title: Effect of cilostazol treatment on adiponectin and soluble CD40 ligand levels in diabetic patients with peripheral arterial occlusion disease.
abstract: BACKGROUND
  Peripheral arterial occlusion disease (PAOD) is caused mainly by chronic inflammation and endothelium dysfunction, and is often treated with cilostazol. However, because this drug's influence on atherogenic cytokines is still not well known, this study examined the effect of cilostazol on the serum levels of soluble CD40 ligand (sCD40L), adiponectin and high-sensitivity C-reactive protein (hs-CRP) in patients with type 2 diabetes and PAOD.
  
  
  RESULTS
  The 92 type 2 diabetics with PAOD and 100 non-PAOD diabetics were enrolled and randomly assigned to a group receiving either cilostazol or placebo for 6 months. The atherogenic cytokines were measured at the beginning and completion of the study. In the PAOD groups, those in the cilostazol group had significant changes in the levels of hs-CRP, sCD40L and adiponectin (P=0.001, P=0.05, P=0.004, respectively). Changes in the levels of adiponectin and sCD40L were more significant in the PAOD group treated with cilostazol than in the non-PAOD group also treated with the drug (P=0.01 and P=0.008, respectively).
  
  
  CONCLUSIONS
  Cilostazol can decrease hs-CPR and sCD40L levels and increase that of adiponectin, and then delay the progression of atherogenesis and chronic inflammation in type 2 diabetics, especially those with PAOD.
authors.affiliation: Division of Endocrinology and Metabolism, Department of Internal Medicine, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan. c2607c@ms56.hinet.net
authors.forename: Ching-Jung
authors.initials: CJ
authors.lastname: Hsieh
authors.forename: Pei-Wen
authors.initials: PW
authors.lastname: Wang
mesh_terms: D052242:Adiponectin / Q000097:blood; D000368:Aged; D000369:Aged, 80 and over; D000842:Ankle / Q000098:blood supply; D001157:Arterial Occlusive Diseases / Q000097:blood / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D001916:Brachial Artery / Q000503:physiopathology; D002097:C-Reactive Protein / Q000378:metabolism; D023201:CD40 Ligand / Q000097:blood*; D000077407:Cilostazol; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D018450:Disease Progression; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D016014:Linear Models; D008297:Male; D008875:Middle Aged; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D018570:Risk Assessment; D012307:Risk Factors; D016037:Single-Blind Method; D013777:Tetrazoles / Q000627:therapeutic use*; D016896:Treatment Outcome; D014665:Vasodilator Agents / Q000627:therapeutic use*
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D015415:Biomarkers; D018836:Inflammation Mediators; D010975:Platelet Aggregation Inhibitors; D013777:Tetrazoles; D014665:Vasodilator Agents; D023201:CD40 Ligand; D002097:C-Reactive Protein; D000077407:Cilostazol