Abstract

The role of hepatitis C virus (HCV) in insulin resistance (IR) is not fully understood. The aim of this study was to determine the impact of amino acid (aa) substitutions in the core region of HCV according to IR and to identify clinical and laboratory associations. Ninety-two treatment-naive HCV patients were recruited to determine laboratory data and blood cell count. IR was determined using Homeostasis Model Assessment (HOMA) index where IR was defined as HOMA ≥2. HCV RNA load and genotype were determined by Abbott Real time HCV. HCV core region was determined by direct nucleotide sequencing. Bivariate analysis was conducted using HOMA IR ≥2 as a dependent factor. IR prevalence was 43.5% (n = 40), vitamin D sufficiency was found in 76.1% (n = 70) and 72.8% (n = 67) had advanced liver fibrosis. In the bivariate analyses, elevated values of γGT (p = 0.024) and fibrosis staging (p = 0.004) were associated with IR, but IR was not related to core mutations. The presence of glutamine in position 70 was associated with low vitamin D concentration (p = 0.005). In the multivariate analysis, no variable was independently associated with HOMA-IR. In conclusion, lack of association between IR and HCV core mutations in positions 70 and 91 suggests that genetic variability of this region has little impact on IR.

Highlights

  • Hepatitis C virus (HCV) infection is a serious health problem affecting over 170 million people worldwide [1]

  • Chronic hepatitis C (CHC) when associated with metabolic diseases may lead to rapid progression of the disease, increasing the risk of developing hepatocellular carcinoma (HCC) and advanced fibrosis [3]

  • Homeostasis Model Assessment (HOMA) index mean was higher than the cutoff established in this study (3.08 ± 2.74), where 43.5% (n = 40) presented insulin resistance (IR)

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Summary

Introduction

Hepatitis C virus (HCV) infection is a serious health problem affecting over 170 million people worldwide [1]. Chronic hepatitis C (CHC) is associated with many extrahepatic manifestations that contribute to morbidity and mortality [2]. CHC when associated with metabolic diseases may lead to rapid progression of the disease, increasing the risk of developing hepatocellular carcinoma (HCC) and advanced fibrosis [3]. These data become extremely relevant due to the high prevalence of obesity and metabolic syndromes observed worldwide [3]. Available antiviral treatment for HCV has been shown to be quite effective (>90%), but it is important to recognize and identify irreversible and associated metabolic damage, thereby reducing the morbidity and mortality associated with HCV [3]

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