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Optimal pharmacologic approach to patients with hypertriglyceridemia and low high-density lipoprotein-cholesterol: randomized comparison of fenofibrate 160 mg and niacin 1500 mg.

DC FieldValueLanguage
dc.contributor.author강석민-
dc.contributor.author김종윤-
dc.contributor.author박성하-
dc.contributor.author심원흠-
dc.contributor.author위진-
dc.contributor.author이상학-
dc.contributor.author장양수-
dc.contributor.author정남식-
dc.contributor.author조승연-
dc.date.accessioned2015-04-23T17:16:05Z-
dc.date.available2015-04-23T17:16:05Z-
dc.date.issued2010-
dc.identifier.issn0021-9150-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/102139-
dc.description.abstractOBJECTIVES: Atherogenic dyslipidemia is emerging as a target of lipid-modifying therapy. However, an optimal pharmacologic approach has not yet been established. The aim of this study is to compare the efficacy and tolerability of the typical doses of fenofibrate and niacin. METHODS: After an eight-week dietary run-in, 201 patients who had triglyceride (TG) levels of 150-499 mg/dL, high-density lipoprotein-cholesterol (HDL-C) levels of <45 mg/dL and low-density lipoprotein-cholesterol (LDL-C) levels of <130 mg/dL were randomly assigned to one of two treatment groups for 16 weeks: fenofibrate 160 mg or niacin extended release 1500 mg (starting at 500 mg and up-titrated at the fifth and ninth weeks). RESULTS: One hundred forty patients completed the study. The percent reductions in apoB/A1 were not different between the two groups (-20% and -22% in the fenofibrate and niacin groups, respectively, p=0.47). The effects of the two regimens on HDL-C were similar (24% and 20%, respectively, p=0.22), while fenofibrate reduced TG more than did niacin (-53% and -48%, respectively, p=0.045). Niacin was more effective at lowering LDL-C, Lp (a), and hs-CRP. However, niacin worsened the parameters of glycemic control, whereas fenofibrate improved them. Niacin showed more frequent adverse events including pruritus and skin flushing. CONCLUSIONS: These two regimens have largely comparable lipid-modifying effects. However, their effects on glucose metabolism and inflammation, and their adverse events need to be considered additionally. Our results underscore more individualized pharmacologic approaches to patients with atherogenic dyslipidemia.-
dc.description.statementOfResponsibilityopen-
dc.format.extent235~240-
dc.relation.isPartOfATHEROSCLEROSIS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdult-
dc.subject.MESHAged-
dc.subject.MESHApolipoprotein A-I/metabolism-
dc.subject.MESHApolipoproteins B/metabolism-
dc.subject.MESHCholesterol, HDL/blood*-
dc.subject.MESHFemale-
dc.subject.MESHFenofibrate/therapeutic use*-
dc.subject.MESHFibric Acids/metabolism-
dc.subject.MESHGlucose/metabolism-
dc.subject.MESHHumans-
dc.subject.MESHHypertriglyceridemia/drug therapy*-
dc.subject.MESHHypolipidemic Agents/therapeutic use-
dc.subject.MESHInflammation-
dc.subject.MESHMale-
dc.subject.MESHMiddle Aged-
dc.subject.MESHNiacin/therapeutic use*-
dc.titleOptimal pharmacologic approach to patients with hypertriglyceridemia and low high-density lipoprotein-cholesterol: randomized comparison of fenofibrate 160 mg and niacin 1500 mg.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorJin Wi-
dc.contributor.googleauthorJong-Youn Kim-
dc.contributor.googleauthorSungha Park-
dc.contributor.googleauthorSeok-Min Kang-
dc.contributor.googleauthorYangsoo Jang-
dc.contributor.googleauthorNamsik Chung-
dc.contributor.googleauthorWon-Heum Shim-
dc.contributor.googleauthorSeung-Yun Cho-
dc.contributor.googleauthorSang-Hak Lee-
dc.identifier.doi10.1016/j.atherosclerosis.2010.08.068-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00037-
dc.contributor.localIdA00926-
dc.contributor.localIdA01512-
dc.contributor.localIdA02202-
dc.contributor.localIdA02450-
dc.contributor.localIdA03448-
dc.contributor.localIdA03585-
dc.contributor.localIdA03844-
dc.contributor.localIdA02833-
dc.relation.journalcodeJ00260-
dc.identifier.eissn1879-1484-
dc.identifier.pmid20855072-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0021915010007161-
dc.contributor.alternativeNameKang, Seok Min-
dc.contributor.alternativeNameKim, Jong Youn-
dc.contributor.alternativeNamePark, Sung Ha-
dc.contributor.alternativeNameShim, Won Heum-
dc.contributor.alternativeNameWi, Jin-
dc.contributor.alternativeNameLee, Sang Hak-
dc.contributor.alternativeNameJang, Yang Soo-
dc.contributor.alternativeNameChung, Nam Sik-
dc.contributor.alternativeNameCho, Seung Yun-
dc.contributor.affiliatedAuthorKang, Seok Min-
dc.contributor.affiliatedAuthorKim, Jong Youn-
dc.contributor.affiliatedAuthorPark, Sung Ha-
dc.contributor.affiliatedAuthorShim, Won Heum-
dc.contributor.affiliatedAuthorWi, Jin-
dc.contributor.affiliatedAuthorJang, Yang Soo-
dc.contributor.affiliatedAuthorChung, Nam Sik-
dc.contributor.affiliatedAuthorCho, Seung Yun-
dc.contributor.affiliatedAuthorLee, Snag Hak-
dc.citation.volume213-
dc.citation.number1-
dc.citation.startPage235-
dc.citation.endPage240-
dc.identifier.bibliographicCitationATHEROSCLEROSIS, Vol.213(1) : 235-240, 2010-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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