TaqIB polymorphism in CETP gene: The influence on incidence of cardiovascular disease in statin-treated patients with familial hypercholesterolemia
article
The effects of Taq1 restriction fragment length polymorphism of the CETP gene on the occurrence of cardiovascular disease (CVD) events were investigated in patients with familial hypercholesterolemia (FH). A total of 300 FH patients, of which 116 (39%) had CVD at the start of the study, were treated with statins during a mean period of 8.5 years. The distribution of Taq1B genotypes was 31% B1B1, 49% B1B2, and 20% B2B2. No differences were found at baseline between the three genotypes, except for an association of the B1 allele with lower high-density lipoprotein (HDL)-cholesterol levels (P= 0.003). All patients were put on statins within 6-8 weeks after the first visit; about 60% received simvastatin (20-40 mg daily) and 40% either pravastatin (40 mg daily) or atorvastatin (20-40 mg daily). The different statin treatments were similar for all groups. The mean change of plasma HDL-cholesterol, low-density lipoprotein-cholesterol, and triglyceride concentration during statin therapy was similar for the three genotypes. During follow-up, new CVD events were recorded in 22 (37%) of the B2B2 patients (n = 59) and in 67 (28%) of B1 allele carriers (n = 241) (P = 0.36). The relative risk for CVD events, after adjustment for age, gender, and CVD at intake, was 1.8 (CI: 1.1-3.0) for B2B2 carriers compared to B1 allele carriers. The Taq1B polymorphism is a significant predictor of future CVD events in statin-treated patients with FH. In spite of similar improvement of the lipoprotein profile during statin therapy, our FH patients with the B2B2 genotype may have a higher CVD risk in comparison with the B1 allele carriers. © 2005 Nature Publishing Group. All rights reserved. Chemicals / CAS: atorvastatin, 134523-00-5, 134523-03-8; pravastatin, 81131-74-0; simvastatin, 79902-63-9; Carrier Proteins; CETP protein, human; Cholesterol Ester Transfer Proteins; Deoxyribonucleases, Type II Site-Specific, EC 3.1.21.4; endodeoxyribonuclease TaqI, EC 3.1.21.-; Glycoproteins; Hydroxymethylglutaryl-CoA Reductase Inhibitors
Topics
Biomedical ResearchCardiovascular diseaseCETPFamilial hypercholesterolemiaPolymorphismProspective follow-upStatinsTaqIBatorvastatincholesterol ester transfer proteinhigh density lipoprotein cholesterolhydroxymethylglutaryl coenzyme A reductase inhibitorlow density lipoprotein cholesterolpravastatinsimvastatintriacylglycerolangina pectorischolesterol blood levelcontrolled studycoronary artery bypass graftdrug dose regimenfamilial hypercholesterolemiafollow upgenetic associationgenetic polymorphismgenetic riskgenetic variabilitygenotypeheart infarctionheterozygoteincidencemajor clinical studyperipheral vascular diseasepredictionrestriction fragment length polymorphismrestriction siterisk assessmenttransluminal coronary angioplastytriacylglycerol blood levelAdolescentAdultAgedCardiovascular DiseasesCarrier ProteinsCholesterol Ester Transfer ProteinsDeoxyribonucleases, Type II Site-SpecificFemaleGene FrequencyGenetic Predisposition to DiseaseGlycoproteinsHumansHydroxymethylglutaryl-CoA Reductase InhibitorsHyperlipoproteinemia Type IIIncidenceMaleMiddle AgedPolymorphism, Genetic
TNO Identifier
238563
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ISSN
10184813
Source
European Journal of Human Genetics, 13(7), pp. 877-882.
Pages
877-882
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