Alcohol does not impact chronic hepatitis C treatment outcomes but increases risk for progressive liver disease: Findings from a prospective multicentre Australian study (OPERA‐C).

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Title: Alcohol does not impact chronic hepatitis C treatment outcomes but increases risk for progressive liver disease: Findings from a prospective multicentre Australian study (OPERA‐C).
Authors: Clark, Paul J. (AUTHOR), Valery, Patricia C. (AUTHOR), Strasser, Simone I. (AUTHOR), Weltman, Martin (AUTHOR), Thompson, Alex (AUTHOR), Levy, Miriam T. (AUTHOR), Leggett, Barbara (AUTHOR), Zekry, Amany (AUTHOR), Rong, Julian (AUTHOR), Sinclair, Marie (AUTHOR), George, Jacob (AUTHOR), Sievert, William (AUTHOR), MacQuillan, Gerry (AUTHOR), Tse, Edmund (AUTHOR), Nicoll, Amanda (AUTHOR), Wade, Amanda (AUTHOR), Cheng, Wendy (AUTHOR), Roberts, Stuart K. (AUTHOR)
Source: Drug & Alcohol Review. Sep2024, Vol. 43 Issue 6, p1559-1572. 14p.
Subjects: Hepatic fibrosis, Chronic hepatitis C, Alcoholism, Alcohol drinking, Hepatitis C virus
Abstract: Introduction: Alcohol use is common in patients with chronic hepatitis C virus (HCV) infection. We examined the impact of alcohol use on direct‐acting antiviral (DAA) therapy outcome and the clinical course of liver disease and 2‐year survival for patients receiving HCV DAA therapy. Methods: Adults (n = 2624) recruited from 26 Australian hospital liver clinics during 2016–2021 were followed up for 2 years. Risky alcohol use was defined by a combination of self‐report (≥40 g/day of ethanol), physician‐reported history of problematic alcohol use, and anti‐craving medication prescription via population‐based database linkage. We examined factors associated with advanced liver fibrosis and survival using multivariable logistic and Cox regression. Results: Among 1634 patients (62.3%) with risky alcohol use, 24.6% reported consuming ≥40 g/day of alcohol, 98.3% physician‐reported problematic alcohol use; only 4.1% were dispensed naltrexone/acamprosate. One hundred and forty‐three patients with cirrhosis reported ≥40 g/day of alcohol, 6 (4.3%) were prescribed naltrexone/acamprosate. Risky alcohol use was associated with advanced fibrosis (adjusted‐odds ratio 1.69, 95% confidence interval 1.32–2.17) and patients were over‐represented for cirrhosis (45.1% vs. 25.6% in no‐risky alcohol use [p < 0.001]) and hepatocellular carcinoma (5.7% vs. 2.5% [p < 0.001]). Sustained viral response (p = 0.319) and 2‐year survival (adjusted‐hazard ratio 1.98, 95% confidence interval 0.84–4.63) after DAA therapy were not associated with risky alcohol use. Discussion and Conclusions: Risky alcohol use in HCV patients was prevalent, but did not reduce HCV cure. Treatment for alcohol dependence was low. Risky alcohol use may be under‐recognised in liver clinics. Better integration of addiction medicine into liver services and increased resourcing and addiction medicine training opportunities for hepatologists may help address this. [ABSTRACT FROM AUTHOR]
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Database: Psychology and Behavioral Sciences Collection
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Abstract:Introduction: Alcohol use is common in patients with chronic hepatitis C virus (HCV) infection. We examined the impact of alcohol use on direct‐acting antiviral (DAA) therapy outcome and the clinical course of liver disease and 2‐year survival for patients receiving HCV DAA therapy. Methods: Adults (n = 2624) recruited from 26 Australian hospital liver clinics during 2016–2021 were followed up for 2 years. Risky alcohol use was defined by a combination of self‐report (≥40 g/day of ethanol), physician‐reported history of problematic alcohol use, and anti‐craving medication prescription via population‐based database linkage. We examined factors associated with advanced liver fibrosis and survival using multivariable logistic and Cox regression. Results: Among 1634 patients (62.3%) with risky alcohol use, 24.6% reported consuming ≥40 g/day of alcohol, 98.3% physician‐reported problematic alcohol use; only 4.1% were dispensed naltrexone/acamprosate. One hundred and forty‐three patients with cirrhosis reported ≥40 g/day of alcohol, 6 (4.3%) were prescribed naltrexone/acamprosate. Risky alcohol use was associated with advanced fibrosis (adjusted‐odds ratio 1.69, 95% confidence interval 1.32–2.17) and patients were over‐represented for cirrhosis (45.1% vs. 25.6% in no‐risky alcohol use [p < 0.001]) and hepatocellular carcinoma (5.7% vs. 2.5% [p < 0.001]). Sustained viral response (p = 0.319) and 2‐year survival (adjusted‐hazard ratio 1.98, 95% confidence interval 0.84–4.63) after DAA therapy were not associated with risky alcohol use. Discussion and Conclusions: Risky alcohol use in HCV patients was prevalent, but did not reduce HCV cure. Treatment for alcohol dependence was low. Risky alcohol use may be under‐recognised in liver clinics. Better integration of addiction medicine into liver services and increased resourcing and addiction medicine training opportunities for hepatologists may help address this. [ABSTRACT FROM AUTHOR]
ISSN:09595236
DOI:10.1111/dar.13914