title: Multifactorial treatment increases endothelial progenitor cells in patients with type 2 diabetes.
abstract: OBJECTIVE
  Endothelial progenitor cells (EPC) augment vascular repair and neovascularisation. Patients with type 2 diabetes have reduced EPC and increased risk of cardiovascular disease (CVD), which is reduced by multifactorial intervention. Our aim, therefore, was to evaluate in type 2 diabetic patients whether the numbers of EPC derived from peripheral blood mononuclear cells is influenced by a multifactorial treatment strategy.
  
  
  METHODS
  We enrolled 28 patients newly referred for initiation of multifactorial treatment, which consisted of improving glycaemic, lipid and blood pressure control, as well as antithrombotic therapy and lifestyle modification. EPC count was assessed by in vitro cultures at baseline and after 90 days of treatment. After 7 days in culture, we identified EPC by fluorescent staining of attached cells. Patients were treated with metformin, aspirin, statins and angiotensin II receptor blockers, and divided accordingly into groups of mono-, dual-, triple- or quadruple therapy.
  
  
  RESULTS
  After 90 days of treatment, glycaemic control improved and total cholesterol decreased. Multifactorial intervention for 90 days significantly increased EPC count in cultures by 35% (from 105 [SE 8] to 140 [11] cells per field [p = 0.002]). The change in EPC among patients with quadruple therapy was higher (63%) than in untreated patients (-32%, p = 0.043).
  
  
  CONCLUSIONS
  Numbers of EPC derived from peripheral blood mononuclear cells increased significantly after multifactorial intervention in type 2 diabetic patients. It remains to be shown whether these changes contribute to the beneficial effects of multifactorial intervention on diabetic micro- and macroangiopathy.
authors.affiliation: Steno Diabetes Center, Niels Steensenvej 1, DK-2820 Gentofte, Denmark. hnri@steno.dk
authors.forename: H
authors.initials: H
authors.lastname: Reinhard
authors.forename: P Karl
authors.initials: PK
authors.lastname: Jacobsen
authors.forename: M
authors.initials: M
authors.lastname: Lajer
authors.forename: N
authors.initials: N
authors.lastname: Pedersen
authors.forename: N
authors.initials: N
authors.lastname: Billestrup
authors.forename: T
authors.initials: T
authors.lastname: Mandrup-Poulsen
authors.forename: H-H
authors.initials: HH
authors.lastname: Parving
authors.forename: P
authors.initials: P
authors.lastname: Rossing
mesh_terms: D057911:Angiotensin Receptor Antagonists / Q000627:therapeutic use; D001241:Aspirin / Q000627:therapeutic use; D002452:Cell Count; D002478:Cells, Cultured; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000628:therapy*; D004038:Diet, Reducing; D042783:Endothelial Cells / Q000166:cytology*; D005081:Exercise Therapy; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007963:Leukocytes, Mononuclear / Q000166:cytology; D008019:Life Style; D008297:Male; D008687:Metformin / Q000627:therapeutic use; D013234:Stem Cells / Q000166:cytology*; D016896:Treatment Outcome
chemical_list: D057911:Angiotensin Receptor Antagonists; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008687:Metformin; D001241:Aspirin