Hepatitis C and Nonalcoholic Fatty Liver Disease

Ramesh, Seela; Sanyal, Arun J.

doi:10.1055/s-2004-860869

Cited by 88 publications

(68 citation statements)

References 76 publications

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“…Pro-inflammatory cytokines such as tumor necrosis factor-␣, monocyte chemoattractant protein-1, and interleukin-6 are up-regulated, whereas adiponectin, an adipokine with insulin-sensitizing effects, is decreased. 14 …”

Section: Steatosis Mediated Via Host Metabolic Factorsmentioning

confidence: 99%

Steatosis and Chronic Hepatitis C Infection: Mechanisms and Significance

Harrison

2005

Clinical Gastroenterology and Hepatology

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Section: Steatosis Mediated Via Host Metabolic Factorsmentioning

confidence: 99%

Steatosis and Chronic Hepatitis C Infection: Mechanisms and Significance

Harrison

2005

Clinical Gastroenterology and Hepatology

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“…The endocrine function of adipose tissue, which produces adipokines, could partially explain these complex associations. The source of adipokines from the obese patients (high BMI) and from visceral fat are being studied to determine their relationship with the severity of liver fibrosis [21][22][23][24][25][26].…”

Section: Discussionmentioning

confidence: 99%

Adipokines, insulin resistance, hepatic steatosis, and necroinflammation in patients with chronic viral hepatitis

Treeprasertsuk

Komolmit

Tanyaowalak³

2014

Asian Biomedicine

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Background: Hypoadiponectinemia and hyperleptinemia, and reductions in the ratio of adiponectin to leptin (A/L ratio) are associated with the development of hepatic necroinflammation in nonalcoholic fatty liver, but the association of the adipokines with hepatic steatosis in chronic viral hepatitis is unclear. Objective: To investigate the relationship between serum A/L ratio, insulin resistance, degree of hepatic steatosis, and necroinflammation in patients with chronic viral hepatitis. Methods: We measured serum adiponectin, leptin, and resistin levels, insulin resistance, and analyzed the association between liver histopathology and the level of the adipokines in 44 patients with chronic viral hepatitis before they started treatment. Results: We found that insulin resistance, leptin, and resistin levels tended to increase in the group with a greater degree of hepatic steatosis and necroinflammation, but that the increase was not significant. The adiponectin/leptin ratio (A/L ratio) in a group with a low degree of hepatic steatosis was significantly higher than it was in the group with a high degree of hepatic steatosis (3.1 ± 3.1 vs 1.2 ± 0.8; P = 0.008). The A/L ratio in a group with low histological activity index (HAI) scores was significantly higher than in the group with high HAI scores (3.7 ± 3.4 vs 1.1 ± 1.1; P = 0.006). Abdominal obesity was the only variable that showed a significant association with the HAI score (P = 0.03). Conclusion:The serum A/L ratio in patients with chronic viral hepatitis showed a significant inverse association with their degree of hepatic steatosis and necroinflammation.

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“…Additionally, the global burden of liver disease is increasing steadily due to the increasing prevalence of hepatitis C and non-alcoholic fatty liver disease. [11][12][13][14] Currently in the US, liver diseases are the 10th most common cause of death and responsible for an associated economic burden of approximately 1% of the total national healthcare expenditure ($1.2 trillion in 1999). 15 These observations clearly underline the potential usefulness of a device for extracorporeal liver support therapy if it can facilitate an improved environment for hepatic regeneration and clinical recovery.…”

Section: Is There a Need For Liver Support/ Replacement Therapies?mentioning

confidence: 99%

Review article: non‐biological liver support in liver failure

Laleman¹,

Wilmer²,

Evenepoel³

et al. 2006

Aliment Pharmacol Ther

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SUMMARYLiver failure, whether acute or acute-on-chronic, remains an important cause of morbidity and mortality. The lack of liver detoxification, metabolic and regulatory functions of the liver leads to life-threatening complications, such as renal failure, altered immune response, hepatic coma and systemic haemodynamic dysfunction, eventually culminating in multiorgan failure.Current medical therapy involves the management of the precipitating event and treatment of complications until the liver eventually recovers, leaving us with no other treatment options than transplantation if these attempts fail. However, the shortage in cadaveric organs and other transplant-related problems, have prompted the need for alternative methods to provide liver support.As liver failure is often potentially reversible, considerable effort has been invested in the development of liver support systems. Currently, most of the experience is available for non-biological support systems. They represent the focus of this review, which aims to define the goals of liver support, to describe the design of the different existing devices and to analyse the available data to determine their current status in the management of patients with liver failure.

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Hepatitis C and Nonalcoholic Fatty Liver Disease

Cited by 88 publications

References 76 publications

Steatosis and Chronic Hepatitis C Infection: Mechanisms and Significance

Steatosis and Chronic Hepatitis C Infection: Mechanisms and Significance

Adipokines, insulin resistance, hepatic steatosis, and necroinflammation in patients with chronic viral hepatitis

Review article: non‐biological liver support in liver failure

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