Glycometabolic Control and Fibrinolysis in Diabetic Patients

We investigated 148 diabetic patients with regard to their relationship between fibrinolysis (D-dimer and plasminogen activator inhibitor; PAI) and glycometabolic control (HbA_1c, HbA₁ and fructosamine). The percentage of moderately controlled patients as indicated by HbA_1c, HbA₁ and fructosamine is relatively high (29.7, 41.7 and 30.4%, respectively). Simultaneously, the D-dimer and PAI levels turned out to be enhanced in 30.8 and 22.4% of the patients. There was a positive nonsignificant correlation between D-dimer and HbA_1c, a highly significant negative correlation between D-dimer and HbA₁ and a nonsignificant negative correlation between D-dimer and fructosamine. According to the upper limits of the distinct reference ranges for HbA_1c, HbA₁ and fructosamine, we splitted up the .D-dimer results and calculated the mean D-dimer values belonging to each category. Comparing the D-dimer means for each parameter, we separately obtained significant differences of the D-dimer means between the lower and higher HbA₁ and fructosamine groups, whereas in the case of HbA_1c the mean D-dimer values of the categories under and over 9% showed no significant difference. For PAI, we found only weak nonsignificant positive correlations to D-dimer and fructosamine and weak but highly significant correlations to HbA_1c. These results are indicative for an increase of PAI with diminished glycometabolic control as measured with the HbA_1c and fructosamine level. Both D-dimer and PAI showed positive, highly significant correlations to the age of the diabetic patients, whereas HbA_1c and fructosamine were age independent. The results described in this report demonstrate that the fibrin degradation to D-dimer fragments by the specific fibrinolytic enzyme plasmin is dependent on the glycometabolic control state as measured with HbA₁ and fructosamine and thus on the nonenzymatic glycosylation, which reduces the susceptibility of fibrin to degradation by plasmin.