We investigated 148 diabetic patients with regard to their relationship between fibrinolysis (D-dimer and plasminogen activator inhibitor; PAI) and glycometabolic control (HbA1c, HbA1 and fructosamine). The percentage of moderately controlled patients as indicated by HbA1c, 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 HbA1c, 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 HbA1c, 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 HbA1c 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 HbA1c. These results are indicative for an increase of PAI with diminished glycometabolic control as measured with the HbA1c and fructosamine level. Both D-dimer and PAI showed positive, highly significant correlations to the age of the diabetic patients, whereas HbA1c 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.