Fibrosis In Chronic Hepatitis B Research Articles

Serum ceruloplasmin levels correlate negatively with liver fibrosis in males with chronic hepatitis B: a new noninvasive model for predicting liver fibrosis in HBV-related liver disease.

AimsThis study aimed to investigate associations between ceruloplasmin (CP) levels, inflammation grade and fibrosis stages in patients with chronic hepatitis B (CHB) and to establish a noninvasive model to predict cirrhosis.MethodsLiver biopsy samples and sera were collected from 198 CHB patients randomized into a training group (n=109) and a validation group (n=89). CP levels were determined using nephelometric immunoassays. Relationships between CP and liver inflammation and fibrosis were analyzed by Spearman rank correlation. Receiver operator characteristic (ROC) curves were used to evaluate the diagnostic value of CP for determining liver fibrosis in CHB. The liver pathology-predictive model was built using multivariate logistic regression analysis to identify relevant indicators.ResultsCP levels were lower in males than in females, lower in patients with inflammation stage G4 compared to other stages and lower in cirrhotic compared to non-cirrhotic patients. Using area under the curve (AUC) values, CP levels distinguished different stages of inflammation and fibrosis. Multivariate analysis showed that CP levels were all significantly associated with cirrhosis in males. A model was developed combining routine laboratory markers APPCI (alpha-fetoprotein [AFP], prothrombin time, and platelets [PLT] with CP) to predict fibrosis in CHB patients. The APPCI had a significantly greater AUC than FIB-4 (aspartate aminotransferase [AST]/ alanine aminotransferase [ALT]/PLT/age), APRI (AST/PLT ratio index), GPI (globin/PLT), and APGA (AST/PLT/gammaglutamyl transpeptidase [GGT]) models (all P-values<0.001).ConclusionsCP levels correlate negatively and indirectly with inflammation and fibrosis stages in male CHB patients. The APPCI model uses routine laboratory variables with CP to accurately predict liver fibrosis in CHB.

Fibroscan can avoid liver biopsy in Indian patients with chronic hepatitis B

Liver fibrosis is an established determinant of prognosis and therapy in chronic hepatitis B (CHB). The role of fibroscan in assessing fibrosis in CHB remains unclear. Present study was designed to correlate fibroscan with liver biopsy and determine whether fibroscan can avoid liver biopsy in patients with CHB. Fibroscan and liver biopsy were performed in 382 consecutive patients with CHB. Biopsies were reviewed by pathologist blinded to the fibroscan value. Discriminant values of liver stiffness measurement (LSM) to reasonably exclude and predict significant fibrosis were calculated from receiver operating characteristic (ROC) curves. The factors affecting LSM independent of fibrosis were assessed. Three hundred fifty-seven patients were included (mean age 30.1 ± 9.7 years, male : female 17 : 3). There was significant correlation between LSM and histological fibrosis (r = 0.58, P < 0.001). The area under ROC curve of LSM for significant fibrosis (F0-1 vs. F2-4), bridging fibrosis (F0-2 vs. F3-4), and cirrhosis (F0-3 vs. F4) was 0.84 (95% CI: 0.78-0.89), 0.94 (95% CI: 0.89-0.99), and 0.93 (95% CI: 0.85-1.00), respectively. LSM < 6.0 KPa could exclude significant (F ≥ 2) and bridging fibrosis (F ≥ 3) with a negative predictive value (NPV) of 92.4% and 99.5%, respectively. Cut-off of 9 KPa could detect significant (F ≥ 2) and bridging fibrosis (F ≥ 3) with specificity of 95% and 97%, respectively, and had a positive predictive value (PPV) of 84.3% in predicting significant fibrosis. LSM < 6 KPa and > 9 KPa matched with histological fibrosis in 227/250 (91%) patients. Therefore, fibroscan could avoid liver biopsy in 70% (250/357) patients with an accuracy > 90%. Histological fibrosis, ALT > 5 times, and age > 40 years were independent determinants of increased liver stiffness. Fibroscan accurately assessed fibrosis and could avoid liver biopsy in more than two-thirds of patients with CHB.

APRI, the FIB-4 score, and Forn’s index have noninvasive diagnostic value for liver fibrosis in patients with chronic hepatitis B

The aim of this study was to evaluate the potential use of serum transforming growth factor-β1 (TGF-β1), tissue inhibitor of metalloproteinase-1 (TIMP-1), fetuin-A, and fibroblast growth factor 21 (FGF21) in the detection of liver fibrosis in patients with chronic hepatitis B (CHB). The value of the noninvasive fibrosis models - that is, the aspartate aminotransferase to platelet ratio index (APRI), the fibrosis index based on the four factors (FIB-4) score, and Forn's index - was also examined. CHB patients who underwent liver biopsy for the evaluation of fibrosis were included in the study. A total of 73 patients were divided into two groups according to their METAVIR scores (F0-1, no/minimal fibrosis; F2-4, significant fibrosis). Serum levels of TGF-β1, TIMP-1, fetuin-A, and FGF21 were measured besides APRI, FIB-4, and Forn's scores. The area under the receiver operating characteristic curve was measured for each parameter, followed by calculation of sensitivity, specificity, and positive and negative predictive values. APRI, FIB-4, and Forn's index scores were significantly higher in patients with significant fibrosis (P<0.05). There was no difference between no/minimal fibrosis and significant fibrosis groups in terms of serum levels of TGFβ-1, TIMP-1, fetuin-A, and FGF21 (P>0.05). The areas under the receiver operating characteristic curve for TGF-β1, TIMP-1, fetuin-A, FGF21, APRI, FIB-4, and Forn's index were 0.445, 0.483, 0.436, 0.585, 0.662, 0.687, and 0.680, respectively. Our results suggest that serum TGF-β1, TIMP-1, fetuin-A, and FGF21 are not useful for the assessment of the extent of liver fibrosis in CHB in this patient group. However, APRI, FIB-4, and Forn's index have a better diagnostic value in patients with significant fibrosis than in those with no/minimal fibrosis.

Magnetic resonance elastography for the detection and staging of liver fibrosis in chronic hepatitis B

We measured the accuracy of magnetic resonance elastography (MRE) for the detection and staging of liver fibrosis in chronic hepatitis B (CHB) and compared it with serum fibrosis markers. Prospective comparison of MRE and routine serum fibrosis markers, namely serum alanine aminotransferase (ALT), serum aspartate aminotransferase (AST), ALT/AST ratio (AAR), AST to platelet ratio index (APRI) and prothrombin index (PI), was performed in 63 consecutive CHB patients who underwent MRE and histological confirmation of liver fibrosis within a 6-month interval. Diagnostic performance of MRE and serum markers for staging fibrosis (≥F1), significant fibrosis (≥F2), advanced fibrosis (≥F3) and cirrhosis (F4) was compared. The study group comprised 63 patients (19 female; mean age ± SD, 50 ± 11.9years). MRE (ρ = 0.94, P < 0.0001), APRI (ρ = 0.42, P = 0.0006), PI (ρ = 0.42, P = 0.0006) and AST (ρ = 0.28, P = 0.028) results correlated significantly with fibrosis stage. MRE was significantly more accurate than serum fibrosis markers for the detection of significant fibrosis (0.99 vs. 0.55-0.73) and cirrhosis (0.98 vs. 0.53-0.77). Sensitivity, specificity, positive predictive and negative predictive values for MRE for significant fibrosis and cirrhosis were 97.4%, 100%, 100% and 96%, and 100%, 95.2%, 91.3% and 100%, respectively. MRE is an accurate non-invasive technique for the detection and staging of liver fibrosis in CHB. • Magnetic resonance elastography is accurate for liver fibrosis detection and staging. • MR elastography is more accurate than serum tests for staging liver fibrosis. • MR elastography can potentially replace liver biopsy in chronic hepatitis B.

Utility of liver stiffness measurement by fibroscan in assessment of fibrosis in patients with chronic hepatitis B

Background and Aim: Assessment of liver fibrosis is an important determinant for staging of disease, prognosis as well as therapeutic decision making in patients with chronic hepatitis B(CHB). Liver biopsy, although is gold standard, has certain limitations. Fibroscan is simple to perform, non-invasive, has good patient acceptance and reproducible. However, role of fibroscan in assessing fibrosis in CHB has remained controversial.

Comparative assessment of liver fibrosis by computerized morphometry in naïve patients with chronic hepatitis B and C

Liver fibrosis, now assessed by liver biopsy or using non-invasive methods, might be different in chronic hepatitis B (CHB) and chronic hepatitis C (CHC). To compare histological amount and pattern of fibrosis in CHB and CHC. Sixty CHB and sixty CHC biopsies from naïve patients, standardized for the spectrum of Metavir fibrosis stages, were analysed for (1) semi-quantitative Metavir activity, steatosis, perisinusoidal fibrosis, alpha-smooth muscle actin immunoreactivity, (2) quantitative morphometry of total and perisinusoidal fibrosis ratio (FR and PFR). Biopsy quality, activity, steatosis, Fibrotest(®) values were not different between the two groups. Correlation between FR and fibrosis stage was stronger in CHB (r = 0.90) than CHC (r = 0.81). Mean FR was 1.5-fold higher in CHC than CHB for early fibrosis stages (F ≤ 2, P = 0.001), with higher PFR in CHC for F0 (P = 0.001), F1 (P = 0.08) and F2 (P = 0.004). Hepatic stellate cell activation index was also higher in CHC than in CHB (P = 0.007). Diagnosis performance of FR for significant fibrosis was not statistically different in CHB than CHC (AUROC 0.92 and 0.87 respectively), but cut-offs optimizing sensitivity and specificity were higher in CHC and their extrapolation to CHB led to 10% decrease in sensitivity. In F ≤ 2 patients, correlation between FR and Fibrotest(®) was only significant in CHC. As compared to CHB, amount of fibrosis is greater in CHC for F ≤ 2 patients, mainly because of higher perisinusoidal fibrosis. These data illustrate difficulty to assess early fibrosis stages by non-invasive methods, and support the need for specific cut-offs in CHB.

DNA methylation patterns of peroxisome proliferator‐activated receptor gamma gene associated with liver fibrosis and inflammation in chronic hepatitis B

Peroxisome proliferator-activated receptor gamma (PPAR gamma) is a nuclear receptor that regulates gene expression of inflammatory mediators in liver injury. Hepatitis B virus (HBV) suppresses the PPAR gamma-mediated transactivation in liver cancerous cell lines. However, the role of PPAR gamma in patients with chronic HBV infection has not fully demonstrated. Our present study was firstly to determine the clinical relevance of peripheral PPAR gamma mRNA levels in chronic hepatitis B (CHB) patients, and then, the DNA methylation of PPAR gamma promoter was investigated. Peripheral blood mononuclear cells (PBMCs) were isolated from 91 CHB patients and 18 healthy controls. The mRNA level of PPAR gamma was determined by quantitative real-time PCR; meanwhile, the CpG island methylation was assessed by methylation-specific PCR. CHB patients showed significantly lower mRNA level of PPAR gamma than healthy controls (P=0.005). The mRNA level was decreased in HBV-DNA-positive group than HBV-DNA-negative group (P=0.041). Interaction analysis demonstrated that the DNA methylation pattern was responsible for the suppression of peripheral PPAR gamma transcription in CHB patients (P=0.003). Furthermore, the hypermethylation of PPAR gamma gene promoter was significantly associated with liver inflammation and fibrosis in CHB. In conclusion, DNA methylation patterns were responsible for the decreased mRNA level of peripheral PPAR gamma in CHB patients. Liver inflammation and fibrosis were found to be associated with hypermethylation of PPAR gamma promoter.

Noninvasive assessment of liver damage in chronic hepatitis B

To evaluate the efficacy of the aspartate aminotransferase/platelet ratio index (APRI) and neutrophil-lymphocyte (N/L) ratio to predict liver damage in chronic hepatitis B (CHB). We analyzed 89 patients diagnosed with CHB by percutaneous liver biopsy and 43 healthy subjects. Liver biopsy materials were stained with hematoxylin-eosin and Masson's trichrome. Patients' fibrosis scores and histological activity index (HAI) were calculated according to the Ishak scoring system. Fibrosis score was recognized as follows: F0-1 No /early-stage fibrosis, F2-6 significant fibrosis, F0-4 non-cirrhotic and F5-6 cirrhotic. Significant liver fibrosis was defined as an Ishak score of ≥ 2. APRI and N/L ratio calculation was made by blood test results. The hepatitis B and control group showed no difference in N/L ratios while there was a significant difference in terms of APRI scores (P < 0.001). Multiple logistic regression analysis revealed that the only independent predictive factor for liver fibrosis in CHB was platelet count. APRI score was significantly higher in cirrhotic patients than in non-cirrhotic patients. However, this significance was not confirmed by multiple logistic regression analysis. The optimum APRI score cut-off point to identify patients with cirrhosis was 1.01 with sensitivity, specificity, positive predictive value and negative predictive value of 62% (36%-86%), 74% (62%-83%), 29% (13%-49%) and 92% (82%-97%), respectively. In addition, correlation analyses revealed that N/L ratio has a negative and significant relationship with HAI (r = -0.218, P = 0.041). N/L ratio was negatively correlated with HAI. APRI score may be useful to exclude cirrhosis in CHB patients.

Reply to Dr Onal: the importance of serum angiotensin-converting enzyme level in chronic hepatitis B

We would like to thank Dr. Onal for his interest in our recent study.1 The non-invasive assessment of liver fibrosis is an ongoing research area of viral hepatitis. Hitherto, these studies have focused mainly on patients infected with hepatitis C.2–4 In this regard, our study is important because we tried to determine whether a new non-invasive fibrosis marker could be possible for patients with chronic hepatitis B as well. Despite our small-sized study, the results were promising. First of all, we did not intend to find a non-invasive marker for discriminating between patients who are in different phases of chronic hepatitis B (CHB). Our main driving force was to discriminate between mild fibrosis and advanced fibrosis using serum angiotensin-converting enzyme level. While in the planning phase of the study, as we mentioned in detailed fashion in the article, we discovered many hypothetical and theoretical facts that could lead to using serum ACE level as a marker of fibrosis in CHB. Although we did not study the power of serum ACE level for discriminating between HbeAg-negative CHB and the inactive hepatitis B virus (HBV) carrier state, we will take Dr. Onal’s valuable opinion into account in our future studies.

Factor XIII Val34Leu mutation accelerates the development of fibrosis in patients with chronic hepatitis B and C

There is considerable variation in liver fibrosis stage and progression to cirrhosis among patients with chronic hepatitis B (CHB) or C (CHC). Coagulation pathway activity due to genetic variations could influence the rate of fibrosis. We investigated thrombotic risk factors and their association with the extent and progression of fibrosis in CHB or CHC patients. In total, 194 patients with CHB (n = 88) or CHC (n = 106) were included. Data on demographic and laboratory findings were collected. Liver biopsies were evaluated according to the Ishak classification system. Fibrosis progression rate (FPR), defined as ratio of fibrosis score to duration of infection, was determined for 131 patients. Prevalence of factor V Leiden, prothrombin G20210A, plasminogen activator inhibitor type-1 (PAI-1) 4G/5G and factor XIIIA Val34Leu mutations was evaluated. Heterozygosity for factor V Leiden, prothrombin G20210A, PAI-1 4G/5G and factor XIIIA Val34Leu mutations was present in 3.1%, 2.1%, 49% and 28% of the patients, respectively. Factor XIII Val34Leu mutation was a risk for enhanced FPR (odds ratio 4.7; P = 0.01). In patients with both factor XIII Val34Leu and PAI-1 4G/5G mutations the risk of an accelerated FPR was further increased (odds ratio 5.0; P = 0.02). Mutations of the other thrombotic genes were not significantly associated with fibrosis stage and FPR. Our data show that factor XIII Val34Leu mutation alone or in combination with PAI-1 4G/5G mutation is a risk factor for an increased rate of liver fibrosis development in patients with CHB or CHC.

Comparison of noninvasive models of fibrosis in chronic hepatitis B

Liver fibrosis influences treatment and surveillance strategies in chronic hepatitis B (CHB). This multicenter study aimed to examine the accuracy of serum fibrosis models in CHB patients including those with low alanine aminotransferase (ALT) levels and serially in those undergoing treatment. We examined noninvasive fibrosis models [Hepascore, Fibrotest, APRI, hepatitis e antigen (HBeAg)-positive and -negative models] in 179 CHB patients who underwent liver biopsy and fibrosis assessment by METAVIR and image morphometry. Serial Hepascore measurements were assessed in 40 subjects for up to 8.7years. Hepascore was more accurate than Fibrotest [area under the curve (AUC) 0.83 vs. 0.72, P=0.05] and HBeAg-positive model (AUC 0.83 vs. 72, P=0.03) for significant fibrosis but was not significantly different to APRI or HBeAg-negative scores. Fibrosis area assessed by morphometry was correlated with Hepascore (r=0.603, P<0.001), Fibrotest (r=0.392, P=0.03), and HBeAg-positive (r=0.492, P=0.001) scores only. Among 73 patients with an ALT <60IU/L, noninvasive models were useful to predict fibrosis (PPV 80-90%) or exclude significant fibrosis (NPV 79-100%). Hepascore increased significantly among patients monitored without treatment and reduced among patients undergoing therapy (0.05/year±0.03 vs. -0.04/year±0.02, P=0.007). Serum fibrosis models are predictive of fibrosis in CHB and assist in identifying subjects with low-normal ALT levels for treatment.

Diagnostic accuracy of transient elastography (FibroScan) versus the aspartate transaminase to platelet ratio index in assessing liver fibrosis in chronic hepatitis B: The role in primary care setting

BackgroundA non-invasive method to assess liver fibrosis by measuring liver stiffness with transient elastography (TE) has been recently introduced. The role of TE among chronic hepatitis B (CHB) patients in...

Noninvasive Markers of Hepatic Fibrosis in Chronic Hepatitis B.

A serum biomarker (FibroTest; Biopredictive, Paris, France; FibroSure; LabCorp, Burlington, USA) and liver stiffness measurement (LSM) by Fibroscan (Echosens, Paris, France) have been extensively validated in chronic hepatitis C. This review updates the clinical validation of serum biomarkers and LSM in patients with chronic hepatitis B (CHB). One meta-analysis combined all published studies and another used a database combining FibroTest individual data. Sensitivity analysis assessed the impact of several factors, including authors’ independence, length of biopsy, ethnicity, hepatitis B early antigen status, viral load, and alanine aminotransferase value. Only two biomarkers had several validations: FibroTest (8 studies, 1,842 patients), and Fibroscan (5 studies, 618 patients). For the diagnosis of advanced fibrosis, the standardized area under the receiver operating curve was 0.84 (0.79–0.86) for FibroTest and 0.89 (0.83–0.96) for LSM, without significant difference. No significant factors of variability were identified for FibroTest’s performance. In conclusion, FibroTest and LSM were the most validated biomarkers of fibrosis in CHB. However, the reliability of Fibroscan must be better assessed.

Mean platelet volume as a fibrosis marker in patients with chronic hepatitis B

Many noninvasive tests have been studied for the diagnosis and determining the liver fibrosis score (LFS). In this study, we aimed to research the correlation of mean platelet volume (MPV) and stage of liver fibrosis in patients with chronic hepatitis B (CHB). Fifty-nine patients with CHB were enrolled retrospectively into the study. Age-sex matched 25 healthy subjects were used as control group. The following data were obtained from computerized patient registry database: HBV-DNA level, hepatitis B e-antigen seropositivity, liver enzymes and function tests, white blood cell count, platelet count, hemoglobin, histological activity index, LFS, and MPV. Patients were divided into two groups: patients without significant fibrosis (F0, F1, or F2) (Group 1) and patients with advanced fibrosis (F3, F4) (Group 2). A statistically significant increase in MPV was seen in patients with CHB compared with healthy controls (8.49±0.84 fl vs.7.65±0.42 fl, P<0.001). Receiver operating characteristic curve analysis suggested that the optimum MPV level cut-off points for CHB was 8.0 fl, with sensitivity, specificity, PPV, and NPV of 68, 76, 86, and 50%, respectively. MPV levels were significantly higher in Group 2 (8.91±0.94 fl, P: 0.009) compared with Group 1 (8.32±0.74 fl). ROC curve analysis suggested that the optimum MPV level cut-off points for Group 2 was 8.45 fl, with sensitivity, specificity, positive and negative predictive value of 77, 59, 45, and 85%, respectively. Multivariable logistic regression model, which consisted of HAI, ALT, HBV-DNA, platelet count, and MPV, was performed. We showed that MPV was independently associated with advanced fibrosis (P: 0.031). We suggest that MPV might help in the assessment of fibrosis in CHB. It should not be considered a stand-alone test for this use owing to nonspecificity with other diseases.

Clinical expression of insulin resistance in hepatitis C and B virus-related chronic hepatitis: Differences and similarities

To investigate the prevalence of the clinical parameters of insulin resistance and diabetes in patients affected by chronic hepatitis C (CHC) or chronic hepatitis B (CHB). We retrospectively evaluated 852 consecutive patients (726 CHC and 126 CHB) who had undergone liver biopsy. We recorded age, sex, ALT, type 2 diabetes and/or metabolic syndrome (MS), body mass index (BMI), and apparent disease duration (ADD). Age, ADD, BMI, prevalence of MS and diabetes in patients with mild/moderate liver fibrosis were significantly higher in CHC. However, the degree of steatosis and liver fibrosis evaluated in liver biopsies did not differ between CHC and CHB patients. At multivariate analysis, age, sex, BMI, ALT and diabetes were independent risk factors for liver fibrosis in CHC, whereas only age was related to liver fibrosis in CHB. We also evaluated the association between significant steatosis (>30%) and age, sex, BMI, diabetes, MS and liver fibrosis. Diabetes, BMI and liver fibrosis were associated with steatosis >30% in CHC, whereas only age and BMI were related to steatosis in CHB. These data may indicate that hepatitis C virus infection is a risk factor for insulin resistance.

Correlation of liver biochemistry with liver stiffness in chronic hepatitis B and development of a predictive model for liver fibrosis

Abstract Aim: To correlate liver stiffness with demographical factors and routine liver biochemistry and to assess the predictive value of these as potential markers of fibrosis. Transient elastography was performed in 1268 chronic hepatitis B (CHB) patients. According to a previous validated study for CHB, liver stiffness of >8.1 and >10.3 kPa were used as cut-off values for defining severe fibrosis and cirrhosis respectively. Liver stiffness correlated positively with bilirubin, alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), globulin, alpha-fetoprotein (AFP) and HBV DNA levels and negatively with albumin and platelet levels (P<0.05 for all correlations). From 13 parameters (age, sex, platelet, AST, ALT, GGT, AFP, albumin, globulin, bilirubin, ALP, HBV DNA and hepatitis B e-antigen), four best parameters (AST, platelet, GGT and AFP) were used to derive a liver stiffness model. Using log (index)=1.44+0.1490(GGT)+0.3308 log (AST)-0.5846 log (platelets)+0.1148 log (AFP+1) to predict both severe fibrosis and cirrhosis had area under the receiver operating characteristics curve of 0.85. Routine liver biochemistry correlated well with liver stiffness in Asian CHB patients. A model using simple serum markers can predict liver stiffness, and further studies are required to validate the usefulness of these simple tests as non-invasive markers of fibrosis in CHB.

Serum hyaluronic acid: A promising marker of hepatic fibrosis in chronic hepatitis B

Serum hyaluronic acid: A promising marker of hepatic fibrosis in chronic hepatitis B

Noninvasive assessment of liver fibrosis with combined serum aminotransferase/platelet ratio index and hyaluronic acid in patients with chronic hepatitis B

To construct a noninvasive assessment model consisting of routine laboratory data to predict significant fibrosis and cirrhosis in patients with chronic hepatitis B (CHB). A total of 137 consecutive patients with CHB who underwent percutaneous liver biopsy were retrospectively analyzed. These patients were divided into two groups according to their aminotransferase (ALT) level. The sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), the likelihood ratio (LR) of aminotransferase/platelet ratio index (APRI) > or = 1.5 or < 1.5 in combination with different hyaluronic acid (HA) cut-off points were calculated for the presence of moderate to severe fibrosis/cirrhosis (fibrosis stages 2 and 4) and no to mild fibrosis/cirrhosis (fibrosis stages 0 and 1). The APRI correlated with fibrosis stage in CHB patients. The APRI > or = 1.5 in combination with a cut-off HA cut-off point > 300 ng/mL could detect moderate to severe fibrosis (stages 2-4) in CHB patients. The PPV was 93.7%, the specificity was 98.9%. The APRI < 1.5 in combination with different HA cut-off points could not detect no to mild fibrosis in CHB patients. The APRI > or = 1.5 in combination with a HA cut-off point > 300 ng/mL can detect moderate to severe fibrosis (stages 2-4) in CHB patients.

Hepatic steatosis in chronic hepatitis B and C: Predictors, distribution and effect on fibrosis

Chronic hepatitis B (CHB) and C (CHC) are commonly associated with hepatic steatosis. The aims of this study were to investigate predictors of hepatic steatosis, and their impact on inflammation and fibrosis in CHB and CHC. Consecutive patients with either CHB or CHC who underwent a liver biopsy at The Alfred Hospital between April and September 2002 were included. Histological analysis of liver biopsies was performed by two hepatopathologists blinded to the clinical data. Ninety-one patients were analysed including 17 patients with CHB and 74 with CHC. CHC genotype 3, C-peptide, glucose and waist circumference were independent predictors of extent of Brunt steatosis grade, while CHC genotype 3, C-peptide and waist circumference were independent predictors of microvesicular steatosis grade. Alcohol intake and age were predictors of hepatic fibrosis. There was a trend toward a correlation between both Brunt steatosis and microvesicular steatosis grades and fibrosis progression rate in CHC genotype non-3. Hepatic steatosis is common in chronic hepatitis B and C, and is associated with waist circumference, glucose, C-peptide and chronic hepatitis C genotype 3. Steatosis grade appears to relate to hepatic fibrosis progression rate in chronic hepatitis C genotype non-3.