The impact of pegylated interferon and ribavirin combination treatment on lipid metabolism and insulin resistance in chronic hepatitis C patients

Jung, Hyun-Joo; Kim, Young Seok; Kim, Sang Gyune; Lee, Yun Nah; Jeong, Soung Won; Jang, Jae Young; Lee, Sae Hwan; Kim, Hong Soo; Kim, Boo Sung

doi:10.3350/cmh.2014.20.1.38

Cited by 35 publications

(30 citation statements)

References 30 publications

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“…Previously identified changes in peripheral lipid profiles included increases in TCHOL and LDL[4,16-18]. It has also been associated with increases in HDL[16,19], though not in all studies[4,17]. In our study, we found that treatment with DAA resulted in increases in TCHOL, LDL, HDL as well as a decrease in TGs in GT1, and increases in TCHOL, HDL, and LDL in GT3.…”

Section: Discussionsupporting

confidence: 56%

Genotype specific peripheral lipid profile changes with hepatitis C therapy

Pedersen¹,

Patel²,

Backstedt³

et al. 2016

WJG

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AIMTo evaluate magnitude/direction of changes in peripheral lipid profiles in patients undergoing direct acting therapy for hepatitis C by genotype.METHODSMono-infected patients with hepatitis C were treated with guideline-based DAAs at a university-based liver clinic. Patient characteristics and laboratory values were collected before and after the treatment period. Baseline demographics included age, ethnicity, hypertension, diabetes, hyperlipidemia, treatment regimen, and fibrosis stage. Total cholesterol (TCHOL), high density lipoprotein (HDL), low density lipoprotein (LDL), triglycerides (TG), and liver function tests were measured prior to treatment and ETR. Changes in lipid and liver function were evaluated by subgroups with respect to genotype. Mean differences were calculated for each lipid profile and liver function component (direction/magnitude). The mean differences in lipid profiles were then compared between genotypes for differences in direction/magnitude. Lipid profile and liver function changes were evaluated with Levene’s test and student’s t test. Mean differences in lipid profiles were compared between genotypes using ANOVA, post hoc analysis via the Bonferroni correction or Dunnett T3.RESULTSThree hundred and seventy five patients enrolled with 321 (85.6%) achieving sustained-viral response at 12 wk. 72.3% were genotype 1 (GT1), 18.1% genotype 2 (GT2), 9.7% genotype 3 (GT3). Baseline demographics were similar. Significant change in lipid profiles were seen with GT1 and GT3 (ΔGT1, p and ΔGT3, p), with TCHOL increasing (+5.3, P = 0.005 and +16.1, P < 0.001), HDL increasing (+12.5, P < 0.001 and +7.9, P = 0.038), LDL increasing (+7.4, P = 0.058 and +12.5, P < 0.001), and TG decreasing (-5.9, P = 0.044 and -9.80 P = 0.067). Among genotypes (ΔGT1 v. ΔGT2 v. ΔGT3, ANOVA), significant mean differences were seen with TCHOL (+5.3 v. +0.1 v. +16.1, P = 0.017) and HDL (+12.3 v. +2 v. +7.9, P = 0.040). Post-hoc, GT3 was associated with a greater increase in TCHOL than GT1 and GT2 (P = 0.028 and P = 0.019).CONCLUSIONSuccessful DAA therapy results in increases in TCHOL, LDL, and HDL and decrease in TG, particularly in GT1/GT3. Changes are most pronounced in GT3.

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Section: Discussionsupporting

confidence: 56%

Genotype specific peripheral lipid profile changes with hepatitis C therapy

Pedersen¹,

Patel²,

Backstedt³

et al. 2016

WJG

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“…It has been shown that HCV nonstructural protein 5A (NS5A) is able to phosphorylate serine residues of IRS-1, thereby interfering with the post receptor downstream cascade of insulin action [68] . In accordance with this fact, treatment of HCV patients with pegylated interferon and ribavirin reduces insulin resistance assessed by homeostasis model for assessment [69] . Moreover, NS5A protein also exerts direct lipogenic effect through activation of LXRs [70] .…”

Section: Insulin Resistancementioning

confidence: 79%

Liver steatosis in hepatitis C patients

González‐Reimers¹

2015

WJH

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would affect HCV patients who are also obese or diabetics. In fact, several genotypes exert metabolic effects which overlap with some of those observed in the metabolic syndrome. In this review we will analyse the pathogenic pathways involved in the development of steatosis in HCV patients. Several cytokines and adipokines also become activated and are involved in "pure" steatosic effects, in addition to inflammation. They are probably responsible for the evolution of simple steatosis to steatohepatitis, making it difficult to explain why such alterations only affect a proportion of steatosic patients. Core tip: Chronic hepatitis C virus (HCV) infection can lead to steatosis and steatohepatitis. Increased liver triglyceride synthesis is mediated by several transcription factors such as sterol regulatory elementbinding protein (SREBP) whose expression is enhanced, in turn, by HCV core protein. Chronic HCV infection is also associated with insulin resistance that seems to be selective because although it activates systemic lipolysis, it increases triglyceride synthesis within the liver. This is due to the stimulatory effect of insulin on SREBP. It remains to be answered why not all patients with HCV infection and steatosis develop steatohepatitis despite early cytokine activation and metabolic derangements. AbstractThere is controversy regarding some aspects of hepatitis C virus (HCV) infection-associated liver steatosis, and their relationship with body fat stores. It has classically been found that HCV, especially genotype 3, exerts direct metabolic effects which lead to liver steatosis. This supports the existence of a so called viral steatosis and a metabolic steatosis, which REVIEWSubmit a

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“…The homeostasis model assessment-estimated HOMA-IR has been widely used, across all ethnic groups, for the estimation of IR and increased cardio-metabolic risk [27,28]. It is calculated by multiplying fasting plasma insulin (FPI) by FPG, then dividing by the constant 22.5, i.e.…”

Section: Figure 2 Iron Load and Glycemic Abnormalities In Thalassemimentioning

confidence: 99%

Diabetes and Glucose Metabolism in Thalassemia Major: An Update

Sanctis¹,

Soliman

Elsedfy

et al. 2016

Expert Review of Hematology

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In patients with TM, uncontrolled iron overload has serious clinical consequences with considerable morbidity and mortality. Complications include liver damage, cardiac disease and endocrine dysfunction. Diabetes is an important complication of TM. The mechanisms of abnormal glucose homeostasis are complex and multifactorial. This review updates the current knowledge about glycemic abnormalities in TM patients and directs the attention to an early diagnosis and proper management.

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The impact of pegylated interferon and ribavirin combination treatment on lipid metabolism and insulin resistance in chronic hepatitis C patients

Cited by 35 publications

References 30 publications

Genotype specific peripheral lipid profile changes with hepatitis C therapy

Genotype specific peripheral lipid profile changes with hepatitis C therapy

Liver steatosis in hepatitis C patients

Diabetes and Glucose Metabolism in Thalassemia Major: An Update

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