Increased Oxidation as an Additional Mechanism Underlying Reduced Clot Permeability and Impaired Fibrinolysis in Type 2 Diabetes

Aims. We sought to investigate whether enhanced oxidation contributes to unfavorable fibrin clot properties in patients with diabetes. Methods. We assessed plasma fibrin clot permeation (Ks, a measure of the pore size in fibrin networks) and clot lysis time induced by recombinant tissue plasminogen...

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Main Authors: Anna Lados-Krupa, Malgorzata Konieczynska, Artur Chmiel, Anetta Undas
Format: Article
Language:English
Published: Wiley 2015-01-01
Series:Journal of Diabetes Research
Online Access:http://dx.doi.org/10.1155/2015/456189
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author Anna Lados-Krupa
Malgorzata Konieczynska
Artur Chmiel
Anetta Undas
author_facet Anna Lados-Krupa
Malgorzata Konieczynska
Artur Chmiel
Anetta Undas
author_sort Anna Lados-Krupa
collection DOAJ
description Aims. We sought to investigate whether enhanced oxidation contributes to unfavorable fibrin clot properties in patients with diabetes. Methods. We assessed plasma fibrin clot permeation (Ks, 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 Ks 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 Ks 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.
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spelling doaj-art-1654d83f5e4e4cd0a44f73a56588ac8e2025-02-03T01:12:20ZengWileyJournal of Diabetes Research2314-67452314-67532015-01-01201510.1155/2015/456189456189Increased Oxidation as an Additional Mechanism Underlying Reduced Clot Permeability and Impaired Fibrinolysis in Type 2 DiabetesAnna Lados-Krupa0Malgorzata Konieczynska1Artur Chmiel2Anetta Undas3Beskid Oncology Center, John Paul II Hospital, Bielsko-Biala, PolandDepartment for Diagnosis, John Paul II Hospital, Krakow, PolandDepartment of Cardiology, Provincial Hospital, Rybnik, PolandInstitute of Cardiology, Jagiellonian University Medical College, Krakow, PolandAims. We sought to investigate whether enhanced oxidation contributes to unfavorable fibrin clot properties in patients with diabetes. Methods. We assessed plasma fibrin clot permeation (Ks, 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 Ks 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 Ks 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.http://dx.doi.org/10.1155/2015/456189
spellingShingle Anna Lados-Krupa
Malgorzata Konieczynska
Artur Chmiel
Anetta Undas
Increased Oxidation as an Additional Mechanism Underlying Reduced Clot Permeability and Impaired Fibrinolysis in Type 2 Diabetes
Journal of Diabetes Research
title Increased Oxidation as an Additional Mechanism Underlying Reduced Clot Permeability and Impaired Fibrinolysis in Type 2 Diabetes
title_full Increased Oxidation as an Additional Mechanism Underlying Reduced Clot Permeability and Impaired Fibrinolysis in Type 2 Diabetes
title_fullStr Increased Oxidation as an Additional Mechanism Underlying Reduced Clot Permeability and Impaired Fibrinolysis in Type 2 Diabetes
title_full_unstemmed Increased Oxidation as an Additional Mechanism Underlying Reduced Clot Permeability and Impaired Fibrinolysis in Type 2 Diabetes
title_short Increased Oxidation as an Additional Mechanism Underlying Reduced Clot Permeability and Impaired Fibrinolysis in Type 2 Diabetes
title_sort increased oxidation as an additional mechanism underlying reduced clot permeability and impaired fibrinolysis in type 2 diabetes
url http://dx.doi.org/10.1155/2015/456189
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