Why
does the usual dose of medication work for a person while another individual
cannot give the expected response to the same drug? On the other hand, how come
half of the usual dose of an analgesic relieves an individual’s pain
immediately, as another man continue to suffer even after taking double dose?
Although a treatment method has been successfully used in majority of the
population for many years, why does the same therapy cause serious side effects
in another region of the world? Most presently approved therapies are not
effective in all patients. For example, 20-40% of patients with depression
respond poorly or not at all to antidepressant drug therapy. Many patients are
resistant to the effects of antiasthmatics and antiulcer drugs or drug treatment
of hyperlipidemia and many other diseases. The reason for all those is basically
interindividual differences in genomic structures of people, which are explained
in this chapter in terms of the systems and the most frequently used drugs in clinical
treatment.
Keywords: Adverse reactions, Carriers, Clinical pharmacology, Cytochrome P- 450 enzyme family, Drug response, Enzyme activity, Extensive metabolizer, Intermediate metabolizer, Metabolism, Optimal dosage, Personalized medicine, Pharmacodynamics, Pharmacogenetics, Pharmacogenomic biomarkers, Pharmacokinetics, Polymorphism, Poor metabolizer, Targeted treatment, Transporter molecules, Ultra-rapid metabolizer.
