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We aimed to investigate the relationship between serum hepatitis B virus (HBV) DNA and alanine transaminase (ALT) levels and the risk of cirrhosis in a large cohort of hepatitis B e antigen (HBeAg)-negative chronic hepatitis B (CHB) patients based on transient elastography.We prospectively studied treatment-naive HBeAg-negative patients recruited based on territory-wide referrals. We defined possible cirrhosis and probable cirrhosis with two different cutoffs according to the results from a subgroup of patients with histologic proof.One thousand one hundred ninety-seven patients with successful liver stiffness measurement (LSM) were studied. In the subgroup of 100 patients with liver biopsy, LSM ofor =8.4 kiloPascal (kPa) had a sensitivity of 90% and LSM ofor =13.4 kPa had a specificity of 94% for liver cirrhosis. Possible and probable cirrhosis were defined as a LSM valueor =8.4 kPa andor =13.4 kPa, and were present in 31% and 11% of the patients, respectively. The risk of cirrhosis was significantly increased when ALT level was0.5x upper limit of normal (ULN) or serum HBV DNA4 log(10) copies/mL. Among patients who have ALTor =0.5 x ULN and HBV DNAor =4 log(10) copies/mL, 10% (26/264) and 3% (7/264) had possible and probable cirrhosis respectively, which were significantly lower when compared with 34% (329/887, P0.001) and 14% (125/887, P0.001) of those who had higher ALT and HBV DNA levels.Liver cirrhosis was common among HBeAg-negative CHB patients. Patients with ALT levels0.5 x ULN and/or serum HBV DNA4 log(10) copies/mL have higher risk of cirrhosis and need further assessment for antiviral therapy.

Histological assessment of liver fibrosis is important in the management of chronic hepatitis B (CHB) infection but poorly accepted by patients because of its invasiveness. The aim of this study was to develop a noninvasive model to assess liver fibrosis in CHB patients using clinical and routine laboratory data.This was a retrospective study on 235 treatment-naive viremic CHB patients. Univariate analysis of data from the training cohort (n = 150) followed by multivariate logistic regression were performed to identify independent predictors of significant fibrosis and generate predictive models. The models were validated with the remaining patients or validation cohort (n = 85) and by receiver operating characteristics (ROC) analysis.Body mass index (BMI), platelet count, serum albumin, and total bilirubin levels were identified as independent predictors of bridging fibrosis or cirrhosis (Ishak stage 3-6). ROC analysis was performed using the predictive probabilities derived from the regression models. The area under the ROC curve of the best model was 0.803 (95% CI: 0.729-0.878) for the training cohort, 0.765 (95% CI: 0.644-0.885) for the validation cohort, and 0.791 (95% CI: 0.728-0.854) for the entire cohort. Using the low cut-off probability of 0.15, significant fibrosis could be excluded in 83 patients of the total patient population (negative predictive value 0.92).Our noninvasive model comprising BMI and three routine laboratory tests was accurate in predicting absence of significant fibrosis. Application of this model could provide useful additional information on the stage of disease, guide future management decisions, and potentially decrease the need for liver biopsy in some CHB patients.

Nonalcoholic fatty liver disease is the most common chronic liver disease. Fatty pancreas has also been described but is difficult to assess. It is now possible to measure pancreatic and liver fat accurately with magnetic resonance imaging (MRI). We aimed to define the normal range of pancreatic fat and identify factors associated with fatty pancreas. In addition, the effect of fatty liver and fatty pancreas on insulin resistance (IR) and pancreatic β-cell function was studied.Fat-water MRI and proton-magnetic resonance spectroscopy were performed on 685 healthy volunteers from the general population to measure pancreatic and liver fat, respectively. On the basis of fasting plasma glucose and insulin levels, the IR and β-cell function were assessed using the homeostasis model assessment (HOMA).Among subjects without significant alcohol consumption or any component of metabolic syndrome, 90% had pancreatic fat between 1.8 and 10.4%. Using the upper limit of normal of 10.4%, 110 (16.1%; 95% confidence interval 13.3-18.8%) subjects had fatty pancreas. On multivariable analysis, high serum ferritin, central obesity, and hypertriglyceridemia were independent factors associated with fatty pancreas. Subjects with both fatty pancreas and fatty liver had higher HOMA-IR than did those with either condition alone. Fatty pancreas was not associated with HOMA-β after adjusting for liver fat and body mass index.In all, 16.1% of this community cohort of adult Hong Kong Chinese volunteers had a fatty pancreas by our definition. Central obesity, hypertriglyceridemia, and hyperferritinemia are associated with fatty pancreas. Individuals with fatty pancreas have increased IR.

Nonalcoholic fatty liver disease (NAFLD) is increasing in prevalence worldwide. This study aimed to validate the NAFLD fibrosis score in the Chinese population.NAFLD patients were prospectively recruited for liver biopsy and blood tests. The NAFLD fibrosis score was calculated as -1.675 + 0.037 x age (yr) + 0.094 x BMI (kg/m(2)) + 1.13 x impaired fasting glucose/diabetes (yes = 1, no = 0) + 0.99 x AST/ALT ratio-0.013 x platelet (x10(9)/L)-0.66 x albumin (g/dL). Advanced fibrosis was defined as stage 3 to 4 fibrosis.One hundred sixty-two patients (age 46 +/- 10 yr, male 59%) were included in the study. Advanced fibrosis was found in 18 (11%) patients. Only 11 of 128 patients with the NAFLD fibrosis score below the proposed low cutoff point (-1.455) were under-staged, resulting in a high negative predictive value of 91%. Only two patients exceeded the proposed high cutoff point (0.676), but neither had advanced fibrosis. If the NAFLD fibrosis score was implemented in the Chinese population, 79% of liver biopsies could be avoided.The NAFLD fibrosis score has high negative predictive value in excluding advanced fibrosis in the Chinese population, and can reduce the burden of liver biopsy in the vast majority of cases. Since there were few cases of advanced fibrosis in this cohort, this study had limited power in validating the high cutoff point.

We aimed to study the predictive ability of model for end-stage liver disease (MELD) for short-term mortality in chronic hepatitis B.All patients admitted from 1996 to 2003 because of chronic hepatitis B and its related complications were identified by electronic search of the hospital database. MELD and Child-Turcotte-Pugh (CTP) scores on initial admissions were calculated. Cox proportional hazard model was used to determine the factors associated with mortality. The area under receiver operator characteristics curve (AUC) was used to determine the predictive abilities of the two models for 3-month and 1-yr mortalities.A total of 2,073 patients was admitted because of liver-related problems and 506 patients had chronic hepatitis B-related complications. Two hundred fifty-six (51%) patients died and 16 (3%) patients underwent liver transplantation. In multivariate analysis, MELD and CTP scores were independent predictors of 3-month and 1-yr mortality. Other independent predictors of mortality included older age, hepatocellular carcinoma (HCC), lamivudine treatment, and lower serum sodium. At both 3 months and 1 yr, the AUC of the MELD score (0.65 and 0.63, respectively) was significantly lower than that of the CTP score (0.75 and 0.77, respectively) (p0.0001). The differences remained significant when only liver cirrhosis patients without HCC at presentation were analyzed, but the AUC of the two scores became comparable when patients on lamivudine were excluded.The MELD score is a valid prognostic model in decompensated chronic hepatitis B. Lamivudine treatment may affect the performance of MELD score. Other variables including those in CTP score may improve its predictive ability.