Traditionally, prescribing has been on a one-size-fits-all basis, with standardised doses of medicines given to all patients. Personalised medicine offers the promise of more effective therapy with fewer side effects by better understanding the genetic causes of disease and different individual reactions to drug treatment. Genetic variants in the genes encoding the cytochrome p450 enzymes, which activate or degrade many commonly used drugs, are increasingly being linked to variations in response to medicines. Separate reports by Collet et al, Mega et al and Simon et al highlight the importance of CYP2C19 polymorphisms in responsiveness to clopidogrel, an oral antiplatelet agent that is commonly prescribed after heart attacks to reduce the likelihood of subsequent cardiovascular events. Clopidogrel is a pro-drug that is inactive until it is metabolised in the liver by cytochrome P450 enzymes, including CYP2C19. All studies found that individuals with loss-of-function variants of CYP2C19 were more likely to die or experience major adverse cardiovascular events than individuals with fully functional CYP2C19.
The FDA and the International Serious Adverse Events Consortium have also recently released the first data on the genetics associated with serious drug-induced skin rashes, such as Stevens-Johnson syndrome and toxic epidermal necrolysis. Understanding which patients are likely to suffer severe reactions to commonly prescribed drugs should reduce the incidence of these life-threatening conditions.