Author information
1Department of Public Health Sciences (M-HT, TW, ST, HCG, ML), Henry Ford Health, Detroit MI. Electronic address: mtao1@hfhs.org.
2Department of Gastroenterology and Hepatology (SCG, HCG), Henry Ford Health, Detroit MI; School of Medicine (SCG, HCG), Wayne State University, Detroit MI.
3Department of Public Health Sciences (M-HT, TW, ST, HCG, ML), Henry Ford Health, Detroit MI.
4Department of Health Policy and Health Services Research (LBR), Henry Ford Health, Detroit MI.
5Department of Public Health Sciences (M-HT, TW, ST, HCG, ML), Henry Ford Health, Detroit MI; Department of Gastroenterology and Hepatology (SCG, HCG), Henry Ford Health, Detroit MI; School of Medicine (SCG, HCG), Wayne State University, Detroit MI.
6Center for Integrated Health Care Research (YGD), Kaiser Permanente Hawaii, Honolulu, HI.
7Center for Health Research (MAS), Kaiser Permanente Northwest, Portland, OR.
Abstract
Objective: Eradication of hepatitis C virus (HCV) infection has been linked with improvement in neurocognitive function, but few studies have evaluated the effect of antiviral treatment/ response on risk of dementia. Using data from the Chronic Hepatitis Cohort Study (CHeCS), we investigated how antiviral therapy impacts the risk of developing dementia among patients with HCV.
Methods: A total of 17,485 HCV patients were followed until incidence of dementia, death, or last follow-up. We used an extended landmark modeling approach, which included time-varying covariates and propensity score justification for treatment selection bias, as well as generalized estimating equations (GEE) with a link function as multinominal distribution for a discrete time-to-event data. Death was considered a competing risk.
Results: After 15 years of follow-up, 342 patients were diagnosed with incident dementia. Patients who achieved sustained virological response (SVR) had significantly decreased risk of dementia compared to untreated patients, with hazard ratios (HRs) of 0.32 (95% CI 0.22-0.46) among patients who received direct-acting antiviral (DAA) treatment and 0.41 (95% CI 0.26-0.60) for interferon-based (IFN) treatment. Risk reduction remained even when patients failed antiviral treatment (HR 0.38, 95% CI 0.38-0.51). Patients with cirrhosis, Black/African American patients, and those without private insurance were at significantly higher risk of dementia.
Conclusion: Antiviral treatment independently reduced the risk of dementia among HCV patients, regardless of cirrhosis. Our findings support the importance of initiation antiviral therapy in chronic HCV-infected patients.