Association of insulin resistance, viral load, and adipokine levels with liver histology in patients with chronic hepatitis C

2012 ◽  
Vol 24 (12) ◽  
pp. 1393-1399 ◽  
Author(s):  
Hasan S. Zeki Aksu ◽  
Behice Kurtaran ◽  
Yusuf Onlen ◽  
Mustafa Namiduru ◽  
Ahmet C. Inkaya ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Chronic Hepatitis ◽  
Viral Load ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Liver Histology

Insulin Resistance in Patients with Chronic Hepatitis C

2016 ◽  
Vol 70 (2) ◽  
pp. 93-98
Author(s):  
Beti Todorovska ◽  
Viktorija Caloska-Ivanova ◽  
Magdalena Dimitrova-Genadieva ◽  
Elena Curakova ◽  
Nenad Joksimovic
Keyword(s):  
Insulin Resistance ◽  
Chronic Hepatitis ◽  
Viral Load ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Liver Steatosis ◽  
Chronic Viral Hepatitis ◽  
Cross Sectional ◽  
Viral Hepatitis C ◽  
Treatment Naïve

Abstract Introduction. Insulin resistance is the most common extrahepatic manifestation associated with hepatitis C virus, which leads to developing more pronounced fibrosis and liver steatosis. The aim of the study was to assess the prevalence of insulin resistance in non-diabetic, treatment naive patients with chronic hepatitis C and to analyze the relation of insulin resistance with genotype, viral load, gender, age, laboratory parameters, inflammatory and fibrotic changes in the liver, body mass index (BMI) and the presence of steatosis. Methods. In this cross sectional study, 224 patients with hepatitis C viral infection were included. The patients were divided into two groups. The first group was with no insulin resistance and the second one with present insulin resistance. They were compared in terms of genotype, viral load, gender, age, inflammatory and fibrotic changes in the liver, BMI and liver steatosis. Results. Insulin resistance was present in 45.5% of patients. The following factors were associated with insulin resistance: age (p=0.0022), inflammatory and fibrotic changes in the liver (p=0.001, p=0.006, respectively), steatosis (p=0.015) and transaminase activities (for AST, p=0,002, for ALT, p=0.001). Conclusion. In the Republic of Macedonia, a high percent of 45.5% among non-diabetic and treatment naïve patients with chronic viral hepatitis C, had insulin resistance. Insulin resistance was more prevalent in older patients, in those with more pronounced inflammatory and fibrotic changes in the liver, in patients with steatosis and in those with higher transaminase activity.

High hepatitis C viral load is associated with insulin resistance in patients with chronic hepatitis C

2007 ◽  
Vol 28 (2) ◽  
pp. 271-277 ◽  
Author(s):  
Ching-Sheng Hsu ◽  
Chun-Jen Liu ◽  
Chen-Hua Liu ◽  
Chia-Chi Wang ◽  
Chi-Ling Chen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Chronic Hepatitis ◽  
Viral Load ◽  
Hepatitis C ◽  
Chronic Hepatitis C

scholarly journals Impaired mitochondrial β-oxidation in patients with chronic hepatitis C: relation with viral load and insulin resistance

2013 ◽  
Vol 13 (1) ◽  
Author(s):  
Chikako Sato ◽  
Takafumi Saito ◽  
Keiko Misawa ◽  
Tomohiro Katsumi ◽  
Kyoko Tomita ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Chronic Hepatitis ◽  
Viral Load ◽  
Hepatitis C ◽  
Chronic Hepatitis C

scholarly journals HOMA, BMI, and Serum Leptin Levels Variations during Antiviral Treatment Suggest Virus-Related Insulin Resistance in Noncirrhotic, Nonobese, and Nondiabetic Chronic Hepatitis C Genotype 1 Patients

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Alessandro Grasso ◽  
Federica Malfatti ◽  
Gabriella Andraghetti ◽  
Simona Marenco ◽  
Chiara Mazzucchelli ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Chronic Hepatitis ◽  
Viral Load ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Antiviral Treatment ◽  
Genotype 1 ◽  
Serum Leptin ◽  
Peginterferon And Ribavirin ◽  
Chronic Hcv

Objective. To investigate the relationship between insulin resistance and viral load decay in nondiabetic and noncirrhotic genotype 1 chronic HCV patients during peginterferon and ribavirin treatment and the possible influence of BMI and leptin as metabolic confounders.Methods. 75 consecutive noncirrhotic, nonobese, and nondiabetic patients with genotype 1 chronic hepatitis C treated with peginterferon alpha 2a plus ribavirin were evaluated. HOMA-IR, serum leptin, and BMI were measured in all patients at baseline and at weeks 12 and 48, whereas viral load was measured at the same time points and then 24 weeks after the end of treatment.Results. HOMA-IR was significantly associated with both BMI and leptin at baseline. During peginterferon plus ribavirin treatment, there was a significant reduction of HOMA-IR at weeks 12 and 48 from baseline (P=0.033and 0.048, resp.) in patients who achieved an early viral load decay (EVR), a trend not observed in patients who not achieved EVR. No variations during treatment were observed regarding BMI and leptin irrespective of EVR.Conclusion. The early reduction of HOMA-IR but not of BMI and leptin during antiviral treatment in noncirrhotic, chronic hepatitis C genotype 1 patients who achieved EVR suggests a viral genesis of insulin resistance in patients with nonmetabolic phenotype.

scholarly journals LIPID METABOLISM DISORDERS IN PATIENTS WITH CHRONIC HEPATITIS C

2015 ◽  
pp. 50-56 ◽  
Author(s):  
L. I. Tkachenko ◽  
V. V. Maleev ◽  
D. M. Sarieva
Keyword(s):  
Insulin Resistance ◽  
Chronic Hepatitis ◽  
Viral Load ◽  
Lipid Metabolism ◽  
Hepatitis C ◽  
Chronic Hepatitis C ◽  
Hdl Cholesterol ◽  
Response To Treatment ◽  
Genotype 3 ◽  
Lipid Metabolism Disorders

Purpose of the study. To study lipid metabolism in chronic hepatitis C and to assess its impact on the formation of insulin resistance, steatosis and progression of liver fibrosis.Materials and methods. The study included 205 patients with chronic hepatitis C (CHC). Conducts research, depending on the genotype C, viral load and body mass index (BMI) of the patients.Results. CHC patients revealed a combined hyperlipoproteinemia on the background of op-pression synthesis of apolipoproteins A1 and B. Formation of hepatic steatosis was associated with HCV genotype 3 virus-induced viral load at ≥ 6 log10 IU/ml and metabolic in VL < 6 log10 IU/ml. In patients with chronic hepatitis C genotype 1, high viral load leads to inhibition of protein synthesis conveyor ApoA1 and increased synthesis of cholesterol, accompanied by abdominal obesity and the formation of insulin resistance. CHC patients with BMI < 25 kg/m2 viral load ≥ 6 log10 ME/ml was associated with dyslipidemia IV type on D. Fredriskson (1970), hyperglycemia, insulin resistance and diabetes. The advanced stage of liver fi brosis (F ≥ 3 on a scale METAVIR) and non-response to treatment were associated with a decrease in HDL cholesterol below normal. With an increase in viral load > 5 log10 ME/ml signifi cantly increased the risk of lipid and carbohydrate metabolism.

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