5 to 24 months (mean, 7 months) following initiation of immunosuppression. Mean follow-up after lamivudine administration was 21 months. Three patients died of lymphoma complications and 10 (77%) survived. None of the patients had clinical or serological evidence of HBV reactivation during or after lamivudine prophylaxis. Of 6 patients who presented with liver function test disturbances, 5 improved during combined lamivudine and immunosuppression treatment. At the end of follow-up, HBV DNA became undetectable in 2 of 10 patients. In 2 patients, seroconversion from HBsAg to anti-HBs was observed. In contrast, 2 of 5 control patients had HBV reactivation. Lamivudine prophylaxis in HBsAg carriers receiving immunosuppressive therapy may prevent HBV reactivation and hepatic failure.

scholarly journals 905. Risk of Hepatitis B Reactivation in Patients Receiving Ibrutinib: The National VA Cohort

2021 ◽  
Vol 8 (Supplement_1) ◽  
pp. S544-S544
Author(s):  
Ting-Yi Chen ◽  
David Jacob ◽  
John David Coppin ◽  
Chetan Jinadatha
Keyword(s):  
At Risk ◽  
Viral Load ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Cumulative Incidence ◽  
Hbv Dna ◽  
Hbv Reactivation ◽  
Virus Surface ◽  
B Virus ◽  
Risk Patients

Abstract Background Ibrutinib, a bruton tyrosine kinase inhibitor was approved by Food and Drug Administration (FDA) in 2013 and became the first-line treatment for chronic lymphocytic leukemia in 2014. The risk Hepatitis B Virus (HBV) reactivation after initiation of ibrutinib is unclear. Here, we report the results of national Veterans Health Administration (VHA) pharmacy database review estimating the incidence of HBV reactivation after initiation of ibrutinib. Methods Veterans who received ibrutinib between Feb 1, 2014 through October 31, 2019 were included in our study. Possible reactivations were identified by change of Hepatitis B Virus surface antigen (HBV sAg), HBV core antibody (Ab) or HBV viral load from no data or negative to positive after starting ibrutinib. Individual chart review was conducted to verify HBV reactivation due to ibrutinib. Cumulative incidence was calculated by identifying HBV reactivation cases among at risk patients, which was defined as prior exposure by positive HBV core Ab regardless of HBV sAg or HBV viral load status. For patients without any HBV serology, an estimated prevalence of HBV exposure in veterans from the literature is used. Results A total of 4130 veterans were on ibrutinib during the study period. Of 4130 patients, 1875 patients with HBV core Ab negative and 68 patients on antivirals against HBV prior to ibrutinib were excluded. Among the remaining 2187 patients, there were 170 patients with positive HBV core Ab and 2017 patients without HBV core Ab tested regardless of HBV sAg or HBV DNA status. We used the estimated 13.6% (95%CI 11.5-16.1) of HBV exposure in veterans and estimated that 274 (95%CI 232-325) out of 2017 patients would be at risk of HBV reactivation. Thirty-nine patients were identified to have HBV reactivation after ibrutinib. After detailed review, 7 HBV reactivations were attributable to initiation of ibrutinib. The cumulative incidence of HBV reactivation after ibrutinib was estimated as 1.5% (95% CI 1.4-1.7). Conclusion In this large VHA study, we identified 7 cases of HBV reactivations among 444 at risk patients. The cumulative incidence of HBV reactivation after ibrutinib was 1.5% in patients with prior HBV exposure with positive HBV core Ab irrespective of HBV sAg or HBV DNA status, indicating a moderate risk of HBV reactivation. Disclosures All Authors: No reported disclosures

scholarly journals Incidence of hepatitis B virus reactivation in patients with resolved infection on immunosuppressive therapy for rheumatic disease: a multicentre, prospective, observational study in Japan

2016 ◽  
Vol 76 (6) ◽  
pp. 1051-1056 ◽  
Author(s):  
Wataru Fukuda ◽  
Tadamasa Hanyu ◽  
Masaki Katayama ◽  
Shinichi Mizuki ◽  
Akitomo Okada ◽  
...  
Keyword(s):  
Risk Factors ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Rheumatic Disease ◽  
Hbv Dna ◽  
Hbv Infection ◽  
Hbv Reactivation ◽  
Virus Reactivation ◽  
Virus Surface ◽  
B Virus

BackgroundAlthough the reactivation of hepatitis B virus (HBV) is recognised as a serious complication in patients with rheumatic disease (RD) receiving immunosuppressive drugs (ISDs), the incidence and risk factors for reactivation remain controversial.ObjectivesTo investigate the incidence and risk factors for HBV reactivation in patients with RD.MethodsWe performed a multicentre, observational, prospective study over 2 years in patients with resolved HBV infection. Patients with RD treated with a dose of ≥5 mg/day prednisolone and/or synthetic or biological ISDs with negative HB virus surface antigen and positive anti-HB virus surface antibody (HBsAb) and/or anti-HB virus core antibody (HBcAb) were enrolled. Quantitative HBV DNA results and related data were regularly recorded.ResultsAmong 1042 patients, including 959 with rheumatoid arthritis, HBV DNA was detected in 35 (1.93/100 person-years), with >2.1 log copies/mL observed in 10 patients (0.55/100 person-years). None of the reactivated patients, including seven treated with a nucleic acid analogue, showed overt hepatitis. Low HBsAb titres and advanced age seemed to be risk factors for HBV reactivation; however, reactivation was observed in three patients with positive HBsAb and negative HBcAb test results. The risk of reactivation was lower with methotrexate but higher with prednisolone among the different types of ISDs. The intervals from the start of ISD to reactivation were relatively long (3–182 months; median, 66 months).ConclusionsThe incidence of HBV reactivation with ISD use was 1.93/100 person-years in patients with RD with resolved HBV infection. No overt hepatitis was observed in the reactivated patients.

scholarly journals Post-Autotransplant Hepatitis B Virus (HBV) Reactivation in Lymphoma and Multiple Myeloma Patients with Hepatitis B Surface Antigen-Positive or Resolved HBV Infection

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 1196-1196
Author(s):  
Jieun Jang ◽  
Hyunsung Park ◽  
Jungyeon Lee ◽  
Yundeok Kim ◽  
Soo Jeong Kim ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Surface Antigen ◽  
Hepatitis B Surface Antigen ◽  
Hbv Infection ◽  
Hbv Reactivation ◽  
B Virus ◽  
Conditioning Regimens ◽  
Anti Cd20

Abstract Background: Although hepatitis B virus (HBV) reactivation in patients with hepatitis B surface antigen (HBsAg)-positive or resolved HBV infection (HBsAg-negative and hepatitis B core antibody [anti-HBc]-positive) undergoing anticancer therapy with or without rituximab has been frequently reported, few studies have evaluated the risk of HBV reactivation in patients receiving autologous stem cell transplantation (ASCT). We studied the rate of hepatitis and HBV reactivation after ASCT in lymphoma and multiple myeloma (MM) patients with HBsAg-positive or resolved HBV infection. Methods & Materials: Medical records of patients who diagnosed with lymphoma or MM and received ASCT between November 2005 and April 2014 in Severance hospital were retrospectively analyzed. HBV status was screened routinely at ASCT and when viral-related hepatitis was suspected after ASCT. Hepatitis was defined as a 3-fold or greater increase in serum alanine transaminase (ALT) that exceeded the reference range (>46 IU/L) or an absolute increase of ALT to more than 100 IU/L. HBV reactivation was defined as elevation of serum HBV-DNA level more than 1 log IU/L from baseline in HBsAg(+) patients. In case of resolved HBV patients, positive conversion of HBsAg (reverse seroconversion) with or without increase of ALT was defined as HBV reactivation. Hepatitis and HBV reactivation occurred before 1 year after ASCT was considered ASCT-related in this study. Result: A total of 297 patients (196 lymphoma and 101 MM) were studied. Median age at diagnosis was 47 years (range 16-64). A male to female ratio was 1.36:1. Most common subtype of lymphoma was diffuse large B-cell lymphoma (DLBCL, n=111). The median duration from diagnosis to ASCT was 475 days (range 105-5230) and 175 days (range 39-5400) in lymphoma and MM patients, respectively. Busulfan-based (n= 161, 82.1%) conditioning regimens were commonly used in lymphoma patients and melphalan-based (n=101, 100%) conditioning regimens were used in MM patients. The patients with HBsAg(-) did not received a routine anti-HBV prophylaxis regardless of the presence of anti-HBc. Nine patients did not tested for HBV at ASCT. Among 274 patients with HBsAg(-), 110 patients were anti-HBc(+) (resolved HBV infection) and 161 patients were anti-HBc(-). Within 1 year after ASCT, 48 of anti-HBc(+) and 71 of anti-HBc(-) patients experienced hepatitis (43.6% vs. 44.1%, p>0.999). The most common cause of hepatitis was drug-related (n= 81, 66.9%). There was no HBsAg reverse seroconversion within 1 year after ASCT. After 1 year, Only one patient with anti-HBc(+) experienced HBV reactivation at days 763 after ASCT and 3 patients with anti-HBc(-) showed HBsAg reverse seroconversion at days 406, 457 and 1172 post-transplant. In the subset of 178 lymphoma patients with HBsAg(-), 90 patients had a history of previous use of anti-CD20 monoclonal antibody, of whom 37 patients were anti-HBc(+). Twelve of anti-HBc(+) and 24 of anti-HBc(-) patients experienced hepatitis (32.4% vs. 45.3%, p=0.276) but there was no HBV reactivation related hepatitis within 1 year after ASCT. Among 14 patients with HBsAg(+) at ASCT, 13 patients received rituximab-containing chemotherapy before ASCT. They had received prophylactic HBV therapy with lamivudine (n=6), telbivudine (n=4), clevudine (n=2), adefovir (n=1) and tenofovir (n=1). Among them, 3 patients with telbivudine (n=1, 25%), clevudine (n=1, 50%) and lamivudine (n=1, 16.7%) experienced HBV reactivation at days 36, 161 and 204 after ASCT. Conclusion: Our data suggest that ASCT-related HBV reactivation is rare in lymphoma and MM patients with resolved HBV infection regardless of previous anti-CD20 therapy. Routine anti-HBV prophylaxis is not necessary for patients with resolved HBV infection. In case of HBsAg(+) patients, antiviral prophylaxis with lamivudine, clevudine, or telbivudine may not be sufficient to prevent HBV reactivation after ASCT. More potent antiviral agents such as adefovir or tenofovir should be considered. Figure 1 Figure 1. Characteristics of 7 patients with HBV reactivation or HBsAg reverse seroconversion after ASCT. Disclosures No relevant conflicts of interest to declare.

scholarly journals Screening for and management of hepatitis B virus reactivation in patients treated with anti-B-cell therapy

Hematology ◽  
2014 ◽  
Vol 2014 (1) ◽  
pp. 576-583 ◽  
Author(s):  
Shigeru Kusumoto ◽  
Kensei Tobinai
Keyword(s):  
Hepatitis B Virus ◽  
High Risk ◽  
Hepatitis B ◽  
Cell Therapy ◽  
B Cell ◽  
Hbv Dna ◽  
Hbv Infection ◽  
Core Antigen ◽  
Hbv Reactivation ◽  
B Virus

Abstract Reactivation of hepatitis B virus (HBV) is a potentially fatal complication after anti-B-cell therapy. It can develop not only in patients seropositive for hepatitis B surface antigen (HBsAg), but also in those with resolved HBV infection who are seronegative for HBsAg but seropositive for antibodies against hepatitis B core antigen (anti-HBc) and/or antibodies against HBsAg (anti-HBs). The risk of HBV reactivation depends on the balance between replication of the virus and the immune response of the host. Anti-CD20 monoclonal antibody—rituximab in combination with steroid-containing chemotherapy (R-CHOP: rituximab + cyclophosphamide + hydroxydaunorubicin + vincristine + prednisone/prednisolone)—is an important risk factor for HBV reactivation in HBsAg-negative patients. More obviously, HBsAg-positive patients are considered to be at very high risk for HBV reactivation and, in the rituximab era, 59%–80% of these patients develop HBV reactivation after R-CHOP-like chemotherapy. Patients with resolved HBV infection should also be considered at high risk of HBV reactivation, the incidence of which is reported to be 9%–24% in such lymphoma patients. All patients should be screened to identify risk groups for HBV reactivation before initiating anti-B-cell therapy by measuring serum HBV markers including HBsAg, anti-HBc and anti-HBs. To prevent the development of hepatitis due to HBV reactivation after anti-B-cell therapy, antiviral prophylaxis is recommended for HBsAg-positive patients and/or patients in whom HBV DNA is detectable at baseline, whereas regular monitoring of HBV DNA-guided preemptive antiviral therapy is a reasonable and useful approach for patients with resolved HBV infection.

Risk of Hepatitis B Virus (HBV) Reactivation and Role of Anti-Viral Prophylaxis in Lymphoma Patients with Past HBV Infection (HBV Antigen negative but anti-Hepatitis B core antibody positive) Receiving Chemo-Immunotherapy

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 3768-3768 ◽  
Author(s):  
Yu Xuan Koo ◽  
Shao Weng Tan ◽  
Bee Huat Tan ◽  
Miriam Tao ◽  
Wan Cheng Chow ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Systemic Treatment ◽  
Hbv Dna ◽  
Hbv Infection ◽  
Hbv Reactivation ◽  
Antiviral Prophylaxis ◽  
Past Infection ◽  
Absolute Increase ◽  
B Virus

Abstract Hepatitis B virus (HBV) infection, defined by the presence of HBV surface antigen (HBsAg), increases the risk of HBV reactivation and current guidelines recommend that patients who are HBV-infected should receive antiviral prophylaxis during and after chemotherapy. As HBV infection is endemic in Asia, a proportion of patients may have had past HBV infection unknowingly. These patients have cleared HBsAg and are HBsAg negative but anti-Hepatitis B core antibody (anti-HBc) positive. The risk of HBV reactivation in lymphoma patients with past HBV infection undergoing immunochemotherapy has not been previously studied. We accrued 430 consecutive patients from our prospectively maintained data-base and an ongoing prospective epidemiological study from May 2006 to May 2008. All patients were tested for HBsAg. Prior to May 2006, anti-HBc test was performed at the discretion of the treating physician. After May 2006, anti-HBc test was performed for all patients. Stored sera from consented patients were genotyped for HBV DNA. Hepatitis attributable to HBV reactivation was defined as an increase in HBV DNA levels of tenfold, or an absolute increase greater than 105 copies/ml in the HBV DNA level. At presentation, characteristics of lymphomas and baseline liver function test in patients with HBV infection were similar to those with past HBV infection. Among the 430 patients tested for HBsAg, the prevalence of HBV infection is 7.2% (31/430). Overall, 233 patients had both tests performed and 80 (34%) were anti-HBc positive only. Among the 80 patients with past HBV infection, 67 patients received systemic treatment. Of these 67 patients, 58 had a HBV DNA test, which was positive in three (5.2%). 46 patients with past HBV infection were treated with rituximab immunochemotherapy. Of these 46 patients, one reactivated and died (1/46; 4.3%); this patient did not receive anti-viral prophylaxis and had undetectable HBV DNA at time of lymphoma diagnosis. Of the 26 patients with HBV infection receiving systemic treatment, 11 (42.3%) reactivated (p<0.0001). 90% of patients with HBV infection received antiviral prophylaxis compared to 10% with past HBV infection. Of note, all 4 patients with HBV infection with mutant HBV on genotyping reactivated despite prophylactic lamivudine usage. The incidence of past HBV infection (34%) is unexpectedly high and a small proportion (5.2%) had occult infection (detectable HBV DNA). These findings have further implications in terms of HBV screening in endemic regions. Our data is the first to suggest that although majority of patients with past infection do not reactivate, the risk is not negligible when rituximab is used (4%). Undetectable HBV DNA does not appear to preclude reactivation. This data is also provocative and suggests that anti-HBc should be routinely tested and those with past infection, with or without detectable HBV DNA, be monitored closely for reactivation. The optimal use of anti-viral prophylaxis, particularly if immunotherapy is given, should be further evaluated. This is particularly relevant in endemic regions where the incidence of past infection is likely to be high. Given the observation that all patients with mutant HBV reactivated despite lamivudine prophylaxis, the optimal anti-viral agents chosen should be further evaluated. Past HBV infection (n=67) HBV–carrier (n=26) p= Prophylactic lamivudine 7 (10.4%) 18 (69.2%) <0.0001 ALT(Baseline) (median/range) 20 (5–118) 21 (6–338) - Received Rituximab 46 (68.7%) 17 (65.4%) 0.8073 Hepatic decompensation 22 (32.8%) 10 (38.5%) 0.633 HBV reactivation 1 (1.5%) 11 (42.3%) <0.0001

scholarly journals Reactivation of Hepatitis B Virus With Immune-Escape Mutations After Ocrelizumab Treatment for Multiple Sclerosis

2018 ◽  
Vol 6 (1) ◽  
Author(s):  
Maria R Ciardi ◽  
Marco Iannetta ◽  
Maria A Zingaropoli ◽  
Romina Salpini ◽  
Marianna Aragri ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Immune Escape ◽  
Hbv Dna ◽  
Hbv Infection ◽  
Hbv Reactivation ◽  
Optimal Management ◽  
B Virus ◽  
Anti Cd20

Abstract Ocrelizumab is an anti-CD20 monoclonal antibody for the treatment of multiple sclerosis (MS) that is closely related to rituximab. We describe a case of hepatitis B virus (HBV) reactivation in an MS patient with resolved HBV infection receiving ocrelizumab. HBV reactivation was monitored with HBV-DNA and HBV surface antigen periodic assessment. Anti-HBV treatment with entecavir was started after HBV-DNA detection. Ocrelizumab can reactivate viral replication in patients with resolved HBV infection. HBV reactivation monitoring seems an effective and safe option for the management of these patients. More studies are needed to assess the optimal management of HBV reactivation in MS patients on ocrelizumab treatment.

scholarly journals Possible role of tocopherols in the modulation of host microRNA with potential antiviral activity in patients with hepatitis B virus-related persistent infection: a systematic review

2014 ◽  
Vol 112 (11) ◽  
pp. 1751-1768 ◽  
Author(s):  
S. Fiorino ◽  
L. Bacchi-Reggiani ◽  
S. Sabbatani ◽  
F. Grizzi ◽  
L. di Tommaso ◽  
...  
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Antiviral Activity ◽  
Hbv Infection ◽  
Cochrane Library ◽  
Viral Pathogen ◽  
Increased Risk ◽  
B Virus ◽  
Chronic Hbv

Hepatitis B virus (HBV) infection represents a serious global health problem and persistent HBV infection is associated with an increased risk of cirrhosis, hepatocellular carcinoma and liver failure. Recently, the study of the role of microRNA (miRNA) in the pathogenesis of HBV has gained considerable interest as well as new treatments against this pathogen have been approved. A few studies have investigated the antiviral activity of vitamin E (VE) in chronic HBV carriers. Herein, we review the possible role of tocopherols in the modulation of host miRNA with potential anti-HBV activity. A systematic research of the scientific literature was performed by searching the MEDLINE, Cochrane Library and EMBASE databases. The keywords used were ‘HBV therapy’, ‘HBV treatment’, ‘VE antiviral effects’, ‘tocopherol antiviral activity’, ‘miRNA antiviral activity’ and ‘VE microRNA’. Reports describing the role of miRNA in the regulation of HBV life cycle,in vitroandin vivoavailable studies reporting the effects of VE on miRNA expression profiles and epigenetic networks, and clinical trials reporting the use of VE in patients with HBV-related chronic hepatitis were identified and examined. Based on the clinical results obtained in VE-treated chronic HBV carriers, we provide a reliable hypothesis for the possible role of this vitamin in the modulation of host miRNA profiles perturbed by this viral pathogen and in the regulation of some cellular miRNA with a suggested potential anti-HBV activity. This approach may contribute to the improvement of our understanding of pathogenetic mechanisms involved in HBV infection and increase the possibility of its management and treatment.

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