A P < 0.05 was considered statistically significant. Data analysis was performed using SPSS 11.5 for Windows (SPSS, Chicago, IL). Table 1shows the baseline characteristics of the 4,302 enrolled patients at initiation of follow-up. The patients

were divided into three groups: with HCC, with malignancies other than HCC, and without events. There were significant selleck products differences in several baseline characteristics among the three groups. The SVR rate was 34.4% (985/2,861) in IFN monotherapy and 63.5% (915/1,441) in combination therapy of IFN and ribavirin. Thus, the number of patients with SVR was 1,900. The mean follow-up was 8.1 (SD 5.0) years. As shown in Table 1, 606 of 4,302 patients developed malignancies: 393 developed HCC and 213 developed malignancies other than HCC. HCC accounted for 33.3% (44/132) of malignancies in patients with SVR and 73.6% (349/474) in patients MAPK Inhibitor Library cost without SVR. The breakdown of malignancies other than HCC was as follows: stomach cancer, n = 36; colon cancer, n = 35; lung cancer, n = 20; malignant lymphoma, n = 19; pancreatic cancer, n = 12; prostatic cancer, n = 16; breast cancer, n = 15; other cancers, n = 60. The cumulative development rate of HCC was 4.3% at 5 years, 10.5% at 10 years, 19.7% at 15 years, and 28.0% at 20 years (Fig.

1A). The factors associated with the development of HCC are shown in Table 2. Multivariate Cox proportional hazards analysis showed that HCC occurred when patients had liver cirrhosis (hazard ratio [HR], 5.01; 95% confidence interval [CI], 3.92-6.40; P < 0.001), non-SVR (HR, 4.93; 95% CI, 3.53-6.89; P < 0.001), age increments of 10 years (HR, 1.97; 95% CI, 1.71-2.28; P < 0.001), T2DM (HR, 1.73; 95% CI, 1.30-2.30; P < 0.001), male sex (HR, 1.67; 95% CI, 1.24-2.23; P = 0.001), and TAI of ≥ 200 kg (HR, 1.45; 95% CI, 1.11-1.88; Parvulin P = 0.007). Fig. 1B-D and Fig. 2A-C show the cumulative development rates of HCC based on difference of IFN efficacy, age, hepatic fibrosis, TAI, sex, and T2DM. The 10-year cumulative rates of HCC after IFN therapy was determined to be 7.1% in 3,869 patients with chronic hepatitis and 37.7% in 433

patients with cirrhosis by using the Kaplan-Meier Method (Fig. 1D). Fig. 2D shows the development rates of HCC in T2DM patients according to difference of mean hemoglobin A1c (HbA1c) level during follow-up. HCC decreased when T2DM patients had a mean HbA1c level of <7.0% during follow-up (HR, 0.56; 95% CI, 0.33-0.89; P = 0.015). The development of HCC was reduced by 44% in T2DM patients with a mean HbA1c level of <7.0% compared with those with a mean HbA1c level of ≥7.0%. Table 3 shows the development rate of HCC and risk factors in four groups classified by the difference of hepatic fibrosis and efficacy of IFN therapy. The development rate of HCC per 1,000 person years was 1.55 in patients with chronic hepatitis (CH) at baseline and SVR (CH+SVR), 18.