Hepatitis B Virus DNA-negative Patients Research Articles

Liver Stiffness Is a Predictor of Rebleeding in Patients With Hepatitis B-Related Cirrhosis: A Real-World Cohort Study.

Background: Esophageal vein rebleeding is a life-threatening complication of liver cirrhosis. However, the role of non-invasive methods that were developed to evaluate the severity of chronic liver disease, especially in rebleeding, remains unclear.Aims: To evaluate the performance of liver stiffness and non-invasive fibrosis scores in predicting esophageal vein rebleeding in hepatitis B virus (HBV) cirrhotic patients.Methods: A prospective analysis of 194 HBV patients between 2017 and 2021 was performed. Receiver operating characteristic (ROC) curves and time-dependent ROC curves were used to assess the power for predicting rebleeding with non-invasive fibrosis score and liver stiffness.Results: During the median follow-up time of 68.28 weeks, 55 patients experienced rebleeding. In the entire cohort, the area under the ROC curve for liver stiffness measurement (LSM) predicting for rebleeding was 0.837, with a cut-off value of 17.79 kPa, and the time-dependent ROC curve also showed stable prediction performance of LSM. The predictive ability of the non-invasive fibrosis score was less than that of LSM, and there were statistical differences. Moreover, patients using non-selective beta-blockers and HBV DNA-negative patients experienced significantly reduced rebleeding.Conclusions: Compared with non-invasive fibrosis scores, LSM can more simply and accurately predict rebleeding events of hepatitis B liver cirrhosis.

Perioperative antiviral therapy improves the prognosis of HBV DNA-negative patients with HBV-related hepatocellular carcinoma

ABSTRACT Objective To investigate the effect of perioperative antiviral therapy on the prognosis of hepatitis B virus (HBV) DNA-negative patients with HBV-related hepatocellular carcinoma (HCC). Methods The clinical data of 140 patients who were positive for hepatitis B surface antigen (HBsAg) but negative for HBV DNA before partial hepatectomy were retrospectively analyzed. Propensity score matching (PSM) was used to eliminate the influence of confounding factors on prognosis. Postoperative liver function, HBV reactivation rate, recurrence-free survival (RFS) and overall survival (OS) were compared between antiviral and non-antiviral therapy groups. Results Compared with the non-antiviral therapy group, the antiviral therapy group had a lower rate of HBV reactivation and better postoperative liver function (P < 0.05). The 1-year, 2-year and 3-year survival rates of the antiviral therapy group were better than those of the non-antiviral therapy group before or after PSM (P < 0.05). Prognostic analysis excluding 11 patients with HBV reactivation showed that perioperative antiviral therapy could significantly improve OS (P = 0.004), but had no significant effect on RFS (P = 0.056). Multivariate analyzes showed that antiviral therapy was associated with better OS. Conclusion Perioperative antiviral therapy can significantly reduce the risk of HBV reactivation and improve postoperative liver function, RFS and OS.

Diagnostic value of gamma-glutamyltransferase/aspartate aminotransferase ratio, protein induced by vitamin K absence or antagonist II, and alpha-fetoprotein in hepatitis B virus-related hepatocellular carcinoma.

BACKGROUNDResearchers have investigated the diagnostic value of protein induced by vitamin K absence or antagonist II (PIVKA-II) and alpha-fetoprotein (AFP) in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC), and obtained abundant clinical diagnostic data. However, PIVKA-II and AFP have unsatisfactory specificity and sensitivity in the diagnosis of early-stage HBV-related HCC. Gamma-glutamyltransferase (γ-GT) and aspartate aminotransferase (AST) are common biomarkers for evaluating liver function, and we hypothesized that the γ-GT/AST ratio in combination with PIVKA-II and AFP would improve the diagnosis of early-stage HBV-related HCC.AIMTo evaluate the diagnostic value of γ-GT/AST ratio alone or in combination with PIVKA-II and AFP in HBV-related HCC.METHODSSerum levels of γ-GT, AST, PIVKA-II, and AFP were detected and analysed in 176 patients with HBV-related HCC and in 359 patients with chronic hepatitis B. According to tumour size and serum level of HBV DNA, HBV-related HCC patients were divided into the following categories: Early-stage HCC patients, HCC patients, HBV DNA positive (HBV DNA+) HCC patients, and HBV DNA negative (HBV DNA-) HCC patients. Receiver-operating characteristic (ROC) curves were used to analyse and compare the diagnostic value of the single and combined detection of various biomarkers in different types of HBV-related HCC.RESULTSTumour size was positively correlated with serum levels of PIVKA-II and AFP in HCC patients (r = 0.529, aP < 0.001 and r = 0.270, bP < 0.001, respectively), but there was no correlation between tumour size and the γ-GT/AST ratio (r = 0.073, P = 0.336). The areas under the receiver-operating characteristic curves (AUROCs) of the γ-GT/AST ratio in early-stage HCC patients, HBV DNA+ HCC patients and HBV DNA- HCC patients were not significantly different from that in the total HCC patients (0.754, 0.802, and 0.705 vs 0.779, respectively; P > 0.05). When PIVKA-II was combined with the γ-GT/AST ratio in the diagnosis of early-stage HCC, HCC, and HBV DNA+ HCC, the AUROCs of PIVKA-II increased, with values of 0.857 vs 0.835, 0.925 vs 0.913, and 0.958 vs 0.954, respectively. When AFP was combined with the γ-GT/AST ratio in the diagnosis of early-stage HCC, HCC, HBV DNA+ HCC, and HBV DNA- HCC, the AUROCs of AFP increased, with values of 0.757 vs 0.621, 0.837 vs 0.744, 0.868 vs 0.757, and 0.840 vs 0.828, respectively.CONCLUSIONThe γ-GT/AST ratio may be better than PIVKA-II and AFP in the diagnosis of early-stage HBV-related HCC, and its combination with PIVKA-II and AFP can improve the diagnostic value for HBV-related HCC.

Hepatitis B virus reactivation in HBV DNA-negative patients with hepatocellular carcinoma after transarterial chemoembolization

Objective To evaluate risk factors of hepatitis B virus (HBV) reactivation after transarterial chemoembolization (TACE) in patients with HBV-related hepatocellular carcinoma (HCC) with undetectable HBV DNA levels. Methods From August 2012 to Sepemter 2015, all patients who underwent TACE for HBV-related HCC with HBV DNA level less than 103 copies/ml in the First Affiliated Hospital of Soochow University were enrolled into the study. These patients were followed-up for at least 6 months after TACE to assess HBV reactivation. Univariate and multivariate logistic regression analyses were done to evaluate the risk factors related to HBV reactivation in these patients. Results With predetermined inclusion and exclusion criteria, 99 patients were enrolled into the study. Twenty-four patients (24.2%) developed HBV reactivation after TACE in the followed-up period. The level of transaminase was significantly higher in the HBV reactivation group than the non HBV reactivation group (P<0.05). HBeAg positivity and tumors more than 3 in number were independent risk factors of HBV reactivation. Conclusion HCC patients with undetectable levels of HBV DNA had a significant risk of HBV reactivation after TACE. Key words: Hepatocellular carcinoma; Transcatheter arterial chemoembolization; Hepatitis B virus; Reactivation

Effects of antiviral therapy on post-hepatectomy HBV reactivation and liver function in HBV DNA-negative patients with HBV-related hepatocellular carcinoma.

The ability of antiviral therapy to reduce risk of post-hepatectomy hepatitis B virus (HBV) reactivation in patients negative for viral DNA is unclear. This prospective study involved 174 consecutive patients with hepatitis B virus related hepatocellular carcinoma who were negative for hepatitis B virus DNA in serum and who underwent hepatic resection. Hepatitis B virus reactivation occurred in 30 patients in the non-antiviral group (27.8%) but in only 2 patients in the antiviral group (3.0%, P < 0.001). Based on multivariate analysis, risk of hepatitis B virus reactivation was associated with minor hepatectomy and absence of antiviral therapy. Liver function indicators at one week after resection did not differ significantly between the two groups, or between patients who experienced hepatitis B virus reactivation or not. Nevertheless, alanine aminotransferase and albumin at 1 month after resection were significantly higher in the antiviral group than in the non-antiviral group, and they were significantly higher in patients who did not experience hepatitis B virus reactivation than in those who did. Therefore, patients with hepatitis B virus related hepatocellular carcinoma face substantial risk of hepatitis B virus reactivation after hepatectomy, even if they are negative for viral DNA at baseline. Antiviral therapy can reduce the risk of reactivation, helping improve liver function after surgery. (Clinicaltrials.gov registration number: NCT02829359).

Can hepatitis B virus DNA in semen be predicted by serum levels of hepatitis B virus DNA, HBeAg, and HBsAg in chronically infected men from infertile couples?

Hepatitis B virus (HBV) in semen is important for father-to-child transmission of HBV and has adverse effects on sperm quality. However, risk factors associated with HBV in semen remain unclear. Serum HBV DNA and hepatitis B e antigen (HBeAg) levels may pose a risk on HBV in semen. This study aims to examine whether serum HBV DNA, HBeAg, and hepatitis B surface antigen (HBsAg) level were associated with HBV DNA in semen. 151 male patients chronically infected with HBV from infertile couples were included. Serum HBsAg and HBeAg were determined using an electrochemiluminescence immune assay (ECLIA). Serum and seminal plasma HBV DNA were detected by the QIAGEN Real-Time HBV DNA assay. Of 151 patients, 143 (94.7%) were serum HBV DNA-positive and 65 (43.0%) were seminal plasma HBV DNA-positive. Serum HBV DNA and HBeAg level of seminal plasma HBV DNA-positive patients were significantly higher (p < 0.001) as compared with those of seminal plasma HBV DNA-negative patients, HBsAg level of seminal plasma HBV DNA-positive patients was significantly lower (p < 0.001) compared with that of seminal plasma HBV DNA-negative patients. The best serum HBV DNA, HBeAg, and HBsAg value for discriminating between seminal plasma HBV DNA-positive and HBV DNA-negative patients were ≥6.9 log10 IU/mL (sensitivity 100.0%, specificity 90.7%), >14.8 S/CO (sensitivity 96.9%, specificity 81.5%), and <1791.5 S/CO (sensitivity 81.5%, specificity 81.2%), respectively. The combination of serum HBV DNA and HBeAg had high diagnostic sensitivity (100.0%) and specificity (95.4%) for the presence of HBV DNA in semen. As such, these serum markers especially the combination of HBV DNA and HBeAg are useful predictors of the presence of HBV DNA in semen in HBV chronically infected men from infertile couples.

Inactıve hepatitis B surface antigen carriers and intrafamilial tramsmission: results of a 10-year study.

Background/AimsThe aims of the present study were to determine the outcomes of inactive hepatitis B virus (HBV) surface antigen (HBsAg) carriers over a 10-year study period and to elucidate the HBV serological profile of their family members.MethodsWe retrospectively analyzed the medical files of inactive HBsAg carriers followed up at the Department of Infectious Diseases of Kocatepe University Medical Faculty Hospital between March 2001 and January 2011.ResultsIn total, 438 inactive HBsAg carriers were enrolled in this trial. The follow-up period was 33.7±22.5 months (mean±SD). Anti-hepatitis-B surface antibody seroconversion occurred in 0.7% of cases, while chronic hepatitis B was found in 0.5%. The anti-hepatitis-D virus (HDV) status was evaluated in 400 patients and anti-hepatitis C virus (HCV) in 430. It was found that 1% and 0.2% were positive for anti-HDV and anti-HCV, respectively. HBV serology was investigated in at least 1 family member of 334/438 (76.3%) patients. The HBsAg positivity rate was 34.6% in 625 family members of 334 patients. A comparison of the HBsAg positivity rates in terms of HBV DNA levels in index cases revealed that HBsAg seropositivity rates were higher in family members of HBV DNA-negative patients than in family members of HBV DNA-positive cases (P=0.0001).ConclusionsThe HBsAg positivity rate was higher in family members of inactive HBsAg carriers than in the general population; these family members therefore have a higher risk of HBV transmission. Furthermore, despite negative HBV DNA levels, transmission risk was not reduced in these patients, and horizontal transmission seems to be independent of the HBV DNA value.

A proposal for management of rheumatic disease patients with hepatitis B virus infection receiving immunosuppressive therapy

Reactivation of hepatitis B virus (HBV) and de novo HBV hepatitis in patients with rheumatic diseases given intensive and long-term immunosuppressive therapy with or without biological disease-modifying antirheumatic drugs is of great concern, especially in regions where the virus is endemic, including Japan. To ascertain a better benefit–risk balance for immunosuppressive therapy for patients with rheumatic diseases, the Japan College of Rheumatology developed this proposal. All patients with rheumatic diseases commencing immunosuppressive therapy should be screened for hepatitis B surface antigen (HBsAg); those who are negative for HBsAg should be screened for hepatitis B core antibody (HBcAb) and hepatitis B surface antibody (HBsAb) as well. HBV carriers and serum HBV DNA positive patients with resolved infection should receive nucleoside analog as soon as possible, prior to commencing immunosuppressive therapy. For serum HBV DNA negative patients with resolved infection, careful monthly monitoring using serum levels of aspartate and alanine aminotransferases and HBV DNA is recommended during and at least 12 months after withdrawal of immunosuppressive therapy. If serum HBV DNA becomes positive, patients should receive nucleoside analog treatment as soon as possible, while ongoing immunosuppressive therapy should be continued to avoid severe or fulminant hepatitis development. To facilitate proper management of patients with HBV infection, collaboration between rheumatologists and hepatologists is strongly encouraged.

Dried Blood Spot Sampling for Hepatitis B Virus Serology and Molecular Testing

Background & AimsDried blood spots (DBS) on filter paper have been successfully used to diagnose and monitor several infectious diseases. The aim was to investigate the performance of DBS in hepatitis B virus (HBV) diagnosis using commercial tests in comparison to standard methods.MethodsPaired DBS and plasma samples were collected from 200 patients: 100 patients with HBsAg negative status and 100 patients with HBsAg positive status. In the latter patient, HBeAg reactivity was tested. Ten samples of anti-HBs were collected from people vaccinated against HBV. We also studied 50 patients with positive HBV DNA viral load in plasma and 10 HBV DNA negative patients. HBV genotypes and gene polymerase mutations were determined in 10 randomly selected HBV-infected patients. The DBS sample consisted of 50 µL of whole blood, i.e. a 12-mm paper card.ResultsThe sensitivity thresholds of HBsAg and anti-HBs antibody were 0.30±0.08 IU/mL and 18.11±6.05 IU/mL, respectively, for DBS with 98% sensitivity and 100% specificity. Sensitivity was 98% and specificity 100% for the detection of HBV DNA on a blotter, considering an HBV DNA threshold of 914.1±157.8 IU/ml. Ten patients had an HBeAg positive status in plasma, all were detected positive using DBS. HBV genotyping and mutation detection were successfully performed on DBS, with full concordance between the 10 paired DBS and plasma samples.ConclusionThis study shows DBS is a reliable alternative to plasma specimens for quantifying and detecting HBsAg, anti-HBs, HBeAg and genotyping. DBS may increase the opportunities for HBV testing and treatment follow-up in hard-to-reach individuals.

Detection of highly prevalent hepatitis B virus co-infection with HIV in Indonesia

The prevalence of hepatitis B virus (HBV) co-infection with HIV is increasing worldwide because of shared transmission routes. This study aimed to assess the prevalence of HBV and HIV co-infection in Indonesia, and its molecular and clinical characteristics. A total of 118 serum samples from HIV-infected patients (age 33.3 ± 8.9 years, 99 male, 19 female) collected in 2009 were serologically examined. HBV DNA was assessed by polymerase chain reaction (PCR) analysis targeting the S region. Overall, 15.3% (18/118) of the patients were hepatitis B surface antigen (HBsAg) positive, whereas 27.1% (32/118) were HBsAg negative but HBV DNA positive, and were considered to have occult HBV infection. HBsAg antibodies and/or HBV core antibodies were detected in 45.6% (31/68) of HBV DNA negative patients. HBV co-infection, including occult HBV infection, was common in Indonesian HIV patients. Hepatic damage by the interaction of host immunity and HBV is still a remaining issue in these immunosuppressive patients, and further study will be needed.

A proposal for management of rheumatic disease patients with hepatitis B virus infection receiving immunosuppressive therapy

Reactivation of hepatitis B virus (HBV) and de novo HBV hepatitis in patients with rheumatic diseases given intensive and long-term immunosuppressive therapy with or without biological disease-modifying antirheumatic drugs is of great concern, especially in regions where the virus is endemic, including Japan. To ascertain a better benefit–risk balance for immunosuppressive therapy for patients with rheumatic diseases, the Japan College of Rheumatology developed this proposal. All patients with rheumatic diseases commencing immunosuppressive therapy should be screened for hepatitis B surface antigen (HBsAg); those who are negative for HBsAg should be screened for hepatitis B core antibody (HBcAb) and hepatitis B surface antibody (HBsAb) as well. HBV carriers and serum HBV DNA positive patients with resolved infection should receive nucleoside analog as soon as possible, prior to commencing immunosuppressive therapy. For serum HBV DNA negative patients with resolved infection, careful monthly monitoring using serum levels of aspartate and alanine aminotransferases and HBV DNA is recommended during and at least 12 months after withdrawal of immunosuppressive therapy. If serum HBV DNA becomes positive, patients should receive nucleoside analog treatment as soon as possible, while ongoing immunosuppressive therapy should be continued to avoid severe or fulminant hepatitis development. To facilitate proper management of patients with HBV infection, collaboration between rheumatologists and hepatologists is strongly encouraged.

Prevalence of hepatitis B virus (HBV) co-infection in HBV serologically-negative South African HIV patients and retrospective evaluation of the clinical course of mono- and co-infection

Hepatitis B virus (HBV) infection with undetectable hepatitis B surface antigen (HBsAg) has been reported in HIV patients, but the clinical significance is unknown. This study presents the prevalence of HBV DNA in HIV-positive patients negative for all HBV serological markers and a retrospective evaluation of the clinical course of mono- and co-infection. Of 502 HIV-positive patients, 222 tested negative for HBsAg, antibody to hepatitis B surface antigen (anti-HBs), and antibody to hepatitis B core antigen (anti-HBc). An in-house real-time PCR targeting the HBV S-region was used to quantify HBV DNA. HBV isolates were genotyped. Baseline demographic and clinical characteristics of HBV DNA-positive and HBV DNA-negative patients were described. Treatment outcomes of patients at 6, 12, and 24 months after initiation of antiretroviral therapy (ART) were summarized. HBV DNA was detected in 5.4% (12/222) of serologically negative patients. Mean HBV viral load was 5359.2 IU/ml (standard deviation (SD) ±12768.27). Eleven HBV isolates belonged to genotype A and one to genotype C. There were no significant differences in baseline characteristics or clinical course between the HBV DNA-positive and HBV DNA-negative groups. We found 5.4% of the HBV serologically-negative HIV-positive patients had low levels of HBV DNA. There were no significant differences in clinical outcome between the mono- and co-infected groups.

Evaluating the risk of hepatitis B reactivation in patients with haematological malignancies: is the serum hepatitis B virus profile reliable?

Patients with an occult hepatitis B virus (HBV) infection undergoing deep immunosuppression are potentially at risk of HBV reactivation. In order to assess whether a polymerase chain reaction (PCR) assay for HBV DNA in serum could be used to predict the reactivation of an occult HBV infection, we performed a retrospective study in a cohort of Sicilian patients with oncohaematological diseases. We studied by a highly sensitive ad hoc nested PCR for serum HBV DNA 75 HBsAg-negative oncohaematological patients requiring chemotherapy. Thirty-three patients (44%) were HBV seronegative (anti-HBc and anti-HBs negative) and 42 patients (56%) were HBV seropositive (anti-HBc and/or anti-HBs positive). Baseline serum HBV DNA was positive in nine out of 33 HBV-seronegative patients and in nine out of 42 HBV-seropositive patients (27.3 vs. 21.4%; P=NS). HBsAg seroconversion was observed in five out of 33 seronegative vs. six out of 42 seropositive patients (15 vs. 14%, P=0.9), and in five out of 18 HBV DNA-positive vs. six out of 57 HBV DNA-negative patients (27.7 vs. 10.6%P=0.11). Hepatitis C virus infection was found in 18 patients (24.3%), although with no correlation to HBV serological status, presence of serum HBV DNA or frequency of HBsAg seroconversion. In oncohaematological patients undergoing chemotherapy, highly sensitive serum HBV DNA testing at baseline has a 28% predictive ability to forecast HBsAg seroconversion in HBV DNA-positive patients, and a 90% ability to forecast persistent HBsAg negativity in HBV DNA-negative patients, a better performance than serological tests.

Hepatitis B Virus DNA in Liver Tissue and Risk for Hepatocarcinogenesis in Patients with Hepatitis C Virus-Related Chronic Liver Disease

Aims: To prospectively study whether occult hepatitis B virus (HBV) infection can promote the development of hepatocellular carcinoma (HCC) in patients with hepatitis C virus (HCV)-related chronic liver disease. In addition, to evaluate the difference among HBV DNA-negative patients and patients with high and low HBV copy numbers. Methods: A total of 167 patients with HCV-related chronic liver disease without HBV surface antigen (HBsAg) were studied. HBV DNA in liver tissue was determined using polymerase chain reaction (PCR). Results: HBV DNA was detected in 9 of 167 patients (5.4%) by single PCR and in 25 patients (15.0%) by nested PCR. HCC developed in 12 of 167 patients (7.2%). Ten of 142 HBV DNA-negative patients (7.0%) and 2 of 9 patients with a high HBV copy number (22.2%) developed HCC, whereas none of 16 patients with a low HBV copy number developed HCC. The incidence rate of HCC in patients with a high HBV copy number was significantly higher than in HBV DNA-negative patients and patients with low HBV copy number. Conclusion: A high amount of HBV DNA in liver tissue of HBsAg-negative patients with HCV-related liver disease might be associated with HCC development.

Influence of Occult Hepatitis B Virus Coinfection on the Incidence of Fibrosis and Hepatocellular Carcinoma in Chronic Hepatitis C

We examined prospectively the influence of occult hepatitis B virus (HBV) infection on the histopathological features and clinical outcome of HCV RNA-positive chronic hepatitis (CH-C) and detected hepatitis B core (HBc) particles in hepatocytes. The subjects were 468 patients with CH-C or liver cirrhosis (LC) who were negative for serum hepatitis B surface antigen (HBsAg) by enzyme-linked immunosorbent assay. HBV DNA was detected in serum by nested PCR. HBsAg and HBc antigen (HBcAg) in liver were investigated using immunohistochemical techniques and light (LM) and electron microscopy (EM). Serum HBV DNA was detected in 43.6% of the patients studied. There were no significant differences between HBV DNA-positive and DNA-negative patients in terms of their clinical profiles. For HBV DNA-positive patients, the degree of inflammatory cell infiltration and irregular regeneration of hepatocytes was significantly greater than for HBV DNA-negative patients. The cumulative probability of development of hepatocellular carcinoma (HCC) was significantly higher for HBV DNA-positive patients than for HBV DNA-negative patients. HBV DNA positivity was a risk factor for the occurrence of HCC according to multivariate analysis. HBsAg and HBcAg were detected in 8.5 and 72.3%, respectively, of the livers of serum HBV DNA-positive individuals. Core particles were detected in the nuclei of the hepatocytes by IEM. The histopathological features and long-term outcome of CH-C or LC could be affected by occult HBV infection.

Analysis of the core gene of hepatitis B virus in Korean patients

As the core gene of hepatitis B virus (HBV) is a major immunological target, its mutation may evoke or evade immune clearance. We investigated the frequency and location of HBV core gene substitutions according to hepatitis B e antigen (HBeAg) status and viral replication status, and evaluated the association of these substitutions with the different stages of chronic HBV infection in Korean patients. The study population included 45 HBeAg-positive/DNA-positive patients (group I), 49 HBeAg-negative/DNA-positive patients (II) and 50 HBeAg-negative/DNA-negative patients (III). The HBV core gene was analysed by polymerase chain reaction (PCR) and sequencing. The frequency of core gene substitutions increased from group I to group III. Substitutions were commonly detected at codons 87, 97, 112 and 130. The frequency of substitutions at codons 87 and 112 was higher in groups II/III than in group I. The frequency of the codon I97F substitutions was the highest in group III. However, the codon 130 substitution was more frequently found in groups I/II than in group III. Core gene substitutions were more frequently detected in HBeAg-negative and/or HBV DNA-negative patients. The substitutional hot spots were codons 87, 97, 112 and 130; substitutions at these codons might play a role in immune-modulation during the course of chronic HBV infection.

Occult HBV infection—both hidden and mysterious

Occult HBV infection—both hidden and mysterious

Lamivudine Therapy in Acute Leukemia Patients who are Hepatitis B Surface Antigen Carriers

Background: Reactivation of hepatitis B in patients receiving chemotherapy for acute leukemia may give rise to a variety of clinical patterns including hepatitis, asymtomatic hepatic dysfunction, massive hepatic necrosis and fatal hepatic failure. Lamivudine is a nucleoside analogue which can directly suppress Hepatitis B virus (HBV) replication. We reviewed our combined experience to evaluate the role of lamivudine as prophylaxis in acute leukemia patients who were HBsAg carriers treated with chemotherapy between July 2000 and October 2002 at the Numune Education and Research Hospitals (Ankara, Turkey) retrospectively.Methods: We investigated 75 acute leukemia patients who received chemotherapy. Thirteen (17.3%) of 75 acute leukemia patients were HbsAg positive and of 7 (53.3%) were HBV DNA positive. Two patients (patients 5 and 6) had a chemotherapy regimen that included corticosteroids and were HBsAg and HBV DNA negative but anti HBc total positive. HBsAg positive patients with or without HBV DNA positivity were treated with a dose of 100 mg/day lamivudine commencing when chemotherapy was initiated. Lamivudine started at the beginning of chemotherapy and was maintained for 6 months following the cessation of chemotherapy. During lamivudine treatment, Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), Gama glutamile transpeptidase (GGT), Alkaline phosphatase (ALP) were followed.Results: Of the 8 patients who presented with hepatic dysfunction during the first chemotherapy cycle, 4 improved during the second course. After completing chemotherapy, the levels of hepatic enzymes were in the normal range in all but one patient. With lamivudune prophylaxis, HBV DNA positivity did not develop in any of the HBV DNA negative patients. The two patients who received corticosteroids with their first chemotherapy cycle became positive for HBsAg and HBV DNA and were given Lamivudine when the seroconversion was established. Median follow up from the diagnosis of leukemia was 14.5 months. Survival rate at the end of follow up was 5 (38%) for the 13 patients.Conclusions: As this infection is endemic in our country and the exposure to blood products is high in these patients, HBV infection is more common. Prophylaxis with daily administration of lamivudine to HBsAg carriers who are candidates for chemotherapy seems to be effective and may prevent chemotherapy induced HBV reactivation and hepatic failure.