1%) had one, and 57 patients (37.7%)

had none of these risk factors (Fig. 3). Patients without these risk factors did not develop HCC during the study period. In patients with 1 or 2 risk factors, the cumulative incidence rates at 1, 2, and 3 years were 1.2%, 3.1%, and 8.2%, respectively, whereas patients with all three risk factors had significantly higher cumulative incidence rates (9.1%, 39.4%, and 59.6% at 1, 2, and 3 years, respectively; log-rank test, P < 0.001) (Fig. 4). Fifty-six patients who received IFN therapy without liver biopsy were enrolled into the validation group for analysis of these three risk Selleckchem EGFR inhibitor factors. The 56 patients (33 male and 23 female) had a median age of 65 years (range 35–79 years) and a median LSM of 8.0 kPa (range 2.6–32.0 kPa). There were no significant differences in clinical, anthropometric, and laboratory findings between the validation and estimation cohorts (data

not shown). In the validation cohort, seven patients (12.5%) had all three risk factors, 25 patients (44.6%) had one or two risk factors, and 24 patients (42.9%) had none of these risk factors. Patients without these risk factors did not develop HCC during the study period. In patients with one or two risk factors, and patients with all three risk factors, the cumulative incidence rates at 3 years were 12.7% and 28.6%, respectively. There was also a significant difference SB203580 nmr in the cumulative incidences of HCC development according to the number of risk factors (P = 0.037, Fig. 5). Patients with liver cirrhosis or pre-existing severe hepatic fibrosis have a higher risk of developing HCC,[2] even after IFN-based therapy with SVR.[9, 10] Clinical diagnosis of liver cirrhosis can be easily made in cases showing stigmata of end-stage liver disease, such as ascites, jaundice, variceal bleeding, and hepatic encephalopathy;

however, diagnosis becomes difficult if the liver shows compensation, and normal or near-normal laboratory findings. Liver biopsy has been considered the only diagnostic method for the assessment of early compensated cirrhosis, although several studies have pointed out sampling Resminostat variability as a potential limitation of biopsy to diagnose cirrhosis.[21, 22] Given the importance of assessing the HCC risk factors in managing CHC patients, we evaluated factors that affect the occurrence of HCC in CHC patients receiving IFN therapy, with a special focus on the predictive value of LSM as an alternative to liver biopsy. Our data identified three risk factors for developing HCC after IFN therapy. Consistent with previous reports,[5-7] we found that failure to achieve SVR was a significant predictor of HCC development among patients receiving IFN therapy. Although it is possible that IFN therapy itself reduces the risk of HCC,[6, 7] non-SVR patients had an approximately eightfold higher risk of developing HCC than SVR patients.