| Comparison of treatment of severe high-density lipoprotein cholesterol deficiency in men with daily atorvastatin (20 mg) versus fenofibrate (200 mg) versus extended-release niacin (2 g). | |
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MedLine Citation:
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PMID: 18993152 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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To determine whether available lipid-modifying medication can increase high-density lipoprotein (HDL) cholesterol in well-defined genetic or familial HDL-deficiency states, we studied 19 men with HDL deficiency (HDL cholesterol <5th percentile for age and gender) 55 +/- 10 years of age. Concomitant risk factors included diabetes (n = 3) and hypertension (n = 7) and 8 patients had coronary artery disease. Molecular analysis revealed that 4 patients had a mutation in the ABCA1 gene. Patients were assigned to sequentially receive atorvastatin 20 mg/day, fenofibrate 200 mg/day, and extended-release niacin 2 g/day for 8 weeks, with a 4-week washout period between each treatment. Patients in whom a statin was required, according to current treatment guidelines, were kept on atorvastatin throughout the study. Baseline HDL cholesterol level was 0.63 +/- 0.12 mmol/L (24 +/- 5 mg/dl), triglycerides 2.01 +/- 0.98 mmol/L (180 +/- 86 mg/dl), and low-density lipoprotein (LDL) cholesterol 2.29 +/- 0.95 mmol/L (94 +/- 39 mg/dl). Mean percent changes in HDL cholesterol on atorvastatin, fenofibrate, and niacin were -6% (p = NS), +6% (p = NS), and +22% (p <0.05), respectively. Furthermore, niacin significantly increased the large alpha-1 apolipoprotein A-I-containing HDL subspecies (12 to 17 nm). In conclusion, niacin was the only effective drug to increase HDL cholesterol. The absolute increase in HDL cholesterol, approximately 0.10 mmol/L (3.9 mg/dl), is of uncertain clinical significance. Biomarkers of HDL-mediated cellular cholesterol efflux were not changed by niacin therapy. Atorvastatin or fenofibrate had little effect on HDL cholesterol; atorvastatin decreased the total cholesterol/HDL cholesterol ratio by 26%. Fenofibrate did not change HDL cholesterol levels and caused an increase in LDL cholesterol. Aggressive LDL cholesterol lowering may be the strategy of choice in such patients. |
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Authors:
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Khalid Alrasadi; Zuhier Awan; Khalid Alwaili; Isabelle Ruel; Anouar Hafiane; Larbi Krimbou; Jacques Genest |
Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't Date: 2008-09-11 |
Journal Detail:
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Title: The American journal of cardiology Volume: 102 ISSN: 1879-1913 ISO Abbreviation: Am. J. Cardiol. Publication Date: 2008 Nov |
Date Detail:
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Created Date: 2008-11-10 Completed Date: 2008-12-04 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0207277 Medline TA: Am J Cardiol Country: United States |
Other Details:
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Languages: eng Pagination: 1341-7 Citation Subset: AIM; IM |
Affiliation:
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Cardiovascular Research Laboratories, McGill University Health Center/Royal Victoria Hospital, Montréal, Québec, Canada. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adult Aged Antilipemic Agents / therapeutic use* Cholesterol, HDL / deficiency* Deficiency Diseases / drug therapy Heptanoic Acids / administration & dosage* Humans Male Middle Aged Niacin / administration & dosage* Pilot Projects Procetofen / administration & dosage* Pyrroles / administration & dosage* Severity of Illness Index |
| Chemical | |
Reg. No./Substance:
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0/Antilipemic Agents; 0/Cholesterol, HDL; 0/Heptanoic Acids; 0/Pyrroles; 110862-48-1/atorvastatin; 49562-28-9/Procetofen; 59-67-6/Niacin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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