Pharmacogenetics individual genetic adverse reactions

Other such enzyme deficiencies have been revealed through an individual s adverse reaction to drugs. More than 90% of Orientals are genetically rapid N-acetylators of isoniazid (6.12), whereas only 40% of black or white citizens of the United States showed this trait (Kalow, 1962). Rapid acetylators produce acetylhydrazine, which can cause liver damage. The same inheritance controls the acetylation (deactivation) of the sulphonamide antibacterials. The rise of intraocular pressure when glucocorticoids are placed in the eye is another pharmacogenetic effect. Low and high responses are shown by 66% and 5%, respectively, of a sample white population. 

Many ongoing clinical trials for efficacy and toxicity of new pharmaceutical products or new indications for previously developed pharmaceuticals have employed pharmacogenetic testing. Thus it is anticipated that pharmacogenetic guidelines and possibly tests will be simultaneously released to market with the pharmaceutical. In addition, medications that were previously removed from development because of adverse reactions may be reconsidered if a genetic test can be demonstrated to identify individuals at high risk for ADRs. 

Antipsychotics are the mainstay treatment for schizophrenia. There is large variability between individuals in their response to antipsychotics, both in efficacy and adverse effects of treatment. While the source of interindividual variability in antipsychotic response is not completely understood, genetics is a major contributing factor. The identification of pharmacogenetic markers that predict antipsychotic efficacy and adverse reactions is a growing area of research, and holds the potential to replace the current trial-and-error approach to treatment selection in schizophrenia with a personalized medicine approach. 

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