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

Abstract EN

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 ( 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.