Mortality Rates in Patients With Chronic Hepatitis C and Cirrhosis Compared With the General Population: A Danish Cohort Study.

BACKGROUND: Knowledge about mortality rates (MRs) in patients with chronic hepatitis C (CHC) with cirrhosis is limited. This study aimed to estimate all-cause MRs among patients with CHC with or without cirrhosis in Denmark compared with the general population. METHODS: Patients registered in the Danish Database for Hepatitis B and C with CHC and a liver fibrosis assessment were eligible for inclusion. Liver fibrosis was assessed by means of liver biopsy, transient elastography, and clinical cirrhosis. Up to 20 sex- and age-matched individuals per patient were identified in the general population. Data were extracted from nationwide registries. RESULTS: A total of 3410 patients with CHC (1014 with cirrhosis), and 67 315 matched individuals were included. Adjusted MR ratios (MRRs) between patients with or without cirrhosis and their comparison cohorts were 5.64 (95% confidence interval [CI], 4.76-6.67) and 1.94 (1.55-2.42), respectively. Cirrhosis among patients was associated with an MRR of 4.03 (95% CI, 3.43-4.72). A cure for CHC was associated with an MRR of 0.64 (95% CI, 0.40-1.01) among cirrhotic patients and 2.33 (1.47-3.67) compared with the general population. CONCLUSIONS: MRs were high among patients with CHC with or without cirrhosis compared with the general population. Curing CHC was associated with a reduction in MR among cirrhotic patients, but the MR remained higher than the general population.

Viral load is a negative predictor of antioxidant levels in hepatitis C patients.

The pathogenesis of chronic hepatitis C (HCV) infection is not fully known, but oxidative stress may play a role. The aim of this study was to assess the relationship between HCV load and antioxidant status among patients with chronic HCV infection. Among 23 patients, HCV load, as well as plasma beta-carotene, retinol, ascorbic acid and alpha-tocopherol were measured. Plasma retinol, ascorbic acid and alpha-tocopherol were low in 17%, 26% and 4% of the patients, respectively. Plasma ascorbic acid and alpha-tocopherol declined 9.7 micromol/l (95% CI 3.3-16.2) and 4.5 micromol/l (95% CI 2.1-7.0), respectively, and plasma beta-carotene declined by a factor of 0.60 (95% CI 0.37-0.98) per log increase in viral load. Smoking was independently associated with 8.9 micromol/l (95% CI 4.1-13.7), lower levels of plasma alpha-tocopherol and with 0.27 (95% CI 0.11-0.71) times lower plasma beta-carotene. The effect on plasma ascorbic acid was not significant (-9.2 micromol/l, 95% CI - 21.9-3.5). The association may reflect consumption of antioxidants due to HCV, although effects of low antioxidant status on viral replication cannot be excluded.