title: Endocan Concentration and Chronic Inflammatory Process Among Heart Transplant Recipients.
abstract: BACKGROUND
  Endocan is a novel soluble dermatan sulfate proteoglycan derived from endothelium. It has the capacity of binding to different biologically active molecules associated with cellular signaling, adhesion, and regulating proliferation, differentiation, migration, and adhesion of different cell types in health and pathology. Its elevated level is connected with endothelial activation, neovascularization, and inflammation or carcinogenesis.
  
  
  METHODS
  The level of serum endocan among 131 heart transplant recipients on 3-drug immunosuppression (calcineurin inhibitor, mycophenolate mofetil/mycophenolic acid, steroid) in correlation with other markers of endothelial damage was determined. In addition, 22 healthy volunteers were studied. In cross-sectional study, markers were measured with the use of commercially available assays of endothelial damage-endocan and von Willebrand factor (VWF)-inflammation-high-sensitivity C-reactive protein (hsCRP), interleukin (IL) 6-and kidney function-cystatin C.
  
  
  RESULTS
  The endocan, VWF, IL-6, hsCRP, and cystatin C levels were significantly higher in heart transplant recipients compared with healthy volunteers. In our cohort, endocan level was correlated with renal function (estimated glomerular filtration rate: r = -0.21; P < .05), creatinine (r = 0.21; P < .05), erythrocyte count (r = -0.24; P < .01), hemoglobin (r = -0.33; P < .01), N-terminal pro-B-type natriuretic peptide (r = 0.25; P < .01), cholesterol (r = -0.22; P < .05), LDL (r = -0.21; P < .05), New York Heart Association functional class (r = 0.21; P < .05), hsCRP (r = 0.32; P < .01), IL-6 (r = 0.31; P < .01), and VWF (r = 0.27; P < .01). In multifactorial analysis, the predictors of endocan levels were cholesterol level, cystatin C, and IL-6, predicting 54% of variability.
  
  
  CONCLUSIONS
  Endocan concentration among heart transplant recipients is potentially connected with endothelial damage caused by subclinical inflammation resulting from hyperlipidemia.
authors: First Chair of General Surgery, Jagiellonian University, Medical College, Krakow, Poland. Silesian Center for Heart Diseases, Zabrze, Poland. Electronic address: piotr.przybylowski@uj.edu.pl.
authors: P
authors: P
authors: Przybylowski
authors: Department of Cardiovascular Surgery and Transplantology, Jagiellonian University, Medical College, John Paul II Hospital, Cracow, Poland.
authors: G
authors: G
authors: Wasilewski
authors: 2nd Department of Nephrology, Medical University of Bialystok, Bialystok, Poland.
authors: E
authors: E
authors: Koc-Żórawska
authors: 2nd Department of Nephrology, Medical University of Bialystok, Bialystok, Poland.
authors: J
authors: J
authors: Malyszko
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D016027:Heart Transplantation / Q000009:adverse effects*; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications; D007249:Inflammation / Q000097:blood* / Q000209:etiology; D008297:Male; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000097:blood*; D011509:Proteoglycans / Q000097:blood*; D066027:Transplant Recipients
chemical_list: D015415:Biomarkers; C101134:ESM1 protein, human; D009363:Neoplasm Proteins; D011509:Proteoglycans