Abstract
Diabetes is associated with disturbances in haemostasis that are thought to result in an increased incidence of thrombotic complications and cardiovascular disease. The aim of this pilot study was to monitor activation of haemostasis using specific markers for platelet activation and coagulation. Plasma samples (all blood collected and plasma prepared in the same hospital under the same conditions) were obtained from twenty diabetic patients (8 with type I and 12 with type II) and twenty one normal control volunteers. To monitor coagulation these samples were evaluated with the partial thromboplastin time (APTT), prothrombin time (PT) and D-dimer (D-Di) - all reagents from Diagnostica Stago, Asniéres, France. Platelet activation was monitored with a novel method for monitoring procoagulant phospholipids microparticles (PPM) using a factor Xa-based coagulation assay. In this assay shortened clotting times are associated with increased levels of PPM and thus platelet activation.
. | APTT Sec. . | PT % . | PPM Sec. . | D-Di μg/l . |
---|---|---|---|---|
Controls | 34.6 (29.4–39.6) | 93.1 (79–109) | 57.5 (51.1–74.9) | 0.22 (0.22–0.45) |
Type I Diabetes | 34.5 (33.1–36.7) | 96.9 (92–102.5) | 33.8 (19.1–44.2) | 1.6 (0.22–3.6) |
Type II Diabetes | 36.8 (33.2–40.4) | 96 (59.4–112.5) | 48.3 (44.2–51.2) | 0.7 (0.22–1.7) |
. | APTT Sec. . | PT % . | PPM Sec. . | D-Di μg/l . |
---|---|---|---|---|
Controls | 34.6 (29.4–39.6) | 93.1 (79–109) | 57.5 (51.1–74.9) | 0.22 (0.22–0.45) |
Type I Diabetes | 34.5 (33.1–36.7) | 96.9 (92–102.5) | 33.8 (19.1–44.2) | 1.6 (0.22–3.6) |
Type II Diabetes | 36.8 (33.2–40.4) | 96 (59.4–112.5) | 48.3 (44.2–51.2) | 0.7 (0.22–1.7) |
Significantly higher levels of both PPM and DD were found in Type I diabetes patients compared with controls (both P<0.001). In type II diabetes the levels of both were lower than those found in Type I diabetes but both were still higher than the controls (PPM and DDi at p<0.001 and p<0.01 level respectively), only the differences in levels of PPM reaching significance between type I and type II diabetes (p<0.01). The more severe the diabetes (type I > type II) the greater the level activation of haemostasis that is observed. The increases in PPM could account in part for the development or progression of arthrosclerosis in patients with diabetes mellitus. The increased level of D-Di confirms the increased hypercoagulability of these patients. Although this was a small pilot study and further studies are needed to confirm these findings it is interesting to speculate on the usefulness of both the PPM assay and D-Di assays in monitoring the development/severity of diabetes and its complications. The PPM assay may prove to be especially useful in monitoring progression of the disease.
Author notes
Corresponding author