scholarly journals Etiology and Viral Genotype in Patients with End-Stage Liver Diseases admitted to a Hepatology Unit in Colombia

2011 ◽  
Vol 2011 ◽  
pp. 1-10 ◽  
Author(s):  
Fabian Cortes-Mancera ◽  
Carmen Luisa Loureiro ◽  
Sergio Hoyos ◽  
Juan-Carlos Restrepo ◽  
Gonzalo Correa ◽  
...  
Keyword(s):  
Risk Factor ◽  
Liver Disease ◽  
Alcohol Consumption ◽  
Liver Diseases ◽  
Core Promoter ◽  
Hepatic Tissue ◽  
Basal Core Promoter ◽  
Tissue Samples ◽  
Viral Aetiology ◽  
End Stage

Hepatitis B virus (HBV) and hepatitis C virus (HCV) infections are the principal risk factor associated to end-stage liver diseases in the world. A study was carried out on end-stage liver disease cases admitted to an important hepatology unit in Medellin, the second largest city in Colombia. From 131 patients recruited in this prospective study, 71% of cases were diagnosed as cirrhosis, 12.2% as HCC, and 16.8% as cirrhosis and HCC. Regarding the risk factors of these patients, alcohol consumption was the most frequent (37.4%), followed by viral etiology (17.6%). Blood and/or hepatic tissue samples from patients with serological markers for HCV or HBV infection were characterized; on the basis of the phylogenetic analysis of HCV 5′ UTR and HBV S gene, isolates belonged to HCV/1 and HBV/F3, respectively. These results confirm the presence of strains associated with poor clinical outcome, in patients with liver disease in Colombia; additionally, HBV basal core promoter double mutant was identified in HCC cases. Here we show the first study of cirrhosis and/or HCC in Colombian and HBV and HCV molecular characterization of these patients. Viral aetiology was not the main risk factor in this cohort but alcohol consumption.

PNPLA3 in end-stage liver disease: Alcohol consumption, hepatocellular carcinoma development, and transplantation-free survival

2014 ◽  
Vol 29 (7) ◽  
pp. 1477-1484 ◽  
Author(s):  
Kilian Friedrich ◽  
Andreas Wannhoff ◽  
Stefan Kattner ◽  
Maik Brune ◽  
Johannes Roksund Hov ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Disease ◽  
Alcohol Consumption ◽  
Free Survival ◽  
End Stage Liver Disease ◽  
End Stage

scholarly journals Stem Cell-Related Studies and Stem Cell-Based Therapies in Liver Diseases

2019 ◽  
Vol 28 (9-10) ◽  
pp. 1116-1122 ◽  
Author(s):  
Wei Zhou ◽  
Erek D. Nelson ◽  
Anan A. Abu Rmilah ◽  
Bruce P. Amiot ◽  
Scott L. Nyberg
Keyword(s):  
Liver Transplantation ◽  
Stem Cell ◽  
Liver Disease ◽  
Liver Failure ◽  
Effective Treatment ◽  
Liver Diseases ◽  
Immunosuppressive Agents ◽  
End Stage Liver Disease ◽  
Effective Interventions ◽  
End Stage

Owing to the increasing worldwide burden of liver diseases, the crucial need for safe and effective interventions for treating end-stage liver failure has been a very productive line of inquiry in the discipline of hepatology for many years. Liver transplantation is recognized as the most effective treatment for end-stage liver disease; however, the shortage of donor organs, high medical costs, and lifelong use of immunosuppressive agents represent major drawbacks and demand exploration for alternative treatments. Stem cell-based therapies have been widely studied in the field of liver diseases and are considered to be among the most promising therapies. Herein, we review recent advances in the application of stem cell-related therapies in liver disease with the aim of providing readers with relevant knowledge in this field and inspiration to spur further inquiry.

Model for end-stage liver disease (MELD) exception for unusual metabolic liver diseases

2006 ◽  
Vol 12 (S3) ◽  
pp. S124-S127 ◽  
Author(s):  
Sue McDiarmid ◽  
Robert G. Gish ◽  
Simon Horslen ◽  
George V. Mazariegos
Keyword(s):  
Liver Disease ◽  
Liver Diseases ◽  
End Stage Liver Disease ◽  
End Stage ◽  
Metabolic Liver Diseases

Fatty liver disease in children

2011 ◽  
Author(s):  
R. Mark Beattie ◽  
Anil Dhawan ◽  
John W.L. Puntis
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Liver Injury ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Alcoholic Hepatitis ◽  
Alcoholic Fatty Liver ◽  
End Stage Liver Disease ◽  
End Stage ◽  
Alcoholic Fatty Liver Disease

Demographics 406Pathophysiology 406Differential diagnoses 407Presenting features 407Investigation 408Management 409Fatty liver disease is now increasingly recognized in children, particularly in the setting of obesity.The term non-alcoholic steatohepatitis (NASH) was first coined in 1980 by Ludwig to describe a pattern of liver injury in adults in which the liver histology was consistent with alcoholic hepatitis, but in whom significant alcohol consumption was denied. NASH can be considered as part of a broader spectrum of non-alcoholic fatty liver disease that extends from simple steatosis through steatohepatitis that is characterized by the potential to progress to fibrosis, cirrhosis and subsequent end stage liver disease....

scholarly journals Liver epigenome changes in patients with hepatopulmonary syndrome: A pilot study

PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0245046
Author(s):  
Nuria Mendoza ◽  
Eva Rivas ◽  
Roberto Rodriguez-Roisin ◽  
Tamara Garcia ◽  
Miquel Bruguera ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Liver Disease ◽  
Vascular Remodeling ◽  
Hepatopulmonary Syndrome ◽  
Neuroendocrine System ◽  
Genomic Variation ◽  
Epigenetic Changes ◽  
Tissue Samples ◽  
Control Comparison ◽  
End Stage

The hepatopulmonary syndrome (HPS) is defined by the presence of pulmonary gas exchange abnormalities due to intrapulmonary vascular dilatations in patients with chronic liver disease. Changes in DNA methylation reflect the genomic variation. Since liver transplant (LT) reverts HPS we hypothesized that it may be associated with specific liver epigenetic changes. Thus, the aim of this study was to investigate the role of the liver epigenome in patients with HPS. We extracted DNA from paraffin embedded liver tissue samples from 10 patients with HPS and 10 age-, sex- and MELD (Model for End-stage Liver Disease)-matched controls. DNA methylation was determined using the 850K array (Illumina). Weighted Gene Co-expression Network Analysis (WGCNA) was used to identify modules related to defining physiologic characteristics of HPS. Only 12 out of the 20 liver biopsies (7 HPS and 5 controls) had sufficient quality to be analyzed. None of the 802,688 DNA probes analyzed in the case control comparison achieved a significant False Discovery Rate (FDR). WGCNA identified 5 co-methylated gene-modules associated to HPS markers, mainly related to nervous and neuroendocrine system, apoptotic processes, gut bacterial translocation, angiogenesis and vascular remodeling ontologies. To conclude, HPS is associated with nervous/neuroendocrine system and vascular remodeling related liver epigenetic changes.

scholarly journals New Insights into the Pathogenesis of Alcohol-Induced ER Stress and Liver Diseases

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Cheng Ji
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Er Stress ◽  
Liver Diseases ◽  
Cell Cycle Progression ◽  
Alcohol Exposure ◽  
Cellular Protein ◽  
Protein Homeostasis ◽  
Lipid Species

Alcohol-induced liver disease increasingly contributes to human mortality worldwide. Alcohol-induced endoplasmic reticulum (ER) stress and disruption of cellular protein homeostasis have recently been established as a significant mechanism contributing to liver diseases. The alcohol-induced ER stress occurs not only in cultured hepatocytes but also in vivo  in the livers of several species including mouse, rat, minipigs, zebrafish, and humans. Identified causes for the ER stress include acetaldehyde, oxidative stress, impaired one carbon metabolism, toxic lipid species, insulin resistance, disrupted calcium homeostasis, and aberrant epigenetic modifications. Importance of each of the causes in alcohol-induced liver injury depends on doses, duration and patterns of alcohol exposure, genetic disposition, environmental factors, cross-talks with other pathogenic pathways, and stages of liver disease. The ER stress may occur more or less all the time during alcohol consumption, which interferes with hepatic protein homeostasis, proliferation, and cell cycle progression promoting development of advanced liver diseases. Emerging evidence indicates that long-term alcohol consumption and ER stress may directly be involved in hepatocellular carcinogenesis (HCC). Dissecting ER stress signaling pathways leading to tumorigenesis will uncover potential therapeutic targets for intervention and treatment of human alcoholics with liver cancer.

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