OBJECTIVETo construct a noninvasive model to predict histological liver cirrhosis in patients with chronic hepatitis B.

METHODS275 patients with chronic hepatitis B were divided into a training group (206 cases) and a validation group (69 cases). The constituent ratios of patients in the fibrosis stages S0-S3, fibrosis stage S4 (early cirrhosis) and active cirrhosis stage were calculated according to the liver biopsy results. 30 noninvasive variables, including age-platelet index (API), aspartate aminotransferase to platelet ratio index (APRI), spleen-platelet ratio index (SRPI) and age-spleen-platelet ratio index (ASPRI), were analyzed by univariate analysis and multivariate logistic regression. Variables that were significantly different between patients with and without cirrhosis were used to construct a noninvasive prediction model, and the model was then tested in the validation group.

RESULTS(1) Of the 275 patients with chronic hepatitis B, 193 (70.2%) were in the fibrosis stages S0-S3, 42 (15.3%) in fibrosis stage S4, 40 (14.5%) in active cirrhosis stage. (2) There were 23 variables that are significantly different between patients with and without cirrhosis by univariate analysis. The 23 variables were further analyzed by multivariate logistic regression, and 4 independent factors, including international normalized ratio (INR), gamma glutamyltranspeptidase (GGT), ASPRI, hepatitis B e antigen (HBeAg) were used to construct a noninvasive prediction model. (3) By receiver operating characteristic curves (ROC) analysis, to discriminate patients in stages S0-S3 from patients in stage S4 and patients in active cirrhosis stage, the area under ROC (AUROC), cut-off value, sensitivity, specificity and accuracy of the model were 0.871, 0.458, 84.4%, 75.7%, and 79.7% respectively. To discriminate patients in active cirrhosis stage from patients in other stages, the AUROC, cut-off value, sensitivity, specificity and accuracy were 0.753, 0.526, 81.8%, 62.9%, and 67.4% respectively. There was no significant difference in AUROC between the training group and the validation group (P less than 0.05).

CONCLUSIONINR, GGT, ASPRI and HBeAg are associated with early cirrhosis and active cirrhosis. Our model can be used to predict early cirrhosis and active cirrhosis.

Adolescent ; Adult ; Biopsy ; Female ; Hepatitis B e Antigens ; blood ; Hepatitis B, Chronic ; blood ; complications ; diagnosis ; Humans ; Liver ; pathology ; Liver Cirrhosis ; blood ; diagnosis ; etiology ; Male ; Middle Aged ; Models, Biological ; Platelet Count ; Predictive Value of Tests ; Prognosis ; ROC Curve ; Sensitivity and Specificity ; Severity of Illness Index ; Young Adult ; gamma-Glutamyltransferase ; blood

OBJECTIVETo study the therapeutic efficacy of 48-week telbivudine treatment on cirrhosis resulting from chronic hepatitis B.

METHODS80 patients were equally divided into two groups, and treated with telbivudine 600 mg or lamivudine 100mg once daily for 48 weeks, respectively. The changes of virological and biochemical markers, PTA, Child-Pugh score, and viral resistance were observed at the different time points after antiviral treatment.

RESULTSThe mean of serum HBV DNA level in telbivudine group before treatment was (6.52+/-1.33) log10 copies/ml, and the mean reduction of serum HBV DNA was (2.09+/-1.30), (2.83+/-1.22), (3.23+/-1.27), (3.42+/-1.32), (3.65+/-1.30), (3.67+/-1.43) log10 copies/ml at 2, 4, 8, 12, 24, 48 weeks, respectively. The proportion of patients with serum HBV DNA undetectable was 92.5% (37/40) at 24, 48 weeks. At week 24 and 48, the rates of HBeAg/anti-HBe seroconversion were 30.0% (6/20), 35.0% (7/20), respectively. ALT, AST, albumin, total bilirubin, PTA, and Child-Pugh score were improved (P less than 0.05). Mutation of YMDD observed in telbivudine group was 5.0%. The mean reduction of serum HBV-DNA and the proportion of patients with undetectable serum HBV-DNA were greater in telbivudine group than in lamivudine group (P less than 0.05).

CONCLUSIONSTelbivudine can rapidly and effectively inhibit the replication of HBV in patients with cirrhosis resulting from chronic hepatitis B, and the resistance mutation rate was low. In addition, telbivudine treatment can improve the liver function.

Adult ; Antiviral Agents ; pharmacology ; therapeutic use ; DNA, Viral ; blood ; Drug Resistance, Viral ; Female ; Hepatitis B e Antigens ; blood ; Hepatitis B virus ; drug effects ; immunology ; Hepatitis B, Chronic ; complications ; drug therapy ; Humans ; Lamivudine ; pharmacology ; therapeutic use ; Liver Cirrhosis ; drug therapy ; etiology ; Male ; Middle Aged ; Nucleosides ; pharmacology ; therapeutic use ; Pyrimidinones ; pharmacology ; therapeutic use ; Thymidine ; analogs & derivatives ; Treatment Outcome ; Virus Replication ; drug effects

OBJECTIVETo investigate the clinicopathological features of infantile cytomegalovirus hepatitis.

METHODLiver biopsies from 30 cases of infantile cytomegalovirus hepatitis were observed under optical microscope and electronic microscope.

RESULTThe main clinical manifestations were jaundice, splenohepatomegaly and hypohepatia. Laboratory test showed dysfunction of liver, high level of CMV DNA, and high titer of anti-CMV antibody. Imaging examination demonstrated hepatomegaly. The histological changes were hepatocellular degeneration, necrosis, apoptosis, and fibrosis. The histological characteristics of cytomegalovirus hepatitis, including intranuclear inclusions in multinucleated giant cells and pseudo-lumens, were also observed under optical microscope. In addition, virion was observed in the nuclei and cytoplasm of hepatocytes under electronic microscope.

CONCLUSIONThe viral DNA and serological tests have limited utility for the diagnosis of infantile cytomegalovirus hepatitis, and the final diagnosis depends on histopathology.

Biopsy, Needle ; Cytomegalovirus Infections ; pathology ; Female ; Hepatitis, Viral, Human ; pathology ; Hepatocytes ; pathology ; ultrastructure ; Humans ; Inclusion Bodies, Viral ; pathology ; Infant ; Infant, Newborn ; Liver ; pathology ; Male ; Mitochondria, Liver ; pathology ; ultrastructure

OBJECTIVETo construct a vector that is competent to support the replication of hepatitis B virus (HBV) of genotype B.

METHODSThe HBV genome of genotype B was amplified by PCR and ligated into pBlueskript II KS(+) vector, the resulting plasmid was verified by enzyme digestion and DNA sequencing. After transfection of this plasmid into Huh7 cells, the HBsAg and HBeAg antigens in culture medium were quantified by ELISA, the transcripts and replication intermediates of HBV were detected by northern blot and southern blot respectively. On the other hand, the plasmid was hydrodynamically injected into BALB/cJ mice via tail vein. Then the HBV DNA in serum was quantified by real-time PCR, and HBcAg expression in liver tissue was detected by immunohistochemistry.

RESULTSAfter transfection of the plasmid into Huh7 cells, the HBsAg and HBeAg antigens were detected in the culture medium, the transcripts and replication intermediates of HBV were detected in the cells. High titer of HBV DNA was detected in the serum of hydrodynamic-injected mice. Immunostaining indicated that HBcAg was expressed in hepatocytes of injected mice.

CONCLUSIONThis construct is competent to support the replication of hepatitis B virus of genotype B.

Animals ; Cell Line, Tumor ; Cloning, Molecular ; Disease Models, Animal ; Genetic Vectors ; Genotype ; Hepatitis B ; metabolism ; virology ; Hepatitis B Antigens ; genetics ; metabolism ; Hepatitis B virus ; genetics ; metabolism ; Liver ; metabolism ; virology ; Mice ; Mice, Inbred BALB C ; Plasmids ; Polymerase Chain Reaction ; Transfection ; Virus Replication

OBJECTIVESTo establish a new grading system to evaluate liver inflammation and necrosis in patients with chronic hepatitis B through clinical biochemical assays.

METHODSClinical and pathological data were collected from 255 cases with chronic hepatitis B. 19 biochemical items were analyzed and 5 items were selected for our grading system. Each of the five items was scored 0 to 4 based on the different values. The extent of liver inflammation and necrosis was evaluated according to the total score.

RESULTSALT, AST, ChE, GGT and TBA were selected for our grading system. The grade of liver inflammation and necrosis was considered less than 2.0 if total score lower than 6, and higher grade was considered with higher total score. The estimated results shared an identity of 82.8% with the real grades of liver inflammation and necrosis. When this grading system was applied to patients with liver inflammation and necrosis equal to or higher than grade 2.0, it exhibited a sensitivity of 83.8%, a specificity of 81.2%, a positive prediction value of 88.6%, a negative prediction value of 74.2% in all cases, and 88.0%, 84.7%, 90.6%, 82.4% respectively in patients older than 12 years.

CONCLUSIONOur data suggest that the grading system can be used to evaluate the extent of liver inflammation and necrosis in patients with chronic hepatitis B.

Adolescent ; Alanine Transaminase ; blood ; Aspartate Aminotransferases ; blood ; Bile Acids and Salts ; blood ; Biomarkers ; blood ; Biopsy, Needle ; methods ; Cholinesterases ; blood ; Female ; Hepatitis B, Chronic ; blood ; pathology ; Humans ; Liver Diseases ; pathology ; Liver Function Tests ; Male ; Necrosis ; Severity of Illness Index ; Young Adult ; gamma-Glutamyltransferase ; blood

Fatty Liver ; drug therapy ; Humans ; Sirtuin 1

Humans ; Interferon-gamma ; therapeutic use ; Liver Cirrhosis ; drug therapy

Enzyme-Linked Immunosorbent Assay ; Hepacivirus ; isolation & purification ; Hepatitis C ; virology ; Humans

Case-Control Studies ; Gene Expression ; Humans ; Liver ; metabolism ; pathology ; Liver Neoplasms ; metabolism ; pathology ; Protein-Serine-Threonine Kinases ; genetics ; metabolism ; Proto-Oncogene Proteins ; genetics ; metabolism

Acetyl-CoA Carboxylase ; metabolism ; Cell Line ; Curcumin ; pharmacology ; Hepatocytes ; drug effects ; metabolism ; Humans