Clinical Significance of Serum CD14 and Its Polymorphism as a Biomarker of Non-Alcoholic Fatty Liver Disease

Background: Liver inflammation is deliberated a risk factor for the ongoing liver damage including non-alcoholic steatohepatitis, cirrhosis, and hepatoma. CD14, an effectual mediator for the monocytes activation, has been postulated as a marker of liver inflammation and fibrosis. This study is constructed to detect the alterations in the CD14 serum levels in 40 NAFLD cases and 14 healthy controls along with to analyze the role of CD14 polymorphisms in the causation and severity of Non-Alcoholic Fatty Liver Disease (NAFLD). Liver enzymes, glycated hemoglobin, together with lipid profile were estimated in all included subjects. The diagnosis of NAFLD depends largely on ultrasonography. NAFLD fibrosis score and FIB-4 score were calculated. Serum CD14 was quantified by EnzymeLinked Immunosorbent Assay (ELISA) and C14-159C/T SNP was genotyped via Polymerase Chain Reaction (PCR) and Restriction Fragment Length Polymorphisms (RFLP). Results: Serum CD14 was markedly higher in the diabetic subjects either lean or overweight/obese than the controls (P<0.05). Receiver Operating Characteristic (ROC) curve showed that the optimum cutoff for CD14 was 2.97 ng/ml for discriminating NAFLD patients from their healthy counterparts with a sensitivity of 76.3% and specificity of 78.6%. There was no discrepancy in the prevalence of CD14 genotypes among NAFLD cases and controls. Moreover, the frequency of the CD14 genotypes was analogous in NAFLD patients with NFS≤0.676 and patients with NFS>0.676 (P=1.000). Conclusion: The former observations advocate the potential role of CD14 in both the pathogenesis and progression of NAFLD. Yet, it didn't correlate with the NFS, consequently it couldn't forecast the severity of the disease. Furthermore, no association was distinguished linking CD14 C-(159) T polymorphism and the risk of NAFLD occurrence.