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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1993-12-30
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pubmed:abstractText |
Previous work suggested an influence of etofibrate, a diester of nicotinic acid and clofibric acid, on lipoprotein receptors. Besides its beneficial effects on plasma lipoprotein levels of decrease in total cholesterol, LDL-cholesterol and triglycerides and increase in HDL-cholesterol, etofibrate was shown to inhibit platelet function. In order to further evaluate platelet-lipoprotein interactions, the effects of etofibrate on plasma lipids and lipoproteins on the specific binding of normal [111In]LDL and [111In]HDL onto platelets as well as its effect on platelet function were evaluated in 8 patients affected by Type II hyperlipoproteinemia (HLP). In all patients binding was saturable and indicated high affinity binding sites capable of binding 927 +/- 233 ng protein of [111In]LDL/10(9) platelets (Kd 12 +/- 3 micrograms protein/ml) and 1496 +/- 435 ng protein of [111In]HDL/10(9) platelets (Kd 14 +/- 3 micrograms protein/ml). The capacity of native LDL (HDL) to displace bound [111In]LDL ([111In]HDL) by half (IC50) amounted to 22 +/- 9 micrograms protein/ml (26 +/- 8 micrograms protein/ml). Following a 6-week treatment period with etofibrate (500 mg twice daily), decrease in plasma total cholesterol, LDL-cholesterol and apolipoprotein (apo) B and increase in HDL-cholesterol and apo AI was correlated to a significant (P < 0.01) increase in LDL- as well as HDL-receptor binding. The platelet binding capacity increased to 1085 +/- 212 ng protein/10(9) platelets (Kd 8 +/- 3 micrograms protein/ml) for [111In]LDL and to 1867 +/- 266 ng protein/10(9) platelets for [111In]HDL (Kd 11 +/- 3 micrograms protein/ml). Platelet function studies demonstrated significantly (P < 0.01) reduced platelet aggregation in response to ADP and thromboxane formation after 6 weeks of etofibrate therapy. These findings in patients with HPL Type II indicate in vivo upregulation of specific [111In]LDL as well as [111In]HDL binding sites on human platelets associated with reduced platelet activation following etofibrate therapy.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Anticholesteremic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoproteins B,
http://linkedlifedata.com/resource/pubmed/chemical/Cholesterol,
http://linkedlifedata.com/resource/pubmed/chemical/Cholesterol, HDL,
http://linkedlifedata.com/resource/pubmed/chemical/Cholesterol, LDL,
http://linkedlifedata.com/resource/pubmed/chemical/Clofibric Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Hypolipidemic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Lipoproteins, HDL,
http://linkedlifedata.com/resource/pubmed/chemical/Lipoproteins, LDL,
http://linkedlifedata.com/resource/pubmed/chemical/etofibrate
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0021-9150
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
102
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
217-26
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:8251008-Adult,
pubmed-meshheading:8251008-Anticholesteremic Agents,
pubmed-meshheading:8251008-Apolipoproteins B,
pubmed-meshheading:8251008-Blood Platelets,
pubmed-meshheading:8251008-Cholesterol,
pubmed-meshheading:8251008-Cholesterol, HDL,
pubmed-meshheading:8251008-Cholesterol, LDL,
pubmed-meshheading:8251008-Clofibric Acid,
pubmed-meshheading:8251008-Female,
pubmed-meshheading:8251008-Humans,
pubmed-meshheading:8251008-Hyperlipoproteinemia Type II,
pubmed-meshheading:8251008-Hypolipidemic Agents,
pubmed-meshheading:8251008-Lipoproteins, HDL,
pubmed-meshheading:8251008-Lipoproteins, LDL,
pubmed-meshheading:8251008-Male,
pubmed-meshheading:8251008-Middle Aged,
pubmed-meshheading:8251008-Platelet Aggregation,
pubmed-meshheading:8251008-Stimulation, Chemical
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pubmed:year |
1993
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pubmed:articleTitle |
Etofibrate increases binding of low and high density lipoprotein to human platelets of patients with type II hyperlipoproteinemia.
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pubmed:affiliation |
Department of Nuclear Medicine, University of Vienna, Austria.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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