Tissue plasminogen activator inhibition in diabetes mellitus.

Diabetes Care. 1989 Oct;12(9):655-8.

Comment in:
    Diabetes Care. 1990 Nov;13(11):1129-30.

Tissue plasminogen activator inhibition in diabetes mellitus.

Small M, Kluft C, MacCuish AC, Lowe GD.

Diabetic Unit, Royol Infirmary , Glasgow, Scotland, United Kingdom.

Depression of fibrinolysis may be relevant to the vascular complications of
diabetes mellitus. Plasminogen activator inhibitor (PAI) is an important
inhibitor of fibrinolysis in humans, and we have found basal activities of PA
inhibition to be elevated in patients with diabetes compared with a reference
group of healthy subjects (mean +/- SD 268 +/- 268 vs. 105 +/- 48%; P less than
.0001). With a monoclonal antibody, it was shown that high inhibition values were
due to PAI-1. No differences in PA inhibition were noted in relation to type of
diabetes, diabetic treatment, or presence or absence of vascular complications.
Basal PA inhibition did not correlate with in vivo (B beta 15-42 antigen) or ex
vivo (fibrin plate) fibrinolytic activity or HbA1. In patients with
non-insulin-dependent diabetes mellitus, treatment with the anabolic steroid
stanozolol significantly reduced PA inhibition. These findings suggest a further
abnormality of fibrinolysis in diabetes, but the lack of a relationship among
other measures of fibrinolysis renders its biologic significance uncertain.