Prothrombotic factors in histologically proven nonalcoholic fatty liver disease and nonalcoholic steatohepatitis

• DOI: 10.1002/hep.26510
• Publication Date: 2013-05-23T20:48:42Z
• Authors: An Verrijken; Sven Francque; Ilse Mertens; Janne Prawitt; Sandrine Caron; Guy Hubens; Eric Van Marck; Bart Staels; Peter Michielsen; Luc Van Gaal
• Keywords: Steatosis; Plasminogen activator inhibitor-1

An independent role of nonalcoholic fatty liver disease (NAFLD) in the development cardiovascular has been suggested, probably mediated through increased levels prothrombotic factors. Therefore, we examined whether NAFLD is linked to a state, independently metabolic risk factors large single-center cohort overweight/obese patients. Patients presenting obesity clinic underwent detailed and assessment, including an extensive panel coagulation If was suspected, biopsy proposed. A series 273 consecutive patients (65% female) with were included (age, 44 ± 0.76 years; body mass index: 39.6 0.40 kg/m2). Increase fibrinogen, factor VIII, von Willebrand decrease antithrombin III correlated features, but not histology. Levels plasminogen activator inhibitor-1 (PAI-1) significantly increasing severity steatosis (P < 0.001), lobular inflammation ballooning = 0.002), fibrosis 0.001). steatohepatitis had higher PAI-1 values than those normal In multiple regression, anthropometric parameters, remained predictor levels, explaining, together fasting C-peptide waist circumference, 21% variance PAI-1. No consistent correlations histology found for other Conclusion: obesity, contributes increase whereas are unaltered. This finding might, part, explain associated NAFLD. (Hepatology 2014;58:121–129)