Диссертация (1139975), страница 18
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2244-2247.105.Human Cytochrome P450 Allele Nomenclature Committee // The humancytochromeP450allelenomenclaturedatabase2013.URL:http://www.cypalleles.ki.se/cyp2c19.htm (Accessed 2.09.2014).106.JeongYH, Cho JH, KangMK, et al. Smoking at least 10 cigarettes per dayincreases platelet inhibition by clopidogrel in patients with ST-segment elevationmyocardial infarction // Thromb Res. – 2010. – Vol.
126. – P. 334–338.121107.Jneid H, Anderson JL, Wright RS, et al. 2012 ACCF/AHA focused update ofthe guideline for the management of patients with unstable angina/non–STelevation myocardial infarction: a report of the American College of CardiologyFoundation/American Heart Association Task Force on Practice Guidelines // J AmColl Cardiol. – 2012. – Vol. 60. – P. 645–681.108.Kaneko A, Lum JK, Yaviong J, et al. High and variable frequencies ofCYP2C19 mutations: medical consequences of poor drug metabolism in Vanuatuand other Pacific islands // Pharmacogenetics. – 1999. – Vol.
5. – P. 581–590.109.Karaźniewicz-Łada M, Danielak D, Rubiś B, et al. Impact of commonABCB1polymorphismonpharmacokineticsandpharmacodynamicsofclopidogrel and its metabolites // J Clin Pharm Ther. – 2015. – Vol.40. – P. 226231.110.Kazui M, Nishiya Y, Ishizuka T, et al. Identification of the humancytochrome P450 enzymes involved in the two oxidative steps in the bioactivationof clopidogrel to its pharmacologically active metabolite // Drug Metab Dispos. –2010.
– Vol. 38. – P. 92–99.111.Khode V, Sindhur J, Kanbur D, et al. Mean platelet volume and otherplatelet volume indices in patients with stable coronary artery disease and acutemyocardial infarction: a case control study // J Cardiovasc Dis Res. – 2012. – Vol.3. – P. 272–275.112.Kirtane AJ, Rinaldi M, Parise H, et al. Impact of Point-of-Care PlateletFunction Testing among Patients with and without Acute Coronary SyndromesUndergoing PCI with Drug-Eluting Stents: an Adapt-Des Substudy // J Am CollCardiol. – 2012.
– Vol.59. – P. E291.113.Klingenberg M. et al. Pigments of liver microsomes // Arch BiochemBiophys. – 1958. – Vol. 75. – P. 376-386.122114.Lamba J, Lin Y, Schuetz E, Thummel K. Genetic contribution to variablehuman CYP3A-mediated metabolism // Adv Drug Deliv Rev. – 2002. – Vol. 54. –P. 1271-1294.115.Lau WC, Gurbel PA, Watkins PB et al. Contribution of hepatic cytochromeP450 3A4 metabolic activity to the phenomenon of clopidogrel resistance.
//Circulation. – 2004. – Vol. 109. – P.166-171.116.Leschziner GD, Andrew T, Pirmohamed M et al. ABCB1 genotype and PGPexpression, function and therapeutic drug response: a critical review andrecommendations for future research // Pharmacogenomics J. – 2007. - Vol. 7. – P.154–179.117.Levine GN, Bates ER, Blankenship JC, et al.
2011 ACCF/AHA/SCAIguideline for percutaneous coronary intervention: a report of the American Collegeof Cardiology Foundation/American Heart Association Task Force on PracticeGuidelines and the Society for Cardiovascular Angiography and Interventions // JAm Coll Cardiol. – 2011.
- Vol. 58. – P. 44–122.118.Lewis JP, Fisch AS, Ryan K, et al. Paraoxonase 1 (PON 1) gene variants arenot associated with clopidogrel response // Clin Pharmacol Ther. – 2011. - Vol. 90.– P. 568–574. Rкарин – лакец Карин-лакец119.Lewis JP, Horensteina RB, Ryana K, et al. The functional G143E variant ofcarboxylesterase 1 is associated with increased clopidogrel active metabolite levelsand greater clopidogrel response // Pharmacogenet Genomics. - 2013. - Vol. 23. 1–8.120.Lewis JP, Stephens SH, Horenstein RB, et al.
The CYP2C19*17 Variant isnot Independently Associated with Clopidogrel Response // J Thromb Haemost. –2013. – Vol. 11. – P. 1640–1646.123121.Li D, Zhang GL, Lou YQ, et al. Genetic polymorphisms in MDR1 andCYP3A5 and MDR1 haplotype in mainland Chinese Han, Uygur and Kazakh ethnicgroups // J Clin Pharm Ther. – 2007. - Vol. 32. – P.
89 – 95.122.Li Y, Tang HL, Hu YF, et al. The gain-of-function variant alleleCYP2C19*17: A double-edged sword between thrombosis and bleeding inclopidogrel-treated patients // Journal of Thrombosis and Haemostasis. – 2012. –Vol. 10. – P. 199-206.123.Li Y, Tang HL, Hu YF, et al. The gain-of-function variant alleleCYP2C19*17: A double-edged sword between thrombosis and bleeding inclopidogrel-treated patients // Journal of Thrombosis and Haemostasis. – 2012.
–Vol. 10. – P. 199-206.124.Li-Wan-Po A, Girard T, Farndon P, et al. Pharmacogenetics of CYP2C19:functional and clinical implications of a new variant CYP2C19*17 // Br J ClinPharmacol. – 2010. – Vol. 69. – P. 222-230.125.Longley DB, Johnston PG. Molecular mechanisms of drug resistance // JPathol. – 2005. – Vol. 205. – P. 275–292.126.Luo HR, Poland RE, Lin KM et al. Genetic polymorphism of cytochromeP450 2C19 in Mexican Americans: a cross-ethnic comparative study // ClinPharmacol Ther. – 2006.
– Vol. 80. – P. 33–40127.Luo X, Li X, Hu Zh et al. Evaluation of CYP3A activity in humans usingthree different parameters based on endogenous cortisol metabolism // ActaPharmacologica Sinica. – 2009. – Vol. 30. – P. 1323–1329.128.Makeeva O, Stepanov V, Puzyrev V, et al. Global pharmacogenetics: geneticsubstructure of Eurasian populations and its effect on variants of drug-metabolizingenzymes // Pharmacogenomics.
– 2008. – Vol. 9. – P. 847-868.124129.Marzolini C, Paus E, Buclin T, et al. Polymorphisms in human MDR1 (P-glycoprotein): recent advances and clinical relevance // Clin Pharmacol Ther. –2004. – Vol. 75. – P. 13–33.130.Mayer K, Schulz S, Bernlochner I, et al. A comparative cohort study onpersonalised antiplatelet therapy in PCI-treated patients with high on-clopidogrelplatelet reactivity. Results of the ISAR-HPR registry // Thromb Haemost. – 2014. –Vol. 112. – P. 342-351.131.Mega JL, Close SL, Wiviott SD, et al. Cytochrome p-450 polymorphismsand response to clopidogrel // N Engl J Med. – 2009.
– Vol. 360. – P. 354–362.132.Mega JL, Close SL, Wiviott SD, et al. Genetic variants in ABCB1 andCYP2C19 and cardiovascular outcomes after treatment with clopidogrel andprasugrel in the TRITON-TIMI 38 trial: a pharmacogenetic analysis // Lancet. –2010. – Vol. 376 . – P. 1312-1329.133.Mega JL, Simon T, Collet JP et al. Reduced-function CYP2C19 genotypeand risk of adverse clinical outcomes among patients treated with clopidogrelpredominantly for PCI: a meta-analysis // JAMA.
– 2010. – Vol. 304. – P. 18211830.134.Mičuda S, Hodač M, Šišpera L et al. Influence of amiodarone on urinaryexcretion of 6β-hydroxycortisol in humans // Physiol Res. – 2001. – Vol. 50. – P.191-196.135.Miura G, Ariyoshi N, Sato Y, et al. Genetic and non-genetic factorsresponsible for antiplatelet effects of clopidogrel in Japanese patients undergoingcoronary stent implantation: An algorithm to predict on-clopidogrel plateletreactivity // Thromb Res.
– 2014. – Vol. 134. – P. 877-883.136.Mokhtar OA, Lemesle G, Armero S, et al. Relationship between plateletreactivity inhibition and non-CABG related major bleeding in patients undergoing125percutaneous coronary intervention // Thromb Res. – 2010. – Vol. 126. – P. 147–149.137.Nakamura K, Goto F, Ray WA, et al. Interethnic differences in geneticpolymorphism of debrisoquine and mephenytoin hydroxylation between Japaneseand Caucasian populations // Clin Pharmacol Ther. – 1985.
– Vol. 38. – P. 402–408.138.Pare G, Mehta SR, Yusuf S, et al. Effects of CYP2C19 genotype onoutcomes of clopidogrel treatment // N Engl J Med. – 2010. – Vol. 363. – P. 1704–1714.139.Park SH, Kim W, Park CS, et al. A comparison of clopidogrelresponsiveness in patients with versus without chronic renal failure // Am J Cardiol.– 2009. – Vol. 104. – P. 1292–1295.140.Park Y, Jeong YH, Tantry US, et al.
Accelerated platelet inhibition byswitching from atorvastatin to a non-CYP3A4-metabolized statin in patients withhigh platelet reactivity (ACCEL-STATIN) study // Eur Heart J. – 2012. – Vol. 33.– P. 2151–2162.141.Parker RS, Sontag TJ, Swanson JE, et al. Discovery, characterization, andsignificance of the cytochrome P450 omega-hydroxylase pathway of vitamin Ecatabolism // Ann N Y Acad Sci. – 2004.
– Vol. 1031. – P. 13-21.142.Parodi G, Bellandi B, Venditti F, et al. Residual platelet reactivity,bleedings, and adherence to treatment in patients having coronary stentimplantation treated with prasugrel // Am J Cardiol. – 2012. – Vol. 109. – P. 214–218.143.Parodi G, Marcucci R, Valenti R, al. High residual platelet reactivity afterclopidogrel loading and long-term cardiovascular events among patients with acutecoronary syndromes undergoing PCI // JAMA.
– 2011. – Vol. 306. – P. 1215-1223.126144.Parodi G, Valenti R, Bellandi B, et al. Comparison of prasugrel andticagrelor loading doses in ST-segment elevation myocardial infarction patients:RAPID (Rapid Activity of Platelet Inhibitor Drugs) primary PCI study // J Am CollCardiol. – 2013. – Vol. 61. – P. 1601–1606.145.Patti G, Pasceri V, Vizzi V, et al. Usefulness of platelet response toclopidogrel by point-of-care testing to predict bleeding outcomes in patientsundergoing percutaneous coronary intervention (from the Antiplatelet Therapy forReduction of Myocardial Damage During Angioplasty-Bleeding study) // Am JCardiol. – 2011. – Vol.
107. – P. 995–1000.146.Pedersen RS, Brasch-Andersen C, Sim SC, et al. Linkage disequilibriumbetween the CYP2C19*17 allele and wildtype CYP2C8 and CYP2C9 alleles:identification of CYP2C haplotypes in healthy Nordic populations // Eur J ClinPharmacol. – 2010. – Vol. 66. – P. 1199-1205.147.Pereillo JM, Maftouh M, Andrieu A, et al. Structure and stereochemistry ofthe active metabolite of clopidogrel // Drug Metab Dispos. – 2002. – Vol. 30. – P.1288–1295.148.Pettersen AÅ, Seljeflot I, Abdelnoor M, et al. High on aspirin plateletreactivity and clinical outcome in patients with stable coronary artery disease:results from ASCET (Aspirin Nonresponsiveness and Clopidogrel Endpoint Trial)// J Am Heart Assoc.















