Genomic medicine has raised many expectations with regard to individualized therapies. Drug response is a complex function of many genes interacting with environmental and behavioral factors. In addition, poor prescribing, interactions between drugs and an incomplete understanding of the metabolism of many drugs, which are administered simultaneously to treat concomitant morbidities, are leading causes of the occurrence of adverse drug reactions in chronic non-inflammatory and autoimmune rheumatic diseases. Symptomatic non-steroidal anti-inflammatory drugs, as well as disease-modifying drugs, are complicated by drop-outs (poor patient compliance) in a large percentage of patients. Even though intensive and careful monitoring is always clearly advisable, preliminary data suggest that typing of genes controlling the effects, metabolism and response of drugs might be of clinical utility to define the 'at-risk' genotype.

Pharmacogenetics/pharmacogenomics and antirheumatic drugs in rheumatology

De Santis, Maria;
2004-01-01

Abstract

Genomic medicine has raised many expectations with regard to individualized therapies. Drug response is a complex function of many genes interacting with environmental and behavioral factors. In addition, poor prescribing, interactions between drugs and an incomplete understanding of the metabolism of many drugs, which are administered simultaneously to treat concomitant morbidities, are leading causes of the occurrence of adverse drug reactions in chronic non-inflammatory and autoimmune rheumatic diseases. Symptomatic non-steroidal anti-inflammatory drugs, as well as disease-modifying drugs, are complicated by drop-outs (poor patient compliance) in a large percentage of patients. Even though intensive and careful monitoring is always clearly advisable, preliminary data suggest that typing of genes controlling the effects, metabolism and response of drugs might be of clinical utility to define the 'at-risk' genotype.
2004
Anti-Inflammatory Agents, Non-Steroidal
Antirheumatic Agents
Cyclooxygenase Inhibitors
Humans
Pharmacogenetics
Rheumatic Diseases
Rheumatology
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11699/68413
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