Fat, diabetes, and liver injury in chronic hepatitis C

Ratziu, Vlad; Trabut, Jean‐Baptiste; Poynard, Thierry

doi:10.1007/s11894-004-0022-5

Cited by 41 publications

(33 citation statements)

References 80 publications

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“…However, we cannot exclude the possibility that synergism between the two diseases (diabetes/nonalcoholic steatohepatitis and virus-related chronic hepatitis) affects the outcome of liver fibrosis [7,11] . Steatosis has been associated with more severe liver fibrosis [23][24][25][26] as well as with a worse response to antiviral therapy. Moreover, steatosis is defined "metabolic steatosis" in non-3-genotype-infected patients as opposed to the viral steatosis typical of genotype 3 patients [11] .…”

Section: Discussionmentioning

confidence: 99%

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Clinical expression of insulin resistance in hepatitis C and B virus-related chronic hepatitis: Differences and similarities

Persico¹,

Masarone²,

Mura³

et al. 2009

WJG

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AIM:To investigate the prevalence of the clinical parameters of insulin resistance and diabetes in patients affected by chronic hepatitis C (CHC) or chronic hepatitis B (CHB). METHODS:We retrospectively evaluated 852 consecutive patients (726 CHC and 126 CHB) who had undergone liver biopsy. We recorded age, sex, ALT, type 2 diabetes and/or metabolic syndrome (MS), body mass index (BMI), and apparent disease duration (ADD). RESULTS:Age, ADD, BMI, prevalence of MS and diabetes in patients with mild/moderate liver fibrosis were significantly higher in CHC. However, the degree of steatosis and liver fibrosis evaluated in liver biopsies did not differ between CHC and CHB patients. At multivariate analysis, age, sex, BMI, ALT and diabetes were independent risk factors for liver fibrosis in CHC, whereas only age was related to liver fibrosis in CHB. We also evaluated the association between significant steatosis (> 30%) and age, sex, BMI, diabetes, MS and liver fibrosis. Diabetes, BMI and liver fibrosis were associated with steatosis > 30% in CHC, whereas only age and BMI were related to steatosis in CHB. CONCLUSION:These data may indicate that hepatitis C virus infection is a risk factor for insulin resistance.

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Section: Discussionmentioning

confidence: 99%

“…We next carried out statistical analyses to evaluate whether age, sex, BMI, ALT or diabetes were related to steatosis, which is a well known negative predictor of both disease outcome and response to therapy in HCV patients [23][24][25][26] . None of these parameters were significantly associated with degree of steatosis.…”

Section: As Shown Inmentioning

confidence: 99%

Clinical expression of insulin resistance in hepatitis C and B virus-related chronic hepatitis: Differences and similarities

Persico¹,

Masarone²,

Mura³

et al. 2009

WJG

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“…Also chronic HCV infection is shown to increase the risk of developing diabetes mellitus by up to 11 times in epidemiological studies [Harrison, 2006;Ratziu et al 2004]. Insulin resistance in chronic HCV infection is important in determining treatment outcome as significant correlation is demonstrated between insulin resistance and extent of liver fibrosis [McCaughan and George, 2004].…”

Section: Obesitymentioning

confidence: 99%

Review: Predicting the probable outcome of treatment in HCV patients

Navaneethan

Kemmer

Neff

2009

Therap Adv Gastroenterol

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Hepatitis C virus (HCV) is a major cause of chronic liver disease infecting more than 170 million people worldwide. HCV produces a wide gamut of manifestations varying from mild self-limiting disease to cirrhosis and hepatocellular carcinoma. A variety of viral, environmental and host genetic factors contribute to the clinical spectrum of patients infected with HCV and influence response to interferon (IFN) therapy. Predicting the probable outcome of treatment in patients with HCV infection has always been a challenging task. Treatment of HCV by pegylated interferon (peg-IFN) plus ribavirin eradicates the virus in approximately 60% of patients HCV genotype 1 (4251% response rates) and genotypes 2 and 3 (7684% response rates); however, a significant number of patients do not respond to therapy or relapse following discontinuation of treatment or have significant side effects that preclude further treatment. Accurately predicting the patients who will respond to therapy is becoming increasingly important, both from the point of patient care and also with respect to the healthcare cost as clinicians need to continue treatment in patients who will respond and stop treatment in patients who are unlikely to respond. Viral RNA measurements and genotyping are used to optimize treatment as a low viral load and nongenotype 1 is more likely to be associated with sustained virological response (SVR). Rapid virological response (RVR) defined by undetectable HCV RNA at 4 weeks of treatment is increasingly being recognized as a powerful tool for predicting treatment response. A variety of host factors including single nuclear polymorphisms (SNPs) of IFN response genes, insulin resistance, obesity, ethnicity, human leukocyte antigens and difference in T-cell immune response has been found to modulate the response to antiviral treatment. The presence of severe fibrosis/cirrhosis on pretreatment liver biopsy predicts a poor response to treatment. Recent studies on gene expression profiling and characterization of the liver and serum proteome provide options to accurately predict the outcome of patients infected with HCV in the future. Future studies on the factors that predict treatment response and tailoring treatment based on this is required if we are to conquer this disease.

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“…Steatosis in genotype 1 infection is instead thought to be an expression of metabolic syndrome caused by the activation of proinflammatory mechanisms as well as underlying obesity and IR [262] . The degree of steatosis in this genotype is independent of the HCV viral load, and antiviral therapy does not improve steatosis in these patients.…”

mentioning

confidence: 99%

Hepatitis C virus infection and type 1 and type 2 diabetes mellitus

Antonelli

Ferrari

Giuggioli

et al. 2014

WJD

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cytokines, chemokines, and other immune-mediated mechanisms. Few data have been reported on the association of CHC and T1DM and reports on the potential association between T1DM and acute HCV infection are even rarer. A small number of studies indicate that interferon-α therapy can stimulate pancreatic autoimmunity and in certain cases lead to the development of T1DM. Diabetes and CHC have important interactions. Diabetic CHC patients have an increased risk of developing cirrhosis and hepatocellular carcinoma compared with non-diabetic CHC subjects. However, clinical trials on HCV-positive patients have reported improvements in glucose metabolism after antiviral treatment. Further studies are needed to improve prevention policies and to foster adequate and cost-effective programmes for the surveillance and treatment of diabetic CHC patients. AbstractHepatitis C virus (HCV) infection and diabetes mellitus are two major public health problems that cause devastating health and financial burdens worldwide. Diabetes can be classified into two major types: type 1 diabetes mellitus (T1DM) and T2DM. T2DM is a common endocrine disorder that encompasses multifactorial mechanisms, and T1DM is an immunologically mediated disease. Many epidemiological studies have shown an association between T2DM and chronic hepatitis C (CHC) infection. The processes through which CHC is associated with T2DM seem to involve direct viral effects, insulin resistance, proinflammatory Submit a

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Fat, diabetes, and liver injury in chronic hepatitis C

Cited by 41 publications

References 80 publications

Clinical expression of insulin resistance in hepatitis C and B virus-related chronic hepatitis: Differences and similarities

Clinical expression of insulin resistance in hepatitis C and B virus-related chronic hepatitis: Differences and similarities

Review: Predicting the probable outcome of treatment in HCV patients

Hepatitis C virus infection and type 1 and type 2 diabetes mellitus

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