@article{open3379,
          volume = {167},
          number = {7},
           month = {December},
          author = {Madhumita Premkumar and Radha K Dhiman and Ajay Duseja and Rohit Mehtani and Sunil Taneja and Ekta Gupta and Pankaj Gupta and Anchal Sandhu and Prerna Sharma and Sahaj Rathi and Nipun Verma and Anand V Kulkarni and Harish Bhujade and Sreedhara B Chaluvashetty and Naveen Kalra and Gagandeep S Grover and Jasvinder Nain and K Rajender Reddy},
            note = {copyright of this article belongs to Elsevier BV},
           title = {Recompensation of chronic hepatitis C-related decompensated cirrhosis following direct-acting antiviral therapy: Prospective cohort study from a hepatitis C virus elimination program},
       publisher = {Elsevier BV},
            year = {2024},
         journal = {Gastroenterology},
           pages = {1429--1445},
        keywords = {Chronic Hepatitis C; DAAs; Decompensated Cirrhosis; Direct-Acting Antivirals; HCV Elimination; Hepatitis C Virus; Punjab Model; Recompensation},
             url = {http://crdd.osdd.net/open/3379/},
        abstract = {BACKGROUND \& AIMS: Chronic hepatitis C-related decompensated cirrhosis is associated with lower sustained virologic response (SVR)-12 rates and variable regression of disease severity after direct-acting antiviral agents. We assessed rates of SVR-12, recompensation (Baveno VII criteria), and survival in such patients. METHODS: Between July 2018 and July 2023, patients with decompensated chronic hepatitis C-related cirrhosis after direct-acting antiviral agents treatment were evaluated for SVR-12 and then had 6-monthly follow-up. RESULTS: Of 6516 patients with cirrhosis, 1152 with decompensated cirrhosis (age 53.2 {$\pm$} 11.5 years; 63\% men; Model for End-stage Liver Disease-Sodium MELD-Na: 16.5 \${$\backslash$}pm\$ 4.6; 87{$\backslash$}\% genotype 3) were enrolled. SVR-12 was 81.8{$\backslash$}\% after 1 course; ultimately SVR was 90.8{$\backslash$}\% after additional treatment. Decompensation events included ascites (1098; 95.3{$\backslash$}\%), hepatic encephalopathy (191; 16.6{$\backslash$}\%), and variceal bleeding (284; 24.7{$\backslash$}\%). Ascites resolved in 86{$\backslash$}\% (diuretic withdrawal achieved in 24{$\backslash$}\% patients). Recompensation occurred in 284 (24.7{$\backslash$}\%) at a median time of 16.5 (interquartile range, 14.5-20.5) months. On multivariable Cox proportional hazards analysis, low bilirubin (adjusted hazard ratio aHR, 0.6; 95{$\backslash$}\% confidence interval CI, 0.5-0.8; P {\ensuremath{<}} 0.001), international normalized ratio (aHR, 0.2; 95{$\backslash$}\% CI, 0.1-0.3; P {\ensuremath{<}} 0.001), absence of large esophageal varices (aHR, 0.4; 95{$\backslash$}\% CI, 0.2-0.9; P = 0.048), or gastric varices (aHR, 0.5; 95{$\backslash$}\% CI, 0.3-0.7; P = 0.022) predicted recompensation. Portal hypertension progressed in 158 (13.7{$\backslash$}\%) patients, with rebleed in 4{$\backslash$}\%. Prior decompensation with variceal bleeding (aHR, 1.6; 95{$\backslash$}\% CI, 1.2-2.8; P = 0.042), and presence of large varices (aHR, 2.9; 95{$\backslash$}\% CI, 1.3-6.5; P {\ensuremath{<}} 0.001) were associated with portal hypertension progression. Further decompensation was seen in 221 (19{$\backslash$}\%); 145 patients died and 6 underwent liver transplantation. A decrease in MELDNa of \${$\backslash$}geq\$3 was seen in 409 (35.5{$\backslash$}\%) and a final MELDNa score of {\ensuremath{<}}10 was seen in 335 (29{$\backslash$}\%), but 2.9{$\backslash$}\% developed hepatocellular carcinoma despite SVR-12. CONCLUSIONS: SVR-12 in hepatitis C virus-related decompensated cirrhosis in a predominant genotype 3 population led to recompensation in 24.7{$\backslash$}\% of patients over a follow-up of 4 years in a public health setting. Despite SVR-12, new hepatic decompensation evolved in 19{$\backslash$}\% and hepatocellular carcinoma developed in 2.9{$\backslash$}\% of patients. (ClinicalTrials.gov, Number: NCT03488485).}
}