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Studies of Apolipoprotein Genotyping on the Drug Treatment of Hyperlipidemic Patients

This study has been completed.
Sponsor:
Information provided by:
National Taiwan University Hospital
ClinicalTrials.gov Identifier:
NCT00451464
First received: March 22, 2007
Last updated: NA
Last verified: July 2005
History: No changes posted

March 22, 2007
March 22, 2007
January 2002
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No Changes Posted
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Studies of Apolipoprotein Genotyping on the Drug Treatment of Hyperlipidemic Patients
Studies of Apolipoprotein Genotyping on the Drug Treatment of Hyperlipidemic Patients

Cardiovascular-related diseases have been the majorities of the leading ten causes of death in Taiwan. Atherosclerotic cardiovascular diseases are multifactorial. Some non-modifiable risk factors (e.g. genetic trait) may attenuate the benefit of risk modification of the modifiable factors (e.g. the effect of drug treatment). Genetic epidemiology has being widely used to analyze the underline risk of cardiovascular diseases and to point the direction of treatment or prevention.

Lipoprotein is composed of lipid and protein. The genetic variation or mutation of apolipoprotein, the protein of lipoprotein, has been linked to some lipid abnormality resulting severe atherosclerotic cardiovascular diseases. ApoA-I, apo A-II, apo A-IV, apo B100, apo B48, apo C-I, apo C-II, apo C-III, apo D, and apo E are currently thought to affect lipid abnormalities. In addition, it has been documented that genetic variations are presented among different races. Apolipoprotein genetic variations or genetic polymorphism study has been emerged as an important role in the field of genetic therapy. The purpose of this 3-year study is to continue the lipid study in our laboratory, identifying the apolipoprotein genotyping in our pooled hyperlipidemic patients and normal control subjects living in Taiwan. We will observe the incidence and link apo A-I, apo A-II, apo A-IV and apo C-III genetic variations to the related lipid abnormality and cardiovascular diseases. The changes of genotyping after lipid lowering drug treatment using statin or fibrate in hypercholesterolemic or hypertriglyceridemic patients is another goal of this project.

Cardiovascular-related diseases have been the majorities of the leading ten causes of death in Taiwan. Atherosclerotic cardiovascular diseases are multifactorial. Some non-modifiable risk factors (e.g. genetic trait) may attenuate the benefit of risk modification of the modifiable factors (e.g. the effect of drug treatment). Genetic epidemiology has being widely used to analyze the underline risk of cardiovascular diseases and to point the direction of treatment or prevention.

Lipoprotein is composed of lipid and protein. The genetic variation or mutation of apolipoprotein, the protein of lipoprotein, has been linked to some lipid abnormality resulting severe atherosclerotic cardiovascular diseases. ApoA-I, apo A-II, apo A-IV, apo B100, apo B48, apo C-I, apo C-II, apo C-III, apo D, and apo E are currently thought to affect lipid abnormalities. In addition, it has been documented that genetic variations are presented among different races. Apolipoprotein genetic variations or genetic polymorphism study has been emerged as an important role in the field of genetic therapy. The purpose of this 3-year study is to continue the lipid study in our laboratory, identifying the apolipoprotein genotyping in our pooled hyperlipidemic patients and normal control subjects living in Taiwan. We will observe the incidence and link apo A-I, apo A-II, apo A-IV and apo C-III genetic variations to the related lipid abnormality and cardiovascular diseases. The changes of genotyping after lipid lowering drug treatment using statin or fibrate in hypercholesterolemic or hypertriglyceridemic patients is another goal of this project.

Our results showed ApoC-III (3175NT C→G) mutation was significantly related to hypertriglyceridemia, the same relation was also found in the Apo B exon 29 (13132 NT C→G; 4311 AA Asn →Ser) mutation. It is interesting to find some hot spot mutation among Caucasian population, such as Apo B exon 26 (10699 NT C→A; 3500 AA Arg →Gln), Apo A-IV (1527-2345 NT) and Apo E exon 2 mutations, were not found in tested samples. Most of presented allele frequencies in apolipoteins genes were different between our population and Caucasian population. The present results strongly suggest that it is necessary to establish our own genetic data which are linked to diseases.

Observational
Observational Model: Case Control
Time Perspective: Cross-Sectional
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Hyperlipidemia
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*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
600
January 2005
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Inclusion Criteria:

  • Hyperlipidemia

Exclusion Criteria:

  • Liver and kidney disease
Both
18 Years and older
Yes
Contact information is only displayed when the study is recruiting subjects
Taiwan
 
NCT00451464
9100205283, NSC93-2314-B-002-016
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National Taiwan University Hospital
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Principal Investigator: Chen Ming-Fong, MD, PhD National Taiwan University Hospital
National Taiwan University Hospital
July 2005

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP