Tissue Plasminogen Activator Inhibition in Diabetes Mellitus
- Michael Small, MD,
- Cornelius Kluft, PhD,
- Angus C MacCuish, MD and
- Gordon D O Lowe, MD
- Diabetic Unit and University Department of Medicine Royal Infirmary, Glasgow, Scotland, United Kingdom; and the Gaubius Institute TNO, Leiden, The Netherlands
- Address correspondence and reprint requests to Michael Small, MD, Gartnavel General Hospital, 1053 Great Western Road, Glasgow G12 OYN, Scotland, UK.
Abstract
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 < .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 (Bβ15-42 antigen) or ex vivo (fibrin plate) fibrinolytic activity or HbA,. In patients with noninsulin- 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
- Copyright © 1989 by the American Diabetes Association
