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Allopurinol improves endothelial function and reduces oxidant-inflammatory enzyme of myeloperoxidase in metabolic syndrome

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dc.contributor.authorŞENER, GÖKSEL
dc.contributor.authorsYiginer, Omer; Ozcelik, Fatih; Inanc, Tugrul; Aparci, Mustafa; Ozmen, Namik; Cingozbay, Bekir Yilmaz; Kardesoglu, Ejder; Suleymanoglu, Selami; Sener, Goksel; Cebeci, Bekir Sitki
dc.date.accessioned2022-03-12T17:35:36Z
dc.date.available2022-03-12T17:35:36Z
dc.date.issued2008
dc.description.abstractObjective 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. Conclusion 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.
dc.identifier.doi10.1007/s00392-007-0636-3
dc.identifier.eissn1861-0692
dc.identifier.issn1861-0684
dc.identifier.pubmed18330493
dc.identifier.urihttps://hdl.handle.net/11424/229184
dc.identifier.wosWOS:000255870500008
dc.language.isoeng
dc.publisherSPRINGER HEIDELBERG
dc.relation.ispartofCLINICAL RESEARCH IN CARDIOLOGY
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectmetabolic syndrome
dc.subjectallopurinol
dc.subjectmyeloperoxidase
dc.subjectendothelial dysfunction
dc.subjectC-reactive protein
dc.subjectSERUM URIC-ACID
dc.subjectC-REACTIVE PROTEIN
dc.subjectXANTHINE-OXIDASE
dc.subjectHYPOCHLOROUS ACID
dc.subjectOXIDATIVE STRESS
dc.subjectDYSFUNCTION
dc.subjectHEART
dc.subjectATHEROSCLEROSIS
dc.subjectRISK
dc.subjectASSOCIATION
dc.titleAllopurinol improves endothelial function and reduces oxidant-inflammatory enzyme of myeloperoxidase in metabolic syndrome
dc.typearticle
dspace.entity.typePublication
local.avesis.ide9d18ced-6eff-4904-856b-ee676c444f9e
local.import.packageSS17
local.indexed.atWOS
local.indexed.atSCOPUS
local.journal.numberofpages7
oaire.citation.endPage340
oaire.citation.issue5
oaire.citation.startPage334
oaire.citation.titleCLINICAL RESEARCH IN CARDIOLOGY
oaire.citation.volume97
relation.isAuthorOfPublication2fd85a89-446e-49e1-98c9-d20b11a1a2b5
relation.isAuthorOfPublication.latestForDiscovery2fd85a89-446e-49e1-98c9-d20b11a1a2b5

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