C von Loeffelholz1,2,3, P Horn2,3, A L Birkenfeld4, R A Claus2,3, B U Metzing2,3, S Döcke1, G Jahreis5, R Heller2,6, S Hoppe7, M Stockmann7, J F Lock8, A Rieger9, M O Weickert10, U Settmacher11, F Rauchfuß11, A F H Pfeiffer1,12, M Bauer2,3, C Sponholz3. 1. a Department of Clinical Nutrition , German Institute of Human Nutrition Potsdam-Rehbruecke , Nuthetal , Germany ; 2. b Integrated Research and Treatment Center, Center for Sepsis Control and Care (CSCC) , Friedrich Schiller University , Jena , Germany. 3. c Department of Anaesthesiology and Intensive Care , Jena University Hospital , Jena , Germany ; 4. d Section of Metabolic and Vascular Medicine, Medical Clinic III , University Hospital Carl Gustav Carus , Dresden , Germany ; 5. e Institute of Nutrition , Friedrich Schiller University , Jena , Germany. 6. f Institute for Molecular Cell Biology , Germany Center for Molecular Biomedicine, Jena University Hospital , Jena , Germany ; 7. g Department of General, Visceral and Transplantation Surgery , Charité-Universitätsmedizin , Berlin , Germany ; 8. h Department of General-, Visceral-, Vascular- and Paediatric Surgery , University Hospital of Wuerzburg , Wuerzburg , Germany ; 9. i Institute of Pathology , Charité-Universitätsmedizin , Berlin , Germany ; 10. j Warwickshire Institute for the Study of Diabetes, Endocrinology and Metabolism , University Hospitals Coventry and Warwickshire , CV2 2DX , Coventry , UK , Division of Metabolic & Vascular Health , University of Warwick , CV4 7AL , Coventry , UK ; 11. k Department of General, Visceral and Transplantation Surgery , Friedrich Schiller University of Jena , Jena , Germany ; 12. l Department of Endocrinology, Diabetes, and Nutrition , Charité-Universitätsmedizin , Berlin , Germany.
Abstract
BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) are frequent comorbidities in perioperative patients. However, the predictive role of the hepatokine fetuin A was not evaluated in this collective. OBJECTIVE: To study fetuin A as predictor of NAFLD/NASH in preoperative patients. METHODS: 58 subjects were included. Fetuin A was studied in patients undergoing open abdominal surgery and in a subset with acute liver failure. Blood and liver specimens were sampled. NAFLD was histologically evaluated. Liver fat was additionally analyzed by an enzymatic approach, circulating fetuin A by enzyme linked-immunosorbent assay, fetuin A mRNA by reverse-transcription PCR. RESULTS: Univariate correlation studies linked fetuin A to liver steatosis (r = 0.40, p = .029) and hepatocellular ballooning degeneration (r = 0.34, p = .026). Compared to non-NAFLD subjects fetuin A was increased in NAFLD (p = .009) and in NASH (p = .029). However, when corrected for main confounders by linear modeling, fetuin A remained related to hepatic steatosis, but not to ballooning degeneration or other NAFLD features. In support of this, biochemically analyzed liver lipids correlated with fetuin A in plasma (r = 0.34, p = .033) and with hepatic fetuin A mRNA (r = 0.54, p < .001). In addition, plasma fetuin A was related to hepatic mRNA (r = 0.32, p = .036), while circulating levels were reduced by 64% with acute liver failure (p < .001), confirming the liver as main fetuin A source. CONCLUSION: Fetuin A is suggested as noninvasive biomarker of hepatic steatosis in preoperative settings.
BACKGROUND:Nonalcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) are frequent comorbidities in perioperative patients. However, the predictive role of the hepatokine fetuin A was not evaluated in this collective. OBJECTIVE: To study fetuin A as predictor of NAFLD/NASH in preoperative patients. METHODS: 58 subjects were included. Fetuin A was studied in patients undergoing open abdominal surgery and in a subset with acute liver failure. Blood and liver specimens were sampled. NAFLD was histologically evaluated. Liver fat was additionally analyzed by an enzymatic approach, circulating fetuin A by enzyme linked-immunosorbent assay, fetuin A mRNA by reverse-transcription PCR. RESULTS: Univariate correlation studies linked fetuin A to liver steatosis (r = 0.40, p = .029) and hepatocellular ballooning degeneration (r = 0.34, p = .026). Compared to non-NAFLD subjects fetuin A was increased in NAFLD (p = .009) and in NASH (p = .029). However, when corrected for main confounders by linear modeling, fetuin A remained related to hepatic steatosis, but not to ballooning degeneration or other NAFLD features. In support of this, biochemically analyzed liver lipids correlated with fetuin A in plasma (r = 0.34, p = .033) and with hepatic fetuin A mRNA (r = 0.54, p < .001). In addition, plasma fetuin A was related to hepatic mRNA (r = 0.32, p = .036), while circulating levels were reduced by 64% with acute liver failure (p < .001), confirming the liver as main fetuin A source. CONCLUSION:Fetuin A is suggested as noninvasive biomarker of hepatic steatosis in preoperative settings.
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