Abstract

Objective. The aim of the present study was to investigate whether pentraxin 3 (PTX3) can be a new noninvasive marker for prediction of liver fibrosis in patients with NAFLD. We also aimed to evaluate the relationship between PTX3 and atherosclerosis in patients with NAFLD. Method. Fifty-four male patients with biopsy-proven NAFLD and 20 apparently healthy male volunteers were included. PTX3 levels were determined, using an ELISA method (R&D Sysytems, Quantikine ELISA, USA). To detect the presence of subclinical atherosclerosis in NAFLD, measurements of CIMT, FMD, and cf-PWV levels were performed. Results. PTX3 levels in NAFLD patients with fibrosis were higher than both NAFLD patients without fibrosis and controls (P = 0.032 and P = 0.028, respectively), but there was no difference between controls and NAFLD patients without fibrosis in terms of PTX3 levels (P = 0.903). PTX3 levels were strongly correlated with cf-PWV (r = 0.359, P = 0.003), whereas no significant correlation was found with other atherosclerosis markers, CIMT and FMD. Conclusion. Elevated plasma PTX3 levels are associated with the presence of fibrosis in patients with NAFLD, independently of metabolic syndrome components. This study demonstrated that for the first time there is a close association between elevated PTX3 levels and increased arterial stiffness in patients with NAFLD.

Highlights

  • The term nonalcoholic fatty liver disease (NAFLD) refers to the fatty infiltration of hepatocytes in the absence of significant alcohol intake [1]

  • We aimed to evaluate the relationship between pentraxin 3 (PTX3) and atherosclerosis in patients with NAFLD, by measuring carotid femoral pulse wave velocity, carotid intima media thickness (CIMT), and flow mediated dilatation (FMD)

  • NAFLD patients, regardless of fibrosis status, had higher Body mass index (BMI), WC, DBP, fasting plasma glucose (FPG), and hs-C reactive protein (CRP) levels but no significant difference in these parameters was found between the NAFLD subgroups

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Summary

Introduction

The term nonalcoholic fatty liver disease (NAFLD) refers to the fatty infiltration of hepatocytes in the absence of significant alcohol intake [1]. A major mechanism is increased hepatic insulin resistance leading to hepatic steatosis. The subclinical inflammation process causes the steatosis to progress to hepatic inflammation and steatohepatitis [2]. Attention has been focused on distinguishing simple steatosis (SS) from nonalcoholic steatohepatitis (NASH) because NASH can lead to liver degeneration and progress to liver cirrhosis [3]. Liver biopsy is accepted as the gold standard for both diagnosis of NAFLD and distinguishing NASH from SS. A noninvasive and clinical useful method is needed because of some limitations of liver biopsy such as being invasive, expensive, and needing hospitalization [4, 5]. Several clinical studies have focused on finding a biomarker which is most closely correlated with the severity of liver fibrosis in patients with NAFLD [6, 7] but already failed to prove a serum biomarker for accurately predicting the severity of liver fibrosis

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