• Ulrike M Stamer and Frank Stüber.
• Department of Anesthesiology and Intensive Care Medicine, Rheinische Friedrich-Wilhelms-Universität, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany. ulrike.stamer@ukb.uni-bonn.de
• Curr Opin Anaesthesiol. 2007 Oct 1; 20 (5): 478-84.

Purpose Of ReviewGenomic variations influencing basal pain sensitivity, the likelihood of developing chronic pain diseases as well as the response to pharmacotherapy of pain are currently under investigation Here, we review examples of promising approaches to diagnose genetic predisposition from recently published studies.Recent FindingsCandidate genes such as those for catechol-O-methyltransferase, melanocortin-1 receptor, guanosine triphosphate cyclohydrolase and mu-opioid receptor have been intensively investigated, and associations were found with sensitivity to pain as well as with analgesic requirements in states of acute and chronic pain. In contrast, the impact of genetic variants of drug-metabolizing enzymes on the response to pharmacotherapy is generally well described. Polymorphisms of the cytochrome P450 enzymes influence the analgesic efficacy of codeine, tramadol, tricyclic antidepressants and nonsteroidal antiinflammatory drugs. Together with further candidate genes, they are major targets of ongoing research in order to identify associations between an individual's genetic profile and drug response (pharmacogenetics).SummaryThe article reviews recent studies on genetic variables influencing pain and pharmacotherapy. Examples of promising candidate genes have been intensively studied during recent years. Although the number of subjects investigated is often small, published data and current advances in genotyping and study design suggest valid and clinically relevant results to date and even more in the future.

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