1.
Renal function is impaired in normotensive chronic HCV patients: role of insulin resistance.
Sciacqua, A, Perticone, M, Tassone, EJ, Cimellaro, A, Caroleo, B, Miceli, S, Andreucci, M, Licata, A, Sesti, G, Perticone, F
Internal and emergency medicine. 2016;(4):553-9
Abstract
Renal dysfunction is an independent predictor for cardiovascular morbidity and mortality. We investigated whether chronic hepatitis C virus (HCV) infection and the related insulin resistance/hyperinsulinemia influence renal function in comparison with a group of healthy subjects and with another group with metabolic syndrome. We enrolled 130 newly diagnosed HCV outpatients matched for age and gender with 130 patients with metabolic syndrome and 130 healthy subjects. Renal function was evaluated by calculation of glomerular filtration rate (e-GFR, mL/min/1.73 m(2)) using the CKD-EPI equation. The following laboratory parameters were measured: fasting plasma glucose and insulin, total, LDL- and HDL-cholesterol, triglyceride, creatinine, and HOMA to evaluate insulin sensitivity. HCV patients with respect to both healthy subjects and metabolic syndrome patients have a decreased e-GFR: 86.6 ± 16.1 vs 120.2 ± 23.1 mL/min/1.73 m(2) (P < 0.0001) and 94.9 ± 22.6 mL/min/1.73 m(2) (P = 0.003), respectively. Regarding biochemical variables, HCV patients, in comparison with healthy subjects, have a higher triglyceride level, creatinine, fasting insulin and HOMA (3.4 ± 1.4 vs 2.6 ± 1.3; P < 0.0001). At linear regression analysis, the correlation between e-GFR and HOMA is similar in the metabolic syndrome (r = -0.555, P < 0.0001) and HCV (r = -0.527, P < 0.0001) groups. At multiple regression analysis, HOMA is the major determinant of e-GFR in both groups, accounting for, respectively, 30.8 and 27.8 % of its variation in the metabolic syndrome and HCV. In conclusion, we demonstrate that HCV patients have a significant reduction of e-GFR and that insulin resistance is the major predictor of renal dysfunction.
2.
Hepatic steatosis in patients coinfected with human immunodeficiency virus/hepatitis C virus: a meta-analysis of the risk factors.
Machado, MV, Oliveira, AG, Cortez-Pinto, H
Hepatology (Baltimore, Md.). 2010;(1):71-8
Abstract
UNLABELLED Hepatic steatosis (HS) is frequent in patients with hepatitis C virus (HCV) infection, occurring in 40%-80%, associating with metabolic and virus-related factors, namely, genotype 3 and viral load. Human immunodeficiency virus (HIV) infection and antiretroviral treatment seem to be risk factors for HS. Several studies addressed this issue in coinfected patients, with discrepant results. A meta-analysis was performed on the HS risk factors in coinfected patients. Eligible studies were identified through structured keywords including coinfection, HCV, HIV, and steatosis in relevant databases including PubMed. Pooled odds ratios (ORs) and confidence limits (CIs) were obtained with the random-effects model and the DerSimonian-Laird method. Twelve studies, including 1,989 coinfected patients, were selected. Twenty percent were infected with HCV genotype 3. The overall prevalence of HS was 50.8% (23%-72%). Four studies also included 1,540 HCV monoinfected patients, not showing an increased risk for HS in coinfected patients (OR 1.61, 95% CI 0.84-3.10, P = 0.151). In coinfected patients, HS was associated with higher body mass index (OR 1.13, 95% CI 1.07-1.19, P < 0.001), diabetes mellitus (OR 2.32, 95% CI 1.32-4.07, P = 0.003), elevated alanine aminotransferase levels (OR 1.28, 95% CI 1.02-1.61, P = 0.035), necroinflammatory activity (OR 1.72, 95% CI 1.11-2.67, P = 0.016), and fibrosis (OR 1.67, 95% CI 1.20-2.34, P = 0.003). No associations were found between HS and gender, other metabolic factors (dyslipidemia, glucose, metabolic syndrome), HCV-related factors (genotype, viral load), or HIV-related factors (viral load, CD4 count, antiretroviral therapy, and class of medication). CONCLUSION In coinfected patients, HS does not seem to be more frequent than in HCV monoinfected patients and is mostly associated with metabolic factors, such as increased weight, diabetes mellitus, and more severe liver disease. The fact that no associations with HCV factors were found may be due to the small percentage of genotype 3-infected patients.
3.
Hepatitis C infection and nonalcoholic fatty liver disease.
Cheung, O, Sanyal, AJ
Clinics in liver disease. 2008;(3):573-85, viii-ix
Abstract
In hepatitis C virus (HCV) infection, significant hepatic steatosis or superimposed nonalcoholic steatohepatitis is associated with disease severity and poor response to antiviral therapy. Nonalcoholic fatty liver disease (NAFLD) and HCV are common causes of chronic liver disease in Western countries and are strongly linked to concurrent obesity, insulin resistance, and the metabolic syndrome. With the escalating prevalence of obesity in North America, insulin resistance and the metabolic syndrome are major public health problems that have a significant impact on morbidity and mortality associated with NAFLD and HCV. This article focuses on the current understanding of the interplay between host and viral factors that are involved in the interaction between NAFLD and HCV.