Mild Alcohol Consumption is Not Associated With Increased Fibrosis in Patients With Chronic Hepatitis C

Cheung, Onpan; Sterling, Richard K.; Salvatori, Jennifer; Williams, Kim A.; Hubbard, Sarah; Luketic, Velimir A.; Stravitz, Todd; Sanyal, Arun J.; Contos, Melissa J.; Mills, Scott; Shiffman, Mitchell L.

doi:10.1097/mcg.0b013e3181e12511

Cited by 15 publications

(11 citation statements)

References 31 publications

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“…Despite the likely contributions of alcohol to hepatic fibrosis, the effect of subclinical/moderate alcohol consumption in the setting of superimposed liver injury is not well understood. There are conflicting findings regarding the impact of moderate alcohol consumption on the progression of chronic liver diseases, particularly from observational studies in patients with non-alcoholic chronic liver disease [31]–[33]. Results between these different studies are difficult to compare due to variation in the definition and quantification of alcohol intake, as well as other dietary confounders.…”

Section: Discussionmentioning

confidence: 99%

Adenosine 2A Receptor Antagonist Prevented and Reversed Liver Fibrosis in a Mouse Model of Ethanol-Exacerbated Liver Fibrosis

et al. 2013

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The effect of moderate alcohol consumption on liver fibrosis is not well understood, but evidence suggests that adenosine may play a role in mediating the effects of moderate ethanol on tissue injury. Ethanol increases the concentration of adenosine in the liver. Adenosine 2A receptor (A2AR) activation is known to enhance hepatic stellate cell (HSC) activation and A2AR deficient mice are protected from fibrosis in mice. Making use of a novel mouse model of moderate ethanol consumption in which female C57BL/6J mice were allowed continued access to 2% (vol/vol) ethanol (11% calories) or pair-fed control diets for 2 days, 2 weeks or 5 weeks and superimposed with exposure to CCl4, we tested the hypothesis that moderate ethanol consumption increases fibrosis in response to carbon tetrachloride (CCl4) and that treatment of mice with an A2AR antagonist prevents and/or reverses this ethanol-induced increase in liver fibrosis. Neither the expression or activity of CYP2E1, required for bio-activation of CCl4, nor AST and ALT activity in the plasma were affected by ethanol, indicating that moderate ethanol did not increase the direct hepatotoxicity of CCl4. However, ethanol feeding enhanced HSC activation and exacerbated liver fibrosis upon exposure to CCl4. This was associated with an increased sinusoidal angiogenic response in the liver. Treatment with A2AR antagonist both prevented and reversed the ability of ethanol to exacerbate liver fibrosis.ConclusionModerate ethanol consumption exacerbates hepatic fibrosis upon exposure to CCl4. A2AR antagonism may be a potential pharmaceutical intervention to decrease hepatic fibrosis in response to ethanol.

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Section: Discussionmentioning

confidence: 99%

Adenosine 2A Receptor Antagonist Prevented and Reversed Liver Fibrosis in a Mouse Model of Ethanol-Exacerbated Liver Fibrosis

et al. 2013

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“…The impact of ongoing alcohol consumption on "all-stages of fibrosis" in HCV-related chronic hepatitis, as defined before the DAA era, is controversial. 87,88 In patients with advanced liver fibrosis, alcohol increases the risk of liver events. In a prospective study conducted in 74 patients with HCV-related cirrhosis, light to moderate alcohol intake and a lack of viral eradication were associated with the risk of HCC (HR for alcohol consumption: 3.43; 95% CI 1.49-7.92; p = 0.004).…”

Section: Assessment Of Portal Hypertensionmentioning

confidence: 99%

Management of patients with pre-therapeutic advanced liver fibrosis following HCV eradication

Nahon

Ganne-Carrié

2019

JHEP Reports

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Patients with HCV-related bridging fibrosis or cirrhosis remain at risk of developing lifethreatening complications even after achieving a sustained virological response. Although it is reduced, the risk of liver-related events in these patients justifies their inclusion in surveillance programmes dedicated to the early detection of hepatocellular carcinoma and the screening for portal hypertension. Biochemical parameters or non-invasive tests might indicate the potential progression of liver injury despite viral clearance. Specific attention must be focused on the management of comorbidities, while dedicated educational programmes must be encouraged to increase compliance and commitment to surveillance. Better knowledge of the long-term evolution of these patients, who now live longer, is essential to improve risk stratification and refine screening strategies in this growing population.

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“…Hezode et al initially reported a progressive increase in histologic severity and fibrosis in relation to the amount of alcohol intake in chronic HCV infection [59,70]. However, in a similar cohort of 857 patients, the degree of fibrosis was independent of mild-moderate alcohol consumption [71]. A similar negative effect is expected to occur with hepatitis B infection, but also in this condition conflicting data have been reported [72], as well as in storage defect disease [73].…”

Section: Cirrhosis By Blood Tests and Clinicalmentioning

confidence: 97%

Moderate Alcohol Intake in Non-Alcoholic Fatty Liver Disease: To Drink or Not to Drink?

et al. 2019

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Nonalcoholic fatty liver disease (NAFLD) is defined by hepatic steatosis in the presence of alcohol intake within safe limits, defined by guidelines of scientific associations (usually 20 g or 2 units/day in women, 30 g or 3 units in men). The diagnosis is usually followed by medical counseling of total abstinence, in order to prevent disease progression. This policy has been challenged by epidemiological studies, suggesting that the risk of liver disease and disease progression is lower in modest drinkers than in total abstainers. We revised the literature on the effects of modest alcohol intake on disease burden. Epidemiological data may suffer from several potential biases (recall bias for retrospective analyses, difficulties in the calculation of g/day), limiting their validity. Prospective data suggest that NAFLD patients with regular alcohol intake, although within the safe thresholds, are at higher risk of liver disease progression, including hepatocellular carcinoma; a detrimental effect of modest alcohol drinking is similarly observed in liver disease of viral etiology. Alcohol intake is also a risk factor for extrahepatic cancers, particularly breast, oral, and pharyngeal cancers, with gender difference and no floor effect, which outweigh the possible beneficial effects on cardiovascular system, also derived from retrospective studies. Finally, the negative effects of the calorie content of alcohol on dietary restriction and weight loss, the pivotal intervention to reduce NAFLD burden, should be considered. In summary, the policy of counseling NAFLD patients for alcohol abstinence should be maintained.Nutrients 2019, 11, 3048 2 of 23 equals mortality in alcohol users) for an average alcohol consumption of approximately 25-30 g in women and 40 g in men [4].All NAFLD studies explicitly report the exclusion of subjects with alcohol intake at risk, defined according to pre-specified criteria, and most clinicians suggest total abstinence from alcohol as therapeutic measure for prevention NAFLD and/or disease progression. More than a decade ago a few epidemiological studies reported an inverse association between moderate alcohol consumption (within presumably safe limits) and the prevalence of NAFLD in the population [5,6], pointing to a favorable effect of moderate alcohol use extending from the cardiovascular system to the setting of metabolic liver disease. This raised a lot of debate on the correct dietary and lifestyle treatment of NAFLD, which has not settled yet. Do we need to counsel our NAFLD patients for total alcohol abstinence to prevent disease progression?This narrative review is intended to summarize the evidence linking moderate alcohol intake with NAFLD, starting from difficulties in the correct assessment of alcohol intake. The conclusions are based on the experience of authors and the general effects of alcohol on the liver and outside the liver, in the hope to generate a common health policy among healthcare professionals. Literature Search

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Mild Alcohol Consumption is Not Associated With Increased Fibrosis in Patients With Chronic Hepatitis C

Abstract: Mild alcohol use does not seem to adversely affect the severity of fibrosis in patients with chronic HCV.

Cited by 15 publications

References 31 publications

Adenosine 2A Receptor Antagonist Prevented and Reversed Liver Fibrosis in a Mouse Model of Ethanol-Exacerbated Liver Fibrosis

Adenosine 2A Receptor Antagonist Prevented and Reversed Liver Fibrosis in a Mouse Model of Ethanol-Exacerbated Liver Fibrosis

Management of patients with pre-therapeutic advanced liver fibrosis following HCV eradication

Moderate Alcohol Intake in Non-Alcoholic Fatty Liver Disease: To Drink or Not to Drink?

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