Predictors of graft and patient survival in subjects transplanted for HCV infection

Audimoolam, Vinod K.; Foxton, Mathew R.; Agarwal, Kosh; O’Grady, John; Heneghan, Michael A.

doi:10.1002/lt.22015

Cited by 2 publications

(3 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A multidisciplinary group of health care professionals involved in the care of OLT patients met on 4 occasions and generated a list of parameters that they considered important in determining where patients would go after discharge. The parameters were identified on the basis of consensus and a knowledge of the predictors of outcomes from the medical literature 16‐21. The group consisted of 2 transplant surgeons, 2 transplant nurses, 1 transplant nurse manager, 2 physical therapists, 1 case manager, 1 home health care professional, 1 rehabilitation physician, and 1 statistician.…”

Section: Methodsmentioning

confidence: 99%

Predicting the discharge status after liver transplantation at a single center: A new approach for a new era

et al. 2012

View full text Add to dashboard Cite

Section: Methodsmentioning

confidence: 99%

Predicting the discharge status after liver transplantation at a single center: A new approach for a new era

et al. 2012

View full text Add to dashboard Cite

“…For reasons that have already been discussed in the context of the native liver, high intrahepatic viral RNA levels after transplantation are also likely to predispose patients to the development of IR. Several studies have shown that in comparison with patients undergoing transplantation for other conditions, HCV‐positive patients have an increased risk (2‐4 times) of developing type 2 diabetes mellitus after transplantation 20‐24. One recent study has suggested that early recurrent viral infection is particularly associated with the development of diabetes 25.…”

Section: Risk Factors Associated With Rapidly Progressive Hcv Infectimentioning

confidence: 99%

“…One recent study has suggested that early recurrent viral infection is particularly associated with the development of diabetes 25. As in the native liver, the presence of diabetes mellitus has been identified as an independent risk factor for rapid progression to advanced fibrosis in HCV‐positive individuals 22, 23, 26‐28…”

Section: Risk Factors Associated With Rapidly Progressive Hcv Infectimentioning

confidence: 99%

Steatosis and fibrosis progression in patients with recurrent hepatitis C infection: Complex interactions providing diagnostic and therapeutic challenges

Hübscher¹

2011

Liver Transpl

View full text Add to dashboard Cite

The relationship between hepatitis C virus (HCV) infection and hepatic steatosis is complex and involves a number of interrelated mechanisms that regulate viral replication, insulin resistance (IR), and lipid metabolism in the liver. The situation becomes even more complex in HCV-positive patients undergoing liver transplantation, largely because of the effects of immunosuppression. In this issue of Liver Transplantation, Brandman et al. 1 from the University of California San Francisco report an investigation of a number of the components of this complex and multifactorial relationship.In the nontransplant setting, HCV infection is recognized as an important risk factor for IR and hepatic steatosis. The prevalence of type 2 diabetes mellitus, an important result of severe IR, is significantly greater in patients with chronic HCV infection (20%-50%) than in those with other chronic liver diseases (approximately 10%). 2 Likewise, steatosis is seen in 40% to 86% of liver biopsy samples from patients with chronic HCV infection, 3 and this rate is considerably higher than the frequency observed in patients with other chronic liver diseases or in the general population. The development of hepatic steatosis can be viewed as a mechanism that promotes viral replication: the HCV core protein is targeted to lipid droplets, which act as intracellular storage organelles and are also required for virus assembly. 4 Two main pathways for HCV-induced hepatic steatosis have been proposed: metabolic and viral. The first involves a number of HCV-mediated mechanisms that result in IR and is seen in individuals infected with a non-3 genotype (particularly genotype 1). 3,5 The factors involved in the pathogenesis of HCVinduced IR are complex and include (1) direct effects on insulin signaling pathways, (2) altered glucose uptake by hepatocytes, and (3) the production of proinflammatory cytokines such as tumor necrosis factor a and reactive oxygen species (both appear to promote IR through mechanisms that are incompletely understood). 2,6,7 HCV infections also appear to promote truncal obesity, which is an important mechanism in the development of hepatic steatosis and inflammation. 8 In this setting, the severity of steatosis correlates with risk factors for metabolic syndrome rather than viral RNA levels. In contrast, in genotype 3-infected individuals, there is a direct correlation between the HCV RNA levels and the severity of steatosis, which diminishes in patients who achieve a sustained virological response to antiviral therapy; this suggests a direct effect of the virus on lipid metabolism. 3,5 The pathogenesis of viral-induced steatosis likely involves a number of effects of HCV on lipid metabolism in hepatocytes; these include increased lipid production by the up-regulation of Abbreviations: HCV, hepatitis C virus; IR, insulin resistance.

show abstract

Predictors of graft and patient survival in subjects transplanted for HCV infection

Cited by 2 publications

References 12 publications

Predicting the discharge status after liver transplantation at a single center: A new approach for a new era

Predicting the discharge status after liver transplantation at a single center: A new approach for a new era

Steatosis and fibrosis progression in patients with recurrent hepatitis C infection: Complex interactions providing diagnostic and therapeutic challenges

Contact Info

Product

Resources

About