Metabolic disorders associated with chronic hepatitis C: impact of genotype and ethnicity

Sersté, Thomas; Nkuize, Marcel; Moucari, Rami; Gossum, M. Van; Scheen, Robert; Vertongen, Françoise; Buset, Michel; Mulkay, Jean Pierre; Marcellin, Patrick

doi:10.1111/j.1478-3231.2010.02291.x

Cited by 20 publications

(11 citation statements)

References 35 publications

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“…Sersté et al (2010) found similar results (12.4%) in a large cohort of patients with chronic hepatitis C (18). The NCEP/ATPIII criteria would not have diagnosed almost 9.5% of the individuals with MS who were diagnosed using the IDF definition (12.1% vs. 21.6%; p <0.006).…”

Section: Discussionmentioning

confidence: 61%

Metabolic syndrome in patients with chronic hepatitis C virus genotype 1 infection who do not have obesity or type 2 diabetes

Oliveira

Jesus

Boulhosa

et al. 2012

Clinics

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OBJECTIVE:The individual components of metabolic syndrome may be independent predictors of mortality in patients with liver disease. We aimed to evaluate the prevalence of metabolic syndrome and its related components in hepatitis C virus–infected patients who are not obese and do not have type 2 diabetes.METHODS:This cross-sectional study included 125 patients infected with hepatitis C virus genotype 1. Metabolic syndrome was defined according to the International Diabetes Federation. Anthropometric data were measured according to standardized procedures. Bioimpedance analysis was performed on all patients.RESULTS:Metabolic syndrome was diagnosed in 21.6% of patients. Of the subjects with metabolic syndrome, 59.3% had hypertension, 77.8% had insulin resistance, 85.2% were overweight, 48.1% had a high waist circumference, 85.2% had an increased body fat percentage, and 92.3% had an elevated waist:hip ratio. In the bivariate analysis, female sex (OR 2.58; 95% CI: 1.09–6.25), elevated gamma-glutamyl transferase (γGT) (OR 2.63; 95% CI: 1.04–7.29), elevated fasting glucose (OR 8.05; 95% CI: 3.17-21.32), low HDL cholesterol (OR 2.80; 95% CI: 1.07–7.16), hypertriglyceridemia (OR 7.91; 95% CI: 2.88–22.71), elevated waist circumference (OR 10.33; 95% CI: 3.72–30.67), overweight (OR 11.33; 95% CI: 3.97–41.07), and increased body fat percentage (OR 8.34; 95% CI: 2.94–30.08) were independent determinants of metabolic syndrome. Using the final multivariate regression model, similar results were observed for abdominal fat (OR 9.98; 95% CI: 2.63–44.41) and total body fat percentage (OR 8.73; 95% CI: 2.33–42.34). However, metabolic syndrome risk was also high for those with blood glucose ≥5.55 mmol/L or HDL cholesterol <0.9 mmol/L (OR 16.69; 95% CI: 4.64–76.35; OR 7.23; 95% CI: 1.86–32.63, respectively).CONCLUSION:Metabolic syndrome is highly prevalent among hepatitis C virus–infected patients without type 2 diabetes or obesity. Metabolic syndrome was significantly associated with hypertension, insulin resistance, increased abdominal fat, and overweight.

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Section: Discussionmentioning

confidence: 61%

Metabolic syndrome in patients with chronic hepatitis C virus genotype 1 infection who do not have obesity or type 2 diabetes

Oliveira

Jesus

Boulhosa

et al. 2012

Clinics

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“…In the published literature, the presence of MeS in patients with HCV varied, 12.4% in Europe and 35% in the United States (14,15). These differences are explained by the Many authors consider that, despite the fact that insulin resistance is the common etiological link, the prevalence of MeS in HCV infection is similar to that of the general population (16).…”

Section: Discussionmentioning

confidence: 99%

Metabolic Syndrome and Genotype 1 Virus C Compensated Liver Cirrhosis in the Era of Directly Acting Antiviral Therapy

et al. 2017

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Objectives: The current study aimed at evaluating the association between metabolic syndrome (MeS) in patients with hepatitis C virus (HCV) liver cirrhosis (compensated, genotype, 1b) and changes after sustained viral response (SVR) following a 12-week therapy with paritaprevir, ritonavir, ombitasvir, dasabuvir, and ribavirin (PrOD+R). Methods: The current multicenter retrospective study included 809 patients diagnosed with compensated HCV cirrhosis (child class A), all 1b genotype treated for 12 weeks with direct acting antiviral agents -PrOD+R -regimen (according to the protocol practiced in Romania) and achieved SVR. The parameters of MeS (according to the definition of the International Diabetes Federation) were collected from medical records before and 12 weeks after the treatment. The results were collected in a central database and analyzed with SPSS 18.0. Statistical analysis used both descriptive and analytical methods with a significance level of 95% (CI 95%). Results: Out of the 809 patients, 105 (13%) demonstrated 3 out of the 5 criteria for MeS. Based on the MeS criteria, the commonest parameters were abnormal glycaemia (54.1%), followed by visceral obesity (38.6%), raised triglycerides (26.1%), high blood pressure (12.1%), and a low high-density lipoprotein (HDL)-cholesterol (4.6%). The re-assessment of MeS parameters after SVR showed favourable changes, which were statistically significant: a siginficanttly lower serum triglyeride level (182.32 vs. 153.50 mg/dL, P = 0.001), lower systolic arterial blood pressure (130.57 vs. 124.85 mmHg; P = 0.001), lower diastolic arterial blood pressure (80.26 vs. 78.42 mmHg; P = 0.001) and lower glyceamic levels (130.06 vs. 120.71 mg/dL; P = 0.001), as well as a significant rise in HDL-cholesterol levels (48.61 vs. 50.50 mg/dL; P = 0.003). Abdominal circumference was the only parameter, which did not change after SVR. Following the changes sustained after SVR, 26.7% of the patients no longer fulfilled the minimum 3 criteria for MeS. No correlation was observed between the presence of MeS and the risk of severe adverse events, but it was noted that 37.5% of the patients who decompensated, 66.7% of the ones who developed hepatocarcinoma and 100% of the ones that died of abnormal glycaemic levels. Conclusions: Hyperglycemia, and not MeS, is associated with HCV compensated liver cirrhosis genotype 1b, and is a risk factor for severe adverse events. The attainment of SVR through PrOD+R regimen results in short-term improvements in MeS parameters.

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“…As a result, we could not further analyze how viral genotype or viral load might influence the change in insulin resistance. From the existing literature, HCV‐related insulin resistance is most likely present across different genotypes [4], although some studies suggest it is more frequent in genotypes 1 and 4 [6,32]. Further studies are warranted to elucidate whether change in insulin resistance during antiviral treatment will differ according to viral genotype.…”

Section: Discussionmentioning

confidence: 99%

Change in insulin resistance according to virological response during antiviral treatment for hepatitis C virus infection

Tseng

Hsu

Chang

et al. 2015

Adv in Digestive Medicine

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Summary Background Hepatitis C virus (HCV) infection can lead to increased insulin resistance, but the dynamics of insulin resistance in HCV‐infected patients receiving pegylated interferon plus ribavirin remain elusive. Methods This prospective study enrolled HCV‐infected patients who received pegylated interferon plus ribavirin. Patients were classified according to the attainment of sustained virological response (SVR). Insulin resistance was measured using homeostatic model assessment‐insulin resistance (HOMA‐IR). The change in HOMA‐IR at baseline, the end of treatment, and 24 weeks after the end of treatment was compared in patients who achieved SVR and those who did not. Results A total of 65 patients participated in this study, of which 46 (71%) achieved SVR. Overall, The HOMA‐IR changed significantly during antiviral therapy, with the median values [interquartile range (IQR)] of 3.7 (1.6–10.0) prior to the treatment, 1.5 (0.8–2.9) at the end, and 1.6 (0.9–3.1) at 24 weeks after completion of therapy. However, only patients who achieved SVR had significant off‐therapy reduction of HOMA‐IR, with median values of 1.3 (IQR, 0.7–2.6) at 24 weeks off therapy and 3.6 (IQR, 1.5–9.9) at baseline (p < 0.0001). In those without SVR, the HOMA‐IR measured 24 weeks after treatment completion (median, 2.2; IQR, 1.9–4.7) did not differ from baseline values (median, 3.9; IQR, 2.2–10.0; p = 0.5). Conclusion Dual therapy with pegylated interferon plus ribavirin ameliorated IR in HCV‐infected patients, but the off‐therapy improvement of IR was limited to those who attained SVR.

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Metabolic disorders associated with chronic hepatitis C: impact of genotype and ethnicity

Abstract: In CHC, insulin resistance is independently associated with the presence of genotypes 1/4. Ethnicity is not independently associated with metabolic disorders in patients with CHC.

Cited by 20 publications

References 35 publications

Metabolic syndrome in patients with chronic hepatitis C virus genotype 1 infection who do not have obesity or type 2 diabetes

Metabolic syndrome in patients with chronic hepatitis C virus genotype 1 infection who do not have obesity or type 2 diabetes

Metabolic Syndrome and Genotype 1 Virus C Compensated Liver Cirrhosis in the Era of Directly Acting Antiviral Therapy

Change in insulin resistance according to virological response during antiviral treatment for hepatitis C virus infection

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