Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/24406
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dc.contributor.authorKostapanos, M. S.en
dc.contributor.authorMilionis, H. J.en
dc.contributor.authorFilippatos, T. D.en
dc.contributor.authorNakou, E. S.en
dc.contributor.authorBairaktari, E. T.en
dc.contributor.authorTselepis, A. D.en
dc.contributor.authorElisaf, M. S.en
dc.date.accessioned2015-11-24T19:40:48Z-
dc.date.available2015-11-24T19:40:48Z-
dc.identifier.issn0149-2918-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/24406-
dc.rightsDefault Licence-
dc.subjectApolipoproteins/blooden
dc.subjectBlood Glucoseen
dc.subjectDieten
dc.subjectDyslipidemias/*drug therapyen
dc.subjectFemaleen
dc.subjectFluorobenzenes/adverse effects/*therapeutic useen
dc.subjectHumansen
dc.subjectHypolipidemic Agents/adverse effects/*therapeutic useen
dc.subjectInsulin/metabolismen
dc.subjectLipoproteins/blood/*metabolismen
dc.subjectMaleen
dc.subjectMiddle Ageden
dc.subjectPatient Complianceen
dc.subjectProspective Studiesen
dc.subjectPyrimidines/adverse effects/*therapeutic useen
dc.subjectSulfonamides/adverse effects/*therapeutic useen
dc.subjectTriglycerides/blood/*metabolismen
dc.titleA 12-week, prospective, open-label analysis of the effect of rosuvastatin on triglyceride-rich lipoprotein metabolism in patients with primary dyslipidemiaen
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primary10.1016/j.clinthera.2007.07.019-
heal.identifier.secondaryhttp://www.ncbi.nlm.nih.gov/pubmed/17825691-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0149291807002111/1-s2.0-S0149291807002111-main.pdf?_tid=8eb042d5e555a4237861bfb57da2b716&acdnat=1332832349_017420ef3cb4d357f6792851b30b46e4-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικήςel
heal.publicationDate2007-
heal.abstractBACKGROUND: Although the effect of statins on lowering low-density lipoprotein cholesterol (LDL-C) has been extensively studied, their hypotriglyceridemic capacity is not fully understood. OBJECTIVE: The present study examined clinical and laboratory factors potentially associated with the triglyceride (TG)-lowering effect of rosuvastatin. METHODS: Eligible patients had primary dyslipidemia and a moderate risk of heart disease. Patients were prescribed rosuvastatin 10 mg/d in an open-label fashion and kept 3-day food diaries. Laboratory measurements, performed at baseline and 12 weeks, included serum lipid parameters (total cholesterol [TC], TGs, LDL-C, high-density lipoprotein cholesterol [HDL-C], and apolipoprotein [apo] levels), non-lipid metabolic variables (including carbohydrate metabolism parameters and renal, liver, and thyroid function tests), and LDL-subfraction profile (by high-resolution 3% polyacrylamide gel electrophoresis). Tolerability was assessed at each visit. RESULTS: Participants were 75 hyperlipidemic patients (39 men and 36 women; mean age, 51.7 years). At 12 weeks, TC levels were reduced by 35.1% (P < 0.001), TGs by 15.2% (P < 0.001), LDL-C by 48.5% (P < 0.001), apoE by 35.4% (P < 0.001), and apoE by 17.3% (P < 0.001) from baseline, whereas HDL-C and apoA1 levels were not significantly changed. Stepwise linear regression analysis showed that baseline TG levels were most significantly correlated (R(2) = 42.0%; P < 0.001) with the TG-lowering effect of rosuvastatin, followed by the reduction in apoCIII levels (R(2) = 13.6%; P < 0.01). Rosuvastatin use was associated with a reduction in cholesterol mass of both large LDL particles (mean [SD], from 150.5 [36.6] to 90.5 [24.3] mg/dL; P < 0.001) and small, dense LDL (sdLDL) particles (from 11.5 [8.4] to 6.6 [4.5] mg/dL; P < 0.001). Rosuvastatin had no effect on cholesterol distribution of the LDL subfractions (mean [SD], large particles, from 90.8% [7.0%] to 91.8% [5.1%]; sdLDL, from 7.1% [4.7%] to 7.5% [4.8%]) or the mean LDL particle size (from 26.5 [4.2] to 26.6 [4.0] rim). A significant increase in mean LDL particle size after rosuvastatin treatment (mean [SD], from 26.4 [0.4] to 26.9 [0.4] rim; P = 0.02) was observed only in patients with baseline TG levels > or =120 mg/dL. No serious adverse events requiring study treatment discontinuation were reported. One patient who presented with headache and 2 patients who presented with fatigue quickly recovered without discontinuing rosuvastatin treatment. A posttreatment elevation in aminotransferase levels <3-fold the upper limit of normal (ULN) was recorded in 5 (6.7%) patients, and 2 (2.7%) patients experienced elevated creatine kinase concentrations <5-fold ULN. CONCLUSION: Baseline TG levels were the most important independent variable associated with the TG-lowering effect of rosuvastatin.en
heal.journalNameClin Theren
heal.journalTypepeer-reviewed-
heal.fullTextAvailabilityTRUE-
Appears in Collections:Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ

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