title: Improved glycemic control and platelet function abnormalities in diabetic patients with microvascular disease.
abstract: Patients with diabetes mellitus have a variety of platelet and coagulation system dysfunctions. At least theoretically, these can contribute to microvascular complications. Intensive glycemic control has been demonstrated to decrease microvascular complications in type 1 diabetics. We studied 16 patients with type 1 diabetes mellitus (11 men and five women; mean age, 39 years) with albuminuria greater than 0.1 g/d and/or proteinuria greater than 0.3 g/d and a creatinine clearance rate higher than 30 mL/min. They received a regimen including three to four injections of insulin per day with or without a weekly infusion of intravenous insulin, and were evaluated for 6 months. We compared the plasma level of von Willebrand factor, platelet aggregation responses to adenosine diphosphate (ADP), epinephrine, and collagen, and platelet adhesion at the beginning of the study and at follow-up intervals. Glycemic control improved significantly. There were no significant differences in the platelet aggregation responses to ADP (1.59 +/- 0.34 v 1.88 +/- 0.23 mmol/L, P = .3; normal, 4.6 +/- 0.2), epinephrine (0.50 +/- 0.20 v 1.11 +/- 0.31 mmol/L, P = .06; normal, 7.6 +/- 1.5), or collagen (92.4 +/- 6.61 v 82.60 +/- 3.78 seconds, P = .6; normal, 79.1 +/- 3.1) or in platelet adhesion (126.31 +/- 16.95 v 195.08 +/- 30.2 platelets, P = .34; normal, 68.6 +/- 1.4). Baseline von Willebrand factor increased, but not significantly (166.38% +/- 10.6% v 142.72% +/- 14.73%, P = .21; normal, 102.0% +/- 6.0%). In type 1 diabetic patients with established microvascular complications of nephropathy, a statistically significant improvement in glycemic control did not improve the in vitro platelet function abnormalities. Improved glycemic control delays the progression of microvascular disease through mechanisms not measured by tests of platelet function.
authors.affiliation: Department of Medicine, Beth Israel Deaconess Hospital, Institute for the Prevention of Cardiovascular Disease, Boston, MA, USA.
authors.forename: B
authors.initials: B
authors.lastname: Roshan
authors.forename: G H
authors.initials: GH
authors.lastname: Tofler
authors.forename: L A
authors.initials: LA
authors.lastname: Weinrauch
authors.forename: R E
authors.initials: RE
authors.lastname: Gleason
authors.forename: J A
authors.initials: JA
authors.lastname: Keough
authors.forename: I
authors.initials: I
authors.lastname: Lipinska
authors.forename: A T
authors.initials: AT
authors.lastname: Lee
authors.forename: J A
authors.initials: JA
authors.lastname: DElia
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology; D000328:Adult; D001791:Blood Platelet Disorders / Q000097:blood; D003094:Collagen / Q000494:pharmacology; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D004837:Epinephrine / Q000494:pharmacology; D005260:Female; D006801:Humans; D006943:Hyperglycemia / Q000097:blood; D007004:Hypoglycemic Agents / Q000627:therapeutic use*; D007328:Insulin / Q000008:administration & dosage / Q000627:therapeutic use*; D008297:Male; D008833:Microcirculation / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects; D011507:Proteinuria / Q000097:blood; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D007004:Hypoglycemic Agents; D007328:Insulin; D014841:von Willebrand Factor; D000244:Adenosine Diphosphate; D003094:Collagen; D004837:Epinephrine