RESUMO
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.
Assuntos
Demência , Hepatite C Crônica , Hepatite C , Humanos , Antivirais/efeitos adversos , Hepacivirus , Estudos de Coortes , Hepatite C Crônica/complicações , Hepatite C Crônica/tratamento farmacológico , Hepatite C Crônica/epidemiologia , Hepatite C/complicações , Hepatite C/tratamento farmacológico , Hepatite C/epidemiologia , Cirrose Hepática/complicações , Cirrose Hepática/tratamento farmacológico , Demência/etiologia , Demência/induzido quimicamenteRESUMO
This study examined overall and sex-specific associations of serum lipid-soluble micronutrients including α- and γ-tocopherols, 25-hydroxy-vitamin D (25(OH)D), retinol, and six major carotenoids with metabolic dysfunction-associated steatotic lever disease (MASLD) using the 2017-2018 National Health and Nutrition Examination Survey. This analysis included 3956 adults (1991 men, 1965 women) aged ≥ 20 years. Steatotic liver disease was determined through transient elastography examination. Odds ratios (ORs) and 95% confidence intervals (95% CIs) for MASLD associated with micronutrients were estimated using logistic regressions. Higher serum α-tocopherol (highest vs. lowest quartile: OR = 1.53, 95% CI = 1.05-2.22, p = 0.03) and γ-tocopherol (highest vs. lowest quartile: OR = 4.15, 95% CI = 3.00-5.74, p < 0.0001) levels were associated with increased odds of MASLD. Higher serum 25(OH)D levels were associated with reduced odds of MASLD (highest vs. lowest quartile: OR = 0.41, 95% CI = 0.27-0.61, p = 0.0001). Inverse associations with the condition were also observed for carotenoids (α-carotene, ß-carotene, α-cryptoxanthin, ß-cryptoxanthin, combined lutein and zeaxanthin, and lycopene) in the serum (Ps < 0.05). The results were comparable between men and women, except for those on α-tocopherol, for which a positive association was only observed for men (p = 0.01). Our results suggest potential protective associations of serum 25(OH)D and carotenoids with MASLD. The positive associations between tocopherols and MASLD may reflect pathophysiological conditions associated with the condition.
Assuntos
Carotenoides , Micronutrientes , Inquéritos Nutricionais , Vitamina D/análogos & derivados , Humanos , Masculino , Feminino , Estados Unidos/epidemiologia , Micronutrientes/sangue , Adulto , Pessoa de Meia-Idade , Carotenoides/sangue , Vitamina A/sangue , Vitamina D/sangue , Fatores Sexuais , alfa-Tocoferol/sangue , Estudos Transversais , Fígado Gorduroso/sangue , Fígado Gorduroso/epidemiologia , Adulto Jovem , Lipídeos/sangue , gama-Tocoferol/sangue , Razão de Chances , IdosoRESUMO
OBJECTIVE: Sleep is a critical health-related behavior; research evidence has shown that sleep duration, poor sleep quality and insomnia are associated with aging and relevant age-related diseases. However, the associations between sleep duration, chronotype, sleep disturbance, and biological age have not been comprehensively assessed. This study aimed to examine sleep characteristics with biological age. METHODS: The study included 6534 participants aged 20 years and older from the National Health and Nutrition Examination Survey between 2017 and March 2020. Sleep questionnaires were used to collect information on sleep duration and wake behavior on workdays and workfree days and sleep disturbance. Phenotypic age acceleration (PhenoAgeAccel) was estimated as a biological age measure using 9 blood chemistry biomarkers. RESULTS: Long sleep (>9 hours) and extremely short sleep (≤4 hours) on workdays were positively associated with PhenoAgeAccel, compared with optimal sleep duration (7-8 hours). Similar positive associations with PhenoAgeAccel were observed for sleep duration on workfree days and across the whole week. Both slightly evening and evening chronotypes were associated with faster PhenoAgeAccel compared to morning chronotype. Social jetlag and sleep disturbance were not associated with PhenoAgeAccel, while long corrected social jetlag was associated with faster PhenoAgeAccel. The associations of sleep duration, chronotype, and corrected social jetlag with PhenoAgeAccel appeared stronger among females than among males. CONCLUSIONS: Findings suggest a U-shape relationship between sleep duration and biological aging; slightly evening and evening chronotypes may be risk factors for aging. Further studies are needed to confirm these findings.