Accès gratuit
Numéro
Med Sci (Paris)
Volume 26, Numéro 6-7, Juin–Juillet 2010
Page(s) 641 - 646
Section M/S revues
DOI https://doi.org/10.1051/medsci/2010266-7641
Publié en ligne 15 juin 2010
  1. Uetrecht J. Idiosyncratic drug reactions: current understanding. Annu Rev Pharmacol Toxicol ; 47 : 513-39.
  2. Weber WW. The molecular basis of hereditary acetylation polymorphisms. DrugMetab Dispos 1986 ; 14 : 377-81.
  3. Bourdi M, Larrey D, Nataf J, et al. Anti-liver endoplasmic reticulum autoantibodies are directed against human cytochrome P-450IA2. A specific marker of dihydralazine-induced hepatitis. J Clin Invest 1990 ; 85 : 1967-73.
  4. Park BK, Pirmohamed M, Kitteringham NR. Role of drug disposition in drug hypersensitivity: a chemical, molecular, and clinical perspective. Chem Res Toxicol 1998 ; 11 : 969-88.
  5. Gallucci S, Lolkema M, Matzinger P. Natural adjuvants: endogenous activators of dendritic cells. Nat Med 1999 ; 5 : 1249-55.
  6. Pichler WJ. Pharmacological interaction of drugs with antigen-specific immune receptors: the p-i concept. Curr Opin Allergy Clin Immunol 2002 ; 2 : 301-5.
  7. Demoly P, Hillaire-Buys D, Raison-Peyron N, et al. Identifier et comprendre les allergies médicamenteuses. Med sci (Paris) 2003; 19 : 327-36.
  8. Harrill AH, Rusyn I. Systems biology and functional genomics approaches for the identification of cellular responses to drug toxicity. Expert Opin Drug Metab Toxicol 2008; 4 : 1379-89.
  9. Wadelius M, Chen LY, Lindh JD, et al. The largest prospective warfarin-treated cohort supports genetic forecasting. Blood 2009 ; 113 : 784-92.
  10. Caldwell MD, Awad T, Johnson JA, et al. CYP4F2 genetic variant alters required warfarin dose. Blood ; 111 : 4106-12.
  11. Takeuchi F, McGinnis R, Bourgeois S, et al. A genome-wide association study confirms VKORC1, CYP2C9, and CYP4F2 as principal genetic determinants of warfarin dose. PLoS Genet 2009 ; 5 : e1000433.
  12. Borgiani P, Ciccacci C, Forte V, et al. CYP4F2 genetic variant (rs2108622) significantly contributes to warfarin dosing variability in the Italian population. Pharmacogenomics 2009 ; 10 : 261-6.
  13. Hetherington S, McGuirk S, Powell G, et al. Hypersensitivity reactions during therapy with the nucleoside reverse transcriptase inhibitor abacavir. Clin Ther 2001 ; 23 : 1603-14.
  14. Hughes AR, Spreen WR, Mosteller M, et al. Pharmacogenetics of hypersensitivity to abacavir: from PGx hypothesis to confirmation to clinical utility. Pharmacogenomics J 2008 ; 8 : 365-74.
  15. Nelson MR, Bacanu SA, Mosteller M, et al. Genome-wide approaches to identify pharmacogenetic contributions to adverse drug reactions. Pharmacogenomics J 2009 ; 9 : 23-33.
  16. Hughes S, Hughes A, Brothers C, et al. PREDICT-1 (CNA106030): the first powered, prospective trial of pharmacogenetic screening to reduce drug adverse events. Pharm Stat 2008 ; 7 : 121-9.
  17. Kindmark A, Jawaid A, Harbron CG, et al. Genome-wide pharmacogenetic investigation of a hepatic adverse event without clinical signs of immunopathology suggests an underlying immune pathogenesis. Pharmacogenomics J 2008 ; 8 : 186-95.
  18. Thome-Kromer B, Bonk I, Klatt M, et al. Toward the identification of liver toxicity markers: a proteome study in human cell culture and rats. Proteomics 2003 ; 3 : 1835-62.
  19. Bandara LR, Kelly MD, Lock EA, Kennedy S. A correlation between a proteomic evaluation and conventional measurements in the assessment of renal proximal tubular toxicity. Toxicol Sci 2003 ; 73 : 195-206.
  20. Séguin B, Boutros PC, Li X, Okey AB, Uetrecht JP. Gene expression profiling in a model of D-penicillamine-induced autoimmunity in the Brown Norway rat: predictive value of early signs of danger. Chem Res Toxicol 2005 ; 18 : 1 193-202.
  21. Lu W, Li X, Uetrecht JP. Changes in gene expression induced by carbamazepine and phenytoin: testing the danger hypothesis. J Immunotoxicol 2008 ; 5 : 107-13.
  22. Pacitto SR, Uetrecht JP, Boutros PC, Popovic M. Changes in gene expression induced by tienilic Acid and sulfamethoxazole: testing the danger hypothesis. J Immunotoxicol 2007 ; 4 : 253-66.
  23. Waring JF, Liguori MJ, Luyendyk JP, et al. Microarray analysis of lipopolysaccharide potentiation of trovafloxacin-induced liver injury in rats suggests a role for proinflammatory chemokines and neutrophils. J Pharmacol Exp Ther 2006 ; 316 : 1080-7.
  24. Shaw PJ, Hopfensperger MJ, Ganey PE, Roth RA. Lipopolysaccharide and trovafloxacin coexposure in mice causes idiosyncrasy-like liver injury dependent on tumor necrosis factor-alpha. Toxicol Sci 2007 ; 100 : 259-66.
  25. Shaw PJ, Ditewig AC, Waring JF, et al. Coexposure of mice to trovafloxacin and lipopolysaccharide, a model of idiosyncratic hepatotoxicity, results in a unique gene expression profile and interferon gamma-dependent liver injury. Toxicol Sci 2009 ; 107 : 270-80.
  26. Kier LD, Neft R, Tang L, et al. Applications of microarrays with toxicologically relevant genes (tox genes) for the evaluation of chemical toxicants in Sprague Dawley rats in vivo and human hepatocytes in vitro. Mutat Res 2004 ; 549 : 101-13.
  27. Cosgrove BD, King BM, Hasan MA, et al. Synergistic drug-cytokine induction of hepatocellular death as an in vitro approach for the study of inflammation-associated idiosyncratic drug hepatotoxicity. Toxicol Appl Pharmacol 2009 ; 237 : 317-30.
  28. Luyendyk JP, Maddox JF, Cosma GN, et al. Ranitidine treatment during a modest inflammatory response precipitates idiosyncrasy-like liver injury in rats. J Pharmacol Exp Ther 2003 ; 307 : 9-16.
  29. Le Bonniec B. La cible de la warfarine identifiée. Med Sci (Paris) 2004 ; 20 : 512-4.

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