Background. Few data are available on liver disease progression following viral eradication due to DAA treatment in HIV/HCV-coinfected patients in real life settings. Methods. Patients consecutively enrolled in the PITER cohort from 2014-2019, with at least 12 weeks follow-up after the end of DAA treatment (median follow-up 38.9 months, range 4.1-60.8), were analysed. Emergence of a liver complication (de novo HCC occurrence or hepatic decompensation) was evaluated in patients with pretreatment diagnosis of liver cirrhosis. Variables independently associated to development of a liver complication after achieving SVR12 were evaluated by Cox regression analysis. Results. We included 244 HIV/HCV-coinfected patients (74.6% men, median age 52, range: 32-77) and 2870 HCV-infected patients (54.1% men, median age 61, range: 20-86). Higher prevalence of HCV genotype 1b was observed in monoinfected patients, whereas genotype 1a and 3 were dominant in coinfected patients. No significant differences in main baseline characteristics and a similar fibrosis stage distribution were observed in both groups. Despite the significant younger age (p<0.001), cirrhotic coinfected patients had higher liver disease severity in terms of Child-Pugh class distribution (p<0.001). Comparable rates of SVR12 were observed in cirrhotic coinfected (93.3%) and monoinfected (94%) patients. The incidence of HCC following SVR12 achievement was 1.9% and 4% in coinfected and monoinfected patients, respectively (p>0.05). Factors independently associated to de novo HCC occurrence were age (increasing years Hazard Ratio [HR]=1.08, 95% CI 1.04-1.12), albumin (decreasing g/dl HR= 3.03, 95% CI=1.46-6.30) and genotype 3 (HR=2.67, 95% CI=1.03-6.96). Occurrence of hepatic decompensation was 9.9% in coinfected and 9.1% in monoinfected patients. Platelet count lower than 100,000 (HR=2.01, 95% CI 1.29-3.12), albumin (decreasing g/dl HR=1.65, 95% CI 1.08-2.54), HCC (HR=1.83, 95% CI 1.02-3.26) and liver decompensation prior to treatment (HR=7.13, 95% CI 4.51-11.27) were independently associated with the appearance of a decompensation event (ascites, hepatic encephalopathy, portal hypertensive gastrointestinal bleeding) after SVR12. Conclusion. These real life data confirm the high effectiveness of DDA treatment in achieving SVR in advanced liver disease patients, despite HIV coinfection. HIV coinfection is not associated with a higher probability of developing liver complications in HCV-infected patients with advanced liver disease, after viral eradication.
Outcomes of advanced liver disease in patients with chronic hepatitis C with and without HIV coinfection following sustained virological response: a real life evaluation in the PITER cohort
L Chessa;
2019-01-01
Abstract
Background. Few data are available on liver disease progression following viral eradication due to DAA treatment in HIV/HCV-coinfected patients in real life settings. Methods. Patients consecutively enrolled in the PITER cohort from 2014-2019, with at least 12 weeks follow-up after the end of DAA treatment (median follow-up 38.9 months, range 4.1-60.8), were analysed. Emergence of a liver complication (de novo HCC occurrence or hepatic decompensation) was evaluated in patients with pretreatment diagnosis of liver cirrhosis. Variables independently associated to development of a liver complication after achieving SVR12 were evaluated by Cox regression analysis. Results. We included 244 HIV/HCV-coinfected patients (74.6% men, median age 52, range: 32-77) and 2870 HCV-infected patients (54.1% men, median age 61, range: 20-86). Higher prevalence of HCV genotype 1b was observed in monoinfected patients, whereas genotype 1a and 3 were dominant in coinfected patients. No significant differences in main baseline characteristics and a similar fibrosis stage distribution were observed in both groups. Despite the significant younger age (p<0.001), cirrhotic coinfected patients had higher liver disease severity in terms of Child-Pugh class distribution (p<0.001). Comparable rates of SVR12 were observed in cirrhotic coinfected (93.3%) and monoinfected (94%) patients. The incidence of HCC following SVR12 achievement was 1.9% and 4% in coinfected and monoinfected patients, respectively (p>0.05). Factors independently associated to de novo HCC occurrence were age (increasing years Hazard Ratio [HR]=1.08, 95% CI 1.04-1.12), albumin (decreasing g/dl HR= 3.03, 95% CI=1.46-6.30) and genotype 3 (HR=2.67, 95% CI=1.03-6.96). Occurrence of hepatic decompensation was 9.9% in coinfected and 9.1% in monoinfected patients. Platelet count lower than 100,000 (HR=2.01, 95% CI 1.29-3.12), albumin (decreasing g/dl HR=1.65, 95% CI 1.08-2.54), HCC (HR=1.83, 95% CI 1.02-3.26) and liver decompensation prior to treatment (HR=7.13, 95% CI 4.51-11.27) were independently associated with the appearance of a decompensation event (ascites, hepatic encephalopathy, portal hypertensive gastrointestinal bleeding) after SVR12. Conclusion. These real life data confirm the high effectiveness of DDA treatment in achieving SVR in advanced liver disease patients, despite HIV coinfection. HIV coinfection is not associated with a higher probability of developing liver complications in HCV-infected patients with advanced liver disease, after viral eradication.
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