Correlation between beta-lipoprotein levels and outcome of hepatitis C treatment

Gopal, K.; Johnson, Timothy C.; Gopal, Saraswathi; Walfish, Aaron; Bang, Christine T.; Suwandhi, Pauline; Pena-Sahdala, Helene N.; Clain, David J.; Bodenheimer, Henry C.; Min, Albert D.

doi:10.1002/hep.21261

Cited by 107 publications

(111 citation statements)

References 26 publications

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“…These data suggested a possible interaction between TC and HCV infection. Our speculations were supported by recent data that higher TC and LDL levels are associated with a better therapeutic outcome of chronic hepatitis C [40].…”

Section: Discussionsupporting

confidence: 85%

Metabolic profiles in patients with chronic hepatitis C: a case–control study

Hsu

Liu

et al. 2008

Hepatol Int

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BackgroundThe clinical implications of metabolic profiles in patients with chronic hepatitis C remain controversial. To study the association of metabolic abnormalities with chronic hepatitis C, we conducted a case-control study with special emphasis on serum lipid pattern, fasting blood glucose, and adiponectin. Methods We enrolled 500 patients with chronic hepatitis C and 536 sex and age-matched controls. Unadjusted and adjusted associations of demographic and metabolic variables were estimated. Results Chronic hepatitis C patients had higher alanine aminotransferase (ALT) and high-density lipoprotein-cholesterol levels, but lower total cholesterol (TC), triglyceride (TG), and low-density lipoprotein-cholesterol levels than controls. Stratifying ALT level according to its upper limit of normal, HCV infection was associated with younger age, female gender, and higher TC levels in chronic hepatitis C patients with normal ALT levels, but with lower TC and lower TG levels in those with abnormal ALT levels. By using multiple linear regression analyses for subjects with available adiponectin data, presence of HCV infection was independently associated with higher serum adiponectin levels. Conclusions Metabolic profiles of chronic hepatitis C patients are affected by age, gender, serum adiponectin, and ALT levels. Further longitudinal studies are needed to clarify the complex interplay between HCV infection and metabolic profiles.

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Section: Discussionsupporting

confidence: 85%

Metabolic profiles in patients with chronic hepatitis C: a case–control study

Hsu

Liu

et al. 2008

Hepatol Int

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“…Smaller previous studies have suggested that this might be the case for LDL, 3,4 but this is the largest trial to date to corroborate these findings and the first published study to our knowledge to show a relationship between HDL and SVR. In a small retrospective study, Gopal et al 4 found that, among patients with EVR, EOT response, and SVR, the LDL and total cholesterol levels were higher, and this was independent of age. 4 Subsequently, Akuta et al 3 found that an LDL level !…”

Section: Discussionsupporting

confidence: 65%

“…In a small retrospective study, Gopal et al 4 found that, among patients with EVR, EOT response, and SVR, the LDL and total cholesterol levels were higher, and this was independent of age. 4 Subsequently, Akuta et al 3 found that an LDL level ! 86 mg/dL was an independent predictor in a multivariate logistic regression analysis of EVR and SVR in 114 Japanese adults with HCV genotype 1 who were treated with PEG-IFN and RBV for 48 weeks.…”

Section: Discussionmentioning

confidence: 99%

“…2 Recent evidence from small retrospective studies suggests that elevated low-density lipoprotein (LDL) levels may be associated with higher SVR rates in patients infected with HCV genotype 1. [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17] In vitro data suggest that lipid-lowering agents (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors or statins) may inhibit viral replication. However, cell culture models of HCV infection have demonstrated that anti-HCV activity is not the same for all statins: fluvastatin, atorvastatin, simvastatin, and lovastatin inhibit viral replication to variable extents, whereas pravastatin and rosuvastatin have little to no anti-HCV activity.…”

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confidence: 99%

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Serum Cholesterol and Statin Use Predict Virological Response to Peginterferon and Ribavirin Therapy†,‡

et al. 2010

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Elevated low-density lipoprotein (LDL) levels and statin use have been associated with higher sustained virological response (SVR) rates in patients receiving chronic hepatitis C therapy. However, these relationships have not been well characterized in randomized controlled trials. Furthermore, little is known about the relationship between high-density lipoprotein (HDL) and virological response. To determine whether baseline LDL or HDL levels and statin use affect SVR rates, we retrospectively evaluated the IDEAL (Individualized Dosing Efficacy Versus Flat Dosing to Assess Optimal Pegylated Interferon Therapy) trial, in which 3070 treatment-naive, hepatitis C virus (HCV) genotype 1-infected patients were treated for up to 48 weeks in one of the following arms: (1) peginterferon (PEG-IFN) alfa-2b at 1.5 lg/kg/week with ribavirin (RBV) at 800 to 1400 mg/day, (2) PEG-IFN alfa2b at 1.0 lg/kg/week with RBV at 800 to 1400 mg/day, or (3) PEG-IFN alfa-2a at 180 lg/week with RBV at 1000 to 1200 mg/day. Virological responses were assessed by pretreatment statin use and baseline elevated LDL levels (!130 mg/dL) or low HDL levels (<40 mg/dL for men and <50 mg/dL for women). In 1464 patients with baseline elevated LDL levels or low HDL levels, the SVR rate was significantly higher than that in patients with normal levels (44.9% versus 34.0%, P < 0.001). In 66 patients receiving a statin pretreatment, the SVR rate was higher than the rate of those not receiving it (53.0% versus 39.3%, P 5 0.02). In a multivariate logistic regression analysis using the stepwise selection method with baseline characteristics, a high LDL level [odds ratio (OR) 5 1.6, 95% confidence interval (CI) 5 1.4-1.8, P < 0.001], a low HDL level (OR 5 0.5, 95% CI 5 0.3-0.8, P 5 0.004), and statin use (OR 5 2.0, 95% CI 5 1.1-3.7, P 5 0.02) were independently associated with SVR. Conclusion: Baseline elevated LDL levels or low HDL levels and preemptive statin usage were associated with higher SVR rates. Prospective studies may be considered to explore the biological impact of these factors on HCV RNA replication and treatment response. (HEPATOLOGY 2010;52:864-874)

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“…The low levels of LDL are caused by geranylgeranyl-diphosphate in viral replication, which is a substrate for the synthesis of cholesterol. The high levels of LDL compete with LDL receptors and reduce viral replication, whilst the high levels of HDL aid the entry of the virus into the hepatocyte (24). In the hepatocyte, HCV interferes with the lipid metabolism of the host to replicate and assemble leading to hepatic steatosis.…”

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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Correlation between beta-lipoprotein levels and outcome of hepatitis C treatment

Cited by 107 publications

References 26 publications

Metabolic profiles in patients with chronic hepatitis C: a case–control study

Metabolic profiles in patients with chronic hepatitis C: a case–control study

Serum Cholesterol and Statin Use Predict Virological Response to Peginterferon and Ribavirin Therapy†,‡

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

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