Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/22049
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dc.contributor.authorMilionis, H. J.en
dc.contributor.authorKakafika, A. I.en
dc.contributor.authorTsouli, S. G.en
dc.contributor.authorAthyros, V. G.en
dc.contributor.authorBairaktari, E. T.en
dc.contributor.authorSeferiadis, K. I.en
dc.contributor.authorElisaf, M. S.en
dc.date.accessioned2015-11-24T19:20:34Z-
dc.date.available2015-11-24T19:20:34Z-
dc.identifier.issn1097-6744-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/22049-
dc.rightsDefault Licence-
dc.subjectFemaleen
dc.subjectHeptanoic Acids/*pharmacology/therapeutic useen
dc.subjectHomeostasis/drug effectsen
dc.subjectHumansen
dc.subjectHydroxymethylglutaryl-CoA Reductase Inhibitors/*pharmacology/therapeutic useen
dc.subjectHyperlipidemias/blood/*drug therapy/metabolismen
dc.subjectHypolipidemic Agents/pharmacology/therapeutic useen
dc.subjectLipids/blooden
dc.subjectLogistic Modelsen
dc.subjectMaleen
dc.subjectMiddle Ageden
dc.subjectPyrroles/*pharmacology/therapeutic useen
dc.subjectSimvastatin/*pharmacology/therapeutic useen
dc.subjectUric Acid/*blood/urineen
dc.titleEffects of statin treatment on uric acid homeostasis in patients with primary hyperlipidemiaen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1016/j.ahj.2004.04.005-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/15459594-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0002870304001930/1-s2.0-S0002870304001930-main.pdf?_tid=1655067b424c589f38d4488b003c0410&acdnat=1333534263_7b77309ea7546fdcffd4abb52b9d2a7b-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2004-
heal.abstractBACKGROUND: Epidemiologic studies have shown that serum uric acid is a risk factor of coronary artery disease. In addition to fenofibrate, there is some evidence that atorvastatin may have a hypouricemic action, but the underlying mechanisms remain speculative. METHODS: This randomized trial was conducted to investigate the effects of atorvastatin and simvastatin on uric acid homeostasis in patients treated for primary hyperlipidemia. A total of 180 patients were enrolled; patients were randomly assigned to 40 mg/d of either atorvastatin or simvastatin. Serum lipid and metabolic parameters were measured at baseline and at 6 and 12 weeks of treatment; random urine samples were simultaneously obtained for creatinine, sodium, and uric acid determinations. RESULTS: Baseline serum uric acid levels correlated positively with the body mass index, serum insulin, creatinine, and triglyceride levels and inversely with serum HDL cholesterol levels. Both statins caused a favorable effect on lipids and a significant decrease in fibrinogen and high-sensitivity CRP levels. However, only atorvastatin reduced serum uric acid levels (from 5.6 +/- 1.7 to 4.9 +/- 1.5 mg/dL, P <.0001) by augmenting its urinary fractional excretion (from 10.4% +/- 7.9% to 12.0% +/- 7.4%, P <.01). In a multivariate logistic regression analysis, the reduction of uric acid levels was independently associated with baseline serum uric acid concentration but not to other variables, including lipid parameters (OR, 1.65; 95% CI, 1.14 to 2.40; P =.008). CONCLUSIONS: Atorvastatin (but not simvastatin) significantly lowered serum uric acid levels. This result may be in favor of a preferable choice of atorvastatin for the treatment of hyperlipidemic patients presenting with hyperuricemia.en
heal.journalNameAm Heart Jen
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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