Antiviral Agents ; therapeutic use ; Female ; Hepatitis B virus ; Hepatitis B, Chronic ; drug therapy ; Humans ; Pregnancy ; Pregnancy Complications ; drug therapy ; virology

<b>OBJECTIVEb>To assess changes of liver function in HIV-positive children with/without HBV/ HCV co-infection after 1 year of highly active antiretroviral therapy (HARRT).

<b>METHODSb>Seventy-eight pediatric AIDS patients with HBV/HCV co-infection,19 pediatric AIDS patients with HBV co-infection and 44 pediatric AIDS patients without HBV/HCV co-infection who received HAART at least for 1 year were enrolled. HIV-1 viral load was quantitatively detected using a standardized reverse transcriptase-polymerase chain reaction assay, and blood cells were determined by three-color flow cytometry. Anti-HCV antibody and HBsAg was detected using an enzyme-linked immunosorbent technique, and ALT, AST and TBIL were detected by automatic biochemical analyzer.

<b>RESULTSb>After 1 year-HAART, the viral load was decreased to the lowest limit of detection in 90.34% patients (t=2.61, P<0.01), and CD4+ T cell counts were increased from 170.187±132.405/ μl to 796.014±158.491/ μl (t=3.17, P<0.01). The levels of ALT and AST were elevated (t=2.02, P<0.05), while the ALT and AST levels in patients receiving nevirapine (NVP) based HAART increased from 18.28±13.74 U/L and 24.23±8.09 U/L to 55.35±22.40 U/L and 69.97±26.72 U/L, respectively(t=3.80,t=4.11;Ps<0.01). The increment of ALT and AST in NVP based HAART were significantly higher than that in the efavirenz based HAART (ALT:46.28±13.35 U/L vs 37.70±15.25 U/L and AST:19.53±7.23 U/L vs 1.25±0.21 U/L, respectively; t=4.53, t=5.79; Ps<0.01), particularly in patients co-infected with HIV/HBV/HCV (ALT:54.32±22.85 U/L vs 16.89±14.42 U/L and AST:41.71±19.26 U/L vs -3.44±15.59 U/L, respectively; t=3.42, t=2.98, Ps<0.01).

<b>CONCLUSIONb>HARRT can repress HIV-1 replication effectively, but it also cause the damage of liver function, especially in patients with HBV and/or HCV co-infection.

Antiretroviral Therapy, Highly Active ; Child ; Coinfection ; drug therapy ; Female ; HIV Infections ; complications ; drug therapy ; physiopathology ; Hepatitis B ; complications ; Hepatitis C ; complications ; Humans ; Liver ; physiopathology ; Male

Antiviral Agents ; administration & dosage ; therapeutic use ; HIV ; HIV Infections ; complications ; Hepacivirus ; Hepatitis B ; complications ; drug therapy ; Hepatitis C ; complications ; Humans ; Superinfection ; drug therapy

Objective:b> To analyze the occurrence of recompensation conditions in patients with chronic hepatitis B virus-related decompensated cirrhosis after entecavir antiviral therapy. Methods:b> Patients with hepatitis B virus-related decompensated cirrhosis with ascites as the initial manifestation were prospectively enrolled. Patients who received entecavir treatment for 120 weeks and were followed up every 24 weeks (including clinical endpoint events, hematological and imaging indicators, and others) were calculated for recompensation rates according to the Baveno VII criteria. Measurement data were compared using the Student t-test or Mann-Whitney U test between groups. Categorical data were compared by the χ (2) test or Fisher's exact probability method between groups. Results:b> 283 of the 320 enrolled cases completed the 120-week follow-up, and 92.2% (261/283) achieved a virological response (HBV DNA 20 IU/ml). Child-Pugh and MELD scores were significantly improved after treatment (8.33 ± 1.90 vs. 5.77 ± 1.37, t = 12.70, P < 0.001; 13.37 ± 4.44 vs. 10.45 ± 4.58, t = 5.963, P < 0.001). During the 120-week follow-up period, 14 cases died, two received liver transplants, 19 developed hepatocellular cancer, 11 developed gastroesophageal variceal bleeding, and four developed hepatic encephalopathy. 60.4% (171/283) (no decompensation events occurred for 12 months) and 56.2% (159/283) (no decompensation events occurred for 12 months and improved liver function) of the patients had achieved clinical recompensation within 120 weeks. Patients with baseline MELD scores > 15 after active antiviral therapy achieved higher recompensation than patients with baseline MELD scores ≤15 [50/74 (67.6%) vs. 109/209 (52.2%), χ (2) = 5.275, P = 0.029]. Conclusion:b> Antiviral therapy can significantly improve the prognosis of patients with hepatitis B virus-related decompensated cirrhosis. The majority of patients (56.2%) had achieved recompensation. Patients with severe disease did not have a lower probability of recompensation at baseline than other patients.
Humans ; Hepatitis B virus/genetics* ; Hepatitis B, Chronic/drug therapy* ; Antiviral Agents/adverse effects* ; Esophageal and Gastric Varices/complications* ; Liver Cirrhosis/complications* ; Treatment Outcome ; Gastrointestinal Hemorrhage/complications* ; Hepatitis B/drug therapy*

<b>OBJECTIVEb>To evaluate the effect of different immune status on the incidence of hepatic lesions in patients with hepatitis B virus (HBV) infection undergoing anti-tuberculosis therapy.

<b>METHODSb>The PubMed (1966-2013), Embase (1966-2013), Wanfang (1998-2013), Chinese National Knowledge Infrastructure (CNKI; 1997-2013), and Chinese Biomedical (CBMdisc; 1860-2013) literature databases were searched for case-control studies of hepatic lesions in patients undergoing anti-tuberculosis therapy with or without concomitant HBV infection. The HBV patients were divided into subgroups according to hepatitis B e antigen (HBeAg) positivity or negativity, all members of the control group were HBsAg⁻. The data from all 7 studies included in the meta-analysis were extracted and analysed using RevMan5.2 soft-ware.

<b>RESULTSb>Patients with HBV infection who were undergoing anti-tuberculosis therapy had a higher risk factor than the control patients (OR =5.81, 95% CI =[4.26, 7.39]). The HBV patients with HBeAg positivity who were undergoing anti-tuberculosis therapy had a high risk factor than the HBV patients with HBeAg negativity (OR =2.56, 95% CI=[1.90, 3.44]).

<b>CONCLUSIONb>HBV infection is a risk factor for hepatic lesions when undergoing anti-tuberculosis therapy, and HBeAg-positive status may put a patient at higher risk.

Antitubercular Agents ; adverse effects ; therapeutic use ; Hepatitis B ; complications ; pathology ; Hepatitis B e Antigens ; blood ; Humans ; Liver ; drug effects ; pathology ; Tuberculosis ; complications ; drug therapy ; pathology

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

Cancer prevention is a challenging project both in the basic and clinical medicine. In particular, prevention of liver cancer is the most urgent task in countries where the incidence of hepatitis virus-related liver cancer is rising. As reviewed in this article, liver cancer is going to be the first cancer that will be actually prevented by primary and secondary interventions. Even the improvement of absolute survival of the patients can be expected by successful prevention, as already demonstrated in a few clinical trials. Thus, prevention of liver cancer is promising to provide not only cost-effectiveness by morbidity reduction but also cost-benefit by mortality improvement.
Animals ; Chemoprevention ; Hepatitis B/complications/drug therapy ; Human ; Liver Neoplasms/etiology/*prevention & control ; Retinoids/*therapeutic use

Antiviral Agents ; therapeutic use ; DNA, Viral ; blood ; Hepatitis B e Antigens ; blood ; Hepatitis B, Chronic ; complications ; drug therapy ; virology ; Humans ; Lamivudine ; therapeutic use ; Liver Cirrhosis ; drug therapy

The incidence of HBV infection in lymphoma patients is much higher than that in the general normal population. HBV reactivation caused by treatment is one of the common complications in considerable amount of lymphoma patients, which can induce fatal fulminating hepatitis in severe cases. The HBV reactivation in lymphoma patients is related to multiple factors, such as age, sex, HBV infectious state, HBV genotypes and gene mutations, and antitumor drugs. It's necessary to strengthen monitoring, prevention and treatment to HBV reactivation in the process of dealing with lymphoma. This review focuses on the epidemiological characteristics of lymphoma and HBV, as well as the risk factors, morbidity, pathogenesis, clinical feature, suggestion on prevention and treatment of HBV reactivation.
Antineoplastic Agents ; therapeutic use ; Hepatitis B ; complications ; drug therapy ; prevention & control ; Hepatitis B Surface Antigens ; Hepatitis B virus ; drug effects ; physiology ; Humans ; Lymphoma ; drug therapy ; virology ; Risk Factors ; Virus Activation ; drug effects

<b>OBJECTIVEb>To investigate the efficacy and safety of adefovir dipivoxil (ADV) in treating hepatic cirrhosis complicated with hepatitis B virus associated glomerulonephritis.

<b>METHODSb>Six hepatic cirrhosis (Child-Pugh A grade, liver function compensated) patients complicated with hepatitis B virus associated glomerulonephritis diagnosed by renal biopsy, real time PCR and urinary protein tests were treated with ADV for one year in addition to a routine treatment. The dosage of ADV was 100mg daily.

<b>RESULTSb>After 3 and 6 months treatment the negative conversion rates of HBV-DNA were 33.3% and 83.3%; the negative conversion rates of HBeAg were 16.7% and 66.7%; the positive conversion rates of HBeAb were both 16.7%; the recovery rates of ALT were 83.3% and 100.0%; and the recovery rates of TBil were 66.7% and 83.3% respectively. Protein in the urine of two patients was decreased to 0.3 g/d and in three patients it was 50% of the original values. After 1 year treatment the disease subsided fully in 3 and partially in 2 patients.

<b>CONCLUSIONb>Treating hepatic cirrhosis complicated with hepatitis B virus associated glomerulonephritis using adefovir dipivoxil is effective and safe.

Adenine ; analogs & derivatives ; therapeutic use ; Adolescent ; Adult ; Antiviral Agents ; therapeutic use ; Female ; Glomerulonephritis ; complications ; drug therapy ; virology ; Hepatitis B ; complications ; drug therapy ; Hepatitis B virus ; Humans ; Liver Cirrhosis ; complications ; drug therapy ; virology ; Male ; Middle Aged ; Organophosphonates ; therapeutic use ; Young Adult