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Clinical outcomes and prognostic factors after HCV clearance with DAA in HIV/HCV coinfected patients with advanced Fibrosis/Cirrhosis.
Hepatology : Official Journal of the American Association for the Study of Liver Diseases 2024 March 8
AIMS AND BACKGROUND: We assessed long-term clinical outcomes and prognostic factors for liver disease progression after sustained viral response (SVR) with direct-acting antivirals (DAAs) in HIV/HCV coinfected patients with advanced fibrosis (AdF) or cirrhosis.
APPROACH AND RESULTS: A total of 1,300 patients who achieved SVR with DAAs from 2014 to 2017 in Spain were included: 1145 with chronically advanced liver disease (cACLD) (384 AdF and 761 compensated cirrhosis [CoC]) and 155 with decompensated cirrhosis (DeC). The median follow-up was 40.9 months. Overall, 85 deaths occurred, 61 due to non-liver non-AIDS-related (NLNA) causes that were the leading cause of death across all stages of liver disease. The incidence (95% confidence interval [CI]) of decompensation per 100 person-years (py) was 0 in patients with AdF, 1.01 (0.68-1.51) in patients with CoC, and 8.35 (6.05-11.53) in patients with DeC. The incidence (95% CI) of hepatocellular carcinoma (HCC) per 100 py was 0.34 (0.13-0.91) in patients AdF, 0.73 (0.45-1.18) in patients with CoC, and 1.92 (1.00-3.70) per 100 py in patients with DeC. Prognostic factors for decompensation in patients with cACLD included serum albumin, liver stiffness measurement (LSM), and FIB-4. In this population, LSM and LSM-based posttreatment risk stratification models showed their predictive ability for decompensation and HCC.
CONCLUSIONS: NLNA events were the leading causes of morbidity and mortality after DAA cure among coinfected patients with AdF/cirrhosis. Among those with cACLD, baseline LSM and posttreatment LSM-based models helped to assess decompensation and HCC risk.
APPROACH AND RESULTS: A total of 1,300 patients who achieved SVR with DAAs from 2014 to 2017 in Spain were included: 1145 with chronically advanced liver disease (cACLD) (384 AdF and 761 compensated cirrhosis [CoC]) and 155 with decompensated cirrhosis (DeC). The median follow-up was 40.9 months. Overall, 85 deaths occurred, 61 due to non-liver non-AIDS-related (NLNA) causes that were the leading cause of death across all stages of liver disease. The incidence (95% confidence interval [CI]) of decompensation per 100 person-years (py) was 0 in patients with AdF, 1.01 (0.68-1.51) in patients with CoC, and 8.35 (6.05-11.53) in patients with DeC. The incidence (95% CI) of hepatocellular carcinoma (HCC) per 100 py was 0.34 (0.13-0.91) in patients AdF, 0.73 (0.45-1.18) in patients with CoC, and 1.92 (1.00-3.70) per 100 py in patients with DeC. Prognostic factors for decompensation in patients with cACLD included serum albumin, liver stiffness measurement (LSM), and FIB-4. In this population, LSM and LSM-based posttreatment risk stratification models showed their predictive ability for decompensation and HCC.
CONCLUSIONS: NLNA events were the leading causes of morbidity and mortality after DAA cure among coinfected patients with AdF/cirrhosis. Among those with cACLD, baseline LSM and posttreatment LSM-based models helped to assess decompensation and HCC risk.
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