Non-alcoholic fatty liver disease (NAFLD) is closely related to insulin resistance, type 2 diabetes mellitus, and obesity. It is nowadays considered a multisystem disease with a strong association with cardiovascular disease and arterial hypertension, which interfere with changes in the coagulation system. Coagulation disorders are common in patients with hepatic impairment and are dependent on the degree of liver damage. Patients with NAFLD may have preserved overall hemostatic profile, but many studies suggest a trend toward a procoagulant state. Hypercoagulable state in NAFLD patients may even induce progression of hepatic injury. Endothelial dysfunction is present in the systemic and portal vein circulation in NAFLD patients, and platelets are being recognized as modulators of liver diseases through various mechanisms. Through a literature review, we discuss possible disorders in the coagulation cascade and fibrinolysis, endothelial dysfunction, and platelet abnormalities in patients with NAFLD. Considering the processes and mechanisms involved in the hemostatic abnormalities associated with NAFLD, directly related to liver disease or indirectly related through inflammatory processes and metabolic disorders, several potential therapeutic targets have been identified and reviewed here.

Non-alcoholic fatty liver disease (NAFLD) is associated with a number of extrahepatic comorbidities and considerable cardiovascular morbidity and mortality, which is possibly related to coagulation changes associated with metabolic syndrome. Coagulation disorders are common in patients with liver disease of any etiology, and here we review possible alterations in coagulation cascade specific to NAFLD. We discuss derangements in the coagulation cascade and fibrinolysis, endothelial dysfunction, and platelet abnormalities as possible culprits for altered coagulation and explore the significance of these changes for potential treatment targets.

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Background and Objective: This study was conducted to evaluate the diagnostic performance of various biomarkers for steatosis, fibrosis, and inflammation in comparison to a liver biopsy (LB) in patients with nonalcoholic fatty liver disease (NAFLD). Materials and Methods: This was a cross-sectional study that included 135 patients with biopsy-proven NAFLD. Fatty liver index (FLI), hepatic steatosis index (HSI), cell death markers (CK-18 M30 and CK-18 M65), FIB-4 index, NAFLD fibrosis score (NFS), BARD, and AST to platelet ratio index (APRI) were calculated and analysed. Results: FLI, HSI scores, and the cell death biomarkers showed poor diagnostic accuracy for steatosis detection and quantification, with an area under the curve (AUC) of <0.70. The cell death biomarkers likewise did not perform well for the detection of nonalcoholic steatohepatitis (NASH) (AUC < 0.7). As for the fibrosis staging, only APRI and the cell death biomarkers had moderate accuracy (AUC > 0.7) for advanced fibrosis, whereas FIB-4, BARD, and NFS scores demonstrated poor performance (AUC < 0.70). However, a combination of FIB-4 and NFS with the cell death biomarkers had moderate accuracy for advanced (≥F3) fibrosis detection, with an AUC of >0.70. Conclusions: In this first study on Croatian patients with NAFLD, serum biomarkers demonstrated poor diagnostic performance for the noninvasive diagnosis of liver steatosis and NASH. APRI and the cell death biomarkers had only moderate accuracy for diagnosing advanced fibrosis, as did the combination of FIB-4 and NFS with the cell death biomarkers. Further studies regarding serum biomarkers for all NAFLD stages are needed.