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Liver fibrosis is a dynamic process consisting of the chronic activation of the wound healing reaction in response to reiterated liver damage, leading to the excessive deposition of fibrillar extracellular matrix into the liver and eventually, if the cause of injury is not removed, to liver cirrhosis. The term "adipokines" identifies a group of polypeptide molecules secreted primarily by adipose tissue, which exert local, peripheral and/or central actions. Additionally to their well-established role in controlling adipose tissue physiology, adipokines have been shown to be involved in different obesity-related diseases, such as hypertension, atherosclerosis and type 2 diabetes. Accumulating data demonstrate that obesity and insulin resistance are associated with a more severe and faster progression of the fibrogenic process in different chronic liver diseases. Therefore, numerous recent studies have analyzed the role played by adipokines in the hepatic wound healing process, identifying novel roles as modulators of liver pathophysiology. This review summarizes the more significant and recent findings concerning the role played by adipocyte-derived molecules, such as leptin, adiponectin and resistin, in the liver fibrogenic process. The actions of different adipokines on the biology of liver resident cells, as well as their effects in different animal models of liver injury are discussed. The variations in the circulating levels and in the intrahepatic expression of these molecules occurring in patients with different chronic liver diseases will be also analyzed.
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PMID:The role of adipokines in liver fibrosis. 1860 1

Transient elastgraphy with use of FibroScan is one of most accurate methods for assessment of liver fibrosis. FibroScan can be readily used with an operator with a short training. In many different studies, liver stiffness measured by transient elastgraphy correlates well with fibrosis stages, and cutoff values of liver stiffness for fibrosis staging are similar even among different diseases. However there is wide variation of stiffness values in the same fibrosis stage, and some overlap between the adjacent stages. In addition, inflammatory activity and size of nodule of cirrhosis affect the liver stiffness values. The reproducibility may be reduced by age, obesity, steatosis, narrow intercostal space and lower degrees of hepatic fibrosis in patients. Thus the estimation of fibrosis stages from liver stiffness should be cautiously done. To improve the accuracy of liver fibrosis staging, the combination of transient elastography with other noninvasive methods such as FibroTest should be required.
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PMID:Transient elastography: Applications and limitations. 1862 15

Hepatic fibrosis is an integral part in the progression of chronic liver disease, ultimately leading to cirrhosis and hepatocellular carcinoma. Globally, alcohol consumption, hepatitis B (HBV) and hepatitis C (HCV) have been the main causes of cirrhosis. More recently, the increasing prevalence of obesity and the metabolic syndrome has resulted in increasing incidence of cirrhosis secondary to nonalcoholic fatty liver disease (NAFLD), especially in developed countries. Chronic liver disease and cirrhosis are important causes of morbidity and mortality in the world. Moreover, the burden of chronic liver disease is projected to increase, due in part to the increasing prevalence of end-stage liver disease and HCC secondary to NAFLD and HCV.
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PMID:The global impact of hepatic fibrosis and end-stage liver disease. 1898 63

Narcotic analgesics are commonly prescribed drugs in patients with chronic hepatitis C (CHC) infection. In vitro data have shown that morphine enhances hepatitis C virus replication in human hepatic cells, however the effect of narcotics on hepatitis C virus disease progression remains uncertain. The aim of this study was to evaluate the potential effects of narcotic analgesic use on the progression of hepatic fibrosis in patients with CHC infection. We identified CHC patients who had been seen at our institution and had undergone a liver biopsy between 1990 and 2005. Their charts were reviewed for the presence of narcotic analgesic and known risk factors for progression of hepatic fibrosis including male sex, age > or =40, obesity, diabetes, and alcohol abuse. All biopsy were reviewed and fibrosis scores were standardized using the Batts and Ludwig scoring system (stage 0 to 4). A total of 1147 evaluable patients were identified and 171 of these had narcotic analgesic use. In univariate analysis, narcotic analgesic use was associated with the presence of alcohol abuse (P<0.001), obesity (P=0.02), and advanced fibrosis defined as stage 3 to 4 fibrosis (P=0.02), but not with male sex or diabetes. In multivariate logistic regression analysis, obesity [odds ratio (OR) 1.68 (confidence interval (CI), 1.21-2.33)], alcohol abuse [OR 1.45 (CI, 1.04-2.02)], age > or =40 [OR 1.85 (CI, 1.22-2.89)], and diabetes [OR 2.43 (CI, 1.41-4.14)] all independently predicted advanced liver fibrosis but narcotic analgesic use did not [OR 1.71 (CI, 0.99-2.89)]. As the amount of narcotic analgesic use increased from no use, to <3 months use, to > or =3 months use, the frequency of obesity, alcohol abuse, and advanced fibrosis increased accordingly (P=0.005), suggesting that it is difficult to separate these known risk factors from narcotic use as the cause for advanced fibrosis in this population.
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PMID:Narcotic analgesics and progression of fibrosis in patients with chronic hepatitis C. 1903 42

The prognosis and management of liver disease greatly depends on the amount of liver fibrosis. Non-alcoholic fatty liver disease (NAFLD), ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), is emerging as a major cause of liver disease in Western countries because of the increasing prevalence of obesity and type 2 diabetes. A key issue in patients with NAFLD is the differentiation of NASH from simple steatosis. It is particularly important to identify NASH patients as they are at greatest risk of developing complications such as cirrhosis, liver failure and hepatocellular carcinoma. The limitations of liver biopsy (invasive procedure, sampling errors, interobserver variability and non-dynamic fibrosis evaluation) have stimulated the search for non-invasive approaches for the assessment of steatosis and liver fibrosis in patients with NAFLD. A variety of methods, including serum markers, imaging techniques such as ultrasound, CT, MRI and measurement of liver stiffness by transient elastography, have been proposed for the non-invasive assessment of steatosis and hepatic fibrosis. This review discusses the advantages and limitations of these different methods in clinical practice.
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PMID:Non-invasive diagnosis of steatosis and fibrosis. 1919 29

Liver fibrosis is the progressive deposition of extracellular matrix in the liver parenchyma that precedes the development of cirrhosis. In the last few years, knowledge of the cellular and molecular bases of liver fibrosis has increased considerably. Environmental and genetic factors have been described that influence the progression of liver fibrosis, while non-invasive methods have been developed that allow the grade of fibrosis to be estimated without the need for liver biopsy. Currently, the only clearly effective treatment to attenuate or reverse liver fibrosis is elimination of the causative agent. When this is not feasible, fibrogenic factors (such as insulin resistance, obesity, alcohol intake, cannabis consumption, etc.) should be identified and treated. However, several agents are able to reduce liver fibrosis in experimental models of chronic liver damage. Few controlled clinical trials have been performed that evaluate the efficacy and safety of these agents and consequently the level of evidence supporting their use as anti-fibrogenic therapy is still low. The efficacy of the anti- fibrogenic drugs, renin-angiotensin system inhibitors, is currently being evaluated.
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PMID:[Treatment of liver fibrosis]. 1964 93

Non-invasive modalities to estimate fibrosis stage are desirable in hepatitis C-infected haemophilia patients. Previous studies found a high rate of significant fibrosis both by Fibrotest (FT) and Fibroscan (FS) in these patients. To estimate liver fibrosis and to assess the concordance between FT and FS in hepatitis C-infected haemophilia patients. FT and FS were performed at different laboratories and were unaware of the results of the alternative test. Three successive liver stiffness measurements (LSM) were performed at different sites on the liver. Two-validated algorithms were used to improve evaluation of fibrosis by non-invasive methods. Fifty-seven hepatitis C-infected haemophilia patients were evaluated by FT and FS. Acquisition of LSMs was not feasible in two patients: obesity--one, surgical scars--one. Fibrosis stage > or=F2, > or =F3 or =F4 were estimated in about a half, about a third and in 15-20% of the evaluated patients by FS and FT respectively. The corresponding concordance rates and kappa score for fibrosis stage > or =F2, > or =F3 or =F4 between FT and FS were 62%, 69%, 85% and 0.24, 0.32, 0.44 respectively. Using the two aforementioned algorithms, additional 14 patients could be reliably estimated for fibrosis stage > or =F2. High proportion hepatitis C-infected haemophilia patients were estimated with significant or advanced stages of liver fibrosis using both tests. Nevertheless, the agreement between modalities was only fair and improved with more advanced stages of fibrosis. Practical algorithms for the accuracy of FT and FS may improve reliable evaluation of fibrosis in this population.
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PMID:Fibrotest or Fibroscan for evaluation of liver fibrosis in haemophilia patients infected with hepatitis C. 1970 31

Hepatitis C virus (HCV) infection is the most important liver disease (LD) after renal transplantation. Liver biopsy is the gold standard for the diagnosis and follow-up of LD. The aim of this retrospective study was to evaluate the correlation between values of Fibroscan (EchoSens, Paris, France), a new noninvasive method to assess liver fibrosis, liver biopsy, and clinical data among HCV-positive renal transplant patients. Twenty-four HCV/RNA-positive patients with a previous liver biopsy were selected to undergo Fibroscan (transient elastography) and a clinical evaluation of liver function. Fibroscan values were expressed in kilopascals (kPa). As 2 patients were eliminated due to obesity or ascites, we analyzed 22 patients. Thirteen patients (59%) with fibrosis F0-F1 (METAVIR score) by biopsy and normal liver function showed a mean Fibroscan score of 5.2 kPa (range, 2.3-6.8 kPa). Three patients (13.6%) exhibited F2 by biopsy and normal liver function with a mean Fibroscan score of 8.2 kPa (range, 7.3-8.9 kPa). Three patients (13.6%) with F3 by biopsy and abnormal liver function showed a high mean Fibroscan score of 10.9 kPa (range, 10.5-11.6 kPa). The last 3 patients (13.6%) with F4 (cirrhosis) by biopsy and abnormal clinical data showed the highest mean Fibroscan value of 14.2 kPa (range, 8.9-18 kPa). In conclusion, among renal transplant patients with HCV the values of Fibroscan seem to correlate with the degree of fibrosis by biopsy and with clinical liver function. Therefore, Fibroscan may be useful to follow patients with LD. However, these results should be analyzed with caution due to the small number of cases and retrospective nature of the study.
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PMID:Correlation between fibroscan, liver biopsy, and clinical liver function in patients with hepatitis C virus infection after renal transplantation. 1971 40

Metabolic syndrome (MS) is one of the most prevalent disease states in the so-called developed countries and is closely associated with the incidence of cardiovascular as well as other diseases. Predominant sign is the abdominal type of obesity with increased visceral fat mass and the associated insulin resistance. Glucose metabolism disorder, dyslipidemia and arterial hypertension are other important attributes. Metabolic syndrome is also closely associated with the liver steatosis, mostly benign and reversible liver disease. Nevertheless, uncomplicated steatosis may, under certain conditions, progress to inflammation and the disease may, through the stage of NASH (nonalcoholic steatohepatitis) and liver fibrosis, result in liver cirrhosis and hepatocellular carcinoma. Anglo-Saxon literature uses the term NAFLD (non-alcoholic fatty liver disease) to refer to these various stages ofthe liver disease (uncomplicated liver steatosis, steatohepatitis, fibrosis and cirrhosis). While simple steatosis is not dangerous for the patient, NASH is the sign of developing cirrhosis. Etiopathogenesis of NASH features identical characteristics as etiopathogenesis of insulin resistance and metabolic syndrome. Even though liver biopsy remains the gold standard in the diagnosis, new diagnostic approaches are emerging that could be useful in distinguishing simple steatosis from NASH. Therapy includes lifestyle changes, insulin resistance-reducing medication (also useful in the treatment of type 2 diabetes) with a range of other agents under development. In the meantime, randomized double-blind placebo-controlled studies with histological proof of the results are still lacking. A range of unresolved issues remains with regards to etiopathogenesis as well as diagnosis and treatment of NAFLD and NASH.
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PMID:[Metabolic syndrome and the liver (NAFLD/NASH)]. 1973 69

Endogenous cannabinoids are ubiquitous lipid-signaling molecules able to partially mimic the actions produced by Delta(9)-tetrahydrocannabinol, the compound responsible for most of the psychological effects of marijuana. Endocannabinoids are derived from arachidonic acid and are involved in many physiological effects. This family of substances includes anandamide (arachidonylethanolamide), 2-arachydonylglycerol, noladin ether and virodhamine. The interaction of these substances with CB1 and CB2 receptors results in most of their biological effects. The endocannabinoid system is involved in the pathogenesis of the cardiovascular dysfunction occurring in advanced liver disease and also plays a role in the pathogenesis of portal hypertension and liver fibrosis. Moreover, this system is also altered in other processes associated with hepatic dysfunction, including encephalopathy, obesity and steatosis. These findings indicate that the endocannabinoid system may open new avenues for the therapeutic regulation of fibrosis and portal hypertension in advanced liver disease.
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PMID:[Endogenous cannabinoids in liver disease: Many darts for a single target]. 1975 27


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