Author information

¹Department of Gastroenterology, Alcohol and Drug Assessment Unit, Princess Alexandra and Mater Hospitals, Brisbane, Australia.

²Faculty of Medicine, The University of Queensland, Brisbane, Australia.

³QIMR Berghofer Medical Research Institute, Brisbane, Australia.

⁴AW Morrow Gastroenterology and Liver Centre, Royal Prince Alfred Hospital, Sydney, Australia.

⁵Hepatology Services, Nepean Hospital, Sydney, Australia.

⁶Department of Gastroenterology, St Vincent's Hospital, Melbourne, Australia.

⁷Department of Gastroenterology and Liver, Liverpool Hospital, Sydney, Australia.

⁸Department of Gastroenterology and Hepatology, Royal Brisbane and Women's Hospital, Brisbane, Australia.

⁹Department of Gastroenterology and Hepatology, St George Hospital, Sydney, Australia.

¹⁰Gippsland Gastroenterology, Latrobe Regional Hospital, Traralgon, Australia.

¹¹Department of Gastroenterology and Hepatology, Austin Hospital, Melbourne, Australia.

¹²Faculty of Medicine, The University of Sydney, Sydney, Australia.

¹³Storr Liver Centre, Westmead Hospital, Sydney, Australia.

¹⁴Gastrointestinal and Liver Unit, Monash Health and Monash University, Melbourne, Australia.

¹⁵Department of Hepatology and Liver Transplant Unit, Sir Charles Gairdner Hospital, Perth, Australia.

¹⁶Hepatology, Royal Adelaide Hospital, Adelaide, Australia.

¹⁷Eastern Health, Melbourne, Australia.

¹⁸Burnet Institute, Melbourne, Australia.

¹⁹Barwon Health Liver Clinic University Hospital, Geelong, Australia.

²⁰Department of Gastroenterology & Hepatology, Royal Perth Hospital, Perth, Australia.

²¹The Alfred Hospital and Monash University CCS, Melbourne, Australia.

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.