title: Clinical parameters and biomarkers for anti-TNF treatment prognosis in rheumatoid arthritis patients.
abstract: Tumor necrosis factor (TNF) plays a pivotal role in the pathogenesis of rheumatoid arthritis (RA). This finding has led to the development of TNF blockers for RA treatment. However, response to these therapies is heterogeneous with success in only two thirds of patient. Some clinical aspects useful in the attempt to predict the response to TNF inhibitors is the promptness and the magnitude of the response at the first weeks and a low basal disease activity, while comorbidities, tobacco, glucocorticoids treatment, and high basal radiological score correlate with a poorer response. The role of TNF promoter polymorphisms in clinical response to anti-TNF therapies is controversial. A correlation between the presence of high baseline titers of rheumatoid factor (RF) and decreased response to anti-TNF treatment has been reported. Most studies show decreased RF titers during anti-TNF treatment mainly in patients who responded to treatment. There is no consensus about the usefulness of basal anti-citrullinated protein antibodies (ACPA) levels, and a decrease in ACPA titers as predictor of clinical response to anti-TNF therapy. Despite some promising markers identified to fulfill this role, currently the predictive value of single markers seems not strong enough to predict treatment response in an individual RA patient.
authors.affiliation: Department of Medicine, Clinical Hospital University of Chile, San Pío X, N 2460, Off 607, Providencia, Santiago, Chile, mcuchaco@gmail.com.
authors.forename: Miguel
authors.initials: M
authors.lastname: Cuchacovich
authors.forename: Daniel
authors.initials: D
authors.lastname: Bueno
authors.forename: Rodrigo
authors.initials: R
authors.lastname: Carvajal
authors.forename: Nicolás
authors.initials: N
authors.lastname: Bravo
authors.forename: Juan Carlos
authors.initials: JC
authors.lastname: Aguillón
authors.forename: Diego
authors.initials: D
authors.lastname: Catalán
authors.forename: Lilian
authors.initials: L
authors.lastname: Soto
mesh_terms: D000068879:Adalimumab; D000911:Antibodies, Monoclonal / Q000008:administration & dosage; D061067:Antibodies, Monoclonal, Humanized / Q000008:administration & dosage; D001172:Arthritis, Rheumatoid / Q000175:diagnosis* / Q000188:drug therapy* / Q000235:genetics; D002097:C-Reactive Protein / Q000378:metabolism; D000068582:Certolizumab Pegol; D016207:Cytokines / Q000378:metabolism; D000068800:Etanercept; D005938:Glucocorticoids / Q000008:administration & dosage / Q000627:therapeutic use; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000008:administration & dosage; D007074:Immunoglobulin G / Q000008:administration & dosage; D000069285:Infliximab; D010597:Pharmacogenetics; D011092:Polyethylene Glycols / Q000008:administration & dosage; D011110:Polymorphism, Genetic; D011237:Predictive Value of Tests; D011379:Prognosis; D011401:Promoter Regions, Genetic; D018124:Receptors, Tumor Necrosis Factor / Q000008:administration & dosage; D014026:Nicotiana / Q000737:chemistry; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D016207:Cytokines; D005938:Glucocorticoids; D007140:Immunoglobulin Fab Fragments; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D011092:Polyethylene Glycols; D002097:C-Reactive Protein; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept; D000068582:Certolizumab Pegol
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