- Email: [email protected]
P714 LIVER GENE EXPRESSION OF VISFATIN, OMENTIN, CHEMERIN AND CHEMERIN RECEPTOR IN CHRONIC HEPATITIS C
POSTERS Results: 1.118 were included in the analysis. There was a slight prevalence of males (51.6%), the mean age (±SD) was 55.5±14.5. The mean body mass index was 25.2±4.3 with no gender differences. The most represented age decade was 60–69 years (23.8%). The diagnosis was CHC without cirrhosis in 981/1118 (87.7%), compensated cirrhosis in 106/1118 (9.5%), decompensated cirrhosis in 24/1118 (2.1%) and HCC in 7/1118 (0.6%). Only 44/1118 (3.9%) were above limit alcohol consumers. Genotype 1 was the most represented (47.3%) followed by 2 (23.8%), 3 (13.1%) and others (15.8%). The most frequent concomitant diseases were vascular (21.4%), metabolic (12.2%) and psychiatric (10.8%). 431/1118 (38.6%) were judged as non-eligible for antiviral therapy. Reasons of noneligibility are analyzed in the table. Conclusions: In Italian clinical practice, almost 40% of patients with CHC are considered non-eligible for treatment. Patient’s age and comorbidity represent the most important reasons of non-eligibility. Considering substantially shorter treatment durations with the addition of direct-acting antivirals, eligibility can be increased with careful evaluation of risk/benefit profile for individual patients along with efficient management of comorbidities. Table: Reasons of non-eligibility Main reasons
N
Therapy not indicated: 247/431 (57.3%) Age 144 Histologically mild disease 77 Substance abuse 17 Other reasons 9 Therapy contraindicated: 184/431 (42.6%) Comorbidity 139 Severe hepatic dysfunction 41 Other reasons 4
% 33.4 17.9 3.9 2.1 32.3 9.5 0.9
P714 LIVER GENE EXPRESSION OF VISFATIN, OMENTIN, CHEMERIN AND CHEMERIN RECEPTOR IN CHRONIC HEPATITIS C M. Kukla1 , B. Adamek2 , M. Hartleb1 , M. Zalewska-Ziob2 , B. SobalaSzczygieł3 , L. Ke˛pa3 , M. Waluga1 , R.J. Buldak4 , J. Kasperczyk5 , A. Wiczkowski2 , A. Gabriel6 , K. Zwirska-Korczala4 . 1 Gastroenterology and Hepatology, Medical University of Silesia in Katowice, Katowice, 2 General Biology, Medical University of Silesia in Katowice, Zabrze, 3 Infectious Diseases, Medical University of Silesia in Katowice, Bytom, 4 Physiology, 5 Environmental Medicine, 6 Pathomorphology, Medical University of Silesia in Katowice, Zabrze, Poland E-mail: [email protected] Background and Aims: Adipokines seem to be a link between metabolic disturbances and disease progression in chronic hepatitis C (CHC). Aims: 1. To assess omentin, visfatin, chemerin serum levels and their gene expression in in CHC patients livers. 2. To evaluate their relationship with histological features, biochemical parameters and insulin resistance. Methods: The study included 70 non-obese CHC patients (31M/39F) infected with genotype 1b (age 46.3±10.3 years, BMI 25.0±3.5 kg/m2 ). Liver tissue mRNA expression of omentin, visfatin, chemerin and chemerin receptor genes were assessed with real time quantitative PCR assay, while adipokines serum concentrations with ELISA method. Results: BMI correlated negatively with serum visfatin (r = −0.55, p = 0.01) and visfatin in patients with BMI < 25 kg/m2 (r = −0.45, p = 0.02) and positively with omentin in those with BMI > 25 kg/m2 (r = −0.55, p = 0.01). Serum chemerin levels were negatively associated with fibrosis stage (r = −0.37, p = 0.01) and inflammatory grade (r = −0.30, p = 0.04), independently of BMI. Serum chemerin
level correlated, but surprisingly negatively, with chemerin (r = −0.43; p = 0.004). Expression of visfatin correlated positively with inflammatory and steatosis grade (r = 0.45, p = 0.02; r = 0.42, p = 0.04; respectively) only in patients with BMI < 25 kg/m2 , while chemerin negatively with steatosis grade in patient with BMI > 25 kg/m2 (r = −0.50, p = 0.01). No association between liver gene expression and liver fibrosis and HOMA-IR was found. Chemerin correlated positively with chemerin receptor (r = 0.41, p = 0.002). Conclusions: BMI is a predictor of some adipokines liver gene expression. Only serum chemerin is associated, although negatively, with its liver gene expression. Serum chemerin is associated with fibrosis and inflammatory process. Liver gene expression of some adipokines may influence steatosis and inflammatory process. P715 A STEADY INCREASE IN PROPORTION OF HCV INFECTIONS DUE TO GENOTYPE 3 IN THE CANADIAN PROVINCE OF ALBERTA FROM 1998 TO 2013: IMPLICATIONS FOR THERAPY S.D. Shafran1 , K.E. Doucette1 , J.W. Tang2 . 1 Medicine, 2 Medical Microbiology and Immunology, University of Alberta, Edmonton, AB, Canada E-mail: [email protected] Background and Aims: Genotyping of HCV is necessary to guide treatment. HCV has been genotyped in the Canadian province of Alberta (population ~4M) since 1998 exclusively by the Alberta Provincial Laboratory for Public Health. Methods: We reviewed all HCV genotypes performed in Alberta since 1998 in persons aged 20–49 years to evaluate the distribution of HCV genotypes over time. We selected “younger” adults since they are likely to be closer to the date of HCV acquisition and therefore more representative of HCV transmission epidemiology. Trend data were examined by the Cochran-Armitage method. Results: HCV genotyping was performed in 8145 unique patients aged 20 to 49 years from 1998 to 2013. There was a steady increase in the proportion of genotype 3 cases from 20.9% in 1998–2000 to 30.1% in 2011–2013, a 44% increase (p < 0.0001), and a steady decrease in the proportion of cases due to genotype 1 from 69.1% in 1998–2000 to 58.4% in 2011–2013 (p < 0.0001). The proportion of cases due to genotype 2 was stable at ~9%. Less than 3% of HCV genotypes were due to non-genotypes 1, 2 and 3. These are displayed in the figure.
Figure: HCV genotype distribution over time.
Conclusions: The significant increase in the proportion of HCV cases due to genotype 3 at the “expense” of genotype 1 cases has implications for treatment, since patients with genotype 3 HCV infection are treated with less expensive antiviral regimens with less intensive laboratory monitoring than patients with HCV genotype 1.
Journal of Hepatology 2014 vol. 60 | S215–S359
S307
N
Therapy not indicated: 247/431 (57.3%) Age 144 Histologically mild disease 77 Substance abuse 17 Other reasons 9 Therapy contraindicated: 184/431 (42.6%) Comorbidity 139 Severe hepatic dysfunction 41 Other reasons 4
% 33.4 17.9 3.9 2.1 32.3 9.5 0.9
P714 LIVER GENE EXPRESSION OF VISFATIN, OMENTIN, CHEMERIN AND CHEMERIN RECEPTOR IN CHRONIC HEPATITIS C M. Kukla1 , B. Adamek2 , M. Hartleb1 , M. Zalewska-Ziob2 , B. SobalaSzczygieł3 , L. Ke˛pa3 , M. Waluga1 , R.J. Buldak4 , J. Kasperczyk5 , A. Wiczkowski2 , A. Gabriel6 , K. Zwirska-Korczala4 . 1 Gastroenterology and Hepatology, Medical University of Silesia in Katowice, Katowice, 2 General Biology, Medical University of Silesia in Katowice, Zabrze, 3 Infectious Diseases, Medical University of Silesia in Katowice, Bytom, 4 Physiology, 5 Environmental Medicine, 6 Pathomorphology, Medical University of Silesia in Katowice, Zabrze, Poland E-mail: [email protected] Background and Aims: Adipokines seem to be a link between metabolic disturbances and disease progression in chronic hepatitis C (CHC). Aims: 1. To assess omentin, visfatin, chemerin serum levels and their gene expression in in CHC patients livers. 2. To evaluate their relationship with histological features, biochemical parameters and insulin resistance. Methods: The study included 70 non-obese CHC patients (31M/39F) infected with genotype 1b (age 46.3±10.3 years, BMI 25.0±3.5 kg/m2 ). Liver tissue mRNA expression of omentin, visfatin, chemerin and chemerin receptor genes were assessed with real time quantitative PCR assay, while adipokines serum concentrations with ELISA method. Results: BMI correlated negatively with serum visfatin (r = −0.55, p = 0.01) and visfatin in patients with BMI < 25 kg/m2 (r = −0.45, p = 0.02) and positively with omentin in those with BMI > 25 kg/m2 (r = −0.55, p = 0.01). Serum chemerin levels were negatively associated with fibrosis stage (r = −0.37, p = 0.01) and inflammatory grade (r = −0.30, p = 0.04), independently of BMI. Serum chemerin
level correlated, but surprisingly negatively, with chemerin (r = −0.43; p = 0.004). Expression of visfatin correlated positively with inflammatory and steatosis grade (r = 0.45, p = 0.02; r = 0.42, p = 0.04; respectively) only in patients with BMI < 25 kg/m2 , while chemerin negatively with steatosis grade in patient with BMI > 25 kg/m2 (r = −0.50, p = 0.01). No association between liver gene expression and liver fibrosis and HOMA-IR was found. Chemerin correlated positively with chemerin receptor (r = 0.41, p = 0.002). Conclusions: BMI is a predictor of some adipokines liver gene expression. Only serum chemerin is associated, although negatively, with its liver gene expression. Serum chemerin is associated with fibrosis and inflammatory process. Liver gene expression of some adipokines may influence steatosis and inflammatory process. P715 A STEADY INCREASE IN PROPORTION OF HCV INFECTIONS DUE TO GENOTYPE 3 IN THE CANADIAN PROVINCE OF ALBERTA FROM 1998 TO 2013: IMPLICATIONS FOR THERAPY S.D. Shafran1 , K.E. Doucette1 , J.W. Tang2 . 1 Medicine, 2 Medical Microbiology and Immunology, University of Alberta, Edmonton, AB, Canada E-mail: [email protected] Background and Aims: Genotyping of HCV is necessary to guide treatment. HCV has been genotyped in the Canadian province of Alberta (population ~4M) since 1998 exclusively by the Alberta Provincial Laboratory for Public Health. Methods: We reviewed all HCV genotypes performed in Alberta since 1998 in persons aged 20–49 years to evaluate the distribution of HCV genotypes over time. We selected “younger” adults since they are likely to be closer to the date of HCV acquisition and therefore more representative of HCV transmission epidemiology. Trend data were examined by the Cochran-Armitage method. Results: HCV genotyping was performed in 8145 unique patients aged 20 to 49 years from 1998 to 2013. There was a steady increase in the proportion of genotype 3 cases from 20.9% in 1998–2000 to 30.1% in 2011–2013, a 44% increase (p < 0.0001), and a steady decrease in the proportion of cases due to genotype 1 from 69.1% in 1998–2000 to 58.4% in 2011–2013 (p < 0.0001). The proportion of cases due to genotype 2 was stable at ~9%. Less than 3% of HCV genotypes were due to non-genotypes 1, 2 and 3. These are displayed in the figure.
Figure: HCV genotype distribution over time.
Conclusions: The significant increase in the proportion of HCV cases due to genotype 3 at the “expense” of genotype 1 cases has implications for treatment, since patients with genotype 3 HCV infection are treated with less expensive antiviral regimens with less intensive laboratory monitoring than patients with HCV genotype 1.
Journal of Hepatology 2014 vol. 60 | S215–S359
S307