Hepatitis B Virus Reactivation Research Articles

Study of hepatitis B virus infection, reactivation among patients with chronic hepatitis C infection treated by direct antiviral agents (DAAs)

BackgroundHepatitis B virus (HBV) may reactivate when treating chronic hepatitis C (CHC) with direct-acting antivirals (DAA). We aimed to investigate the risk of HBV infection and reactivation during DAA therapy by performing a prospective observational study carried on 200 patients positive for chronic HCV who were candidates for treatment by DAA therapy according to the Egyptian guidelines from February 2019 to December 2019; the patients identified to carry HBsAg at baseline or with positive HBc Abs were further assessed for other HBV markers: hepatitis B e antigen at baseline, and serum HBV DNA quantitative measurement at baseline, week 4 of treatment, end of treatment. On the other hand, recent infection by HBV among those patients was observed.ResultsOf all participants, 49% were males and 51% were females, aged above 18 years. There is a highly statistically significant difference (p-value < 0.05) between HCV RNA PCR (at the beginning, at the end of 4 weeks, and at the end of 12 weeks) in studied patients. There was a highly statistically significant difference found between the liver function tests at the beginning, at the end of 4 weeks, and at the end of 12 weeks of treatment where it shows improvement except for serum albumin. At beginning of the study, there were 34 patients who are co-infected with HCV and HBV with quantitative PCR test for HBV DNA ≥ 20 IU/ml. After 1 month of DAA therapy, reactivation was detected in 6 cases (4 occult cases show reverse seroconversion (became HBs Ag positive), and 2 co-infected cases show increased HBV DNA > 1000 IU/L above the baseline level). In addition, 3 new cases acquired recent infection with the positivity of HBc IgM and detectable levels of HBV DNA. After 3 months of study, reactivation was detected in one patient with co-infection (where increased HBV DNA > 1000 IU/L above the baseline level), and 5 new cases acquired recent infection late in the study.ConclusionScreening for HBV infection prior to DAA therapy is required to detect recent infection of reactivation of previous infection during or after DAA therapy.

Determination of reactivation rate and risk factors for Hepatitis B virus reactivation in low-positive cases: A retrospective cohort study

IntroductionIn quantitative assays for hepatitis B virus (HBV) DNA, although the amplification reaction signal is detected for low-positive cases, quantification remains challenging. HBV reactivation has been reported in many studies, but only a few have focused on HBV low-positive cases. This study aimed to determine the reactivation rate and risk factors for HBV reactivation in low-positive cases. MethodsIn this retrospective cohort study, we analyzed 7498 patients who had their HBV DNA measured at Sapporo Medical University Hospital between April 2008 and November 2020. Patient selection criteria were defined as follows: hepatitis B surface antigen was negative; HBV DNA was detectable but not quantifiable at least once. HBV DNA was monitored according to the guidelines for HBV reactivation. ResultsIn total, 49,086 HBV DNA quantitative tests were performed. HBV DNA levels of 2578 tests were detectable but not quantifiable. Eighty patients met the criteria in this study. The median observation period was 497 days, and the 2-year reactivation rate was 15%. Ten patients had low HBV DNA positivity at baseline. Malignant lymphoma was observed in 15 patients; chemotherapy was used to treat other solid tumors in 35 patients, and immunosuppressive therapy was used in 30 patients. Multivariate analysis revealed that HBV DNA detected below the quantification level at baseline was an independent risk factor for HBV reactivation (adjusted hazard ratio 5.82; P = 0.010). ConclusionsPatients with low HBV DNA positivity, especially at baseline, are at high risk for HBV reactivation and therefore require closer monitoring.

Treatment or Prophylaxis against Hepatitis B Virus Infection in Patients with Rheumatic Disease Undergoing Immunosuppressive Therapy: An Update.

Chronic hepatitis B virus (HBV) flares or reactivations are serious causes of morbidity or mortality in rheumatologic patients undergoing immunosuppressive therapy. The recent insights in the pathogenesis of rheumatic diseases led to the use of new immunosuppressive therapies indicated in case of failure, partial response, or intolerance of conventional synthetic disease-modifying anti-rheumatic drugs. Based on these premises, this review examines and discusses the main rheumatologic treatments that could require the initiation of prophylactic treatment or close monitoring of occult HBV infection in patients beginning antiviral therapy at the first signs of HBV reactivation, or antiviral treatment in chronic HBV-infected patients. We searched for relevant studies published in the last five years. Studies suggested that the presence of HBV infection is common in rheumatic patients and HBV reactivation during these immunosuppressant treatments is quite frequent in these kinds of patients. Therefore, before starting an immunosuppressive therapy, patients should be screened for HBsAg, anti-HBs, and anti-HBc and, on the basis of markers positivity, they should be carefully characterized for HBV infection phases. In conclusion, screening of HBV infection in patients undergoing immunosuppressive therapy with subsequent HBV monitoring, prophylaxis or treatment consistently reduces the risk of clinical consequences.

Direct antiviral agents in hepatitis C virus related liver disease: Don't count the chickens before they're hatched.

Since molecules with direct-acting antiviral (DAA) became available, the landscape of the treatment of hepatitis C virus (HCV) infection has completely changed. The new drugs are extremely effective in eradicating infection, and treatment is very well tolerated with a duration of 8-12 wk. This review aims to report the outstanding clinical benefits of DAA and to highlight their critical disadvantages, identifying some clinically relevant hot topics. First, do the rates of virological response remain as high when patients with more advanced cirrhosis are considered? Large studies have shown slightly lower but still satisfactory rates of response in these patients. Nevertheless, modified schedules with an extended treatment duration and use of ribavirin may be necessary. Second, does the treatment of HCV infection affect the risk of occurrence and recurrence of liver cancer? Incidence is reduced after viral eradication but remains high enough to warrant periodic surveillance for an early diagnosis. In contrast, the risk of recurrence seems to be unaffected by viral clearance; however, DAA treatment improves survival because of the reduced risk of progression of liver disease. Third, can HCV treatment also have favorable effects on major comorbidities? HCV eradication is associated with a reduced incidence of diabetes, an improvement in glycemic control and a decreased risk of cardiovascular events; nevertheless, a risk of hypoglycemia during DAA treatment has been reported. Finally, is it safe to treat patients with HCV/ hepatitis B virus (HBV) coinfection? In this setting, HCV is usually the main driver of viral activity, while HBV replication is suppressed. Because various studies have described HBV reactivation after HCV clearance, a baseline evaluation for HBV coinfection and a specific follow-up is mandatory.

Outcome after kidney transplantation in hepatitis B surface antigen-positive patients

Few reports detail the actual outcome of Hepatitis B Surface Antigen-positive patients after kidney transplant. HBsAg-positive patients who underwent kidney transplant between January, 1999, and December, 2018, were reviewed retrospectively. Outcomes including hepatitis B reactivation rate, risk factors for reactivation, and patient and graft survival rates were analyzed. Seventy-seven patients were enrolled (47.1 ± 11.5 years old). Patients received ABO-incompatible (n = 5), crossmatch positive transplant (n = 2), and re-transplant (n = 4). Forty-six patients received prophylactic; 19, medication at least 3 months before the transplant; and 12, did not receive medication. Seventeen out of 76 patients developed reactivation post-transplant. 52.9% of HBV reactivation was accompanied by hepatitis. Inappropriate, other than lifelong prophylactic, antiviral agents (HR = 7.34, 95% CI 1.51–35.69, P = 0.01) and high hepatitis DNA (≥ 1000 IU/ml) pre-transplant (HR = 4.39, 95% CI 1.08–17.81, P = 0.04) increased reactivation risk. There was no significant difference in patient and graft survival between antigen positive patients who received antiviral agent and propensity score matched negative patients. HBsAg positivity in kidney transplant recipients is associated with substantial HBV reactivation rate. Lifelong antiviral therapy is mandatory, and patients with high preop HBV titer should be monitored closely for HBV reactivation.

The consensus on the prophylaxis and treatment of HBV reactivation in B or plasma cell-directed CAR-T cell therapy(2021)

The consensus on the prophylaxis and treatment of HBV reactivation in B or plasma cell-directed CAR-T cell therapy(2021)

Hepatitis B Seropositive Status in Recipients or Donors Is Not Related to Worse Outcomes after Haploidentical Hematopoietic Stem Cell Transplantation

Hepatitis B virus (HBV) has a high rate of chronic infection in Asian populations, and only limited studies have been performed to analyze the impact of HBV-seropositive haploidentical hematopoietic stem cell transplantation (haplo-HSCT) recipients and donors. The present study aimed to evaluate the effect on clinical outcomes in those patients. We conducted a retrospective study enrolling 237 consecutive patients undergoing first haplo-HSCT. The patients were classified into 3 groups: recipient HBV-positive group (R+D-; n=62), donor HBV-positive group (D+; n=83), and HBV-negative group (R-D-; n=92). Corresponding prophylactic antiviral treatment was given in the R+D- and D+ groups. The results were compared among the 3 groups using the Kruskal-Wallis test for continuous variables, Pearson's chi-square test for categorical variables, the competing-risk method to evaluate cumulative incidence, Kaplan-Meier curves to estimate overall survival (OS) and disease-free survival (DFS), and a Cox proportional hazard model to analyze multivariable influences. The 3-year cumulative HBV reactivation rate was 4.2%. The median time to HBV reactivation was 845 days (range, 545 to 1439 days) after haplo-HSCT. The R+D- group tended to have a higher cumulative incidence of HBV reactivation compared with the D+ group (11.8% versus 3.1%; P=.080). Significant differences in the causes of hepatic damage were observed among the 3 groups (P=.017), and all patients with acute hepatitis B after haplo-HSCT were from the R+D- group. Multivariate analysis showed that pretransplantation HBV status was associated with cytomegalovirus reactivation (R+D- versus R-D-: hazard ratio, 1.514; 95% confidence interval, 1.060 to 2.163; P=.023). The 3-year OS and DFS, 3-year cumulative incidence of nonrelapse mortality (NRM), rates of relapse and graft-versus-host disease (GVHD), and causes of death were comparable among the 3 groups. Pretransplantation HBV serostatus had no significant effect on OS, DFS, NRM, relapse, or GVHD in the multivariate analysis. Based on our data, seropositivity for hepatitis B surface antigen (HbsAg) or core antibody (HBcAb) in donors or recipients before transplantation did not negatively affect the overall outcome after haplo-HSCT under the premise of proper antiviral prophylaxis along with regular post-transplantation surveillance, and HBV seropositivity should not be considered a contraindication to haplo-HSCT.

HBsAg Loss Due to Tenofovir Treatment for HBV Reactivation Following DAAs Therapy in One Patient with HBV-HCV Coinfection

Abstract Hepatitis B virus (HBV) reactivation induced by administration of direct-acting antiviral agents (DAAs) to treat hepatitis C virus (HCV) infection has been reported in previous studies, the subsequent clinical outcomes varied from no symptom to liver failure or death, however, the timing of anti-HBV treatment is controversial. We report the clinical HBV reactivation in a 51 years old female fibrotic patient with chronic HBV-HCV infection during the paritaprevir/ritonavir/ombitasvir and dasabuvir (PrOD) therapy. Her baseline HCV RNA, HBV DNA, alanine aminotransferase (ALT), and liver stiffness measurement levels were 5,560,000 IU/mL, &lt;15 IU/mL, 48 U/L, and 11.8 kPa, respectively. At 8 weeks of PrOD treatment, her HCV RNA, HBV DNA, and ALT levels were &lt;15 IU/mL, 2,880,000 IU/mL, and 837 U/L, respectively, and clinical reactivation was diagnosed. Meanwhile, tenofovir was immediately used for anti-HBV treatment. Fortunately, HBV DNA and ALT were undetectable and normalized after 16 weeks of anti-HBV therapy, and unexpectedly, hepatitis B surface antigen loss occurred at 80 weeks of anti-HBV treatment. This study may extend our understanding of the timing of anti-HBV therapy to prevent potential HBV reactivation during DAAs treatment in HBV-HCV coinfected patients, and proper initiation timing may lead to functional cure of chronic HBV infection.

P322 Hepatitis B reactivation under biologic therapy in patients with HBsAg negative phase of chronic HBV infection

Abstract Background Biologic agents are widely used in immune mediated inflammatory diseases (IMID). The risk and consequences of hepatitis B reactivation in hepatitis B surface antigen (HBsAg) negative phase of hepatitis B virus (HBV) exposed patients is not clear. We aim to investigate the reactivation rate in biologic exposed patients within surface antigen negative phase of HBV infection. Methods We identified patients followed up at gastroenterology, rheumatology and dermatology out-patient clinics with a diagnosis of IMID from clinical charts. Patients exposed to biologic agents with a negative HBsAg and positive Anti-HBc IgG were included. Primary outcome was HBV reactivation, which was defined as reverse seroconversion of HBsAg. Results We screened 8266 IMID patients and 2484 of them were exposed to biologic agents. A total of 221 patients were included in the study. The mean age was 54.08 ± 11.69 years and 115 (52.0%) patients were female. The median number of different biologic subtype use was 1 (range: 1 – 6). The mean biologic agent exposure time was 55 (range: 2 – 179) months. One hundred and fifty-two (68.8%) patients were using concomitant immunomodulatory agents and 84 (38.0%) patients were exposed to corticosteroids during biologic use. No hepatitis B reactivation with a reverse seroconversion of HBsAg positivity was observed in the whole cohort. Antiviral prophylaxis for hepatitis B was given to 48 (21.7%) patients with entecavir, tenofovir or lamivudine. HBV-DNA was screened in 56 (25.3%) patients prior to the biologic exposure. Two patients had HBV-DNA reactivation with a negative HBsAg during exposure to the biologic agent. Conclusion Though only 21.7% of our patients used prophylaxis, we found only two reactivations (1%) and no HBsAg seroconversion in our cohort. Our results suggest a re-assessment of antiviral prophylaxis for anti-HBc Ag (+) patients exposed to biologic agents. Current guidelines would be updated in the light of future studies.

P358 An observational, prospective cohort study to evaluate the long term safety and effectiveness of intravenous CT-P13 (biosimilar of infliximab) in patients with Crohn’s Disease or Ulcerative Colitis

Abstract Background CT-P13 is the world’s first approved biosimilar infliximab for all indications of the reference infliximab. The purpose of this study was to assess long term safety and effectiveness of CT-P13 intravenous (IV) in patients with Crohn’s Disease (CD) and Ulcerative Colitis (UC). We now present the result of safety and effectiveness of CT-P13 in patient with CD, UC for up to 5 years from this longitudinal, observational, prospective cohort Phase IV study. Methods The study was conducted from 17 April 2014 to 28 February 2020 in 22 and 21 study centres, in Korea and European Union, respectively. Patients were administered 5 mg/kg of CT-P13 by IV at weeks 0, 2 and 6 and every 8 weeks thereafter. The primary objective was to evaluate adverse events of special interest (AESI) including HBV reactivation, congestive heart failure, opportunistic infections, serious infection including sepsis, tuberculosis, serum sickness (delayed hypersensitivity reactions), hematologic reactions, systemic lupus erythematosus/lupus like syndrome, demyelinating disorders, lymphoma, hepatobiliary events, hepatosplenic T cell lymphoma (HSTCL), intestinal or perianal abscess (in CD), serious infusion reactions during a re-induction regimen following disease flare, sarcoidosis/sarcoid-like reactions, paediatric malignancy, leukaemia, malignancy, colon carcinoma, dysplasia (in UC), skin cancer, pregnancy exposure and bowel stenosis, stricture and obstruction (in CD). Results A total of 470 patients with inflammatory bowel disease (IBD) were analysed. Overall 352 (74.9%) patients have been continuously treated for more than 1 year and the mean duration of drug exposure was 26.3 months. The safety profile of CT-P13 and switching from the reference infliximab to CT-P13 was well-tolerated. A total of 329 (70.0%) patients experienced at least one treatment-emergent adverse event (TEAE). Adverse events of special interest of CT-P13 were analysed by safety analysis set (Table 1). Immunogenicity testing was optional and 72 (15.3%) patients had at least one ADA positive after first infusion of study drug. The incidence of TEAEs in ADA positive subset (83.3%) were slightly higher compared to the incidence of TEAEs in ADA negative subset (76.6%). The effectiveness results of clinical remission for each indication was generally well maintained after the study drug administration (Table 2). Conclusion The results show that CT-P13 was well-tolerated and efficacious in IBD patients. There was no new safety and effectiveness findings in patients who have been exposed to CT-P13 or patients who have switched treatment from the reference infliximab to CT-P13.

Entecavir Monotherapy Prevents Hepatitis B Virus Recurrence After Liver Transplant for Chronic Hepatitis B Patients: A Long-Term Retrospective Study

Limited data are available on the use of oral antiviral therapy, particularly the long-term use of entecavir monotherapy in patients with hepatitis B virus (HBV)-related diseases after liver transplant (LT). The clinical data on consecutive patients who underwent LT for HBV-related diseases from 2011 to 2019 were prospectively collected and retrospectively analyzed. All patients received entecavir monotherapy alone during the follow-up period; viral serology/load and liver biochemical tests were performed regularly. Among the total of 89 patients were patients with decompensated cirrhosis (n=27 [30%]), acute-on-chronic HBV (n=21 [24%]), and hepatocellular carcinoma (HCC) (n=41 [46%]). The median age of the patients was 50 years (range, 42-58 years), and the median follow-up was 37 months (range, 1-96 months). Before LT, 45 (51%) patients did not receive, whereas 44 (49%) were currently receiving, oral antiviral therapy. At the time of LT, serum level of HBV DNA of 34 (38%) patients was >20 IU/mL, with the median level being 270,000 IU/mL (range, 4270-2,020,000), and 53 patients (59%) had undetectable levels of HBV DNA (≤20 IU/mL). The cumulative rate of hepatitis B surface antigen loss was 79.8%, 100%, and 100% after 1 month, 1 year, and 5 years, respectively. Hepatitis B surface antigen positivity returned after seroclearance in 1 patient, who died of HCC recurrence with an undetectable level of HBV DNA. The overall survival rates at 1, 3, and 5 years after LT were 94.51%, 86.84%, and 85.27%, respectively. During the follow-up period, no entecavir adverse reactions or dose reductions were observed. Long-term entecavir monotherapy was highly effective in preventing HBV reactivation and HBV-related diseases.

Risk of hepatitis B virus reactivation in patients with autoimmune diseases undergoing non-tumor necrosis factor-targeted biologics.

Hepatitis B virus reactivation (HBVr) can occur in patients treated with immunosuppressive medications. Risk stratification for HBVr based on hepatitis B virus (HBV) serology and viral load is an important strategy to determine appropriate HBV monitoring and antiviral prophylaxis use. Recent advances in the understanding of pathophysiology of autoimmune diseases have led the development of cytokine-targeted therapies. Tumor necrosis factor (TNF)-α inhibitors have been widely used for patients with inflammatory bowel disease, psoriasis, and rheumatic diseases. Further, the clinical benefits of interleukin (IL)-12/23, IL-17, or Janus kinases inhibitors have been demonstrated in these patients. It is well known that TNF-α inhibitor use can lead to HBVr, however, the risk of HBVr in patients undergoing non-TNF-targeted biologics have not been fully understood. In this review, we discuss the risk of HBVr in patients treated with non-TNF-targeted biologics, and immunological mechanisms of these medications causing HBVr.

Reactivation of Resolved Hepatitis B After Daratumumab for Multiple Myeloma

The risk of reactivation of resolved HBV in HBsAg-negative multiple myeloma patients after daratumumab has not been reported. Among 93 patients with daratumumab treatment, reactivation occurred in 6 patients (6.5%) with one hepatic failure. This is the first report demonstrating a considerable risk of reactivation of resolved HBV after daratumumab.

Risk factors for losing hepatitis B virus surface antibody in patients with HBV surface antigen negative/surface antibody positive serostatus receiving biologic disease-modifying anti-rheumatic drugs: a nested case-control study

BackgroundHepatitis B virus (HBV) reactivation consequent to immunosuppressive therapy is an increasingly prevalent problem with serious clinical implications. Treatment with biologic agents conduces to the loss of protective antibody to HBV surface antigen (anti-HBs), which significantly increases the risk of HBV reactivation. Hence, we investigated the risk factors for losing anti-HBs in patients with rheumatic diseases and HBV surface antigen negative/anti-HBs positive (HBsAg−/anti-HBs+) serostatus during treatment with biologic disease-modifying anti-rheumatic drugs (DMARDs).MethodsUsing a nested case-control design, we prospectively enrolled patients with rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis/psoriasis, or juvenile idiopathic arthritis, who were treated with biologic DMARDs at Changhua Christian Hospital, Taiwan, from January 2013 to June 2019 and had HBsAg−/anti-HBs+ serostatus; the analytic sample excluded all patients with HBsAg+ or anti-HBs− serostatus. Anti-HBs titers were monitored 6-monthly and cases were defined as anti-HBs < 10 mIU/ml during follow-up. Cases were matched one-to-all with controls with anti-HBs ≥ 10 mIU/ml on the same ascertainment date and equivalent durations of biologic DMARDs treatment (control patients could be resampled and could also become cases during follow-up). Between-group characteristics were compared and risk factors for anti-HBs loss were investigated by conditional logistic regression analyses.ResultsAmong 294 eligible patients, 23 cases were matched with 311 controls. The incidence of anti-HBs loss was ~ 2.7%/person-year during biologic DMARDs treatment. Besides lower baseline anti-HBs titer (risk ratio 0.93, 95% CI 0.89–0.97), cases were significantly more likely than controls to have diabetes mellitus (risk ratio 4.76, 95% CI 1.48–15.30) and chronic kidney disease (risk ratio 14.00, 95% CI 2.22–88.23) in univariate analysis. Risk factors remaining significantly associated with anti-HBs loss in multivariate analysis were lower baseline anti-HBs titer (adjusted risk ratio 0.93, 95% CI 0.88–0.97) and chronic kidney disease (adjusted risk ratio 45.68, 95% CI 2.39–871.5).ConclusionsBesides lower baseline anti-HBs titer, chronic kidney disease also strongly predicts future anti-HBs negativity in patients with HBsAg−/anti-HBs+ serostatus who receive biologic DMARDs to treat rheumatic diseases. Patients with low anti-HBs titer (≤ 100 mIU/ml) and/or chronic kidney disease should be monitored during biologic DMARDs therapy, to enable timely prophylaxis to preempt potential HBV reactivation.

Management of Hepatitis B Virus Reactivation in Malignant Lymphoma Prior to Immunosuppressive Treatment

Hepatitis B reactivation is a common complication in lymphoma patients under immunosuppressive treatment with potentially serious and life-threating consequences. In this review, we discuss the basis of chronic Hepatitis B virus (HBV) infection, the definition and risk factors for HBV reactivation. We overview the management of HBV reactivation based on virological status and immunosuppressive regimen risk stratification. We also highlight and update information about the HBV reactivation in lymphoma patients under novel agent treatment, including newer monoclonal antibodies, small molecule inhibitors, and even chimeric antigen receptor T-cell immunotherapy.

POS-768 Hepatitis B reactivation in kidney transplant recipients treated with belatacept

Hepatitis B virus (HBV) reactivation in kidney transplant recipients is a serious and understudied complication which seems to occur in 3 to 6% of HBs antigen (HBsAg)-negative patients. No data exists regarding HBV reactivation in patients receiving belatacept, an alternative to calcineurin inhibitors in renal transplantation but with which viral infections seem more frequent.

Safety and efficacy of anti-PD-1 inhibitors in Chinese patients with advanced lung cancer and hepatitis B virus infection: a retrospective single-center study.

BackgroundProgrammed death protein (ligand) 1 [PD-(L)1] inhibitors have provided new therapeutic options for advanced lung cancer. However, patients with hepatitis B virus (HBV) infection have been traditionally excluded from most registered trials of this form of treatment.MethodsWe performed a retrospective analysis of patients with HBV and advanced lung cancer who received anti-PD-1 immunotherapy from September 2018 to May 2020 in our department. Treatment-related hepatotoxicity was evaluated and recorded. Overall response rate and progression free survival were also assessed in the patients using iRECIST.ResultsSeventeen patients were evaluated in this analysis. Of these, six (35.3%) experienced hepatic transaminase elevation during immunotherapy. Three of these patients developed Grade 3 hepatic immune-related adverse events and received systemic corticosteroids, following which aminotransferase levels recovered to normal in all patients and no adverse events were observed in subsequent treatment. No patient experienced HBV reactivation or flare. One patient developed active pulmonary tuberculosis (TB). Other adverse events were mild, well tolerated and short term. The objective response rate (ORR) of the cohort was 62.5%, and the median progression-free survival (PFS) was 3 months.ConclusionsLung cancer patients can be treated safely with anti-PD-1 inhibitors in the context of HBV infection. Close monitoring for hepatotoxicity and prophylactic antiviral therapy is advised. Further studies on the use of anti-PD-1 inhibitors in HBV-infected patients are needed.

Progress in the research of HBV reactivation in patients undergoing hematopoietic stem cell transplantation

Progress in the research of HBV reactivation in patients undergoing hematopoietic stem cell transplantation

Real-World Experience of Telbivudine and Lamivudine as Antiviral Prophylaxis for Chemotherapy-Related Hepatitis B Reactivation

Background: There is currently no data regarding the efficacy of prophylactic telbivudine in hepatitis B patients undergoing chemotherapy. This study aims to describe the results of preemptive telbivudine and lamivudine to prevent chemotherapy-related HBV reactivation.Methods: The medical records of all patients with HBsAg positive or HBs-Ag negative, anti-HBc positive, who were referred to the hepatology clinic between May 2014 and December 2016, were retrospectively reviewed. As this is a descriptive study, no statistical analysis was done.Results: A total of 52 patients with prophylactic telbivudine or lamivudine therapy were included, with 26 patients in each group. Rituximab-based treatment was given in nine and five patients in the telbivudine and lamivudine group, respectively. The number of patients who completed antiviral treatment up to six months after chemotherapy was 17 patients in each group. There was less incidence of HBV reactivation in the telbivudine group (2 of 17 patients, 11.8%) than in the lamivudine group (7 of 17 patients, 41.2%). Delayed reactivation was noticed in 1 of 2 patients in the telbivudine group and 3 of 7 patients in the lamivudine group. The median log10[HBV DNA] at reactivation was 4.52 (1.70 – 8.35) IU/mL. Severe hepatitis was observed in two patients in the lamivudine group and one patient in the telbivudine group. Of 34 patients who completed antiviral treatment, two patients died due to primary cancer. No interruption of chemotherapy or mortality due to hepatitis was noticed in both groups.Conclusions: Preemptive telbivudine or lamivudine in HBsAg positive or HBsAg negative, anti-HBc positive patients seems to be a good treatment option.

Prophylactic Antiviral Therapy in Low-Risk Patients infected with the Hepatitis B Virus with Solid Tumors

IntroductionThis study aimed to evaluate the prophylactic antiviral therapy in low-risk patients with the Hepatitis B Virus (HBV) infections during chemotherapy.Material and methodsFrom January 2011 to March 2018, HBsAg-positive patients were analyzed in this retrospective study. The HBV reactivation, related hepatitis, chemotherapy delay, and fulminant hepatic failure in low-risk patients between the prophylactic anti-HBV therapy (prophylaxis group) and the non-prophylactic anti-HBV therapy group (control group) were compared.ResultsThere were 68 patients in the prophylaxis group and 102 patients in the control group. The rusult showed that the HBV reactivation was not significantly different between the prophylaxis group and the control group (P=0.741). Three and 5 patients with HBV-related hepatitis were detected in the prophylaxis and control groups, respectively. Moreover, 2 and 4 patients with HBV activation-related chemotherapy delay were detected in the two groups, respectively, without any significant difference (P&gt;0.05). Multivariate analysis showed that HBV DNA titer was associated with HBV reactivation in low-risk patients (P=0.001).ConclusionsProphylactic antiviral therapy might not reduce the HBV reactivation of low-risk solid malignancies (non-HCC, non-hematological lymphatic cancer, and HBV DNA titer &lt;100 IU/ml). For low-risk patients, monitoring the HBV DNA titers and liver function tests in the follow-up observations might be an optimal and cost-effective strategy.