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PubMed2004

Insulin resistance and the pathogenesis of nonalcoholic fatty liver disease.

The prevalence of obesity has reached epidemic proportions in most of the western world. Current estimates suggest that 22.5%of the population of the United States suffers from obesity and is at risk for development of obesity-related complications, including hypertension, coronary artery disease, diabetes, hyperlipidemia,increased predisposition for various cancers, and nonalcoholic fatty liver disease. Fatty liver disease is currently the most common abnormality observed in hepatology practice. Since it was first reported in the 1980s in obese diabetic females, our understanding of nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH) has undergone significant metamorphosis. It is now universally accepted that insulin resistance and subsequent hyperinsulinemia are key factors that lead to both NAFL and NASH.This article reviews the role of insulin resistance in the genesis of these conditions.

Carbohydrate Metabolism↗

PubMed2004

Non-alcoholic steatohepatitis in patients cared in metabolic units.

The clinical significance of liver disease is frequently underestimated in patients with metabolic disorders. In patients followed up in a metabolic unit for diabetes, obesity or hyperlipidemia (n=147), we studied the prevalence and the severity of liver disease, and its relationship with the metabolic syndrome (MS). Cases cared for in a liver unit (n=179) were used as controls. Patients in the metabolic series were older and had a higher prevalence of coronary heart disease. Criteria for the metabolic syndrome were fulfilled in 64% and 22% of cases, respectively (P<0.0001). Liver biopsy was obtained in 44 and 66% of cases. Metabolic patients had a more severe steatosis score (P<0.0001), whereas the scores of fibrosis and necroinflammation were less severe (P=0.0059 and 0.0007, respectively). Histological criteria for non-alcoholic steatohepatitis (NASH) were present in 82% of metabolic cases and 68% cases in the liver series (P=0.057). Liver disease in patients routinely cared for in metabolic units is similar to that observed in patients cared for in liver units, and potentially may progress to terminal liver failure. Liver biopsy is recommended for diagnostic and prognostic purposes, as well as for testing treatment effects in controlled trials.

Adult↗

PubMed2005

Interaction of stress proteins with misfolded keratins.

Misfolded and aggregated proteins are a characteristic feature of a variety of chronic diseases. Examples include neurofibrillary tangles in Alzheimer disease, Lewy bodies in Parkinson disease and Mallory bodies (MBs) in chronic liver diseases, particularly alcoholic and non-alcoholic steatohepatitis (ASH and NASH). MB formation is at least in part the result of chronic oxidative cell stress in hepatocytes and can be induced in mice by long-term intoxication with 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC). Proteomic analysis revealed that MBs consist of ubiquitinated keratins and the stress proteins Hsp70, Hsp25, and p62. Furthermore, marked overexpression of clusterin, which shares functional properties with small heat shock proteins, was identified by gene expression profiling of DDC-treated mice livers. To investigate whether clusterin has a function in the stress response to misfolded keratins, we performed transfection studies utilizing expression constructs encoding ubiquitin, p62, Hsp27, clusterin, keratin 8, and keratin 18. Ubiquitin was found in a strong and constant association with keratin aggregates, whereas binding of p62 to keratin was variable. Hsp27 did not colocalize with keratin aggregates under these experimental conditions. In contrast, clusterin associated with misfolded keratin only if its signal peptide was deleted and its secretion inhibited. This suggests that clusterin has ability to bind misfolded proteins, including keratins but its physiological function is restricted to the extracellular space. The extracellular localization of clusterin was underlined by immunohistochemical studies in Alzheimer disease brains, where clusterin was constantly found in association with amyloid plaques; in contrast, cytoplasmic inclusions such as neurofibrillary tangles as well as MBs in ASH were negative. Furthermore, we found clusterin in association with elastic fibers in the extracellular matrix in several chronic liver diseases, including ASH and alpha1-antitrypsin deficiency, implying a possible role of clusterin in liver fibrosis.

Adaptor Proteins, Signal Transducing↗

PubMed2006

Effects of bezafibrate, PPAR pan-agonist, and GW501516, PPARdelta agonist, on development of steatohepatitis in mice fed a methionine- and choline-deficient diet.

We evaluated the effects of bezafibrate, a peroxisome proliferator-activated receptor (PPAR) pan-agonist, and GW501516, a PPARdelta agonist, on mice fed a methionine- and choline-deficient (MCD) diet, a model of non-alcholic steatohepatitis (NASH), to investigate (a) the efficacy of bezafibrate against non-alcholic steatohepatitis and (b) the relation between non-alcholic steatohepatitis and the functional role of PPARdelta. Bezafibrate (50 or 100 mg/kg/day) and GW501516 (10 mg/kg/day) were administered by gavage once a day for 5 weeks. Hepatic lipid contents, plasma triglyceride, high density lipoprotein (HDL)-cholesterol and alanine aminotransferase (ALT) concentrations were evaluated, as were histopathological changes in the liver and hepatic mRNA expression levels. Bezafibrate and GW501516 inhibited the MCD-diet-induced elevations of hepatic triglyceride and thiobarbituric acid-reactants contents and the histopathological increases in fatty droplets within hepatocytes, liver inflammation and number of activated hepatic stellate cells. In this model, bezafibrate and GW501516 increased the levels of hepatic mRNAs associated with fatty acid beta-oxidation [acyl-CoA oxidase (ACO), carnitine palmitoyltransferase-1 (CPT-1), liver-fatty acid binding protein (L-FABP) and peroxisomal ketothiolase], and reduced the levels of those associated with inflammatory cytokines or chemokine [transforming growth factor (TGF)-beta1, interleukin (IL)-6, IL-1beta, monocyte chemoattractant protein (MCP)-1, tumor necrosis factor (TNF) alpha and nuclear factor (NF)-kappaB1]. In addition, bezafibrate characteristically reduced the elevation in the level of plasma ALT, but enhanced that in plasma adiponectin and increased the mRNA expression levels of its receptors (adiponectin receptors 1 and 2). These results suggest that (a) bezafibrate (especially) and GW501516 might improve hepatic steatosis via an improvement in fatty acid beta-oxidation and a direct prevention of inflammation, (b) treatment with a PPARdelta agonist might improve non-alcholic steatohepatitis, (c) bezafibrate may improve non-alcholic steatohepatitis via activation not only of PPARalpha but also of PPARdelta, because bezafibrate is a PPAR pan-agonist.

Acyl-CoA Oxidase↗

PubMed2006

Hydrogen sulfide inhibits nitric oxide production and nuclear factor-kappaB via heme oxygenase-1 expression in RAW264.7 macrophages stimulated with lipopolysaccharide.

Hydrogen sulfide (H(2)S), a regulatory gaseous molecule that is endogenously synthesized by cystathionine gamma-lyase (CSE) and/or cystathionine beta-synthase (CBS) from L-cysteine (L-Cys) metabolism, is a putative vasodilator, and its role in nitric oxide (NO) production is unexplored. Here, we show that at noncytotoxic concentrations, H(2)S was able to inhibit NO production and inducible NO synthase (iNOS) expression via heme oxygenase (HO-1) expression in RAW264.7 macrophages stimulated with lipopolysaccharide (LPS). Both H(2)S solution prepared by bubbling pure H(2)S gas and NaSH, a H(2)S donor, dose dependently induced HO-1 expression through the activation of the extracellular signal-regulated kinase (ERK). Pretreatment with H(2)S or NaHS significantly inhibited LPS-induced iNOS expression and NO production. Moreover, NO production in LPS-stimulated macrophages that are expressing CSE mRNA was significantly reduced by the addition of L-Cys, a substrate for H(2)S, but enhanced by the selective CSE inhibitor beta-cyano-L-alanine but not by the CBS inhibitor aminooxyacetic acid. While either blockage of HO activity by the HO inhibitor, tin protoporphyrin IX, or down-regulation of HO-1 expression by HO-1 small interfering RNA (siRNA) reversed the inhibitory effects of H(2)S on iNOS expression and NO production, HO-1 overexpression produced the same inhibitory effects of H(2)S. In addition, LPS-induced nuclear factor (NF)-kappaB activation was diminished in RAW264.7 macrophages preincubated with H(2)S. Interestingly, the inhibitory effect of H(2)S on NF-kappaB activation was reversed by the transient transfection with HO-1 siRNA, but was mimicked by either HO-1 gene transfection or treatment with carbon monoxide (CO), an end product of HO-1. CO treatment also inhibited LPS-induced NO production and iNOS expression via its inactivation of NF-kappaB. Collectively, our results suggest that H(2)S can inhibit NO production and NF-kappaB activation in LPS-stimulated macrophages through a mechanism that involves the action of HO-1/CO.

Animals↗

PubMed2005

The characteristics and natural history of Japanese patients with nonalcoholic fatty liver disease.

AIMS: The aim of our study was to elucidate the characteristics and natural history of Japanese nonalcoholic fatty liver disease (NAFLD). PATIENTS AND METHODS: Two hundred and forty-seven patients were diagnosed as having biopsy-proven NAFLD at Tokyo Women's Medical University or an affiliated hospital from 1990 to June 2004. Biopsies were scored for the severity of steatosis, necro-inflammation, and fibrosis according to modified Brunt criteria. We assessed the clinicopathological features and natural history of NAFLD in patients stratified by the stage of their fibrosis. Univariate and multivariate logistic analyses were performed, and the diagnostic ability was assessed by the area under the receiver operating characteristic curve. RESULTS: Clinicopathological features: The median age of the patients was 53 years, with a range from 10 to 89 years. There were 130 males and 117 females. Histologically, 46 patients were classified as F3 (bridging fibrosis), and 43 patients had F4 (cirrhosis). Females and older patients were more common in the F3-4 patients. Most of the F3-4 patients showed mild elevation of transaminases with significant deterioration of liver function tests compared with F0-2 patients. Ten patients were simultaneously diagnosed as having cirrhotic NASH and hepatocellular carcinoma (HCC). Natural history: During follow-up (median 44 months) of the F3-4 patients, 10 patients developed liver-related morbidity and five patients developed HCC. In the F3-4 patients, the 5-year cumulative incidence of HCC was 20%. Eight patients died (two of liver failure, four of HCC and two of other carcinomas). Serum markers for detecting F3-4: Serum hyaluronic acid levels can accurately evaluate NAFLD patients with F3-4. CONCLUSIONS: The most important consequence of NAFLD patients with advanced fibrosis was HCC. Regular screening for this complication is extremely important.

Journal Article↗

PubMed2005

Epidemiological aspects of obesity and NASH/NAFLD in Japan.

Although the characteristics of non-alcoholic steatohepatitis (NASH) and non-alcoholic fatty liver disease (NAFLD) have become well recognized, mainly in the clinical and pathological fields, epidemiological findings, including magnitude of the disease in a population (prevalence, outcomes, and mortality) and risk factors (relative risk and population attributable risk) are scarce in the Asia-Oceania region. Obesity is known to be one of the most important risk factors for NASH/NAFLD, and observed increases in NASH/NAFLD in selected areas or settings may be linked to the increase in overweight and obesity in Japanese adults in the last few decades. Obesity could be a major key to explaining NASH/NAFLD, because of the complex causal web that includes obesity, insulin resistance, dyslipidemia, high blood pressure, etc. In this paper epidemiological data on overweight and obesity were summarized as underlying factors for NAFLD with special reference to yearly trends and regional differences in the prevalence of obesity and overweight in Japanese adults using large-scale representative samples from the National Nutrition Surveys. Unfortunately, as very few published reports on population-based epidemiological data for NAFLD are currently available, we referred to selected data obtained from field settings to estimate the prevalence of NAFLD in the general population and its risk factors or associated factors. It is important to understand NASH/NAFLD as a common "burden of disease" in the populations if effective strategies to control these disorders are to be devised as part of public health initiatives.

Journal Article↗

PubMed2005

CYP17 polymorphism and tamoxifen-induced hepatic steatosis.

Hepatic steatosis is a frequent complication, which sometimes develops nonalcoholic steatohepatitis (NASH), in breast cancer patients treated with tamoxifen, a potent antagonist of estrogen. Recently we reported the impairment of fatty acid beta-oxidation and the enhancing fatty infiltration to hepatocytes in aromatase deficiency (ArKO) mice as the estrogen deficiency models. This experimental observation let us speculate strong link between estrogen and hepatic steatosis. In this study, we investigated whether a polymorphism in the cytochrome P450c17alpha gene (CYP17), which is associated with circulating estrogen levels, influences the development of tamoxifen-induced hepatic steatosis. This consecutive study included 180 breast cancer patients undergoing tamoxifen treatment. Genomic DNA extracted from the peripheral blood of each patient was analyzed by restriction fragment length polymorphism (defined as the A1 and A2 alleles). The extent of hepatic steatosis was assessed by computed tomography (CT) as the liver/spleen (L/S) ratio. While receiving adjuvant tamoxifen, 57 of 180 patients developed hepatic steatosis (L/S ratio <0.9) without obvious changes in body mass index (BMI). We observed a significant association between the A2/A2 genotype and the development of hepatic steatosis compared with the A1/A1 genotype [odds ratio (OR), 3.60; 95% confidence interval (C.I.)=1.42-9.10]. The A1/A2 genotype was at an intermediately increased risk of hepatic steatosis (OR, 2.24; 95% C.I.=0.99-5.08). The presence of the A2 allele possibly increased the progression of hepatic steatosis with a gene dosage effect (P=0.06). Our results suggest that functional polymorphism in CYP17 may be involved in determining susceptibility of tamoxifen-induced hepatic steatosis.

Journal Article↗

PubMed2005

Randomized evaluation of the TriActiv balloon-protection flush and extraction system for the treatment of saphenous vein graft disease.

OBJECTIVES: The Protection During Saphenous Vein Graft Intervention to Prevent Distal Embolization (PRIDE) study compared outcomes with the TriActiv System (Kensey Nash Corp., Exton, Pennsylvania), a balloon-protection flush and extraction device, with an embolic protection group during treatment of saphenous venous grafts (SVGs). BACKGROUND: Treatment of SVGs with embolic protection reduces adverse cardiac events. METHODS: We conducted a prospective trial randomizing 631 patients with coronary ischemia and lesions in SVGs to embolic protection with the TriActiv System or control group (Guardwire System [Medtronic AVE, Santa Rosa, California] or Filterwire EX [Boston Scientific Corp., Maple Grove, Minnesota]). RESULTS: The incidence of major adverse cardiac events at 30 days was 11.2% for the TriActiv group and 10.1% for the control group (relative risk = 1.1%; 95% confidence interval 0.67 to 1.76; p = 0.65; p = 0.02 for non-inferiority). Safety and efficacy end points were similar between groups except that patients randomized to the TriActiv System had more hemorrhagic complications (10.9% vs. 5.4%; p = 0.01). CONCLUSIONS: The TriActiv System was not inferior to approved embolic protection devices for the treatment of diseased SVGs.

Adult↗

PubMed2005

cDNA microarray analysis of autoimmune hepatitis, primary biliary cirrhosis and consecutive disease manifestation.

While autoimmune hepatitis (AIH) and primary biliary cirrhosis (PBC) usually have distinct clinical manifestations, some patients present with features of both conditions. Using cDNA microarrays, we analyzed and compared gene expression profiles in 8 patients with AIH, 9 with PBC, 8 with chronic hepatitis C (CHC), 8 with non-alcoholic steatohepatitis (NASH) and 9 with normal livers. We subsequently applied this method to a tissue sample from a 61-year-old woman with overlapping features of both AIH and PBC. A 61-year-old woman was admitted to our hospital for evaluation of elevated serum alkaline phosphatase. A liver biopsy showed accumulation of mononuclear cells around the bile duct cells, a feature characteristic of chronic non-suppurative destructive cholangitis (CNSDC). Three years later, her serum alanine aminotransferase (ALT) level had increased, and a liver biopsy demonstrated evidence of a severe form of hepatitis. A cDNA microarray analysis of both biopsies identified the molecular events associated with her altered histology. The expression profile of this patient, which was originally different from that of the other PBC patients, changed to an AIH pattern. Our results suggest that this patient has characteristics of both AIH and PBC.

Aged↗

PubMed2005

Landfill space consumption dynamics in the Lower Rio Grande Valley by grey integer programming-based games.

The Lower Rio Grande Valley (LRGV) region in South Texas emerges as a warehouse and transportation center between Central America and the US with positive growth impacts due to the North American Free Trade Agreement (NAFTA). In 10 years time, a 39.8% population increase has resulted in a 25% boost in solid waste per capita disposal rate in the region. A landfill space shortage drives a need for landfill operators to understand their optimal management strategies in this highly-competitive market. Initially, a strategic plan for optimal solid waste pattern distribution minimizes net costs for cities. This is accomplished through a grey integer programming algorithm that encapsulates all uncertainty present in the solid waste system. Secondly, a series of grey integer submodels construct payoff matrices for a zero-sum two-person game. The ensuing game theoretic analysis is critical for evaluating optimal pricing strategies for tipping fees available to the most significant regional landfills (e.g. Browning-Ferris Industries (BFI) and City of Edinburg) as they compete over disposal contracts. The BFI landfill intrinsically benefits from its competitive pricing policy and central location to solid waste generators. The City of Edinburg landfill, on the other hand, wishes to secure its lucrative solid waste management revenue. It desires a gaming strategy backed by optimality that integrates ambiguity in solid waste generation, design capacity boundaries, and unitary shipping costs. Results show that a two-tiered analysis via grey integer programming-based games may pave the way for 'grey Nash equilibria' pricing tactics that will help the Edinburg landfill maintain its waste contracts.

Algorithms↗

PubMed2006

Competition among differentiated health plans under adverse selection.

Market power and adverse selection are prevalent features of the market for pre-paid health plans. However, most of the literature on adverse selection considers extreme cases: either perfect competition or monopoly. If instead health plans are horizontally differentiated, then (i) profits derived from each low risk are higher than from each high risk and (ii) when the profits derived from each high risk are negative (cross-subsidization), a health authority as informed as the health plans can implement a Pareto-improvement. Both local and global deviations from cross-subsidization are addressed within a Nash equilibrium framework.

Economic Competition↗

PubMed2006

Diagnostic and predictive factors of significant liver fibrosis and minimal lesions in patients with persistent unexplained elevated transaminases. A prospective multicenter study.

BACKGROUND/AIMS: In patients with unexplained elevated transaminases, prognosis of the liver disease and factors associated with increased risk of liver fibrosis and normal/subnormal liver are unknown. The aim of this prospective study was to identify diagnosis and clinical and biological factors associated with significant (bridging) fibrosis and minimal lesions of the liver in patients with persistent unexplained elevated ALT levels. METHODS: From July 2002 through October 2004, all consecutive asymptomatic patients with unexplained chronically elevated ALT levels were included. All patients had clinical, biological, ultrasonographic examination and a liver biopsy. RESULTS: 272 patients (60.3% males, mean age 46.4 years, BMI 26.7) were included. Pathological findings were: minimal lesions (18.7%), steatosis (26.8%), NASH (32.7%), and miscellaneous (21.7%). Significant fibrosis was found in 27.4% of cases, including 9 cases of cirrhosis. By multivariate analysis, independent predictors of significant fibrosis were tobacco use (OR 2.5, 95% CI 1.34-4.74 p=0.04), BMI>25 (2.49, 1.31-4.73 p=0.005) and diabetes (4.41, 1.73-11.29 p=0.002). Independent factors associated with minimal lesions were female gender (OR 3.4 95% CI 1.73-6.75 p<0.0001) and BMI<25 (3.55, 1.8-6.98, p<0.0001). CONCLUSIONS: In patients with unexplained chronically elevated transaminases, significant fibrosis is statistically associated with tobacco use, BMI>25 and diabetes, and minimal lesions are significantly associated with female gender and BMI<25.

Adult↗

PubMed2005

Leptin enhances TNF-alpha production via p38 and JNK MAPK in LPS-stimulated Kupffer cells.

Leptin is now recognized as a proinflammatory cytokine and thought to be a progressive factor for non-alcoholic steatohepatitis (NASH). Here we showed the effects of leptin on the production of TNF-alpha (tumor necrosis factor-alpha) by Kupffer cells (KCs) with signal transduction. Leptin enhanced TNF-alpha production accompanied by a dose-dependent increase of MAPK activity in lipopolysaccharide (LPS)-stimulated KCs. SB203580 and JNK inhibitor I, specific inhibitors of P38 and JNK, inhibited TNF-alpha production in KCs but PD98059, an inhibitor of the ERK pathway, did not affect TNF-alpha production by KCs. Recombinant constitutively active adenovirus (Ad)-MKK6 and-MKK7 increased TNF-alpha production in KCs with activation of P38 and JNK without any change by Ad-MEK1 delivery. On the other hand, KCs isolated from the Zucker rat (fa/fa), a leptin receptor-deficient rat, showed reduced production of TNF-alpha on stimulation with LPS. The delivery of Ad-MKK6 and-MKK7, but not Ad-MEK1, increased TNF-alpha production in KCs of Zucker rats with activation of P38 and JNK. Addition of leptin to normal rats increased LPS-induced hepatic TNF-alpha production in vivo and leptin receptor-deficient Zucker rats showed reduced hepatic TNF-alpha production on addition of LPS in vivo. These findings indicate that P38 and JNK pathways are involved in the signal transduction of leptin enhancement of LPS-induced TNF-alpha production.

Animals↗

PubMed2006

The role of triiodothyronine-induced substrate cycles in the hepatic response to overnutrition: thyroid hormone as an antioxidant.

Overnutrition, by generating reactive oxygen species (ROS), produces oxidative stress - an important cause of cellular injury. In the liver, overnutrition begins in the perivenous hepatocytes. To prevent injury, cells must protect themselves against ROS accumulation. Overnutrition also activates the enzyme deiodinase-1 (D1), which catalyzes the conversion of T4 to T3. D1 is primarily located in the PV region of the liver. Thyroid hormone is known to generate substrate cycling. The hypothesis of this paper is that a nutrient-induced increase in intracellular T3 acts as an antioxidant by inducing substrate cycles that reduce ROS accumulation. These cycles do this by: (i) reducing ROS formation by hydrolyzing excess ATP, thus enhancing oxidative phosphorylation and reducing the proton motive force on the electron transport chain (ETC), and; (ii) enhancing the removal (reduction) of ROS by producing the NADPH required for regeneration of reduced glutathione, a potent endogenous antioxidant. Oxidative stress is an important factor in the etiology of a number of hepatic injuries, including nonalcoholic steatohepatitis (NASH) and hepatocarcinogenesis. In the latter, the frequency of mutations in thyroid hormone receptors (TRs) supports the concept that thyroid hormone acts as a tumor suppressor by reducing oxidative stress. This paper reviews the substrate cycles involved in this process. It also describes other mechanisms that permit rapid availability of T3 to cells undergoing oxidative stress.

Antioxidants↗

PubMed2006

Symbiotic adaptive neuro-evolution applied to rainfall-runoff modelling in northern England.

This paper uses a symbiotic adaptive neuro-evolutionary algorithm to breed neural network models for the River Ouse catchment. It advances on traditional evolutionary approaches by evolving and optimising individual neurons. Furthermore, it is ideal for experimentation with alternative objective functions. Recent research suggests that sum squared error may not result in the most appropriate models from a hydrological perspective. Models are bred for lead times of 6 and 24 hours and compared with conventional neural network models trained using backpropagation. The algorithm is also modified to use different objective functions in the optimisation process: mean squared error, relative error and the Nash-Sutcliffe coefficient of efficiency. The results show that at longer lead times the evolved neural networks outperform the conventional ones in terms of overall performance. It is also shown that the sum squared error objective function does not result in the best performing model from a hydrological perspective.

Algorithms↗

PubMed2004

Activity in posterior parietal cortex is correlated with the relative subjective desirability of action.

Behavioral studies suggest that making a decision involves representing the overall desirability of all available actions and then selecting that action that is most desirable. Physiological studies have proposed that neurons in the parietal cortex play a role in selecting movements for execution. To test the hypothesis that these parietal neurons encode the subjective desirability of making particular movements, we exploited Nash's game theoretic equilibrium, during which the subjective desirability of multiple actions should be equal for human players. Behavior measured during a strategic game suggests that monkeys' choices, like those of humans, are guided by subjective desirability. Under these conditions, activity in the parietal cortex was correlated with the relative subjective desirability of actions irrespective of the specific combination of reward magnitude, reward probability, and response probability associated with each action. These observations may help place many recent findings regarding the posterior parietal cortex into a common conceptual framework.

Animals↗

PubMed2006

[Results and place of Fibroscan in the non-invasive diagnosis of hepatic fibrosis].

BACKGROUND AND AIMS: Diagnosis of liver fibrosis by transient elastography (Fibroscan) is a new and non-invasive method. We report its results, and compare them with the non-invasive biological tests. RESULTS: Fibroscan is validated for chronic hepatitis C, allowing to diagnose the fibrosis (Métavir) F2, F3 and F4 with areas under the ROC curve of 0.79-0.83, 0.90-0.91 and 0.91-0.97 respectively. The non-invasive diagnosis of the cirrhosis can be made with positive and negative predictive values from 70 to 95% and 77 in 95%. Preliminary data concern the HCV-HIV co-infections, primary biliary cirrhosis, NASH, portal hypertension, and the follow-up of the hepatic fibrosis. These results are altogether comparable to the various non-invasive biological tests, for cirrhosis diagnosis. CONCLUSIONS: It's remain to determine the respective places of Fibroscan and non-invasive biological tests, in the liver fibrosis diagnosis.

Elasticity↗