Increased H-FABP concentrations in nonalcoholic fatty liver disease Possible marker for subclinical myocardial damage and subclinical atherosclerosis

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disorder which is reported as the hepatic manifestation of metabolic syndrome with an increased risk of cardiovascular events. Patients with NAFLD are also at risk of future cardiac events independently of metabolic syndrome. The aim of this study was to examine serum concentrations of heart type fatty acid binding protein (H-FABP) in NAFLD and to investigate its correlations with metabolic parameters and subclinical atherosclerosis. A total of 34 patients with NAFLD and 35 healthy subjects were enrolled in the study. NAFLD patients had elevated liver enzymes and steatosis graded on ultrasonography. Healthy subjects had normal liver enzymes and no steatosis on ultrasonography. H-FABP levels were measured using an enzyme linked immunosorbent assay (ELISA) method and correlations with metabolic parameters and subclinical atherosclerosis were examined. Subclinical atherosclerosis was determined with carotid artery intima-media thickness (CIMT) which was measured by high resolution B mode ultrasonography. H-FABP levels were elevated in patients with NAFLD (16.3 +/- 4.0 ng/ml) when compared with healthy controls (13.8 +/- 2.1 ng/ml; p < 0.001). NAFLD patients had significantly higher CIMT than the controls had (0.64 +/- 0.17 mm vs. 0.43 +/- 0.14 mm, p = 0.009). The H-FABP concentrations were significantly positively correlated with body mass index (r = 0.255, p = 0.042), fasting blood glucose level (r = 0.300, p = 0.013), CIMT (r = 0.335, p = 0.043), and homeostasis model assessment-estimated insulin resistance (HOMA-IR; r = 0.156, p = 0.306). In multiple linear regression analysis, H-FABP levels were only independently associated with CIMT (p = 0.04) Serum H-FABP concentrations increase in patients with NAFLD. Our results may not only suggest that H-FABP is a marker of subclinical myocardial damage in patients with NAFLD but also of subclinical atherosclerosis, independent of metabolic syndrome and cardiac risk factors.