HBV-related Chronic Liver Disease Research Articles

Screening for and surveillance of high-risk patients with HBV-related chronic liver disease: Promoting the early detection of hepatocellular carcinoma in China

In China, hepatocellular carcinoma (HCC) is the second most common cancer in urban areas and first most common in rural areas. It ranks as the second leading cause of cancer-related deaths in males and the third leading cause of cancer-related deaths in females, with the total mortality rate of 26.26 per 100,000. Currently, people with hepatitis B virus (HBV) infection are a major population at risk of developing HCC in China. In fact, there are 93 million Chinese who are HBV carriers, and about 20 million of them have chronic HBV infection. Several cohort studies have shown that screening high-risk patients with HBV-or HCV-related chronic liver disease may improve the rate of early HCC detection and the rate of curative treatment. However, a government-funded national program to screen for high-risk patients with HBV-related chronic liver disease has yet to be established in China. Although several remarkable advances in HCC management have been made during the past few decades, most patients with HCC still present with advanced-stage disease, thus reducing the chance of curative treatment. Based on firsthand experience in Japan and other countries or areas, this work examined the current status, challenges, and prospects for the future of early detection of HCC in China. Findings suggested the need for a systematic guideline for the standardized management of HCC, a government-funded nationwide screening and surveillance program for high-risk patients with HBV-related chronic liver disease, and extensive use of des-γ-carboxyprothrombin (DCP) as a screening tool in China in order to facilitate the early detection of HCC in China.

Carbohydrate 19.9 Antigen Serum Levels in Liver Disease

Background. Carbohydrate 19.9 antigen (CA19.9) has been used in the diagnosis and followup of gastrointestinal tumours. The aim of this prospective longitudinal study was the evaluation of CA19.9 levels in patients with chronic hepatitis and hepatic cirrhosis hepatitis C virus and B virus correlated. Materials and Methods. 180 patients were enrolled, 116 with HCV-related chronic liver disease (48% chronic hepatitis, 52% cirrhosis) and 64 with HBV-related chronic liver disease (86% chronic hepatitis, 14% cirrhosis). Patients with high levels of CA19.9 underwent abdominal ecography, gastroendoscopy, colonoscopy, and abdominal CT scan. Results. 51.7% of patients with HCV-related chronic liver disease and 48.4% of those with HBV-related chronic liver disease presented high levels of CA19.9. None was affected by pancreatic or intestinal neoplasia, cholestatic jaundice, or other diseases potentially able to induce Ca19.9 elevations. CA19.9 levels were elevated in 43.3% of HCV chronic hepatitis, in 56.3% of HCV cirrhosis, in 45.1% of HBV chronic hepatitis, and in 58% of HBV cirrhosis. Conclusions. CA19.9 commonly increases in the serum of patients with chronic viral hepatitis. Elevation of CA 19.9 is not specific for neoplastic disease and is related to the severity of fibrosis and to the viral aetiology of hepatitis.

Liver transplantation for HBV-related cirrhosis in Europe: An ELTR study on evolution and outcomes

HBV-related chronic liver disease is one of the most common indications for liver transplantation (LT) in Europe. The ELTR database was used to evaluate outcomes and evolution over 20 years (01/1988 and 12/2010). HBV transplanted patients were analysed according to indication for LT: decompensated cirrhosis (HBVdec) or hepatocellular carcinoma (HBV/HCC). These groups were compared with co-infected patients HBV/HDV (HBDV), HBV/HCV (HBCV), HBV/HDV/HCV (HBDCV); n = 16,664 and with HCV patients (n = 2452) according to LT indication. 5912 patients were transplanted for HBV (78% HBVdec, 22% HBV/HCC), with HBV/HCC patients who increased from 15.8% in 1988-1995 to 29.6% in 2006-2010 (p < 0.001). In HBVdec patients, 1, 3, 5, and 10 year patient and graft survival was 83%, 78%, 75%, 68%, and 80%, 74%, 71%, 64%, respectively, significantly better than HBV/HCC (84%, 73%, 68%, 61%, and 81%, 70%, 65%, 58% respectively; p = 0.001 and p = 0.026). In 2006-2010 patient and graft survival significantly improved compared to 1988-1995, both for HBVdec and HBV/HCC (each p < 0.001). A better patient and graft survival was seen in HBV/HCC patients with HBV-DNA(-) compared to HBV-DNA(+) at the time of LT (p < 0.001). Disease recurrence, as cause of death/graft loss, was significantly reduced in recent years compared to the past: currently <1% for HBVdec and 3% for HBV/HCC. Outcomes of LT for HBV have improved in recent years, with disease recurrence being no longer a significant cause of death/graft loss. HBV-DNA at the time of LT seems to influence survival only in HBV/HCC patients.

Etiologic types of end-stage chronic liver disease in adults

Whole native livers from orthotopic liver transplant (LT) recipients provide an ideal resource material for the proper identification and etiologic evaluation of end-stage liver diseases in these patients. This study determined the etiologic types of chronic liver disease (CLD) in adults of our geographic region receiving living donor LT and projected approximate estimates of their current prevalence and temporal changes in these in the general population. The final etiologic categorization of CLD in 372 adult LT recipients was made only after correlating the morphologic findings on explanted whole native livers with all pre-LT data and diagnosis. The final etiologic categorizations of end-stage CLD in the majority (88.4%) of explanted livers in our series were as follows: hepatitis virus related--48.6% [hepatitis C virus (HCV)--31.1%, hepatitis B virus (HBV)--15.9%, HCV and HBV--1.6%]; alcohol related--23.1%; and NALD related--16.7%. Of 84 cases clinically considered as cryptogenic cirrhosis, 57 and nine were finally categorized as nonalcoholic fatty liver disease (NAFLD) cirrhosis and noncirrhotic portal fibrosis, respectively. Hepatocellular carcinoma (HCC) was found in 20.7% of all livers, 81.8% of these tumors developing in HBV-related and/or HCV-related CLD and 9.1% each in alcohol-related and NAFLD-related CLD. The etiology of end-stage CLD in adults of our region has changed over time. HCV, more than HBV, is now the major cause of both CLD and HCC; alcohol-related CLD has increased significantly and several cases of cirrhosis clinically considered as cryptogenic, some of them with HCC, evolve from NAFLD. A proportion of cryptogenic cirrhosis cases that require LT are constituted by the noncirrhotic disease noncirrhotic portal fibrosis.

Impact of hepatitis B virus (HBV) preS/S genomic variability on HBV surface antigen and HBV DNA serum levels

To evaluate whether hepatitis B virus (HBV) preS/S gene variability has any impact on serum hepatitis B surface antigen (HBsAg) levels and to analyze the replication capacity of naturally occurring preS/S variants, sera from 40 untreated patients with HBV-related chronic liver disease (hepatitis B e antigen [HBeAg]-positive, n = 11; HBeAg-negative, n = 29) were virologically characterized. Additionally, phenotypic analysis of three different preS/S variant isolates (carrying a 183-nucleotide deletion within the preS1 region, the deletion of preS2 start codon, and a stop signal at codon 182 within the S gene, respectively) was performed. HBV infecting 14 (35%) patients had single or multiple preS/S genomic mutations (i.e., preS1 and/or preS2 deletions, preS2 start codon mutations, C-terminally truncated and/or "a" determinant mutated S protein). Presence of preS/S variants negatively correlated with HBsAg titers (r = -0.431; P = 0.005) and its prevalence did not significantly differ between HBeAg-positive and HBeAg-negative patients. No correlation was found between HBsAg and HBV DNA levels in patients infected with preS/S mutants, whereas a significant correlation was found between HBsAg and viremia levels (r = 0.607; P = 0.001) in patients infected with wild-type HBV strains. HepG2 cells replicating the above-mentioned three preS/S variants showed significant reduction of HBsAg secretion, retention of envelope proteins in the endoplasmic reticulum, less efficient virion secretion and nuclear accumulation of significantly higher amounts of covalently closed circular DNA compared with wild-type HBV replicating cells. In patients infected with preS/S variants, HBV DNA replication and HBsAg synthesis/secretion appear to be dissociated. Therefore, the use of HBsAg titer as diagnostic/prognostic tool has to take into account the frequent emergence of preS/S variants in chronic HBV infection.

Predictive value of serum gelsolin in hepatitis B virus (HBV)-related chronic liver disease

Gelsolin, an actin-binding protein, which serves as a substrate of caspase in tissue injury has been proposed as a prognostic marker in acute liver injury, but its relationship with human hepatitis B virus (HBV)-related hepatitis at various stages is still unclear. This study was conducted in order to investigate the predictive value of serum gelsolin in HBV-related chronic liver disease. The observation group included 101 patients with HBV-related chronic liver disease and 96 healthy adults were selected as the control group. The enzyme linked immunosorbent assay (ELISA) method was used to detect the gelsolin level in the serum. The concentration of serum gelsolin level of the observation group (54.099 ± 23.688 ig/ml) was much lower (P = 0.000) than that of the control group (186.372 ± 37.549 ig/ml). The concentration of serum gelsolin in chronic HBV hepatitis patients (64.158 ± 21.389 ig/ml), liver cirrhosis patients (50.067 ± 21.658 ig/ml) and acute-on-chronic liver failure patients (37.012 ± 21.231 ig/ml) was considerably different (P =0.013) and decreased as the severity of the pathogenetic condition increased. Serum gelsolin levels of patients with HBV-related chronic liver disease had negative correlations with model for end-stage liver disease (MELD) scores (r = -0.348, P = 0.001) and Child-Pugh scores (r = -0.487, P = 0.001). The serum gelsolin level may be a potential marker of the severity of hepatic injury. Key words : Gelsolin, hepatitis B virus (HBV)-related chronic liver disease, predictive value.

The Seroconversion Rate of Hepatitis A Virus Vaccination among Patients with Hepatitis B Virus-Related Chronic Liver Disease in Korea

Background/AimsThe aim of this study was to evaluate the seroconversion rate of a hepatitis A virus (HAV) vaccination in patients with hepatitis B virus (HBV)-related chronic liver disease (CLD).MethodsAnalyses were conducted using clinical records from 94 patients with chronic HBV infection who were seronegative for IgG anti-HAV antibodies between September 2008 and June 2009. Two doses of an HAV vaccine were administered 24 weeks apart. A third vaccine dose was administered only for patients seronegative for anti-HAV antibodies at week 48.ResultsThe seroconversion rate of anti-HAV following the two-dose vaccination was 86.17%. The seroconversion rate of anti-HAV was not significantly different according to age or status of liver disease. The rate was higher in female than in male patients. A third HAV vaccine dose was administered to 13 patients seronegative for anti-HAV after the two-dose regimen, and 84.62% of these patients showed seroconversion at week 72.ConclusionsHAV vaccination is effective in most Korean patients with HBV-related CLD, and it might be necessary to evaluate three-dose vaccination approach for non-responders to the conventional regimen to maximize the success of an HAV vaccination program.

IL-17 expression is correlated with hepatitis B‑related liver diseases and fibrosis

IL-17-producing T cells (Th17) have been found to play important roles in several liver diseases, but few studies have evaluated the function of such cells in hepatitisB (HBV)‑related diseases, especially in hepatic fibrosis. In this study, we examined the expression of IL‑17 in patients with different chronic HBV-related diseases, and assessed the association between IL-17 expression and the degree of fibrosis. The method of immunohistochemistry was used to evaluate the localization of intrahepatic IL-17. We demonstrated significantly increased expression of IL‑17 in HBV-related chronic liver diseases, especially in liver fibrosis, and that the level of IL-17 is strongly correlated with the degree of fibrosis. Furthermore, we found that intrahepatic IL‑17 was mainly localized in the fibrosis region. Our data reveal important roles of IL-17 and IL-17-producing cells in the progression of HBV related chronic liver diseases, especially in the formation of liver fibrosis.

Update on the Recommended HBV Screening in the United States

Hepatitis B virus (HBV) infection is a serious public health problem that can be associated with HBV-cirrhosis and hepatocellular carcinoma (HCC). HBV-related chronic liver disease is particularly prevalent in the Asian population with significant disparity. Although convenient HBV screening and diagnosis tests are safe and effective, HBV vaccination have been available for many years, under-screening and under-diagnosis of HBV infection is still a serious problem in the USA and worldwide. This article systemically reviewed effectiveness of universal HBV vaccination programs that have been implemented in many countries and regions, the facts of HBV under-screening in the U.S., especially in Asian Americans, and the updated recommendations of HBV screening and vaccination by Center of Disease Control and Prevention (CDC). [N A J Med Sci. 2011;4(1):18-22.]

Steatosis in chronic hepatitis B: Prevalence and correlation with biochemical, histologic, viral, and metabolic parameters

Hepatic steatosis (HS) is highly prevalent in chronic hepatitis C and is an important variable predicting progression of histological injury, insulin resistance, and reduced response to antiviral therapy. There are limited data on HS in patients with chronic hepatitis B (CHB). This is relevant since response to current antiviral therapies for CHB is rather limited. We investigated the spectrum and predictors of HS in CHB patients. Liver biopsies of consecutive patients of chronic Hepatitis B Virus (HBV) infection were studied and were categorized as: Group I - hepatosteatosis (>5%) and Group II - no steatosis (£5%). Anthropometric, histological, biochemical, virological, and metabolic determinants were compared. Logistic regression analysis was applied to identify variables that were independently associated with the presence of steatosis. Of the 350 patients, 118 (33.7%) liver biopsies showed steatosis (Group I); 65 (55.1%) had mild (6 to <25%) and 53 (44.9%) had moderate to severe steatosis ((3)25%). Patients in group I, compared with group II, were older (35.5 ± 10.5 vs 27.9 ± 14.0 years, P < 0.01), predominantly male (M: F, 10.8: 1 vs 4.8: 1, P = 0.035), obese (75.0% vs 23.4%, P P < 0.01), with higher triglycerides (138.8 ± 62.1 vs 88.0 ± 27.9, P = 0.02), with higher cholesterol (171.9 ± 43.5 vs 139.3 ± 37.6, P = 0.017), and with higher serum insulin (13.1 ± 9.1 vs 9.1 ± 6.0, P < .027) levels. HBV DNA level was significantly lower in group I than group II; however, HBV genotype did not influence HS. By multivariate regression analysis, only high serum triglyceride level was independent parameter associated with HS. Steatosis is seen in one-third cases with HBV-related chronic liver disease and is associated with host metabolic factors, especially serum triglyceride levels, whereas HBV DNA level negatively correlated with HS.

Update on Chronic Hepatitis B

Chronic hepatitis B virus (HBV) infection affects over 350 million people worldwide and over 1 million die annually of HBV-related chronic liver disease. The prolonged immunologic response to HBV infection leads to the development of cirrhosis, liver failure, or hepatocellular carcinoma (HCC) in up to 40% of patients. The implementation of mass immunization programs has dramatically decreased the incidence of HBV infection among infants, children, and adolescents in many countries, but there remains a large number who were infected with HBV before such programs. A variety of host, viral, and external factors influence HBV disease progression and the risk of chronic infection. Six drugs are currently FDA-approved for the treatment of chronic HBV infection. While novel antiviral drugs have improved the management of cirrhosis, strategies to prevent and treat HCC remain inadequate.

Hepatitis B virus BCP, precore/core, X gene mutations/genotypes and the risk of hepatocellular carcinoma in India

The study aims to characterize mutations of the HBV genome involving BCP, Precore/core and X regions and also defines HBV genotypes in patients of hepatocellular carcinoma (HCC). The study involved 150 HBV-related HCC cases and 136 HBV-related chronic liver disease patients without HCC as controls. HBV DNA was subjected to mutational analysis using SSCP technique, genotyping by RFLP, and direct nucleotide sequencing. HBV DNA was found in 58.7% (88/150) of the HCC cases and 74.3% (101/136) of controls. HBV mutants were observed in 44.3% of HCC cases and 43.2% of controls. HBV/D was prevalent amongst the patients and controls, followed by HBV/A. The prevalence of the TT1504 mutation in the X gene, the V1753 and T1762/A1764 mutations in the BCP region, and G1914 mutation in the core gene were significantly higher in the HCC group than in the non-HCC group. Multivariate analyses showed that the TT1504, V1753, A1762T/G1764A, and the G1914 mutations and the patient's age, sex, and HBeAg status increased the risk of HCC development significantly. Also, patients with HCC had lower levels of serum albumin, viral load, and platelet counts but higher values of alkaline phosphatase, alanine aminotransferase, aspartate aminotransferase, bilirubin, and Alpha feto-protein than those of controls (P < 0.001 for all comparisons). HBV/D was the predominant genotype associated with HCC cases seen in India. The presence of different types of HBV mutations, age, sex, HBeAg status, and viral load was found to increase significantly the risk of HCC development in India.

OL-058 Methylation status of hepatic IGF-II promoter 3 in HBV-related chronic liver diseases

OL-058 Methylation status of hepatic IGF-II promoter 3 in HBV-related chronic liver diseases

Variability in liver stiffness values from different intercostal spaces

To investigate the variability in liver stiffness measurement (LSM) values from the fifth, sixth and seventh intercostal space (ICS) and examine whether LSM better predicts significant fibrosis (F2-4) and cirrhosis when LSM is performed at the same site as liver biopsy (LB). This study enrolled 91 consecutive patients with hepatitis B virus (HBV)-related chronic liver disease (CLD) who underwent both LB and LSM between September 2007 and January 2009. The mean age of the patients was 45.4 years (66 men and 25 women). F1 fibrosis was noted in 12 patients (13.2%), F2 in 28 (30.7%), F3 in 15 (16.5%) and F4 in 36 (39.6%). The mean LSM values from the fifth, sixth and seventh ICS were 11.6, 11.1 and 10.9 kPa respectively. The mean LSM value from the same site as LB was 11.0 kPa. An interclass correlation analysis showed no significant difference in LSM values from the fifth, sixth and seventh ICS and the same site as LB. The area under the receiver operating characteristic curves of LSM values from the fifth, sixth and seventh ICS and the same site as LB for predicting significant fibrosis were 0.815, 0.838, 0.818 and 0.837, respectively, and those for cirrhosis were 0.919, 0.916, 0.907 and 0.913, respectively, with all overlapping confidence intervals. Any LSM value from the fifth, sixth or seventh ICS can predict significant fibrosis and cirrhosis with considerable accuracy without statistical differences regardless of correspondence with LB site in patients with HBV-related CLD.

Management of HBV-related cirrhosis: Role of nucleoside analogs

In the management of HBV related cirrhosis of the liver, viral suppression with safe and effective antiviral agents is essential. Besides, antiviral therapy for long term use in cirrhotics should be safe and affordable with low risk of drug resistance. Treatment of compensated HBV cirrhosis can diminish the risk of hepatic decompensation and progression to hepatocellular carcinoma [HCC]. Regression of fibrosis and reversal of cirrhosis have also been reported with antiviral therapy. Further, in decompensated cirrhosis, although liver transplantation is considered as the definitive therapy, inhibition of viral replication before transplantation can delay the need for liver transplant and also prevent HBV recurrence in the post-transplantation period. These patients while on antiviral therapy need close monitoring for viral resistance and adverse events, besides continued surveillance for HCC. This article reviews the literature on the role of nucleoside analogues in the management of HBV related chronic liver disease.

Polymorphisms and plasma soluble levels of E-selectin in patients with chronic hepatitis B virus infection

Infections with hepatitis B virus (HBV) may lead to a distinct clinical outcome which is partially related to host genetic variability. Our aim was to investigate the relationships between the polymorphisms of the E-selectin gene and disease progression in a HBV-infected Chinese Han population, and also to determine the plasma soluble E-selectin (sE-selectin) levels in this population. Genomic DNA was extracted from the peripheral blood of 367 HBV carriers and 281 healthy controls. Two polymorphisms (PstI for A561C and HphI for G98T) of the E-selectin gene were analyzed by polymerase chain reaction-restriction fragment length polymorphism. Circulating sE-selectin levels were measured by specific enzyme-linked immunosorbent assay (ELISA). The frequency of the C allele (AC or CC) of the A561C polymorphism was significantly higher in patients with liver cirrhosis (LC) compared to controls (p=0.002). There was no difference in allele distribution of the G98T polymorphism. But in patients with LC, classified according to the Child-Pugh classification, the frequency of the T carrier (GT and TT) was significantly different between Child-Pugh class A and class B plus C (p=0.009). Levels of plasma soluble E-selectin (sE-selectin) were significantly increased in HBV carriers with chronic hepatitis (CH) and LC (mean+/-SD 68.94+/-34.09 and 43.39+/-18.00 ng/mL) compared to controls (13.96+/-7.50 ng/mL) (p<0.01). In the LC subgroup, levels of sE-selectin were significantly decreased from Child-Pugh class A to class C (p<0.05). In each group, individuals with the C allele showed higher sE-selectin levels than those with the A allele (p<0.05). This is the first report describing the association between E-selectin polymorphisms and HBV-related chronic liver diseases. Our data suggest that the A561C polymorphism of the E-selectin gene may be associated with disease progression in patients with chronic HBV infection and control the expression of plasma soluble levels, while the G98T polymorphism may be related to fibrotic severity in the Chinese population.

Aetiology, complications, and preventive measures of liver cirrhosis; Elobeid Hospital; West Sudan

Objectives: to determine the common causes of liver cirrhosis, identify the common complications, and to find the possible preventive measures of the disease at Elobeid Hospital; West Sudan. Patients and method: This is a retrospective hospital based study. It was carried out in Elobeid Teaching Hospital. The medical and socio-demographic data of 61 patients who were admitted to the medical wards in the period from January 2006 to June 2007 with liver cirrhosis were retrieved and reviewed. Results: Out of the 61 patients 38(62%) were males. The age of the patients ranged from 17 to 80 years, with mean (± SD) of 49 ± 12.9 years. Alcohol consumption was found to be the commonest cause of liver cirrhosis, followed by hepatitis B infection. Hepatitis C infection determined as a cause of liver cirrhosis in only one patient. Common complications included ascites (92%), hepatic encephalopathy (19%), portal hypertension (8%), hepatocellular carcinoma (5%), and spontaneous bacterial peritonitis (3%). In the majority of patients, management was based on diuretics (furosemide and spironolactone) and dietary sodium restriction. Few patients received albumin infusion before therapeutic ascitic fluid aspiration. Silymarin in combination with multivitamins was commonly used in management of our patients. Conclusion: Ethanol consumption and HBV infection were the commonest causes of liver cirrhosis in our patients. Religious and Health education to abandon ethanol intake and prohibit traditional practices that could predispose individuals to hepatitis B infection should be emphasized. Universal immunization with hepatitis B vaccine should be commenced to reduce the incidence of HBVrelated chronic liver diseases. Keywords: alcohol, hepatitis B, Hepatitis C, hepatocellular carcinoma.Sudan Journal of Medical Sciences Vol. 3 (1) 2008: pp. 25-28

Genetic Variability of Hepatitis B virus and Response to Antiviral Therapy

Hepatitis B virus (HBV) infection is a global health issue. Effective and individualized treatment of chronic hepatitis B to prevent progression to end-stage liver diseases and hepatocellular carcinoma is needed. HBV can be classified into eight genotypes (A-H) on the basis of genome sequence divergence. In addition, several naturally occurring HBV mutants have also been identified. The epidemiology of HBV genotypes and their implications for response to antiviral therapy have become increasingly recognized. Recent studies suggested that responses to standard interferon treatment in patients with genotype A or B are better than those with genotype C or D; however, conflicting results exist regarding the response to pegylated interferon. The influence of dose and duration on interferon-based therapy remains to be clarified. In addition to genotype, naturally occurring mutations such as precore and core promoter mutations have also attracted much attention, because they have been shown to affect the disease progression of HBV-related chronic liver disease and possibly the response to antiviral therapy. Here, we review the differences in antiviral theraputic response among HBV genotypes and discuss the role of precore or core promoter mutations in response to antiviral therapy.

Prognostic system for hepatitis B virus (HBV)-related hepatocellular carcinoma- Prospective validation of the Chinese University Prognostic Index

4591 Background: Prognosis of patients with HBV-related chronic liver disease and hepatocellular carcinoma (HCC) depends on both extent of tumor involvement and functional hepatic reserve. The Chin...

Hepatic venous pressure gradient as a predictor of fibrosis in chronic liver disease because of hepatitis B virus

Liver biopsy has been considered to be a gold standard for assessing hepatic fibrosis. Sample variability, interobserver variability and step-wise evaluation limit its use. Hepatic venous pressure gradient (HVPG) correlates with hepatic fibrosis in chronic liver disease (CLD) because of hepatitis C. To evaluate the utility of HVPG for assessing hepatic fibrosis in patients with hepatitis B virus (HBV)-related CLD. Sixty-one patients with HBV-related CLD who underwent both liver biopsy and hepatic haemodynamic studies were studied. Forty-nine (80.3%) patients had clinically significant portal hypertension (PHT) (HVPG>or=10 mmHg), 39 (63.9%) severe PHT (i.e. HVPG>or=12 mmHg), six (9.8%) HVPG<or=5 mmHg and another six (9.8%) had preclinical PHT (i.e. HVPG>5 but <10 mmHg). A positive correlation between HVPG and fibrosis score was found (r=0.436, P<0.001). In patients with HVPG<10 or <12 mmHg there was a significant correlation with fibrosis score (r=0.603, P=0.029 and r=0.887, P<0.001 respectively). A positive correlation also existed in patients with HVPG>or=10 mmHg and in patients with HVPG>or=12 mmHg (r=0.512, P<or=0.001 and r=0.543, P<0.001 respectively). Receiver operating characteristic curve of HVPG for the prediction of advanced fibrosis (stage>or=3) had an area under curve of 0.906. HVPG value above 13.0 mmHg had a sensitivity of 79% and a specificity of 89% for predicting advanced fibrosis on histology. HVPG correlates well with the degree of histological fibrosis in patients with HBV-related CLD.