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Annals of the Rheumatic Diseases 2004;63(Supplement 2 ):ii25-ii27; doi:10.1136/ard.2004.028217
Copyright © 2004 BMJ Publishing Group Ltd & European League Against Rheumatism.
Annals of the Rheumatic Diseases 2004;63:ii25-ii27
© 2004 by BMJ Publishing Group Ltd & European League Against Rheumatism

REPORT

Genetics

Pharmacogenetics in the rheumatic diseases

B N Cronstein

Correspondence to:
Correspondence to:
Professor B N Cronstein
New York University School of Medicine, 550 First Ave., New York, NY 10016; cronsb01@med.nyu.edu

Abbreviations: AICAR, aminoimidazolecarboxamidoribonucleotide; MTHFR, methylene tetrahydrofolate reductase; RA, rheumatoid arthritis; TPMT, thiopurine methyl transferase

Keywords: azathioprine; folic acid; methotrexate

The first 150 words of the full text of this article appear below.

One of the promises of the human genome project is individualised pharmacological therapy. An individual’s genetic type would be determined, and the resulting diseases which the person was susceptible to would be determined. In addition, the drugs to which an individual would respond well would be enumerated, and the drugs which were more likely to be toxic could be established. At present we are just beginning to determine those associations which would help us tailor an individual’s pharmacological therapy so as to maximise efficacy and minimise toxicity. In this report we review the considerations involved in determining the pharmacogenetic profile of any given drug and to review the current level of understanding of the association between genetic polymorphisms and drug toxicity/efficacy in rheumatology.

Establishing an association between genetic types and toxicity is perhaps an easier task to accomplish than understanding the association between a given genetic type and drug . . . [Full text of this article]


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