Reappearance Of Hepatitis B Surface Antigen Research Articles

Post-transplant hepatitis B virus reactivation impacts the prognosis of patients with hepatitis B-related hepatocellular carcinoma: a dual-centre retrospective cohort study in China.

Highly active hepatitis B virus (HBV) is known to be associated with poor outcomes in patients with hepatocellular carcinoma (HCC). This study aims to investigate the relationship between HBV status and HCC recurrence after liver transplantation. The study retrospectively analyzed HCC patients undergoing liver transplantation in two centres between January 2015 and December 2020. The authors reviewed post-transplant HBV status and its association with outcomes. The prognosis of recipients with hepatitis B surface antigen (HBsAg) reappearance ( n =58) was poorer than those with HBsAg persistent negative ( n =351) and positive ( n =53). In HBsAg persistent positive group, recipients with HBV DNA reappearance or greater than 10-fold increase above baseline had worse outcomes than those without ( P <0.01). HBV reactivation was defined as (a) HBsAg reappearance or (b) HBV DNA reappearance or greater than 10-fold increase above baseline. After propensity score matching, the 5-year overall survival rate and recurrence-free survival rate after liver transplantation in recipients with HBV reactivation were significantly lower than those without (32.0% vs. 62.3%; P <0.01, and 16.4% vs. 63.1%; P <0.01, respectively). Moreover, HBV reactivation was significantly related to post-transplant HCC recurrence, especially lung metastasis. Cox regression analysis revealed that beyond Milan criteria, microvascular invasion and HBsAg-positive graft were independent risk factors for post-transplant HBV reactivation, and a novel nomogram was established accordingly with a good predictive efficacy (area under the time-dependent receiver operating characteristic curve=0.78, C-index =0.73). Recipients with HBV reactivation had worse outcomes and higher tumour recurrence rates than those without. The nomogram could be used to evaluate the risk of post-transplant HBV reactivation effectively.

Does hepatic steatosis impact chronic hepatitis B?

Does hepatic steatosis impact chronic hepatitis B?

Low but Long-lasting Risk of Reversal of Seroconversion in Patients With Rheumatoid Arthritis Receiving Immunosuppressive Therapy

In patients who have resolved hepatitis B virus (HBV) infection, treatment of rheumatoid arthritis (RA) can result in reappearance of hepatitis B surface antigen (HBsAg), called reverse seroconversion. We investigated clinical features and outcomes of reverse seroconversion in patients who received immunosuppressant or biologic therapy for RA. We identified 1494 patients with RA (925 who resolved HBV infection) and available data on levels of antibody to HB core antigen and HBsAg who had attended Taipei Veterans General Hospital from January 2007 through December 2017. We identified 17 cases (median age, 66 years) who were negative for HBsAg before treatment of RA and reverse seroconversion (HBsAg reappearance) after glucocorticoid treatment (n = 13) and/or biologic therapy (adalimumab, n= 2; etanercept, n = 1; rituximab, n = 9; or abatacept, n = 4). Four patients were positive for antibodies against HBsAg (seroconverted) before the immunosuppressive treatment. The median time from immunosuppressive treatment to reverse seroconversion was 120 months (range, 20-264 months), whereas the time from biologic therapy treatment to reverse seroconversion was 66 months (range, 10-105 months). After reverse seroconversion, 8 individuals (47.1%) were positive for HB e antigen; 9 cases (52.9%) did not have a flare of alanine transaminase. However, 3 patients (17.6%) developed liver decompensation. In patients who resolved HBV infection and received immunosuppressant treatment of RA, risk of reversal of seroconversion is low but persists for up to 10 years. Patients with RA who previously resolved HBV infections should be monitored for levels of HBsAg and HBV DNA once immunosuppressive treatment of RA begins.

Hepatitis B surface antigen loss after discontinuing nucleos(t)ide analogue for treatment of chronic hepatitis B patients is persistent in White patients.

The objective of this study was to determine the long-term clinical outcome and persistence of hepatitis B surface antigen (HBsAg) loss after discontinuation of treatment. The prognosis of patients with chronic hepatitis B (CHB) treated with nucleos(t)ide analogues (NAs) who discontinue treatment after loss of HBsAg remains largely unknown, particularly in White patients. We analysed a cohort of patients with CHB who discontinued NA treatment after loss of HBsAg. A total of 69 patients with hepatitis-B-e antigen-positive or hepatitis-B-e antigen-negative CHB with undetectable HBsAg during NA treatment were included after discontinuation of treatment, and followed up for a median period of 37.8 months (interquartile range: 23.8-54.6 months). At the end of follow-up, none of the patients showed spontaneous reappearance of HBsAg and only one patient had detectable hepatitis B virus DNA (22 IU/ml). Another patient negative for HBsAg and anti-HBs developed hepatitis B virus reactivation without elevated transaminases after treatment with corticosteroids and vincristine for dendritic cell neoplasm, 38 months after withdrawal of the antiviral treatment. Regarding clinical outcome, a patient with cirrhosis developed hepatocellular carcinoma, 6.6 years after discontinuing treatment. None of the patients had hepatic decompensation or underwent liver transplantation. HBsAg clearance after discontinuing NAs in patients with CHB is persistent and associated with good prognosis. The risk for developing hepatocellular carcinoma persists among patients with cirrhosis.

Risk factors and outcomes of hepatitis B virus reactivation in hepatitis B surface antigen negative patients with hematological malignancies.

Current guidelines recommend all patients scheduled to receive chemotherapy should be screened for hepatitis B surface antigen (HBsAg) and antibodies to hepatitis B virus core antigen (anti-HBc) status. However, still, more research is needed to identify the risk factors for hepatitis B virus (HBV) reactivation. We retrospectively investigated the incidence, risk factors and outcome of HBV reactivation in HBsAg negative patients with hematological malignancies. Seven hundred and thirty-eight HBsAg negative patients with hematological malignancies were included in the study. HBV reactivation was defined as reverse seroconversion of HBsAg (HBsAg reappearance). Risk factors, cumulative incidence and overall survival of HBV reactivation were analyzed. Reactivation occurred in 23 of the 738 (3.1%) enrolled patients. As expected, the reactivation rate of the anti-HBc positive group was significantly higher than that of the anti-HBc negative group (5.4% vs 0.8%). Multivariate analysis indicated that loss of antibody to the hepatitis B surface antigen (anti-HBs) was an independent risk factor. Patients with acute lymphoblastic leukemia and multiple myeloma showed significantly higher reactivation rate than those with other diseases. The cumulative incidence of HBV reactivation after starting chemotherapy in the anti-HBc positive subgroup was 0.3% at 1year, 1.7% at 2years and 10.5% at 3years. Close monitoring of HBV markers, including anti-HBs, should be performed for longer than 24months. Further study is needed to establish a strategy to prevent HBV reactivation after chemotherapy in HBsAg negative patients with hematological malignancies.

Antiviral Combination Therapy With Low-Dose Hepatitis B Immunoglobulin for the Prevention of Hepatitis B Virus Recurrence in Liver Transplant Recipients: A Single-Center Experience

ObjectivesThis study presents the overall long-term hepatitis B virus (HBV) recurrence rate with possible associated factors after hepatitis B immunoglobulin (HBIG) was given in combination with 4 different antiviral (lamivudine, adefovir, entecavir, and tenofovir) drugs. Patients and MethodsBetween September 2000 and October 2013, the medical records of 42 adult patients who underwent liver transplantation at the Cukurova University Medical Hospital for chronic liver failure or hepatocellular carcinoma (HCC) secondary to chronic HBV were reviewed retrospectively. The analyses of risk factors for recurrence were performed based on the efficacy of hepatitis B envelope antigen (HBeAg), hepatitis B core antibody (anti-HBc), HBV DNA, preoperative prophylaxis, and the presence of HCC. Posttransplantation HBV recurrence was defined as persistence of hepatitis B surface antigen (HBsAg) positivity after orthotopic liver transplantation, or the reappearance of HBsAg and HBV DNA after initial HBsAg undetectability despite prophylaxis. ResultsThe mean follow-up of 28 patients having HBIG and lamivudine prophylaxis was 73.25 ± 37.5 months with a recurrence rate of 3.5%. The mean follow-up of 2 patients having HBIG and adefovir prophylaxis was 90 ± 46.6 months with a 50% recurrence rate. The mean follow-up of each 6 patients who received prophylaxis with entecavir and tenofovir groups were 27.5 ± 16.1 and 16.17 ± 5.3 respectively, with no posttransplantation recurrence for both groups. On univariate analysis, preoperative factors such as anti-HBc, HBV DNA, preoperative prophylaxis, and the presence of HCC did not show any correlation with recurrence. However, HBeAg showed statistical significance for recurrence. ConclusionsLow-dose HBIG in combination with antiviral agents (lamivudine, entecavir, and tenofovir) is efficacious in preventing recurrence of HBV in posttransplantation patients.

Long‐term outcome in Caucasian patients with chronic hepatitis B virus infection after HBsAg seroclearance

The natural course after hepatitis B surface antigen (HBsAg) seroclearance in Caucasian patients with chronic hepatitis B virus (HBV) infection is not well-defined. To investigate the clinical characteristics and outcome in a series of European Caucasian patients with chronic HBV infection according to HBsAg response over time. A total of 612 patients with compensated chronic HBV infection and without other cause of liver disease were prospectively followed up. Seventy-eight subjects cleared HBsAg and 534 remained HBsAg-positive. Clinical and virological examinations were periodically performed and development of cirrhosis and liver-related complications was monitored during a mean follow-up time of 9.9 years. After HBsAg seroclearance, serum HBV DNA was undetectable in 38 patients in whom it was tested and HBsAg reappearance was observed in two subjects (2.6%). At 15 years of follow-up, the cumulative probability of developing a liver-related complication was 11.6% in HBsAg-positive patients and 1.8% in those with HBsAg loss (P = 0.03), although this benefit was limited to patients with cirrhosis (P < 0.001) and to those who received therapy (P < 0.01). Among patients without cirrhosis and among those who did not receive therapy, the probability was not different between those who cleared the HBsAg and those who did not (P = 0.3 and P = 0.5 respectively). Hepatitis B surface antigen loss confers a significant clinical benefit in Caucasian subjects with HBV-related cirrhosis and in those with chronic HBV infection who receive antiviral therapy. However, HBsAg reappearance can be observed in selected cases.

Entecavir and hepatitis B immune globulin in patients undergoing liver transplantation for chronic hepatitis B

For patients undergoing liver transplantation (LT) for hepatitis B virus (HBV)–related liver disease, the current standard of care for preventing reinfection of the allograft is nucleoside analogue therapy combined with hepatitis B immune globulin (HBIG). Entecavir has demonstrated high efficacy and a favorable safety profile for chronic hepatitis B (CHB) treatment, but data for patients undergoing HBV-related LT are limited. This study assessed the safety and efficacy of entecavir combined with various HBIG regimens after CHB-related LT. In this phase 3b, single-arm, open-label study, 65 patients undergoing LT for CHB-related liver disease with an HBV DNA load <172 IU/mL at LT received entecavir (1.0 mg daily) for 72 weeks after LT. The primary endpoint was the proportion of evaluable patients (treated for ≥4 weeks) with virological recurrence (HBV DNA level ≥50 IU/mL) through week 72. Concomitant HBIG therapy was received by 64 of the 65 enrolled patients, and 44% of these patients received high-dose HBIG (any HBIG dose in the specified interval ≥10,000 IU). Through week 72, all 61 patients evaluable for the efficacy analysis had undetectable HBV DNA. The Kaplan-Meier estimate of patients without hepatitis B surface antigen (HBsAg) recurrence at week 72 was 0.9655. Two patients experienced a reappearance of HBsAg, but both remained HBV DNA− until the last follow-up. The frequency and nature of adverse events were consistent with those expected for this patient population. Serum creatinine increments ≥0.3 mg/dL and ≥0.5 mg/dL occurred in 62% and 39% of the patients, respectively, and all of these patients received calcineurin inhibitor therapy. In conclusion, in this population of patients treated with entecavir after CHB-related LT, entecavir was well tolerated and effective in maintaining viral suppression, even in individuals who experienced a reappearance of HBsAg. Liver Transpl 19:887–895, 2013. © 2013 AASLD.

Viral Hepatitis in Liver Transplantation

Liver transplantation is the only alternative for patients with end-stage liver disease. Viral hepatitis B and C are among the most common causes of cirrhosis and hepatocellular carcinoma and a frequent indication for liver transplantation. Hepatitis B virus immunoglobulin and nucleot(s)ide analogues have facilitated the management of patients with hepatitis B who have received liver transplants and resulted in excellent long-term outcomes. On the contrary, recurrence of hepatitis C is the main cause of graft loss in most transplant programs. Current therapeutic approaches are far from optimal, because sustained virologic responses are only achieved in one-third of treated patients, and adverse effects are common and severe. However, the rapid development of direct-acting antivirals against hepatitis C virus will change the management of this disease and in a few years prevent graft infection with this virus.

Covering the Cover

Covering the Cover

Entecavir Monotherapy Is Effective in Suppressing Hepatitis B Virus After Liver Transplantation

We investigated the efficacy of entecavir, a cyclopentyl guanosine nucleoside analogue, as monoprophylaxis in patients with chronic hepatitis B who received a liver transplant. We studied data from 80 consecutive patients who received a liver transplant (47 from living donors and 33 from deceased donors) for hepatitis B-related disease and entecavir monotherapy as prophylaxis. None of the patients received hepatitis B immunoglobulin. Indications for transplant included decompensation from cirrhosis (27.5%), acute-on-chronic hepatitis B (47.5%), and hepatocellular carcinoma (25%). The median follow-up time was 26 months (range, 5-40 months). Before transplant, 33 patients were not on antiviral therapy and 47 were on oral therapy (18 had received less than 3 months of treatment). At the time of transplant, the median log HBV DNA level was 3.5 copies/mL (range, 1.54-8.81); 21 patients (26%) had undetectable levels of HBV DNA. The cumulative rate of hepatitis B surface antigen (HBsAg) loss was 86% and 91% after 1 and 2 years, respectively. Ten patients had reappearance of HBsAg. Eighteen patients (22.5%) were HBsAg positive at the time of their last examination; 17 of these had undetectable levels of HBV DNA, and the remaining patient had a low level of HBV DNA (217 copies/mL). There was no evidence of mutations at sites that confer resistance to entecavir among patients who were HBsAg positive. Although only 26% of patients had complete viral suppression at the time of transplant, 91% lost HBsAg, with 98.8% achieving undetectable levels of HBV DNA. A hepatitis B immunoglobulin-free regimen of entecavir monotherapy is effective after liver transplantation for chronic hepatitis B.

Prevention of recurrent hepatitis B virus infection after liver transplantation: hepatitis B immunoglobulin, antiviral drugs, or both? Systematic review and meta-analysis

To evaluate antiviral prophylaxis against hepatitis B virus (HBV) following liver transplantation. Systematic review and meta-analysis. Clinical trials and comparative cohort studies comparing the use of hepatitis B immunoglobulin (HBIg), antivirals, or both following liver transplantation for HBV infection were included. The primary outcome was reappearance of hepatitis B surface antigen (HBsAg). Other outcomes included all-cause and HBV-related mortality, HB-related active liver disease, and reappearance of HBV DNA after transplantation. Relative risks (RR) with 95% confidence intervals (CIs) are reported. Twenty studies (22 comparisons) were included. Ten studies compared HBIg to combination treatment, 9 compared antivirals to combination treatment, and 3 compared lamivudine (LAM) to HBIg. Combination treatment reduced HBsAg reappearance (RR 0.28; 95% CI 0.12-0.66), and was superior to HBIg alone in all other outcome measures. Combination treatment was significantly better than antivirals in preventing reappearance of HBsAg (RR 0.31; 95% CI 0.22-0.44), even when low-dose HBIg was given. No significant difference was found between HBIg and LAM monotherapy for all measured outcomes. Major limitations with regard to comparability of the study groups in non-randomized trials were revealed. Combination treatment with HBIg and LAM reduced HBV recurrence following liver transplantation, compared with HBIg or LAM alone, and reduced mortality compared with HBIg alone.

Hepatitis B Virus Reactivation After 23 Months of Rituximab-based Chemotherapy in an HBsAg-negative, Anti-HBs-positive Patient With Follicular Lymphoma

A 72-year-old female negative for hepatitis B surface antigen (HBsAg) and positive for antibody to hepatitis B surface antigen (anti-HBs) was diagnosed to have follicular lymphoma in 2006. Seventeen cycles of rituximab-based chemotherapy were administered over 23 months. Twelve days after the last cycle of chemotherapy, serum aminotransferase levels were elevated, and hepatitis serology tests revealed reappearance of HBsAg and hepatitis B e antigen (HBeAg), loss of anti-HBs, and positivity for hepatitis B virus (HBV) DNA. Antiviral treatment with entecavir was administered immediately, and the hepatitis flare was controlled. Rituximab-based chemotherapy can induce HBV reactivation even in HBsAg-negative, anti-HBs-positive patients. Early recognition and prompt antiviral treatment is crucial for patients with HBV reactivation during anticancer therapy.

Risk of Hepatitis B Virus (HBV) Reactivation and Efficacy of Antiviral Preemptive Therapy in Malignant Lymphoma Patients Who Have Resolved HBV.

Abstract 2918Poster Board II-894 INTRODUCTION:Reactivation of hepatitis B virus (HBV) is a well-described complication for hepatitis B surface antigen (HBsAg) positive patients undergoing systemic chemotherapy or immunosuppressive therapy. Recently, especially under use of rituximab, HBV reactivation has been increasingly reported in patients who have resolved HBV (HBsAg negative and hepatitis B core antibody [HBcAb] positive and/or hepatitis B surface antibody [HBsAb] positive). However the risk of HBV reactivation in malignant lymphoma patients with past HBV infection has not been well studied. PATIENTS AND METHODS:Eight hundred and forty-eight (848) patients were newly diagnosed with malignant lymphoma at Kurashiki Central Hospital from January 2001 to December 2008. We analyzed patients who received both HBsAg and HBcAb test; who underwent systemic chemotherapy; who were alive for >100 days after treatment; who were not administered antiviral prophylaxis for HBV. A total of 582 patients fulfilled these criteria, HBsAg detected in 10 patients (1.7%) and 175 (30.1%) were HBcAb positive only. Of these 175patients, 72 had HBV DNA test prior to systemic chemotherapy, no patients showed a detectable level of HBV serum DNA. Serial monthly HBV DNA monitoring was performed in 46 patients. HBV reactivation was defined as the reappearance of HBsAg or HBV DNA. RESULTS;Of the 175 HBsAg-negative/HBcAb-positive patients (Diffuse large B cell lymphoma [DLBCL]; 91, Follicular lymphoma [FL]; 29, Mantle cell lymphoma [MCL]; 8, Maltoma [MALT]; 6, Hodgkin lymphoma [HL]; 6, Adult T cell leukemia/lymphoma [ATLL]; 8, Peripheral T cell lymphoma [PTCL]; 8, others; 20), 135 were treated with chemotherapy including rituximab, 11 patients received stem cell tarnsplantation (7 autologus, 4 allogenic). HBV reactivation was found in 6 patients (DLBCL; 2, FL; 2, MCL; 1, MALT; 1), all of them were treated with rituximab. Although the rate of reactivation with and without use of rituximab was 4.1%, 0%, respectively, there was no apparent statistical difference (p=0.12), probably due to the smaller number of reactivated patients. Age at diagnosis, sex, subtype of lymphoma, pretreatment liver function test, and type of treatment including allogenic stem cell taransplantation were not significantly associated with HBV reactivation. Three patients had reactivation occurred during chemotherapy, whereas other 3 patients developed reactivation after completion of treatment at median interval of 42 days (range, 19-162 days). At the reactivation, 3 were HbsAg positive/HBV-DNA positive and others, under serial monitoring, were HbsAg negative/HBV-DNA positive. The former group developed de novo HBV hepatitis, among whom 1 died as a result of hepatic failure despite of antiviral therapy. None of the latter group developed hepatitis following antiviral preemptive therapy. CONCLUSIONS;Rituximab-containig regimens may increase the risk of HBV reactivation in lymphoma patients who have resolved HBV. And when molecular reactivation is recognized, prompt administration of preemptive antiviral therapy may prevent the development of de novo HBV hepatitis. For patients who are planned to receive rituximab therapy, HbsAg and HBcAb should be routinely tested, and HBsAg-negative/HBcAb-positive patients should be closely monitored with HBV DNA during at least 6 months after the end of chemotherapy, because the most delayed onset occurred 162 days in our study. Further studies are required to determine optimal monitoring and preemptive therapy. Disclosures:No relevant conflicts of interest to declare.

Diagnosis, prevention and management of hepatitis B virus reactivation during anticancer therapy

Diagnosis, prevention and management of hepatitis B virus reactivation during anticancer therapy

A novel concept: occult HBV infection in the western region of Turkey

Recent studies suggest that reappearance of hepatitis B surface antigen (HBsAg) and loss of anti-HBs antibodies may be common events in bone marrow recipients and patients with chemotherapy. In this study, we reviewed the virologic laboratory records from kidney recipients. Out of 1512 patients, 228 had been diagnosed with resolved HBV infection (anti-HBc positive, HBsAg negative) but normal liver enzyme levels prior to kidney transplantation. Reappearance of HBsAg after kidney transplantation was observed in two (0.9%) of those patients, which may be attributed to reactivation of a latent infection or to a new HBV infection. In both of the patients, HBV infection may have been reactivated although immunosuppression was just on a low level over the whole period. We conclude that natural immunity to HBV may not protect against reactivation in patients with suppression of the immune system. Periodic follow-up of HBV serology for early diagnosis of reactivation is highly recommended in transplant recipients.

HBV reactivation after kidney transplantation

Recent studies suggest that reappearance of hepatitis B surface antigen (HBsAg) and loss of anti-HBs antibodies may be common events in bone marrow recipients and patients with chemotherapy. In this study, we reviewed the virologic laboratory records from kidney recipients. Out of 1512 patients, 228 had been diagnosed with resolved HBV infection (anti-HBc positive, HBsAg negative) but normal liver enzyme levels prior to kidney transplantation. Reappearance of HBsAg after kidney transplantation was observed in two (0.9%) of those patients, which may be attributed to reactivation of a latent infection or to a new HBV infection. In both of the patients, HBV infection may have been reactivated although immunosuppression was just on a low level over the whole period. We conclude that natural immunity to HBV may not protect against reactivation in patients with suppression of the immune system. Periodic follow-up of HBV serology for early diagnosis of reactivation is highly recommended in transplant recipients.

Liver transplantation in Asia: Problems and practice.

Liver transplantation in Asia has been difficult to establish due to: a reluctance in Asians to donate organs; a lack of financial support; and the predominance of hepatitis B in the population, which effectively reduces the number of cadaveric organs. To overcome the problem of organ shortage, living-related liver transplantation for paediatric patients was rapidly established initially at Kyoto University, Japan, and then in several centres in Asia. Living-related liver transplantation was extended to adults using the left lobe in 1994 and using the right lobe in 1996. Up to May 1998, 785 liver transplantations had been performed in major centres in Asia with a patient survival rate approaching 80%. To overcome the problem of hepatitis B viral infection, lamivudine is now used peri-operatively. Lamivudine is shown to be very effective in preventing graft reinfection. Of the 15 patients who received lamivudine and liver transplantation at Queen Mary Hospital, hepatitis B surface antigen (HBsAg) disappeared in 11 patients and hepatitis B virus DNA was not detectable in any of them. Two patients had a reappearance of HBsAg after an initial loss, but their liver grafts were not affected by hepatitis. Compared with hepatitis B immunoglobulin, lamivudine is definitely cheaper and more convenient. In conclusion, even though there are major obstacles to liver transplantation in Asia, steady progress is being made. Hopefully, when the number of cadaveric grafts increases in future, an increasing number of patients can benefit.

Liver transplantation in Asia: Problems and practice

Liver transplantation in Asia has been difficult to establish due to: a reluctance in Asians to donate organs; a lack of financial support; and the predominance of hepatitis B in the population, which effectively reduces the number of cadaveric organs. To overcome the problem of organ shortage, living‐related liver transplantation for paediatric patients was rapidly established initially at Kyoto University, Japan, and then in several centres in Asia. Living‐related liver transplantation was extended to adults using the left lobe in 1994 and using the right lobe in 1996. Up to May 1998, 785 liver transplantations had been performed in major centres in Asia with a patient survival rate approaching 80%. To overcome the problem of hepatitis B viral infection, lamivudine is now used peri‐operatively. Lamivudine is shown to be very effective in preventing graft reinfection. Of the 15 patients who received lamivudine and liver transplantation at Queen Mary Hospital, hepatitis B surface antigen (HBsAg) disappeared in 11 patients and hepatitis B virus DNA was not detectable in any of them. Two patients had a reappearance of HBsAg after an initial loss, but their liver grafts were not affected by hepatitis. Compared with hepatitis B immunoglobulin, lamivudine is definitely cheaper and more convenient. In conclusion, even though there are major obstacles to liver transplantation in Asia, steady progress is being made. Hopefully, when the number of cadaveric grafts increases in future, an increasing number of patients can benefit.

Prophylaxis in liver transplant recipients using a fixed dosing schedule of hepatitis B immunoglobulin

Prophylactic hepatitis B immunoglobulin (HBIg) reduces the risk of reinfection in hepatitis B surface antigen (HBsAg)-positive liver transplant recipients. In the medical center of this study, high-dose HBIg immunoprophylaxis is administered at a fixed dose of 10,000 IU monthly, and in this study, the long-term efficacy of this treatment regimen was examined. Of 52 HBsAg-positive liver transplant recipients, 24 were administered HBIg immunoprophylaxis, and 28 were administered no specific therapy; the 2-year recurrence rates (defined by the reappearance of HBsAg) were 19% and 76%, respectively. Fifty-four percent of the HBIg-treated patients were positive for HBeAg or hepatitis B virus (HBV) DNA (by hybridization assay) pretransplantation. In patients administered monthly HBIg, intrapatient and interpatient variability in trough antibody to HBsAg (anti-HBs) titer was significant, highlighting the potential difficulties of using anti-HBs titer to guide therapy. Trough anti-HBs titers were less in patients who became HBsAg positive than in patients who remained HBsAg-negative (490 vs. 1290 mIU/mL) (P = .0001), reflecting either the cause or effect of HBV reinfection. Of 9 patients who remained HBsAg-negative and who were administered monthly HBIg for at least 1 year, HBV DNA by polymerase chain reaction amplification was detectable in the sera of 67%, the lymphocytes of 50%, and the liver of 57%. In conclusion, a fixed monthly dose of HBIg reduces the recurrence of HBs antigenemia, even in patients with indices of active viral replication pretransplantation. The presence of residual virus in the majority of patients administered HBIg suggests that long-term HBIg administration may be necessary.