Pharmacogenomics can show what your bodymakes of a drug
药物基因组学能够揭示你的身体是如何利用药物的
That provides safer, more effectiveprescriptions
从而为你提供更安全、有效的处方
Doctors have long appreciated that the samedose of medicine will not necessarily have the same effect on differentpatients. Today they are able to predict how patients will respond to hundredsof drugs.
医生们早就认识到,相同剂量的药物未必能对不同患者产生相同的效果。如今,人们已经能够预测成百上千种药物作用于不同患者可能出现的药物反应了。
One of the ways in which people differbiologically is in how they metabolise drugs, a process largely dependent onenzymes in the liver that can vary a lot from person to person, and which aregenetically determined.
人与人之所以会在生物学上存在差异,原因之一在于药物代谢过程,其在很大程度上依赖于肝脏中的酶,人与人之间酶的差异很大,而酶是由基因决定的。
Differences in enzymes can lead twopatients with the same disease, and the same treatment, to end up with afive-fold difference in the amount of working drug molecules in their blood.
对于两名患有相同疾病、接受相同治疗的患者,酶的差异最终会导致他们血液中起作用的药物分子的数量相差五倍。
Sometimes such differences will mean thatthe drug is not circulating at a high enough level to work. Sometimes it iscirculating at too high a level and causing toxic side-effects. Thoughside-effects sound peripheral they are a huge medical problem. In Britain 6.5%of hospital admissions are related to adverse drug reactions.
这种差异意味着,药物有时会因转化水平过低而无法发挥药效,有时则会因转化水平过高而产生毒副作用。虽然副作用听起来好像无关紧要,但这其实是一个巨大的医学问题。在英国,6.5%的住院患者存在药物不良反应。
The study of how genes affect anindividual’s response to drugs is known as pharmacogenetics, and it isflourishing. The NHS in Britain is looking at applying pharmacogenetic tests tothe treatment of 65 different medical conditions within the next few years.
药物基因学是研究基因如何影响个体药物反应的一门学科,这一学科目前正在蓬勃发展。英国国家医疗服务体系正在考虑在未来几年内对65种不同疾病的治疗采取药物遗传测试。
One example of the technique’s potential isfound with warfarin, a commonly used blood thinner that has what doctors call a“narrow therapeutic window”: the distance between a level in the blood too lowto do good and a level too high for safety is small.
被医生们称为“窄治疗指数药物”的常用抗凝剂华法林正是证明该技术潜力的一个例子:它在血液中的含量过低则不起作用,过高则不安全,其中间范围很窄。
Variations in an enzyme gene called CYP2C9,which allow warfarin to stay in the blood for longer, are quite common in whiteEuropeans and Americans. This makes it harder to find the best therapeutic doseand increases the likelihood of adverse effects such as bleeding on the brain.Complications with warfarin cause about one-third of emergency hospital visitsfor older Americans.
酶基因 CYP2C9 的变异在欧美白人中很普遍,而这一基因的变异会使华法林在血液中维持的时间更长。这不仅使最佳治疗剂量更难被把握了,而且还会增加脑出血等副作用发生的可能性。美国大约三分之一的老年人急诊就医正是由于华法林并发症。
Part of the problem with warfarin is thatfor a long time there was no real substitute, so it was used despite itsdrawbacks. The various selective serotonin-reuptake inhibitors used to treatdepression offer a different challenge. Both their effectiveness and theirside-effects are influenced by enzymes produced in the liver.
华法林的问题在一定程度上是由于人们长期以来没能找到合适的替代药,因此尽管它存在缺点,却仍然在被使用。但用于治疗抑郁症的各种选择性血清素再吸收抑制剂则有所不同了。这些药物的有效性和副作用均受到肝脏所产生的酶的影响。
A test produced by Myriad, agenetic-testing company, makes it possible to look at the genes for suchenzymes before an antidepressant is prescribed and appears to limitside-effects and improve clinical outcomes.
基因检测公司 Myriad 能够在医生开处方之前对患者体内的这些酶进行检测,从而让人们能够选择副作用轻、临床效果好的药物。
注:双语全文源自经济学人
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