title: Allopurinol improves endothelial function and reduces oxidant-inflammatory enzyme of myeloperoxidase in metabolic syndrome.
abstract: OBJECTIVE
  In this study, we tested in patients with metabolic syndrome whether allopurinol through decreasing oxidative stress improves endothelial function, and ameliorates inflammatory state represented by markers of myeloperoxidase, C-reactive protein (CRP) and fibrinogen.
  
  
  METHODS
  In a randomized, double-blind fashion; subjects with metabolic syndrome were treated with allopurinol (n = 28) or placebo (n = 22) for one month. Before and after treatment, blood samples were collected and the flow-mediated dilation (FMD) and isosorbide dinitrate (ISDN)-mediated dilation of the brachial artery were performed.
  
  
  RESULTS
  Baseline clinical characteristics of the allopurinol and placebo groups demonstrated no differences in terms of clinical characteristics, endothelial function and inflammatory markers. After the treatment with allopurinol, FMD was increased from 8.0 +/- 0.5 % to 11.8 +/- 0.6% (P < 0.01), but there were no change in the placebo group. In both groups, ISDN-mediated dilation is unaffected by the treatment. As a marker of oxidative stress, allopurinol significantly reduced malondialdehyde. Moreover, myeloperoxidase levels were reduced by the treatment with allopurinol (56.1 +/- 3.4 ng/ml vs. 44.4 +/- 2.4 ng/ml, P < 0.05) but there were no change in the placebo group. Surprisingly, neither CRP nor fibrinogen levels were affected by the treatment in both groups.
  
  
  CONCLUSIONS
  Xanthine oxidoreductase inhibition by allopurinol in patients with metabolic syndrome reduces oxidative stress, improves endothelial function, ameliorates myeloperoxidase levels and does not have any effect on CRP and fibrinogen levels.
authors.affiliation: Gumussuyu Military Hospital, Istanbul, Turkey. oyiginer@yahoo.com
authors.forename: Omer
authors.initials: O
authors.lastname: Yiginer
authors.forename: Fatih
authors.initials: F
authors.lastname: Ozcelik
authors.forename: Tugrul
authors.initials: T
authors.lastname: Inanc
authors.forename: Mustafa
authors.initials: M
authors.lastname: Aparci
authors.forename: Namik
authors.initials: N
authors.lastname: Ozmen
authors.forename: Bekir Yilmaz
authors.initials: BY
authors.lastname: Cingozbay
authors.forename: Ejder
authors.initials: E
authors.lastname: Kardesoglu
authors.forename: Selami
authors.initials: S
authors.lastname: Suleymanoglu
authors.forename: Goksel
authors.initials: G
authors.lastname: Sener
authors.forename: Bekir Sitki
authors.initials: BS
authors.lastname: Cebeci
mesh_terms: D000368:Aged; D000493:Allopurinol / Q000627:therapeutic use*; D001783:Blood Flow Velocity / Q000187:drug effects; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000503:physiopathology; D002097:C-Reactive Protein / Q000378:metabolism; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000503:physiopathology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005500:Follow-Up Studies; D016166:Free Radical Scavengers / Q000627:therapeutic use*; D006801:Humans; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects*; D009195:Peroxidase / Q000097:blood*; D013053:Spectrophotometry; D016896:Treatment Outcome; D014463:Ultrasonography; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D016166:Free Radical Scavengers; D000493:Allopurinol; D005340:Fibrinogen; D002097:C-Reactive Protein; D009195:Peroxidase