title: Increased Oxidation as an Additional Mechanism Underlying Reduced Clot Permeability and Impaired Fibrinolysis in Type 2 Diabetes.
abstract: OBJECTIVE
  We sought to investigate whether enhanced oxidation contributes to unfavorable fibrin clot properties in patients with diabetes.
  
  
  METHODS
  We assessed plasma fibrin clot permeation (K s , a measure of the pore size in fibrin networks) and clot lysis time induced by recombinant tissue plasminogen activator (CLT) in 163 consecutive type 2 diabetic patients (92 men and 71 women) aged 65 ± 8.8 years with a mean glycated hemoglobin (HbA1c) of 6.8%. We also measured oxidative stress markers, including nitrotyrosine, the soluble form of receptor for advanced glycation end products (sRAGE), 8-iso-prostaglandin F2α (8-iso-PGF2α ), oxidized low-density lipoprotein (oxLDL), and advanced glycation end products (AGE).
  
  
  RESULTS
  There were inverse correlations between K s and nitrotyrosine, sRAGE, 8-iso-PGF2α , and oxLDL. CLT showed a positive correlation with oxLDL and nitrotyrosine but not with other oxidation markers. All these associations remained significant for K s after adjustment for fibrinogen, disease duration, and HbA1c (all P < 0.05), while oxLDL was the only independent predictor of CLT.
  
  
  CONCLUSIONS
  Our study shows that enhanced oxidative stress adversely affects plasma fibrin clot properties in type 2 diabetic patients, regardless of disease duration and glycemia control.
authors.affiliation: Beskid Oncology Center, John Paul II Hospital, Bielsko-Biala, Poland.
authors.forename: Anna
authors.initials: A
authors.lastname: Lados-Krupa
authors.affiliation: Department for Diagnosis, John Paul II Hospital, Krakow, Poland.
authors.forename: Malgorzata
authors.initials: M
authors.lastname: Konieczynska
authors.affiliation: Department of Cardiology, Provincial Hospital, Rybnik, Poland.
authors.forename: Artur
authors.initials: A
authors.lastname: Chmiel
authors.affiliation: Institute of Cardiology, Jagiellonian University Medical College, Krakow, Poland.
authors.forename: Anetta
authors.initials: A
authors.lastname: Undas
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001777:Blood Coagulation; D001786:Blood Glucose / Q000737:chemistry; D003924:Diabetes Mellitus, Type 2 / Q000097:blood*; D015237:Dinoprost / Q000031:analogs & derivatives / Q000378:metabolism; D005260:Female; D005337:Fibrin / Q000737:chemistry*; D005342:Fibrinolysis; D005919:Glomerular Filtration Rate; D006442:Glycated Hemoglobin / Q000378:metabolism; D017127:Glycation End Products, Advanced / Q000378:metabolism; D006801:Humans; D007700:Kinetics; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D010100:Oxygen / Q000737:chemistry*; D010539:Permeability; D000067759:Receptor for Advanced Glycation End Products / Q000378:metabolism; D011994:Recombinant Proteins / Q000378:metabolism; D011795:Surveys and Questionnaires; D010959:Tissue Plasminogen Activator / Q000097:blood; D014443:Tyrosine / Q000031:analogs & derivatives / Q000737:chemistry
chemical_list: D001786:Blood Glucose; D015237:Dinoprost; D005337:Fibrin; D006442:Glycated Hemoglobin; D017127:Glycation End Products, Advanced; D008077:Lipoproteins, LDL; D010100:Oxygen; D000067759:Receptor for Advanced Glycation End Products; D011994:Recombinant Proteins; D010959:Tissue Plasminogen Activator; D014443:Tyrosine; C517652:hemoglobin A1c protein, human; C099252:oxidized low density lipoprotein; C075750:8-epi-prostaglandin F2alpha; C002744:3-nitrotyrosine