Suchergebnisse

In Japan, the estimated number of chronic hepatitis B virus infections was 1.1 to 1.4 million, and that of chronic hepatitis C virus was 1.9 to 2.3 million in 2000. The mortality of hepatocellular carcinoma had been increasing and hit the peak at around 2002, which subsequently started to decrease. Japan has a national action plan for addressing viral hepatitis called Basic Act on Hepatitis Measures, established in 2009. In 2011, basic guidelines for promotion of control measures for hepatitis were issued, comprising nine principles in order to promote measures to prevent hepatitis B and C. According to these guidelines, national and local governments share screening costs for testing hepatitis B and C in residents who are over 40 years old. Thus, out-of-pocket expenses from examinees are nil or reduced to the minimum. In addition, for patients with chronic hepatitis B or C and on treatment, drug prices of nucleotide analogs, interferon (IFN) treatment, or IFN-free direct antiviral agents along with examination expenses should be covered by special programs for viral hepatitis. The national and local governments cover the amount in excess of 100 to 200 USD of the cost of treatment. The proportion of liver cancer with nonviral etiology has been increasing in Japan. For the screening and follow-up of patients with nonalcoholic fatty liver disease, we demonstrated that interleukin 34 is a feasible fibrosis marker. Several advantages have prevailed in the Japanese health care systems for patients with viral liver disease compared with those in countries in the Western Pacific region. Therefore, Japan should take a lead in helping the implementation of practical hepatitis action plans in every country when in need.

Nonalcoholic fatty liver disease (NAFLD) can progress from simple steatosis (i.e., nonalcoholic fatty liver [NAFL]) to nonalcoholic steatohepatitis (NASH), cirrhosis, and cancer. Currently, the driver for this progression is not fully understood; in particular, it is not known how NAFLD and its early progression affects the distribution of lipids in the liver, producing lipotoxicity and inflammation. In this study, we used dietary and genetic mouse models of NAFL and NASH and translated the results to humans by correlating the spatial distribution of lipids in liver tissue with disease progression using advanced mass spectrometry imaging technology. We identified several lipids with distinct zonal distributions in control and NAFL samples and observed partial to complete loss of lipid zonation in NASH. In addition, we found increased hepatic expression of genes associated with remodeling the phospholipid membrane, release of arachidonic acid (AA) from the membrane, and production of eicosanoid species that promote inflammation and cell injury. The results of our immunohistochemistry analyses suggest that the zonal location of remodeling enzyme LPCAT2 plays a role in the change in spatial distribution for AA-containing lipids. This results in a cycle of AA-enrichment in pericentral hepatocytes, membrane release of AA, and generation of proinflammatory eicosanoids and may account for increased oxidative damage in pericentral regions in NASH. CONCLUSION: NAFLD is associated not only with lipid enrichment, but also with zonal changes of specific lipids and their associated metabolic pathways. This may play a role in the heterogeneous development of NAFLD. (Hepatology 2017;65:1165-1180). ; Medical Research Council (MRC). Horizon 2020 Framework Program of the European Union.

Background: The knowledge of distribution and pattern of liver disease in a tertiary care center provides an overview of disease pattern in a community. It also helps in planning and prioritizing strategies to treat the diseases and reduce their burden in the community. Methods: A retrospective study was conducted among patients admitted to the Liver unit, Bir Hospital from April 13, 2008 to October 16, 2008. Demographic profile and disease pattern was studied. Descriptive analysis was used to calculate frequencies and percentage and their relations. Results: Male to female ratio was 2.3:1. The mean age was 41.9 (SD 14.8). Median hospital stay was 8.0 days (Q25-75 6.0-12.0). The top three diseases were alcoholic liver disease 50 (38.5%), viral hepatitis 44 (33.8%), and liver abscess 11 (8.5%). Fifty (38.5%) patients had acute, 74 (56.9%) had chronic liver disease and 6 (4.6%) were malignancy. The main cause of acute disease were infections 41 (82.0%) especially Hepatitis E Virus (HEV). HEV was associated with acute liver failure and pregnancy which was 4 (18.2%) and 2 (12.5%) respectively. Chronic diseases were caused by alcohol 45 (60.8%) followed by infection of hepatitis B and C viruses 11 (14.8%). Cirrhosis was diagnosed in 37 (28.5%) with alcohol as the main cause. Conclusions: Majority had chronic liver disease (CLD), mostly due to alcohol, HBV and HCV. Alcohol was the leading cause of cirrhosis. Prevalence of Hepatitis E was found to be high in acute illness. Therefore, an initiative needs to be taken to decrease alcohol consumption along with HEV, HBV and HCV transmission through community health program. Key words: Alcohol, cirrhosis, hepatitis, liver disease DOI: 10.3126/jnhrc.v7i1.2273 Journal of Nepal Health Research Council Vol. 7, No. 1, 2009 April 14-18

An increasing percentage of people have or are at risk to develop non-alcoholic fatty liver disease (NAFLD) worldwide. NAFLD comprises different stadia going from isolated steatosis to non-alcoholic steatohepatitis (NASH). NASH is a chronic state of liver inflammation that leads to the transformation of hepatic stellate cells to myofibroblasts. These cells produce extra-cellular matrix that results in liver fibrosis. In a normal situation, fibrogenesis is a wound healing process that preserves tissue integrity. However, sustained and progressive fibrosis can become pathogenic. This process takes many years and is often asymptomatic. Therefore, patients usually present themselves with end-stage liver disease e.g., liver cirrhosis, decompensated liver disease or even hepatocellular carcinoma. Fibrosis has also been identified as the most important predictor of prognosis in patients with NAFLD. Currently, only a minority of patients with liver fibrosis are identified to be at risk and hence referred for treatment. This is not only because the disease is largely asymptomatic, but also due to the fact that currently liver biopsy is still the golden standard for accurate detection of liver fibrosis. However, performing a liver biopsy harbors some risks and requires resources and expertise, hence is not applicable in every clinical setting and is unsuitable for screening. Consequently, different non-invasive diagnostic tools, mainly based on analysis of blood or other specimens or based on imaging have been developed or are in development. In this review, we will first give an overview of the pathogenic mechanisms of the evolution from isolated steatosis to fibrosis. This serves as the basis for the subsequent discussion of the current and future diagnostic biomarkers and anti-fibrotic drugs. ; The Ph.D. authors of this paper are part of the Limburg Clinical Research Center (LCRC), supported by the foundation Limburg Sterk Merk, province of Limburg, Flemish government, Hasselt University, Ziekenhuis Oost-Limburg, and Jessa Hospital. ; Francque, S (corresponding author), Antwerp Univ Hosp, Dept Gastroenterol & Hepatol, Antwerp, Belgium ; Univ Antwerp, Fac Med & Hlth Sci, Lab Expt Med & Paediat, Antwerp, Belgium. sven.francque@uza.be

Cerium oxide nanoparticles; Non-alcoholic fatty liver disease; Antioxidant agent ; Nanopartículas de óxido de cerio; Enfermedad del hígado graso no alcohólico; Agente antioxidante ; Nanopartícules d'òxid de ceri; Malalties hepàtiques no alcohòliques; Agent antioxidant ; Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease worldwide, ranging from steatosis to non-alcoholic steatohepatitis (NASH). Recently, cerium oxide nanoparticles (CeO2NPs) have emerged as a new antioxidant agent with hepatoprotective properties in experimental liver disease. The aim of the current investigation was to elucidate whether CeO2NPs display beneficial effects in an experimental model of NAFLD.Therefore, fifteen Wistar rats were subjected to a methionine and choline deficient diet (MCDD) for 6 weeks and intravenously treated with CeO2NP or vehicle during the weeks three and four of the diet. The effect of CeO2NPs on serum biochemistry, hepatic steatosis, inflammation, fatty acid content and expression of reactive oxygen species (ROS) and lipid metabolism related genes was assessed. MCDD fed rats showed increased inflammation, enhanced hepatic lipid accumulation of both saturated and unsaturated fatty acids (FAs) and overexpression of genes related to fatty liver and ROS metabolism. Treatment with CeO2NPs was able to reduce the size and content of hepatocyte lipid droplets, the hepatic concentration of triglyceride- and cholesterol ester-derived FAs and the expression of several genes involved in cytokine, adipokine and chemokine signaling pathways. These findings suggest that CeO2NPs could be of beneficial value in NAFLD. ; This research was supported by grants to W. Jiménez from Ministerio de Economia y Competitividad [grants SAF2015-64126R, 12-35979, BES-2013-063685, SAFRTI2018-094734-B-C21], to M. Morales-Ruiz [grant SAF2016-75358-R] and to G. Casals [grant P74844I/15/00777]; Cofinanced by FEDER, European Union, a way of making Europe, Agència de Gestió d'Ajuts Universitaris i de Recerca [grant SGR 2014/219]. The Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd) is funded by the Instituto de Salud Carlos III.