Objective To explore the clinical characteristics of metabolic disorder and the incidence rate of metabolic syndrome (MS) in the patients with posthepatitic cirrhosis.Methods Four hundred and fifty-five patients with posthepatitic cirrhosis were included in the study and divided into hepatitis B related cirrhosis group (LCB group,351 cases) and hepatitis C related cirrhosis group (LCC group,104cases).The prevalence of metabolic disorder was recorded and the characteristics of posthepatitic cirrhosis with MS and without MS were compared and analysed.Results The prevalence of hyperglycemia,hypertension,hyperlipemia,obesity and MS in the posthepatitic cirrhosis patients was 46.59% (212/455),15.16% (69/455),15.38% (70/455),22.64% ( 103/455),12.53% (57/455) respectively.The prevalence of MS in LCB and LCC was 8.26% (29/351) and 26.92% (28/104).The levels of body mass index (BMI),fasting blood glucose,hypertension,cholesterol,aminotransferase (ALT) in LCB with MS patients were significantly higher than those in LCB without MS patients.There were no differences in the levels of HBeAg and HBV DNA between LCB with MS patients and LCB without MS patients.The levels of BMI,hypertension,triglyceride in LCC with MS patients were significantly higher than those in LCC without MS patients.There were no differences in fasting blood glucose,cholesterol and ALT between LCC with MS patients and LCC without MS patients.Logistic regression revealed that BMI was the independent factor in LCB and LCC with MS.Conclusions The prevalence of hyperglycemia and obesity are higher in LCB and LCC.The incidence rate of MS in LCB is less than that in the general population,while the incidence rate of MS in LCC is significantly higher than that in the general population,and it's nothing to do with the viral replication.BMI is an important factor affected in posthepatitic cirrhosis with MS.

Objective To investigate the regulation of interferon α-1b (IFNα-1b) on protein kinase Cε(PKCε) and protein kinase Cα(PKCα) which inhibit the fibrosis of hepatic stellate cells (HSC) ,and to explore its mechanism .Methods HSC-T6 cells were treated with different levels of IFNα-1b (100 , 200 ,400 ,800 and 1000 U/mL) and the proliferation of HSC-T6 cells was analyzed by methyl thiazol tetrazolium (MTT) assay .Changes of hydroxyproline level were analyzed .The expressions of PKCεand PKCαwere detected by immunofluorescence staining . PKCε, PKCα,β-catenin and Survivin mRNA levels were detected by RT-PCR . PKCε, PKCα,β-catenin and Survivin protein levels were detected by Western blot . Variance analysis was conducted by using one-way ANOVA approach . Results The inhibition rates of 100 , 200 , 400 , 800 and 1000 U/mL IFNα-1b treatment after 24 hours of administration were (15 .85 ± 1 .05)％ ,(36 .59 ± 1 .03)％ ,(45 .12 ± 1 .05)％ ,(50 .00 ± 1 .01)％ and (62 .20 ± 1 .02)％ ,respectively ,with statistically significant differences among groups (F=27 .478 , P<0 .01) .The 48h inhibition rates were (20 .87 ± 1 .09)％ ,(43 .96 ± 1 .08)％ ,(53 .85 ± 1 .08)％ ,(64 .84 ± 1 .06)％ and (74 .72 ± 1 .07)％ ,respectively ,with statistically significant differences among groups (F=25 .321 , P< 0 .01 ) . half maximal inhibitory concentration at 48 h was 343 .47 U/mL . The levels of hydroxyproline in 100 ,200 and 400 U/mL IFNα-1b groups were (7 .48 ± 0 .28) ,(6 .26 ± 0 .17) and (3 .86 ± 0 .20) μg/mL ,respectively ,which were lower than that in control group (8 .47 ± 0 .32) μg/mL .The differences were all statistically significant (t=4 .033 ,10 .564 and 21 .160 ,respective ,all P<0 .05) .The fluorescence intensities of PKCεin 100 ,200 and 400 U/mL IFNα-1b groups were all lower than that of control group .The differences were statistically significant (t=1 .984 ,2 .457 and 7 .771 ,respectively ,all P<0 .05) .The fluorescence intensities of PKCαwere also significantly lower than that of control group (t=9 .232 ,15 .921 and 22 .222 ,respectively ,all P< 0 .01) .With the increase of IFNα-1b level ,the levels of HSC-T6 PKCε,PKCα,β-catenin and survivin were significantly lower than those of control group (t=7 .020 ,24 .562 ,45 .701 and 14 .241 ,respectively ,all P<0 .01) .With the increase of IFNα-1b ,the levels of HSC-T6 PKCε,PKCα,β-catenin and survivin were significantly lower than those of control group (t=9 .564 ,4 .409 ,10 .036 and 6 .794 ,respectively ,all P<0 .01) .Conclusions IFNα-1b can down-regulate the expression of collagen in hepatic stellate cells in a dose-dependent manner ,reduce the expressions of PKCε,PKCα,β-catenin and Survivin ,and inhibit the proliferation of HSC-T6 hepatic stellate cells .