Insulin resistance, hepatitis c, and liver transplantation

Alsatie, Mazen; Pandya, Prashant; Chalasani, Naga

doi:10.1002/lt.21318

Cited by 10 publications

(4 citation statements)

References 12 publications

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“…Many studies have shown that HCV is associated with insulin resistance and an increased risk of NODAT . In a study of kidney transplantation, HCV‐positive recipients showed significantly lower insulin sensitivity compared with HCV‐negative recipients; however, insulin secretion and hepatic insulin uptake were not significantly different .…”

Section: Discussionmentioning

confidence: 98%

Incidence and risk factors for new‐onset diabetes in living‐donor liver transplant recipients

Honda

Asonuma

Hayashida

et al. 2013

Clinical Transplantation

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With the increased number of long-term survivors after liver transplantation, new-onset diabetes after transplantation (NODAT) is becoming more significant in patient follow-up. However, the incidence of new-onset diabetes after living-donor liver transplantation (LDLT) has not been well elucidated. The aim of this study was to evaluate the incidence and risk factors for NODAT in adult LDLT recipients at a single center in Japan. A retrospective study was performed on 161 adult patients without diabetes who had been followed up for ≥three months after LDLT. NODAT was defined according to the 2003 American Diabetes Association/World Health Organization guidelines. The recipient-, donor-, operation-, and immunosuppression-associated risk factors for NODAT were assessed. Overall, the incidence of NODAT was 13.7% (22/161) with a mean follow-up of 49.8 months. In a multivariate analysis, the identified risk factors for NODAT were donor liver-to-spleen (L-S) ratio (hazard ratio [HR] = 0.022, 95% confidence interval [CI] = 0.001-0.500, p = 0.017), and steroid pulse therapy for acute rejection (HR = 3.320, 95% CI = 1.365-8.075, p = 0.008). In conclusion, donor L-S ratio and steroid pulse therapy for acute rejection were independent predictors for NODAT in LDLT recipients. These findings can help in screening for NODAT and applying early interventions.

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Section: Discussionmentioning

confidence: 98%

Incidence and risk factors for new‐onset diabetes in living‐donor liver transplant recipients

Honda

Asonuma

Hayashida

et al. 2013

Clinical Transplantation

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“…Interactions between hepatitis C infection, insulin resistance, and NAFLD also appear to be important in the pathogenesis of recurrent HCV and de novo NAFLD [126,[128][129][130][131].…”

Section: De Novo Non-alcoholic Fatty Liver Disease (Nafld)mentioning

confidence: 97%

What is the long-term outcome of the liver allograft?

Hübscher

2011

Journal of Hepatology

122

127

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With improved long-term survival following liver transplantation (LT), issues relating to the assessment of the liver allograft in long-term survivors are becoming increasingly relevant. Histological abnormalities are commonly present in late post-transplant biopsies, including protocol biopsies from patients who appear to be well with good graft function. Recurrent disease is the commonest recognised cause of abnormal graft histology, but may be modified by the effects of immunosuppression or interactions with other graft complications, resulting in complex or atypical changes. Other abnormalities seen in late post-transplant biopsies include rejection (which often has different appearances to those seen in the post-transplant period), de novo disease, "idiopathic" post-transplant hepatitis (IPTH) and nodular regenerative hyperplasia. In many cases graft dysfunction has more than one cause and liver biopsy may help to identify the predominant cause of graft damage. Problems exist with the terminology used to describe less well understood patterns of graft injury, but there is emerging evidence to suggest that late rejection, de novo autoimmune hepatitis and IPTH may all be part of an overlapping spectrum of immune-mediated injury occurring in the late post-transplant liver allograft. Careful clinico-pathological correlation is very important and the wording of the biopsy report should take into account therapeutic implications, particularly whether changes in immunosuppression may be indicated. This article will provide an overview of the main histological changes occurring in long-term survivors post-LT, focusing on areas where the assessment of late post-transplant biopsies is most relevant clinically.

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“…This is, however, restored after clearance of the virus. HCV causes proteasomal degradation of IRS1 and IRS2 that are essential for further insulin signaling through phosphoinositide 3-kinase (PI3K) and Akt (Alsatie et al 2008 ; Kawaguchi et al 2004 , 2007 ). Furthermore, diabetic hepatitis C patients exhibit increased levels of soluble TNF-α receptors.…”

Section: Virusesmentioning

confidence: 99%

Infections at the nexus of metabolic-associated fatty liver disease

et al. 2021

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Metabolic-associated fatty liver disease (MAFLD) is a chronic liver disease that affects about a quarter of the world population. MAFLD encompasses different disease stadia ranging from isolated liver steatosis to non-alcoholic steatohepatitis (NASH), fibrosis, cirrhosis and hepatocellular carcinoma. Although MAFLD is considered as the hepatic manifestation of the metabolic syndrome, multiple concomitant disease-potentiating factors can accelerate disease progression. Among these risk factors are diet, lifestyle, genetic traits, intake of steatogenic drugs, male gender and particular infections. Although infections often outweigh the development of fatty liver disease, pre-existing MAFLD could be triggered to progress towards more severe disease stadia. These combined disease cases might be underreported because of the high prevalence of both MAFLD and infectious diseases that can promote or exacerbate fatty liver disease development. In this review, we portray the molecular and cellular mechanisms by which the most relevant viral, bacterial and parasitic infections influence the progression of fatty liver disease and steatohepatitis. We focus in particular on how infectious diseases, including coronavirus disease-19, hepatitis C, acquired immunodeficiency syndrome, peptic ulcer and periodontitis, exacerbate MAFLD. We specifically underscore the synergistic effects of these infections with other MAFLD-promoting factors. Keywords Metabolic-associated fatty liver disease (MAFLD) • Non-alcoholic steatohepatitis (NASH) • Infectious diseases • Lipid metabolism • Liver • SARS-CoV-2 • Human immunodeficiency virus • Hepatitis C • Helicobacter pylori • Klebsiella pneumoniae

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Insulin resistance, hepatitis c, and liver transplantation

Cited by 10 publications

References 12 publications

Incidence and risk factors for new‐onset diabetes in living‐donor liver transplant recipients

Incidence and risk factors for new‐onset diabetes in living‐donor liver transplant recipients

What is the long-term outcome of the liver allograft?

Infections at the nexus of metabolic-associated fatty liver disease

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