Hepatitis C and alcohol

Schiff, Eugene R.

doi:10.1002/hep.510260707

Cited by 173 publications

(118 citation statements)

References 20 publications

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“…[5][6][7][8][9] In rodents, ethanol feeding was also shown to accelerate CCl 4 -induced liver fibrosis. 10 It is generally believed that ethanol feeding enhances CCl 4 metabolism by induction of cytochrome P450 2E1 expression and, subsequently, enhances CCl 4 -induced liver injury.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] Alcohol consumption, hepatitis C viral (HCV) infection, and nonalcoholic steatohepatitis are currently the 3 main causes of chronic liver injury leading to liver fibrosis. 4 Interestingly, alcohol consumption was shown to accelerate liver fibrosis in patients with chronic HCV infection [5][6][7][8][9] and in animals treated with hepatotoxins. 10 The obvious underlying cause for this is enhanced liver injury induced by alcohol; however, this does not fully explain the acceleration of liver fibrosis observed.…”

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confidence: 99%

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Abrogation of the Antifibrotic Effects of Natural Killer Cells/Interferon-γ Contributes to Alcohol Acceleration of Liver Fibrosis

2008

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Abrogation of the Antifibrotic Effects of Natural Killer Cells/Interferon-γ Contributes to Alcohol Acceleration of Liver Fibrosis

2008

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“…Alcohol also exacerbates the hepatopathy of chronic HCV infection. 41 It is probable that many patients with PCT who formerly were thought to have alcohol-induced liver injury in fact had chronic hepatitis C or combined chronic HCV-and alcoholinduced injury. Alcohol, iron, and chronic HCV infection all produce increased oxidative stress in liver cells, [21][22][23]42 perhaps increasing the likelihood that uroporphyrinogen in hepatocytes will oxidize to uroporphyrin, which is not a substrate for Uro-D and therefore will accumulate.…”

Section: Discussionmentioning

confidence: 99%

Porphyria cutanea tarda, hepatitis C, and HFE gene mutations in north america†

et al. 1998

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In some, but not all countries, porphyria cutanea tarda (PCT) has been associated with chronic infection with the hepatitis C virus (HCV). Recently, PCT has also been associated with mutations in the HFE gene that are associated with HLA-linked hereditary hemochromatosis. Until now, few studies of these associations have been reported from North America. The aims of this study were: 1) to assess the prevalence of HCV infection and HFE mutations in North American patients with PCT; 2) to compare demographic and laboratory features between those who are HCV-positive and HCV-negative; and 3) to study urinary porphyrin excretions in American HCV-positive patients without clinically manifest PCT. Clinical and laboratory data, including tests for HCV and urinary porphyrins, were collected from 70 unselected patients with typical PCT. Urinary porphyrins were also measured in 110 non-PCT patients with chronic hepatitis C. Mutational analyses of the HFE gene were performed in 26 PCT patients. Thirtynine of 70 (56%) of the PCT patients had evidence of HCV infection. Thirty-two of 39 PCT patients with HCV were men, all of whom used alcohol. In contrast, 22 of 31 PCT patients without HCV infection were women, 12 of whom had taken estrogens. The HCV-positive group was more likely to have used illicit intravenous drugs (45% vs. 0%; P ‫؍‬ 0.01), to have had several (G4) sex partners (48% vs. 13%; P ‫؍‬ 0.005), and less likely to have no known risk factors for HCV infection (33% vs. 78%; P ‫؍‬ 0.004). Total urinary porphyrin excretion was the same in the two groups, but those with HCV infection had a significantly lower percentage of uroporphyrin and higher percentages of hepta-and hexa-carboxy porphyrins in urine. Sixteen of 110 (15%) HCV-positive subjects without PCT had increased urinary porphyrins, but, unlike PCT, these were mainly coproporphyrin. Forty-two percent of PCT patients carried the C282Y mutation of HFE (15% homozygous), and another 31% carried the H63D mutation (8% homozygous). Thus, 73% of PCT patients had one of these mutations. The prevalence of HCV infection (56%) and mutations in the HFE gene (73%) are high among North American patients with PCT. Alcohol and estrogen use are important additional risk factors. All PCT patients should be tested for HCV infection and for HFE gene mutations. Although HCV infection is a trigger for PCT, preclinical PCT is rare in chronic HCV hepatitis C in the United States. (HEPATOLOGY 1998;27:1661-1669.)

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“…The rate of disease progression to cirrhosis is highly variable and the host and viral factors that modify the course are poorly understood. Alcohol ingestion is a major cofactor [5], but how other factors, such as male gender and age at acquisition, impact liver injury are at present not understood. Although current therapies can cure HCV infection in approximately one half of infected persons [6], therapy is difficult and not tolerated by many patients.…”

Section: Introductionmentioning

confidence: 99%

Immune responses during acute and chronic infection with hepatitis C virus

Ishii

Koziel

2008

Clinical Immunology

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Hepatitis C virus (HCV) induces persistent infection and causes chronic liver disease in most infected patients. Vigorous HCV-specific CD4+ and CD8+ T cell responses against HCV multiple epitopes are necessary for spontaneous viral clearance during the acute phase, but the virus appears to have multiple strategies to evade these defenses. There are relatively few studies on the role of immune responses during the chronic phase of infection. CD4+ T cell responses appear to protect against liver injury and may be important to clearance during interferon and ribavirin based therapy. Classic cytotoxic T cells (CTL) may primarily damage the liver in chronic HCV, but there may be subpopulations of T cells that protect against liver inflammation. Resolution of these outstanding questions is important to the development of a prophylactic vaccine as well as improving therapeutic options for those with chronic infection.

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Hepatitis C and alcohol

Cited by 173 publications

References 20 publications

Abrogation of the Antifibrotic Effects of Natural Killer Cells/Interferon-γ Contributes to Alcohol Acceleration of Liver Fibrosis

Abrogation of the Antifibrotic Effects of Natural Killer Cells/Interferon-γ Contributes to Alcohol Acceleration of Liver Fibrosis

Porphyria cutanea tarda, hepatitis C, and HFE gene mutations in north america†

Immune responses during acute and chronic infection with hepatitis C virus

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