1909-P: The Platelet-Derived Growth Factor a—An Additional Pathophysiological Factor in Hepatic Steatosis and Fibrosis Development Both in Patients with Hepatitis C and Patients with Prediabetes

Abstract

Insulin resistance (IR) represents one of the key regulatory mechanisms in the development of non - alcoholic fatty liver disease. It is a common hepatocyte injury in hepatitis C virus (HCV) infection and type 2 diabetes mellitus (T2DM). Higher plasma platelet-derived growth factor A (PDGF- A) concentration is associated with increased hepatic steatosis and fibrosis in T2DM. PDGFs are key regulators of the connective tissue formation and potent mitogens for hepatic stellate cells. We investigated whether there is an association between PDGF-A serum concentration, IR and HCV mediated hepatic steatosis and fibrosis. This cross-sectional study comprised 90 nondiabetic participants aged 47.11±1.54 years divided into 3 groups: HCV negative group with IR (HCV-/IR-, N=12), HCV positive group without IR (HCV+/IR-, N=34), HCV positive group with IR (HCV+/IR+, N=44). The fasting PDGF-A concentration was determined by enzyme-linked immunoadsorbent assay. Homeostatic Model Assessment of IR score over 1.64 was categorised as IR. Fibrosis and steatosis were evaluated by elastography. Steatosis severity accessed by Controlled Attenuation Parameter (p<0.001) had the mean value of 15.9 kPa in the HCV+/IR+ (p<0.001) revealing the highest value in HCV-/IR+ (296.5 dB/m) group. The PDGF-A concentration correlated positively with steatosis (r=0.341, p=0.007) and fibrosis (r=0.264, p=0.071). Both IR positive groups had higher PDGF-A compared to HCV+/IR- group (p=0.006). In accordance with more pronounced steatosis, the HCV-/IR+ group revealed the highest PDGF-A. Concentration of PDGF-A is associated with the severity of hepatic steatosis in HCV and non-HCV patients with IR; i.e., that PDGF-A could represent one of the key regulatory mechanisms in the pathway from hepatic steatosis towards fibrosis. These results provide better understanding of pathways that regulate fibrosis. Disclosure K. Blaslov: None. V. Kokic Males: None. S. Kokic: None. I. Kruljac: None.