The −514C/T polymorphism of the hepatic lipase gene significantly modulates the HDL-cholesterol response to statin treatment

Lahoz, Carlos; Peña, Rocı́o; Mostaza, J.M.; Laguna, Fernando Ballester; García-Iglesias, M.F.; Taboada, Manuel; Pintó, Xavier

doi:10.1016/j.atherosclerosis.2005.02.001

Cited by 25 publications

(18 citation statements)

References 24 publications

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“…The lack of full responsiveness to the principal mechanism of action of a specific drug is not rare in clinical practice; it may occur with other antiplatelet drugs such as clopidogrel, an inhibitor of platelet adenosine diphosphate receptors [35] or with antiatherosclerotic drugs, including statins [36].…”

Section: Resultsmentioning

confidence: 99%

Aspirin resistance: is this term meaningful?

Violi

Pignatelli

2006

Current Opinion in Hematology

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Given the multifactorial nature of atherothrombosis, recurrence of cardiovascular events in aspirin-treated patients does not necessarily suggest 'drug failure'. A cause-effect relationship between platelet insensitivity to aspirin and cardiovascular recurrence has not been defined overall because aspirin compliance has been scarcely considered. Until this information is taken into account, the existence of 'clinical resistance' to aspirin should be reconsidered.

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Section: Resultsmentioning

confidence: 99%

Aspirin resistance: is this term meaningful?

Violi

Pignatelli

2006

Current Opinion in Hematology

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“…Carriers of the APOE ε 2 (*2) allele demonstrated a 6–10% greater reduction in Tc and LDL cholesterol levels, as compared with noncarriers . The −514C>T variant in the gene‐encoding hepatic lipase was also associated with a significantly greater HDL‐level increase, despite the lack of impact on other lipid parameters . In a study evaluating the impact of pravastatin therapy of progression of coronary atherosclerosis, the Taq1B B1 allele (rs708272) of the CETP gene was associated with less progression of disease …”

Section: Pravastatinmentioning

confidence: 99%

“…21 The À514C>T variant in the gene-encoding hepatic lipase was also associated with a significantly greater HDL-level increase, despite the lack of impact on other lipid parameters. 26 In a study evaluating the impact of pravastatin therapy of progression of coronary atherosclerosis, the Taq1B B1 allele (rs708272) of the CETP gene was associated with less progression of disease. 22 With regard to cardiovascular outcomes, one variation in the gene encoding the toll-like receptor 4 (rs4986790) was associated with a greater reduction in cardiovascular events in response to pravastatin therapy than carriers of nonvariant alleles (CV event rate 2.0% vs 11.5%, p=0.045).…”

Section: Pravastatin Pharmacogenetics: Efficacymentioning

confidence: 99%

Impact of Pharmacogenetics on Efficacy and Safety of Statin Therapy for Dyslipidemia

et al. 2017

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Interindividual variability in response to 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, or statins, with regard to both efficacy and safety is an obvious target for pharmacogenetic research. Many genes have been identified as possible contributors to variability in statin response and safety. Genetic polymorphisms may alter the structure or expression of coded proteins, with potential impacts on lipid and statin absorption, distribution, metabolism, and elimination as well as response pathways related to the pharmacologic effect. Many studies have explored the variation in statins' pharmacokinetic and pharmacodynamic parameters; however, to our knowledge, few have established definitive relationships between the genetic polymorphisms and patient outcomes, such as cardiovascular events. In this review article, we provide a statin-based summary of available evidence describing pharmacogenetic associations that may be of clinical relevance in the future. Although currently available studies are often small or retrospective, and may have conflicting results, they may be useful in providing direction for future confirmatory studies and may point to associations that could be confirmed in the future when more patient outcomes-based studies are available. We also summarize the clinically relevant evidence currently available to assist clinicians with providing personalized pharmacotherapy for patients requiring statin therapy.

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“…Single studies have reported that a promoter variant in MTP is associated with triglyceride response and recurring risk of coronary events, an LPL variant may alter TC or HDLC response, and an LIPC variant may alter HDLC response. [79][80][81][82][83][84][85] Removal of cholesterol from peripheral cells requires active transport and is mediated by ABCA1. Preliminary pharmacogenetic analysis suggests that an ABCA1 haplotype may attenuate ApoAI response to statin treatment.…”

mentioning

confidence: 99%