Evaluation of Plasma Urokinase-Type Plasminogen Activator Receptor (UPAR) in Patients With Chronic Hepatitis B, C and Non-Alcoholic Fatty Liver Disease (NAFLD) as Serological Fibrosis Marker

被引:7
作者
Akdogan, Ozlem [1 ]
Yucel, Ayegul Atak [2 ]
Sargin, Zeynep Gok [1 ]
Sonmez, Cemile [3 ]
Yilmaz, Guldal Esendagli [4 ]
Ozenirler, Seren [1 ]
机构
[1] Gazi Univ, Dept Gastroenterol, Fac Med, TR-06510 Ankara, Turkey
[2] Gazi Univ, Dept Immunol, Fac Med, Ankara, Turkey
[3] Natl Publ Hlth Inst Turkey, Sexually Transmitted Res Lab, Ankara, Turkey
[4] Gazi Univ, Dept Med Pathol, Fac Med, Ankara, Turkey
关键词
non-alcoholic fatty liver disease; hepatitis B; hepatitis C; urokinease-type plasminogen activator receptor; MATRIX DEGRADATION; PANCREATITIS; PATHOGENESIS; EXPRESSION; INHIBITOR; SYSTEM;
D O I
10.1016/j.jceh.2018.02.001
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background/aims: Progressive hepatic fibrosis is the main predictor of outcome and prognosis in chronic liver diseases. The importance of the coagulation cascade has been defined in liver fibrosis; however, the role of the fibrinolytic pathway has not been clear yet. We aimed to evaluate the association between the plasma levels of soluble urokinase Plasminogen Activator Receptor (uPAR) and the severity of liver fibrosis in chronic hepatitis B, C and Non-Alcoholic Fatty Liver Disease (NAFLD). Methods: 96 chronic hepatitis B, 22 chronic hepatitis C and 11 NAFLD patients together with 47 healthy controls were enrolled in the study. uPAR plasma levels were detected by Enzyme-Linked Immunosorbent Assay (ELISA) method. Results: The plasma levels of uPAR in patients with chronic hepatitis B and C significantly exceeded those of healthy controls (P < 0.001) while mean uPAR levels in patients with NAFLD were not different from healthy controls. Mean uPAR levels in chronic viral hepatitis patients with F1-F3 fibrosis and F4-F6 fibrosis were higher than those of control group (P < 0.001). Mean uPAR level in patients with F4-F6 fibrosis was significantly higher than that of patients with F1-F3 fibrosis (P < 0.001). Conclusion: This is the first study that investigated uPAR as a fibrosis marker in NAFLD and chronic hepatitis B patients. It is suggested that plasma levels of uPAR are closely related to the fibrosis stage in chronic hepatitis B and C and that uPAR might be a noninvasive marker of liver fibrosis.
引用
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页码:29 / 33
页数:5
相关论文
共 33 条
[1]   Extracellular matrix degradation and the role of hepatic stellate cells [J].
Benyon, RC ;
Arthur, MJP .
SEMINARS IN LIVER DISEASE, 2001, 21 (03) :373-384
[2]   Soluble Urokinase Plasminogen Activator Receptor is Associated With Progressive Liver Fibrosis in Hepatitis C Infection [J].
Berres, Marie-Luise ;
Schlosser, Beate ;
Berg, Thomas ;
Trautwein, Christian ;
Wasmuth, Hermann E. .
JOURNAL OF CLINICAL GASTROENTEROLOGY, 2012, 46 (04) :334-338
[3]   uPAR: A versatile signalling orchestrator [J].
Blasi, F ;
Carmeliet, P .
NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2002, 3 (12) :932-943
[4]   THE UROKINASE RECEPTOR - INVOLVEMENT IN CELL-SURFACE PROTEOLYSIS AND CANCER INVASION [J].
ELLIS, V ;
PYKE, C ;
ERIKSEN, J ;
SOLBERG, H ;
DANO, K .
ANNALS OF THE NEW YORK ACADEMY OF SCIENCES, 1992, 667 :13-31
[6]   Urokinase Plasminogen Activator Is a Central Regulator of Macrophage Three-Dimensional Invasion, Matrix Degradation, and Adhesion [J].
Fleetwood, Andrew J. ;
Achuthan, Adrian ;
Schultz, Heidi ;
Nansen, Anneline ;
Almholt, Kasper ;
Usher, Pernille ;
Hamilton, John A. .
JOURNAL OF IMMUNOLOGY, 2014, 192 (08) :3540-3547
[7]   Enhanced urokinase plasminogen activation in chronic pancreatitis suggests a role in its pathogenesis [J].
Friess, H ;
Cantero, D ;
Graber, H ;
Tang, WH ;
Guo, XZ ;
Kashiwagi, M ;
Zimmermann, A ;
Gold, L ;
Korc, M ;
Buchler, MW .
GASTROENTEROLOGY, 1997, 113 (03) :904-913
[8]  
Friess H, 1998, SURGERY, V124, P79, DOI 10.1016/S0039-6060(98)70078-9
[9]   Pathogenesis of Liver Fibrosis [J].
Hernandez-Gea, Virginia ;
Friedman, Scott L. .
ANNUAL REVIEW OF PATHOLOGY: MECHANISMS OF DISEASE, VOL 6, 2011, 6 :425-456
[10]   Models of liver fibrosis: exploring the dynamic nature of inflammation and repair in a solid organ [J].
Iredale, John P. .
JOURNAL OF CLINICAL INVESTIGATION, 2007, 117 (03) :539-548