OBJECTIVE: To define the course of HIV-HCV-coinfected patients with compensated and decompensated liver cirrhosis and to investigate the survival and the risk factors for death. PATIENTS AND METHODS: Ninety-two HIV-infected patients with HCV-related cirrhosis (50 of them without and 42 with previous decompensations) were prospectively followed up during a median period of 20 months. Clinical, biochemical, virological and immunological factors were analysed. Multivariate analyses were performed of those factors associated with decompensations and mortality. RESULTS: There were 168 readmissions due to liver-disease-related causes. A Child-Pugh index > or =6 in those without previous decompensations (hazard ratio [HR] 7.94, 95% confidence interval [CI] 1.59-39.58; P = 0.014), and Child-Pugh index > or =9 (HR 2.68, 95% CI 1.13-6.33; P = 0.003) and absence of HAART (HR 0.44, 95% CI 0.19-0.98; P = 0.048) in those with previous decompensations were independently associated with decompensation during the follow up. There were 27 deaths, 22 of them attributable to liver disease. Independent factors associated with liver-related mortality were a Child-Pugh index > or =9 (HR 6.24, 95% CI 2.31-16.85; P < 0.001), progression of Child-Pugh index during the follow up (HR 4.27, 95% CI 1.54-11.80; P = 0.008), more than one decompensation (HR 24.25, 95% CI 7.27-40.45; P < 0.001) and absence of HAART (HR 0.35, 95% CI 0.12-0.98; P = 0.002). CONCLUSIONS: Evolution from compensated to decompensated cirrhosis and death is influenced by markers of liver function and the absence of HAART. The importance of this last element must be adequately stressed.
OBJECTIVE: To define the course of HIV-HCV-coinfected patients with compensated and decompensated liver cirrhosis and to investigate the survival and the risk factors for death. PATIENTS AND METHODS: Ninety-two HIV-infected patients with HCV-related cirrhosis (50 of them without and 42 with previous decompensations) were prospectively followed up during a median period of 20 months. Clinical, biochemical, virological and immunological factors were analysed. Multivariate analyses were performed of those factors associated with decompensations and mortality. RESULTS: There were 168 readmissions due to liver-disease-related causes. A Child-Pugh index > or =6 in those without previous decompensations (hazard ratio [HR] 7.94, 95% confidence interval [CI] 1.59-39.58; P = 0.014), and Child-Pugh index > or =9 (HR 2.68, 95% CI 1.13-6.33; P = 0.003) and absence of HAART (HR 0.44, 95% CI 0.19-0.98; P = 0.048) in those with previous decompensations were independently associated with decompensation during the follow up. There were 27 deaths, 22 of them attributable to liver disease. Independent factors associated with liver-related mortality were a Child-Pugh index > or =9 (HR 6.24, 95% CI 2.31-16.85; P < 0.001), progression of Child-Pugh index during the follow up (HR 4.27, 95% CI 1.54-11.80; P = 0.008), more than one decompensation (HR 24.25, 95% CI 7.27-40.45; P < 0.001) and absence of HAART (HR 0.35, 95% CI 0.12-0.98; P = 0.002). CONCLUSIONS: Evolution from compensated to decompensated cirrhosis and death is influenced by markers of liver function and the absence of HAART. The importance of this last element must be adequately stressed.
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