Pharmacogenetics of anti-TNF treatment in patients with rheumatoid arthritis.
SourcePharmacogenomics, 8, 7, (2007), pp. 761-773
Article / Letter to editor
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Scanning Probe Microscopy
SubjectDCN 1: Perception and Action; DCN 2: Functional Neurogenomics; EBP 1: Determinants in Health and Disease; IGMD 3: Genomic disorders and inherited multi-system disorders; N4i 1: Pathogenesis and modulation of inflammation; N4i 4: Auto-immunity, transplantation and immunotherapy; NCMLS 1: Immunity, infection and tissue repair; NCMLS 1: Infection and autoimmunity; NCMLS 6: Genetics and epigenetic pathways of disease; Scanning Probe Microscopy; UMCN 4.2: Chronic inflammation and autoimmunity; UMCN 5.1: Genetic defects of metabolism
TNF-blocking strategies are widely used in the treatment of rheumatoid arthritis (RA). Three anti-TNF agents are registered for use in RA: etanercept, infliximab and adalimumab. Although anti-TNF therapy is very effective in controlling disease activity and slowing down radiological damage, prolonged response is only seen in approximately 70% of the patients. The causes for nonresponse in the remaining patients have not yet been elucidated. Pharmacogenetic studies focusing on genes involved in RA etiology (and/or progression) and in the pharmacokinetics of TNF-blocking agents have identified markers associated with anti-TNF treatment outcome. In the future, more exhaustive, less hypothesis-driven search strategies are expected to discover additional markers. Identification of these markers might be viewed as the first step towards tailored TNF-blocking therapy for patients with RA. Nevertheless, replication and large prospective studies will be needed to demonstrate the validity of the identified genetic markers before implementation into daily clinical practice.
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