PMID- 24683220
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20140331
LR  - 20211021
IS  - 0011-393X (Print)
IS  - 0011-393X (Linking)
VI  - 70
IP  - 2
DP  - 2009 Apr
TI  - Effects of atorvastatin 10 mg and fenofibrate 200 mg on the low-density 
      lipoprotein profile in dyslipidemic patients: A 12-week, multicenter, randomized, 
      open-label, parallel-group study.
PG  - 71-93
LID - 10.1016/j.curtheres.2009.03.002 [doi]
AB  - BACKGROUND: Elevated plasma low-density lipoprotein cholesterol (LDL-C) 
      concentrations are highly atherogenic, especially the small, dense LDL (sdLDL) 
      species. Fenofibrate has been reported to shift the LDL profile by decreasing the 
      sdLDL subfraction and increasing larger LDL subclasses. Atorvastatin, 
      anantihyperlipidemic agent, has been reported to reduce plasma total cholesterol 
      (TC) and triglyceride (TG) concentrations and thus could modify the LDL profile. 
      OBJECTIVE: The aim of this study was to compare the effects of fenofi brate and 
      atorvastatin on standard lipid concentrations and the LDL profile. METHODS: In 
      this randomized, open-label, parallel-group study, men and women aged 18 to 79 
      years with type II primary dyslipidemia, defined as LDL-C >/=160 and TG 150 to 400 
      mg/dL, after a 4- to 6-week washout period while eating an appropriate diet, were 
      randomized to receive either atorvastatin 10 mg once daily or fenofi-brate 200 mg 
      once daily. Plasma lipid concentrations and cholesterol and apolipoprotein (apo) 
      B (reflecting the LDL particle number) in each LDL subfraction prepared by 
      ultracentrifiigation were determined at baseline and after 12 weeks of treatment. 
      Tolerability was assessed using adverse events (AEs) obtained on laboratory 
      analysis and vital sign measurement. Adherence was assessed by counting unused 
      drug supplies. RESULTS: A total of 165 patients (117 men, 48 women; mean [SD] 
      age, 50.1 [10.7] years; mean TC concentration, 289 mg/dL) were randomized to 
      receive atorvastatin (n = 81) or fenofibrate (n = 84). Compared with fenofibrate, 
      atorvastatin was associated with a significantly greater mean (SD) percentage 
      decrease in TC (27.0% [12.3%] vs 16.5% [12.9%]; P < 0.001), calculated LDL-C 
      (35.4% [15.8%] vs 17.3% [17.2%]; P < 0.001), TC/high-density lipoprotein 
      cholesterol (HDL-C) ratio (29.1% [16.3%] vs 22.9% [15.9%]; P = 0.001), and apoB 
      (30.3% [12.7%] vs 19.6% [15.5%]; P < 0.001). Compared with atorvastatin, 
      fenofibrate was associated with a significantly greater decrease in TG (37.2% 
      [25.9%] vs 20.2% [27.3%]; P < 0.001) and a significantly greater increase in 
      HDL-C concentration (10.4% [15.7%] vs 4.6% [12.1%]; P = 0.017). Fibrinogen 
      concentration was significantly different between the 2 groups (P = 0.002); it 
      was decreased with fenofibrate use (4.6% [23.7%]) and was increased with 
      atorvastatin use (5.7% [23.5%]). Atorvastatin did not markedly affect the LDL 
      distribution; it was associated with a homogeneous decrease in cholesterol and 
      apoB concentrations in all subfractions, whereas fenofibrate was associated with 
      a marked movement toward a normalized LDL profile, shifting the sdLDL 
      subfractions toward larger and less atherogenic particles, particularly in those 
      patients with baseline TG >/=200 mg/dL. No serious AEs related to the study 
      treatments were reported. A total of 5 AEs were observed in 8 patients, 
      including: abdominal pain, 3 patients (2 in the atorvastatin group and 1 in the 
      fenofibrate group); abnormal liver function test results, 1 (fenofibrate); 
      increased creatine Phosphokinase activity, 2 (atorvastatin); gastrointestinal 
      disorders, 1 (fenofibrate); and vertigo, 1 (fenofibrate). CONCLUSION: In these 
      dyslipidemic patients, fenofibrate treatment was associated with an improved LDL 
      subfraction profile beyond reduction in LDL-C, particularly in patients with 
      elevated TG concentration, whereas atorvastatin was associated with equally 
      reduced concentrations of cholesterol and apoB in all LDL subfractions 
      independent of TG concentrations.
FAU - Ansquer, Jean-Claude
AU  - Ansquer JC
AD  - Laboratoires Fournier SA, Daix, France.
FAU - Corda, Christophe
AU  - Corda C
AD  - Laboratoires Fournier SA, Daix, France.
FAU - Le Malicot, Karine
AU  - Le Malicot K
AD  - Laboratoires Fournier SA, Daix, France.
FAU - Jessent, Valerie
AU  - Jessent V
AD  - Laboratoires Fournier SA, Daix, France.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Curr Ther Res Clin Exp
JT  - Current therapeutic research, clinical and experimental
JID - 0372621
PMC - PMC3967351
OTO - NOTNLM
OT  - LDL profile
OT  - atorvastatin
OT  - fenofibrate
OT  - small dense LDL particles
EDAT- 2009/04/01 00:00
MHDA- 2009/04/01 00:01
PMCR- 2009/04/01
CRDT- 2014/04/01 06:00
PHST- 2008/12/08 00:00 [accepted]
PHST- 2014/04/01 06:00 [entrez]
PHST- 2009/04/01 00:00 [pubmed]
PHST- 2009/04/01 00:01 [medline]
PHST- 2009/04/01 00:00 [pmc-release]
AID - S0011-393X(09)00031-9 [pii]
AID - 10.1016/j.curtheres.2009.03.002 [doi]
PST - ppublish
SO  - Curr Ther Res Clin Exp. 2009 Apr;70(2):71-93. doi: 
      10.1016/j.curtheres.2009.03.002.