A 12-week, prospective, open-label analysis of the effect of rosuvastatin on triglyceride-rich lipoprotein metabolism in patients with primary dyslipidemia
| dc.contributor.author | Kostapanos, M. S. | en |
| dc.contributor.author | Milionis, H. J. | en |
| dc.contributor.author | Filippatos, T. D. | en |
| dc.contributor.author | Nakou, E. S. | en |
| dc.contributor.author | Bairaktari, E. T. | en |
| dc.contributor.author | Tselepis, A. D. | en |
| dc.contributor.author | Elisaf, M. S. | en |
| dc.date.accessioned | 2015-11-24T19:40:48Z | |
| dc.date.available | 2015-11-24T19:40:48Z | |
| dc.identifier.issn | 0149-2918 | - |
| dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/24406 | |
| dc.rights | Default Licence | - |
| dc.subject | Apolipoproteins/blood | en |
| dc.subject | Blood Glucose | en |
| dc.subject | Diet | en |
| dc.subject | Dyslipidemias/*drug therapy | en |
| dc.subject | Female | en |
| dc.subject | Fluorobenzenes/adverse effects/*therapeutic use | en |
| dc.subject | Humans | en |
| dc.subject | Hypolipidemic Agents/adverse effects/*therapeutic use | en |
| dc.subject | Insulin/metabolism | en |
| dc.subject | Lipoproteins/blood/*metabolism | en |
| dc.subject | Male | en |
| dc.subject | Middle Aged | en |
| dc.subject | Patient Compliance | en |
| dc.subject | Prospective Studies | en |
| dc.subject | Pyrimidines/adverse effects/*therapeutic use | en |
| dc.subject | Sulfonamides/adverse effects/*therapeutic use | en |
| dc.subject | Triglycerides/blood/*metabolism | en |
| dc.title | A 12-week, prospective, open-label analysis of the effect of rosuvastatin on triglyceride-rich lipoprotein metabolism in patients with primary dyslipidemia | en |
| heal.abstract | BACKGROUND: 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.access | campus | - |
| heal.fullTextAvailability | TRUE | - |
| heal.identifier.primary | 10.1016/j.clinthera.2007.07.019 | - |
| heal.identifier.secondary | http://www.ncbi.nlm.nih.gov/pubmed/17825691 | - |
| heal.identifier.secondary | http://ac.els-cdn.com/S0149291807002111/1-s2.0-S0149291807002111-main.pdf?_tid=8eb042d5e555a4237861bfb57da2b716&acdnat=1332832349_017420ef3cb4d357f6792851b30b46e4 | - |
| heal.journalName | Clin Ther | en |
| heal.journalType | peer-reviewed | - |
| heal.language | en | - |
| heal.publicationDate | 2007 | - |
| heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής | el |
| heal.type | journalArticle | - |
| heal.type.el | Άρθρο Περιοδικού | el |
| heal.type.en | Journal article | en |
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