Evaluation of endothelial dysfunction in patients with nonalcoholic fatty liver disease: Association of selenoprotein P with carotid intima-media thickness and endothelium-dependent vasodilation

Background: In patients with NAFLD, there is an increased risk of cardiovascular disease (CVD). Selenoprotein P (SelP), a hepatokine, is associated with insulin resistance (IR) and serum SelP was found to be elevated in patients with NAFLD.& para;& para;Aim: This study aimed to determine the risk of CVD in NAFLD patients and the association of serum SelP levels with this NAFLD related CVD risk.& para;& para;Methods: Ninety-three patients with NAFLD and 37 healthy controls were included in the study. Complete blood count, C-reactive protein (CRP), fasting glucose, serum lipid levels, and SelP levels were tested from fasting blood samples. Moreover, body mass index (BMI), HOMA-IR, carotid intima-media thickness (cIMT) and flow-mediated dilatation (FMD) were measured.& para;& para;Results: In patients with NAFLD, the FMD ratio was significantly lower than in controls (P = 0.027) . cIMT measurements were similar in both groups (P = 0.996). Serum SelP levels were significantly higher than controls (P<0.001 ). SelP levels were significantly correlated with BMI, fasting glucose, LDL-cholesterol and HOMA-IR (r = 0.395, P<0.001; r = 0.322, P = 0.002; r = 0.353, P<0.001 ; r = 0.521, P<0.001, respectively). Also, SelP levels were significantly lower andcorrelated with FMD (r= -0.674, P<0.001 ). SelP, ESR and CRP were significantly higher (P<0.05) and FMD ratios were significantly lower (P<0.05) in patients with nonalcoholic steatohepatitis (NASH) when compared to patients with simple steatosis.& para;& para;Conclusion: These results suggest that in young NAFLD patients without additional comorbidi ties, there is an increased risk of CVD. FMD may be a better predictor for assessment of CVD risk when compared with cIMT. We assume that there could also be an important role of SelP in the pathogenesis of NASH. (C) 2017 Elsevier Masson SAS. All rights reserved.