Pharmacogenomics: Difference between revisions
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imported>Robert Badgett |
imported>Robert Badgett |
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Among drugs frequently cited in adverse drug reactions, 60% are metabolized by enzymes with genetic variations in metabolism. 7% to 22% of randomly selected have such variation.<ref name="pmid11710893">{{cite journal |author=Phillips KA, Veenstra DL, Oren E, Lee JK, Sadee W |title=Potential role of pharmacogenomics in reducing adverse drug reactions: a systematic review |journal=JAMA |volume=286 |issue=18 |pages=2270–9 |year=2001 |pmid=11710893 |doi=}}</ref> | Among drugs frequently cited in adverse drug reactions, 60% are metabolized by enzymes with genetic variations in metabolism. 7% to 22% of randomly selected have such variation.<ref name="pmid11710893">{{cite journal |author=Phillips KA, Veenstra DL, Oren E, Lee JK, Sadee W |title=Potential role of pharmacogenomics in reducing adverse drug reactions: a systematic review |journal=JAMA |volume=286 |issue=18 |pages=2270–9 |year=2001 |pmid=11710893 |doi=}}</ref> | ||
Examples include: | |||
* The SLCO1B1 Variants and statin-induced myopathy<ref name="pmid18650507"> The SEARCH Collaborative Group. (2008) [http://content.nejm.org/cgi/content/full/NEJMoa0801936 SLCO1B1 Variants and Statin-Induced Myopathy]. New Eng J Med. PMID 18650507</ref> | |||
* [[Toxic epidermal necrolysis]] (TEN) and [[Stevens-Johnson syndrome]] (SJS) patients with [[HLA]]-B*1502 allele who take [[carbamazepine]]<ref>Anonymous. [http://www.fda.gov/cder/genomics/genomic_biomarkers_table.htm Table of Valid Genomic Biomarkers in the Context of Approved Drug Labels]. U.S. Food and Drug Administration</ref>. | |||
==Drug efficacy== | ==Drug efficacy== | ||
Revision as of 12:26, 24 July 2008
Pharmacogenomics, or pharmacogenetics, is the "branch of genetics which deals with the genetic variability in individual responses to drugs and drug metabolism (biotransformation)."[1]
Drug toxicity
Among drugs frequently cited in adverse drug reactions, 60% are metabolized by enzymes with genetic variations in metabolism. 7% to 22% of randomly selected have such variation.[2]
Examples include:
- The SLCO1B1 Variants and statin-induced myopathy[3]
- Toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS) patients with HLA-B*1502 allele who take carbamazepine[4].
Drug efficacy
Heart failure and hypertension may be an examples were there are racial variations in responses to drugs. Presumably these variations are due to pharmacogenomics.
References
- ↑ Anonymous. Pharmacogenetics. National Library of Medicine. Retrieved on 2008-01-22.
- ↑ Phillips KA, Veenstra DL, Oren E, Lee JK, Sadee W (2001). "Potential role of pharmacogenomics in reducing adverse drug reactions: a systematic review". JAMA 286 (18): 2270–9. PMID 11710893. [e]
- ↑ The SEARCH Collaborative Group. (2008) SLCO1B1 Variants and Statin-Induced Myopathy. New Eng J Med. PMID 18650507
- ↑ Anonymous. Table of Valid Genomic Biomarkers in the Context of Approved Drug Labels. U.S. Food and Drug Administration
External links
- http://www.pharmgkb.org/ - Pharmacogenetics Research Network and Database (Standford University)
- http://medicine.iupui.edu/flockhart/ - Cytochrome P450 interactions (Indiana University Department of Medicine)
- http://www.fda.gov/cder/genomics/genomic_biomarkers_table.htm - Table of Valid Genomic Biomarkers in the Context of Approved Drug Labels. U.S. Food and Drug Administration.