No abstract available.
Hepatitis B virus/isolation & purification ; Hepatitis B, Chronic/diagnosis/*drug therapy/virology ; Humans ; Serologic Tests

BACKGROUND/AIMS: The post-treatment relapse patterns and efficacy of lamivudine re-treatment for relapsed patients have not been clarified. The aims of this study were to evaluate the relapse patterns after discontinuing therapy and the effects of lamivudine re-treatment for relapsed patients after HBeAg seroconversion. METHODS: Therapy was discontinued after HBeAg seroconversion in 121 patients. Sixty-six patients were relapsed and included in this study. The duration of lamivudine re-treatment therapy was from 6-35 (mean: 16) months. Post-retreatment monitoring continued for 1-40 (mean: 8.9) months. RESULTS: Among the relapsed 66 patients, 50 (75.8%) had HBeAg reappearance while 16 (24.2%) remained HBeAg negative and anti-HBe positive. The cumulative relapse rates at 3, 6, 12 and 24 months were 27%, 47%, 60% and 66%, respectively. Forty-two relapsers received lamivudine re-treatment. Among them, 33 were HBeAg positive and 9 were HBeAg negative and anti-HBe positive, Response was achieved in 31 of the 42 patients (73.8%). The cumulative response rates at 6, 9 and 12 months were 62%, 69% and 72%, respectively. Six patients (14.3%) developed viral breakthrough. All patients were HBeAg positive chronic hepatitis B. The duration of lamivudine re-treatment was the only predictable factor for response of lamivudine re-treatment. Therapy was discontinued after response in 21 patients. Eleven patients were relapsed, including 6 who were HBeAg positive and 5 who were HBeAg negative. Predictive factors for post-retreatment relapse were age and the duration of additional lamivudine therapy after response. CONCLUSIONS: The response rate of lamivudine re-treatment was significantly higher than in initial lamivudine treatments. The breakthrough and relapse rates, however, were similar in both initial and retreated lamivudine therapy.
Adult ; Antiviral Agents/*therapeutic use ; Female ; Hepatitis B e Antigens/blood ; Hepatitis B, Chronic/diagnosis/*drug therapy/virology ; Humans ; Lamivudine/*therapeutic use ; Male ; Recurrence ; Retreatment

BACKGROUND: Hepatitis B virus (HBV) detected in Korean patients almost belongs to genotype C, which is subdivided into subgenotype C1 (or Cs) and C2 (or Ce). It was recently reported that the risk of hepatocellular carcinoma is different between subgenotype C1 and C2. Thus, we studied the distribution of subgenotypes of HBV in Korean chronic hepatitis B (CHB) patients. METHODS: Specimens of 421 patients, who were diagnosed as CHB and underwent antiviral treatment, were used. After sequence analysis for HBV S gene, subgenotype was identified through phylogenetic analysis. Utilizing the same sequence data, the distribution of serotypes was also investigated. RESULTS: Among 421 patient specimens, genotype C was found in 419 (99.5%) and genotype B in 2 (0.5%). Among the genotype C strains, 417 strains were C2 subgenotype and 2 strains were mixed subgenotypes. However, C2 was evidently found even in the mixed sequences. Serotypes of 419 HBV with genotype C were classified as follows: adr, 385 (91.9%), adw, 22 (5.3%), ayr, 2 (0.4%) and mixed serotype, 10 (2.3%). Serotype of both HBV with genotype B was adw. CONCLUSIONS: It was found that HBV detected in Korean CHB patients under treatment almost all belong to the C2 (Ce) genotype.
Antiviral Agents/therapeutic use ; Blood Specimen Collection ; Genotype ; Hepatitis B virus/*classification/genetics ; Hepatitis B, Chronic/diagnosis/drug therapy/*virology ; Humans ; Korea ; Phylogeny ; Sequence Analysis, DNA ; Serotyping

Occult HBV infection is defined as the presence of HBV DNA in the liver (with or without detectable or undetectable HBV DNA in the serum) of individuals testing negative for HBsAg. Studies on occult HBV infection in hepatitis C patients have reported highly variable prevalence, because the prevalence of occult HBV infection varies depending on the hepatitis B risk factors and methodological approaches. The most reliable diagnostic approach for detecting occult HBV detection is through examination of liver DNA extracts. HCV has been suspected to strongly suppress HBV replication up to the point where it may be directly responsible for occult HBV infection development. However, more data are needed to arrive at a definitive conclusion regarding the role of HCV in inducing occult HBV infection. Occult HBV infection in chronic hepatitis C patients is a complex biological entity with possible relevant clinical implications. Influence of occult HBV infection on the clinical outcomes of chronic hepatitis C may be considered negative. However, recent studies have shown that occult HBV infection could be associated with the development of hepatocellular carcinoma and contribute to the worsening of the course of chronic liver disease over time in chronic hepatitis C patients. Nevertheless, the possible role of occult HBV infection in chronic hepatitis C is still unresolved and no firm conclusion has been made up until now. It still remains unclear how occult HBV infection affects the treatment of chronic hepatitis C. Therefore, in order to resolve current controversies and understand the pathogenic role and clinical impacts of occult HBV infection in chronic hepatitis C patients, well-designed clinical studies are needed.
Carcinoma, Hepatocellular/complications ; DNA, Viral/analysis ; Hepacivirus/genetics ; Hepatitis B/*complications/*diagnosis/drug therapy ; Hepatitis B virus/genetics ; Hepatitis C, Chronic/*complications/*diagnosis/drug therapy ; Humans ; Interferon-alpha/therapeutic use ; Liver/virology ; Liver Neoplasms/complications

Acute-On-Chronic Liver Failure ; diagnosis ; virology ; Antiviral Agents ; therapeutic use ; Hepatitis B, Chronic ; drug therapy ; Humans ; Nucleosides ; therapeutic use ; Nucleotides ; therapeutic use ; Prognosis

<b>OBJECTIVEb>To evaluate the antiviral efficacy of Bushen Granule (BSG) combined with Marine Injection (MI) in treating patients with chronic hepatitis B of Gan-shen deficiency with Damp-Heat (GSD) syndrome type.

<b>METHODSb>A total of 90 patients, who were HBV DNA, HBsAg, and HBeAg positive and of GS-DD type, were enrolled, and they were randomly assigned into 2 groups. The 49 patients in the treated group were treated with the combined therapy of BSG and MI and the 41 were administered with lamivudine, the therapeutic course for both groups was 1 year. The negative conversion rate of HBeAg and HBV DNA and the changes in HBV DNA titre, liver function, symptoms and physical signs were observed in the two groups before and after treatment.

<b>RESULTSb>In the treated group, the negative conversion rate of HBV DNA was 42.6% (20/ 47), insignificantly different to that in the control group (61.0%, 25/41, P > 0.05); the negative conversion rate of HBeAg and HBeAg/anti-HBe sero-conversion rate was 42.6% and 36.2%, respectively, significantly higher than those in the control group (22.0% and 17.0%, P < 0.05); the ALT normalizing rate was 74.4%, higher than that in the control group (51.4%, P < 0.05); the improvement of liver function (ALB and GLB) and clinical symptoms, especially the dizziness, soreness of waist, hypochondrial distending pain, and yellowish urine, were significantly superior to those in the control group(P < 0.01 or P < 0.05); and the partial response rate was 29.8%, insignificant different to that in the control group (14.6%, P > 0.05).

<b>CONCLUSIONSb>Combined treatment of BSG and MI has an ideal short-term effect in treating patients with chronic hepatitis B of Gan-shen deficiency with Damp-Heat syndrome type, it can inhibit HBV replication and improve patients' liver function and physical signs.

Adolescent ; Adult ; Diagnosis, Differential ; Drugs, Chinese Herbal ; administration & dosage ; therapeutic use ; Female ; Hepatitis B, Chronic ; drug therapy ; virology ; Humans ; Injections, Intravenous ; Male ; Medicine, Chinese Traditional ; Middle Aged ; Phytotherapy

Dermatomyositis is an idiopathic inflammatory myopathy with typical cutaneous manifestations. It has been proposed that dermatomyositis may be caused by autoimmune responses to viral infections. Previous studies have shown an association between dermatomyositis and malignant tumors such as ovarian cancer, lung cancer, and colorectal cancer. However, a chronic hepatitis B virus (HBV) infection associated with dermatomyositis and hepatocellular carcinoma (HCC) has been very rarely reported. Here, we report a rare case of dermatomyositis coinciding with HBV-associated HCC. A 55-year-old male was confirmed to have HCC and dermatomyositis based on proximal muscle weakness, typical skin manifestations, elevated muscle enzyme levels, and muscle biopsy findings. This case suggests that HCC and/or a chronic HBV infection may be factors in the pathogenesis of dermatomyositis through a paraneoplastic mechanism.
Antiviral Agents/therapeutic use ; Biopsy ; Carcinoma, Hepatocellular/diagnosis/*virology ; Dermatomyositis/diagnosis/drug therapy/*virology ; Disease Progression ; Fatal Outcome ; Glucocorticoids/therapeutic use ; Hepatitis B, Chronic/*complications/diagnosis/drug therapy ; Humans ; Liver Neoplasms/diagnosis/*virology ; Male ; Middle Aged ; Paraneoplastic Syndromes/diagnosis/drug therapy/*virology ; Risk Factors ; Time Factors ; Tomography, X-Ray Computed ; Treatment Outcome

Antiviral Agents ; pharmacology ; therapeutic use ; Congresses as Topic ; Drug Resistance, Viral ; Hepatitis B, Chronic ; diagnosis ; drug therapy ; virology ; Hepatitis C, Chronic ; diagnosis ; drug therapy ; virology ; Humans ; Liver Cirrhosis ; diagnosis ; therapy ; Liver Failure ; prevention & control ; Liver Neoplasms ; surgery ; therapy ; Nucleosides ; pharmacology ; therapeutic use

It is generally accepted that seroconversion of hepatitis B virus (HBV) surface antigen (HBsAg) to an antibody to HBsAg (anti-HBs) indicates clearance of HBV. Here we report a case of severe hepatitis that manifested during chemotherapy in a female patient with chronic lymphocytic leukemia (CLL) who had been initially seronegative for HBsAg and seropositive for anti-HBs. The patient received chlorambucil and prednisolone for the treatment of CLL. After 6 months the serum levels of aminotransferases were increased, and HBsAg and HBV DNA were present in serum. Lamivudine was administered immediately after confirming the HBV reactivation, which considerably improved jaundice and aminotransferase levels after 3 weeks. The patient was able to resume the chemotherapy whilst continuing lamivudine treatment. This case report highlights the need for physicians to be aware of the potential risk of HBV reactivation even in an HBsAg-negative person but with detectable anti-HBc and/or anti-HBs, underscoring the need for future studies that explore the role of antiviral prophylaxis in this setting.
Aged ; Antineoplastic Combined Chemotherapy Protocols/*therapeutic use ; Chlorambucil/*therapeutic use ; Female ; Hepatitis B/*diagnosis/virology ; Hepatitis B Antibodies/*blood/immunology ; Hepatitis B Surface Antigens/*blood/immunology ; Hepatitis B virus/isolation & purification/physiology ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/complications/*drug therapy ; Prednisolone/*therapeutic use ; Virus Activation

BACKGROUND/AIMS: Lamivudine (LAM) plus adefovir (ADV) combination therapy has been accepted as one of the best treatments for LAM-resistant chronic hepatitis B (CHB). The aim of this study was to determine the efficacy of this combination therapy in hepatocellular carcinoma (HCC) patients. METHODS: The medical records of CHB patients who developed LAM resistance and were treated with LAM plus ADV combination therapy for more than 6 months were reviewed. Their virological response (VR; undetectable HBV DNA) and biochemical response (BR; alanine aminotransferase normalization) were evaluated, and the findings of HCC and non-HCC patients were compared. RESULTS: The data from 104 patients (19 with HCC and 85 without HCC) were analyzed. The VR rates did not differ significantly between the HCC and non-HCC groups: 33.3% vs. 55.6% at 12 months (P=0.119), 58.3% vs. 67.2% at 24 months (P=0.742), 50% vs. 69.8% at 36 months (P=0.280), and 66.7% vs. 71.0% at 48 months (P=1.000). The BR rates also did not differ significantly between the groups: 55.6% vs. 84.0% at 12 months (P=0.021), 58.3% vs. 83.8% at 24 months (P=0.057), 70.0% vs. 77.8% at 36 months (P=0.687), and 66.7% vs. 80.6% at 48 months (P=0.591). CONCLUSIONS: The efficacy of LAM plus ADV combination therapy is comparable in HCC and non-HCC patients.
Adenine/*analogs & derivatives/therapeutic use ; Adult ; Antiviral Agents/*therapeutic use ; Carcinoma, Hepatocellular/*diagnosis/epidemiology/etiology ; DNA, Viral/analysis ; Drug Administration Schedule ; Drug Resistance, Viral ; Drug Therapy, Combination ; Genotype ; Hepatitis B virus/genetics ; Hepatitis B, Chronic/*drug therapy/virology ; Humans ; Incidence ; Lamivudine/*therapeutic use ; Liver Cirrhosis/diagnosis/epidemiology/etiology ; Liver Neoplasms/*diagnosis/epidemiology/etiology ; Middle Aged ; Organophosphonates/*therapeutic use ; Retrospective Studies ; Treatment Outcome