What will be the role of pharmacogenetics in evaluating drug safety and minimising adverse effects?

被引:32
作者
Ozdemir, V
Shear, NH
Kalow, W
机构
[1] Univ Toronto, Dept Pharmacol, Toronto, ON M5S 1A8, Canada
[2] Univ Toronto, Dept Psychiat, Toronto, ON M5S 1A8, Canada
[3] Univ Toronto, Sunnybrook & Womens Hlth Sci Ctr, Div Clin Pharmacol, Toronto, ON M5S 1A8, Canada
关键词
D O I
10.2165/00002018-200124020-00001
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
In the US, adverse drug reactions (ADRs) rank between the fourth to sixth leading cause of death, ahead of pneumonia and diabetes mellitus. An important reason for the high incidence of serious and fatal ADRs is that the existing drug development paradigms do not generate adequate information on the mechanistic sources of marked variability in pharmacokinetics and pharmacodynamics of new therapeutic candidates, precluding treatments from being tailored for individual patients. Pharmacogenetics is the study of the hereditary basis of person-to-person variations in drug response. The focus of pharmacogenetic investigations has traditionally been unusual and extreme drug responses resulting from a single gene effect. The Human Genome Project and recent advancements in molecular genetics now present an unprecedented opportunity to study all genes in the human genome, including genes for drug metabolism, drug targets and postreceptor second messenger machinery, in relation to variability in drug safety and efficacy. In addition to sequence variations in the genome, high throughput and genome-wide transcript profiling for differentially regulated mRNA species before and during drug treatment will serve as important tools to uncover novel mechanisms of drug action. Pharmacogenetic-guided drug discovery and development represent a departure from the conventional approach which markets drugs for broad patient populations, rather than smaller groups of patients in whom drugs may work more optimally. Pharmacogenetics provides a rational framework to minimise the uncertainty in outcome of drug therapy and clinical trials and thereby should significantly reduce the risk of drug toxicity.
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页码:75 / 85
页数:11
相关论文
共 84 条
[1]  
Aklillu E, 1996, J PHARMACOL EXP THER, V278, P441
[2]   CYP2D6 inhibition by fluoxetine, paroxetine, sertraline, and venlafaxine in a crossover study: Intraindividual variability and plasma concentration correlations [J].
Alfaro, CL ;
Lam, YWF ;
Simpson, J ;
Ereshefsky, L .
JOURNAL OF CLINICAL PHARMACOLOGY, 2000, 40 (01) :58-66
[3]  
[Anonymous], 1994, Adv Drug Res
[4]   Neurotransmitter-related genes and antipsychotic response: pharmacogenetics meets psychiatric treatment [J].
Arranz, MJ ;
Kerwin, RW .
ANNALS OF MEDICINE, 2000, 32 (02) :128-133
[5]   Association of the MscI polymorphism of the dopamine D3 receptor gene with tardive dyskinesia in schizophrenia [J].
Basile, VS ;
Masellis, M ;
Badri, F ;
Paterson, AD ;
Meltzer, HY ;
Lieberman, JA ;
Potkin, SG ;
Macciardi, F ;
Kennedy, JL .
NEUROPSYCHOPHARMACOLOGY, 1999, 21 (01) :17-27
[6]   CRITERIA FOR THE CHOICE AND DEFINITION OF HEALTHY-VOLUNTEERS AND OR PATIENTS FOR PHASE-I AND PHASE-II STUDIES IN DRUG DEVELOPMENT - COMMENTARY ON AN ACTION FOR COOPERATIVE RESEARCH [J].
BECHTEL, PR ;
ALVAN, G .
EUROPEAN JOURNAL OF CLINICAL PHARMACOLOGY, 1989, 36 (06) :549-550
[7]   Polymorphic drug oxidation - Relevance to the treatment of psychiatric disorders [J].
Bertilsson, L ;
Dahl, ML .
CNS DRUGS, 1996, 5 (03) :200-223
[8]   GEOGRAPHICAL INTERRACIAL DIFFERENCES IN POLYMORPHIC DRUG OXIDATION - CURRENT STATE OF KNOWLEDGE OF CYTOCHROMES P450 (CYP) 2D6 AND 2C19 [J].
BERTILSSON, L .
CLINICAL PHARMACOKINETICS, 1995, 29 (03) :192-209
[9]   Drug-metabolizing enzymes and therapeutic drug monitoring in psychiatry [J].
Brosen, K .
THERAPEUTIC DRUG MONITORING, 1996, 18 (04) :393-396
[10]   Extension of a pilot study: Impact from the cytochrome P450 2D6 polymorphism on outcome and costs associated with severe mental illness [J].
Chou, WH ;
Yan, FX ;
de Leon, J ;
Barnhill, J ;
Rogers, T ;
Cronin, M ;
Pho, M ;
Xiao, V ;
Ryder, TB ;
Liu, WW ;
Teiling, C ;
Wedlund, PJ .
JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY, 2000, 20 (02) :246-251