***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background : Patient adherence to screening for hepatocellular carcinoma ( HCC ) is not well known . Our aims were to analyze the adherence to a surveillance program in a prospect i ve cohort of cirrhotic patients and to examine its association with HCC stage at diagnosis . Material s and Methods : A total of 770 patients with cirrhosis were examined semiannually by ultrasound and alpha-fetoprotein at a tertiary center . We collected data on 17 variables at baseline . Suboptimal adherence was defined as failure to complete 2 consecutive screening rounds . Results : Over a median follow-up period of 42.0 months ( interquartile range : 60.0 ) , 125 patients ( 16.2 % ) had suboptimal adherence . Active or previous intravenous drug use [ hazard ratio ( HR ) , 5.33 ; 95 % confidence interval ( CI ) , 3.07 - 9.23 ] , active alcohol consumption ( HR , 3.03 ; 95 % CI , 2.03 - 4.51 ) , absence of liver decompensation before the inclusion in the program ( HR , 1.65 ; 95 % CI , 1.07 - 2.55 ) and aspartate transaminase/alanine transaminase ratio ≥1.6 ( HR , 1.82 ; 95 % CI , 1.23 - 2.70 ) were independent predictors of suboptimal adherence . Compared with those with optimal adherence , patients with suboptimal adherence had a more advanced HCC stage at diagnosis ( P=0.015 ) , they were less frequently treated with curative intention ( P=0.078 ) and survived less ( median : 14.2 mo ; IQR : 36.0 vs. 22.7 mo ; IQR : 47.4 ; P=0.160 ) , although these differences were not significant . Conclusions : The adherence to the process of HCC surveillance can be considered as adequate among cirrhotic patients . Active alcohol consumption and a history of intravenous drug use are the strongest predictors of suboptimal adherence . These patients have a more advanced HCC stage at diagnosis and tend to be less frequently treated with curative intention BACKGROUND & AIMS We performed a prospect i ve study to investigate the effects of a sustained viral response ( SVR ) on outcomes of patients with hepatitis C virus ( HCV ) infection and compensated cirrhosis . METHODS We collected data from 1323 patients included in the prospect i ve Agence Nationale pour la Recherche sur le SIDA et les hépatites virales ( ANRS ) viral cirrhosis ( CirVir ) cohort , recruited from 35 clinical centers in France from 2006 through 2012 . All patients had HCV infection and biopsy-proven cirrhosis , were Child-Pugh class A , and had no prior liver complications . All patients  received anti-HCV treatment before or after inclusion ( with interferon then with direct antiviral agents ) and underwent an ultrasound examination every 6 months , as well as endoscopic evaluations . SVR was considered as a time-dependent covariate ; its effect on outcome was assessed by the Cox proportional hazard regression method . We used a propensity score to minimize confounding by indication of treatment and capacity to achieve SVR . RESULTS After a median follow-up period of 58.2 months , 668 patients ( 50.5 % ) achieved SVR . SVR was associated with a decreased incidence of hepatocellular carcinoma ( hazard ratio [ HR ] compared with patients without an SVR , 0.29 ; 95 % confidence interval [ CI ] , 0.19 - 0.43 ; P < .001 ) and hepatic decompensation ( HR , 0.26 ; 95 % CI , 0.17 - 0.39 ; P < .001 ) . Patients with SVRs also had a lower risk of cardiovascular events ( HR , 0.42 ; 95 % CI , 0.25 - 0.69 ; P = .001 ) and bacterial infections ( HR , 0.44 ; 95 % CI , 0.29 - 0.68 ; P < .001 ) . Metabolic features were associated with a higher risk of hepatocellular carcinoma in patients with SVRs , but not in patients with viremia . SVR affected overall mortality ( HR , 0.27 compared with patients without SVR ; 95 % CI , 0.18 - 0.42 ; P < .001 ) and death from liver-related and non-liver-related causes . Similar results were obtained in a propensity score-matched population . CONCLUSIONS We confirmed a reduction in critical events , liver-related or not , in a prospect i ve study of patients with HCV infection and compensated cirrhosis included in the CirVir cohort who achieved an SVR . We found an SVR to reduce overall mortality and risk of death from liver-related and non-liver-related causes . A longer follow-up evaluation is required to accurately describe and assess specific risk factors for complications in this population BACKGROUND Gastrointestinal haemorrhage from ruptured esophageal varices ( EV ) is a significant cause of morbidity and mortality in patients with HCV-related cirrhosis . The risk of developing EV and bleeding is influenced by hepatitis severity , which can be attenuated by successful interferon ( IFN ) therapy . Our aim was to prospect ively assess whether a successful IFN therapy modifies development and /or progression of EV in patients with HCV-related compensated cirrhosis . METHODS Child-Pugh A patients with either no or small ( F1 ) EV underwent surveillance with repeated endoscopy during and after completion of IFN-based therapy . RESULTS A total of 127 patients ( 59 years , 79 males , 65 HCV-1/4 and 17 F1 EV ) received weight-based ribavirin ( RBV ) combined with either IFN-α2b 3 MU three times per week ( n=36 ) , weekly pegylated (PEG)-IFN-α2b 1.5 μg/kg ( n=68 ) or weekly PEG-IFN-α2a 180 μg ( n=23 ) . Patients were followed-up for 18 - 108 months after treatment completion with a median endoscopic follow-up of 68 months for the 62 patients with a sustained virological response ( SVR ) and 57 months for the 65 non-SVR patients ( P=0.3 ) . De novo EV developed in 10 ( 9.1 % ) patients including 2/57 SVR and 8/53 non-SVR ( 3.5 % versus 15.1 % ; P=0.047 ) , whereas EV progressed in size in 3 patients , including 1/5 SVR and 2/12 non-SVR ( P=0.87 ) . Two non-SVR patients bled from EV and one died . CONCLUSIONS A successful IFN therapy prevents or delays the de novo onset of EV in patients with compensated cirrhosis due to HCV , but does not abrogate the need for continued endoscopic surveillance Chronic hepatitis C virus ( HCV ) infection with advanced cirrhosis or post‐liver transplantation recurrence represents a high unmet medical need with no approved therapies effective across all HCV genotypes . The open‐label ALLY‐1 study assessed the safety and efficacy of a 60‐mg once‐daily dosage of daclatasvir ( pan‐genotypic NS5A inhibitor ) in combination with sofosbuvir at 400 mg once daily ( NS5B inhibitor ) and ribavirin at 600 mg/day for 12 weeks with a 24‐week follow‐up in two cohorts of patients with chronic HCV infection of any genotype and either compensated/decompensated cirrhosis or posttransplantation recurrence . Patients with on‐treatment transplantation were eligible to receive 12 additional weeks of treatment immediately after transplantation . The primary efficacy measure was sustained virologic response at posttreatment week 12 ( SVR12 ) in patients with a genotype 1 infection in each cohort . Sixty patients with advanced cirrhosis and 53 with posttransplantation recurrence were enrolled ; HCV genotypes 1 ( 76 % ) , 2 , 3 , 4 , and 6 were represented . Child‐Pugh classifications in the advanced cirrhosis cohort were 20 % A , 53 % B , and 27 % C. In patients with cirrhosis , 82 % ( 95 % confidence interval [ CI ] , 67.9%‐92.0 % ) with genotype 1 infection achieved SVR12 , whereas the corresponding rates in those with genotypes 2 , 3 , and 4 were 80 % , 83 % , and 100 % , respectively ; SVR12 rates were higher in patients with Child‐Pugh class A or B , 93 % , versus class C , 56 % . In transplant recipients , SVR12 was achieved by 95 % ( 95 % CI , 83.5%‐99.4 % ) and 91 % of patients with genotype 1 and 3 infection , respectively . Three patients received peritransplantation treatment with minimal dose interruption and achieved SVR12 . There were no treatment‐related serious adverse events . Conclusion : The pan‐genotypic combination of daclatasvir , sofosbuvir , and ribavirin was safe and well tolerated . High SVR rates across multiple HCV genotypes were achieved by patients with post‐liver transplantation recurrence or advanced cirrhosis . ( Hepatology 2016;63:1493‐1505 Flaws in the design , conduct , analysis , and reporting of r and omised trials can cause the effect of an intervention to be underestimated or overestimated . The Cochrane Collaboration ’s tool for assessing risk of bias aims to make the process clearer and more Background and Aims : A sustained virological response ( SVR ) decreases the incidence of hepatocellular carcinoma ( HCC ) in patients with hepatitis C. We investigated the long-term outcomes of patients who developed HCC after achieving SVR with interferon therapy .  Patients : Of 75 patients who developed HCC after SVR , 40 patients underwent radical therapies ( SVR group ) . From 436 patients undergoing surgical resection for hepatitis C virus-positive HCC , 80 patients were r and omly chosen as a control cohort , after adjusting for age , gender , and extent of hepatic fibrosis ( non-SVR group ) . Patients were observed for a median of 5.08 years . Results : HCC recurrence was found in 16 SVR patients and in 66 non-SVR patients . The respective HCC recurrence rates of SVR and non-SVR patients were 23 and 56 % at 3 years , 42 and 77 % at 5 years , and 53 and 90 % at 10 years ( p = 0.001 ) . The respective overall survival rates in the SVR and non-SVR groups were 93 and 68 % at 5 years , 88 and 34 % at 10 years , and 53 and 21 % at 15 years ( p = 0.001 ) . Conclusion : Although SVR patients had a significantly lower HCC recurrence rate than the non-SVR patients , the cumulative recurrence rate of SVR patients increased to 86 % at 15 years Background Novel direct-acting antivirals ( DAAs ) have completely changed the panorama of hepatitis C due to their high efficacy and optimal safety profile . Unfortunately , an unexpectedly high rate of early recurrence of hepatocellular carcinoma has been reported within weeks of starting treatment , but the mechanism is not known . Methods We monitored the serum level of vascular endothelial growth factor ( VEGF ) and changes in the pattern of circulating interleukins in 103 chronic hepatitis C patients during antiviral treatment with DAA-regimens .  VEGF , epidermal growth factor ( EGF ) , and several interleukins were assessed at baseline , during treatment , and after treatment . The biological effect of DAA-treated patient serum on human umbilical vein endothelial cell ( HUVEC ) proliferation was also confirmed . Results After 4 weeks of therapy , VEGF increased approximately 4-fold compared to baseline , remained elevated up to the end of treatment , and returned to the pre-treatment level after the end of therapy . In contrast , interleukin-10 and tumor necrosis factor-alpha significantly decreased during therapy , which was coincident with HCV clearance . The levels of both remained low after treatment . The addition of serum from patients collected during therapy induced HUVEC proliferation ; however , this disappeared after the end of therapy . Conclusions DAA administration induces an early increase in serum VEGF and a change in the inflammatory pattern , coinciding with HCV clearance . This may alter the balance between inflammatory and anti-inflammatory processes and modify the antitumor surveillance of the host . Fortunately , such modifications return reverse to normal after the end of treatment BACKGROUND Interferon-containing regimens for the treatment of hepatitis C virus ( HCV ) infection are associated with increased toxic effects in patients who also have cirrhosis . We evaluated the interferon-free combination of the protease inhibitor ABT-450 with ritonavir ( ABT-450/r ) , the NS5A in 
    Output:
    
There is no evidence for differential HCC occurrence or recurrence risk following SVR from DAA and IFN-based therapy .
There is no evidence that HCC occurrence or recurrence is different between patients receiving DAA or IFN therapy