title: Biologic therapies for spondyloarthritis: what is new?
abstract: The course of axial spondyloarthritis (axSpA), including ankylosing spondylitis (AS), is strongly influenced by the degree of disease activity over time, which is mainly based on inflammation, and by the impairment of function, which is based on structural damage-mainly, new bone formation-and inflammation. In AS, nonsteroidal anti-inflammatory agents are currently recommended as the first choice of medical therapy, and there is also a clear role for regular exercise and physiotherapy in order to preserve and prevent loss of spinal mobility. For patients who have insufficiently responded to conventional medications, there are now four biologics approved for the treatment of patients with active AS in many countries, all directed against TNFα: infliximab, etanercept, adalimumab, and golimumab; studies with certolizumab are currently ongoing. Several studies with patients classified as nonradiographic axSpA have also shown a good response to TNF blockers; in patients with early disease and high CRP levels, the response rates were even better. Long-term studies with TNF blockers have shown declining retention rates over time but sustained clinical efficacy in the patients who remained on treatment. States of drug-free remission are rarely reached and only for relatively short periods of time. More studies including magnetic resonance imaging (MRI) are needed to further examine the lack of effect of anti-TNF treatment on radiographic progression in the axial skeleton. Whether the effect of an early intervention with biologics will prevent the development of bone growth in patients with nonradiographic axial SpA remains to be seen. Biologics other than TNF blockers are currently not recommended for the treatment of patients with axSpA, because of insufficient evidence of clinically relevant efficacy. The anti-IL-17a antibody secukinumab may be efficacious, on the basis of a proof-of-concept trial. Finally, first data on biosimilars of TNF blockers have recently been presented.
authors.affiliation: Rheumazentrum Ruhrgebiet, Ruhr-University Bochum, Landgrafenstr. 15, 44652 Herne, Germany.
authors.forename: Xenofon
authors.initials: X
authors.lastname: Baraliakos
authors.forename: Juergen
authors.initials: J
authors.lastname: Braun
mesh_terms: D000068879:Adalimumab; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D000068582:Certolizumab Pegol; D018450:Disease Progression; D000068800:Etanercept; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000627:therapeutic use; D007074:Immunoglobulin G / Q000627:therapeutic use; D007249:Inflammation; D000069285:Infliximab; D011092:Polyethylene Glycols / Q000627:therapeutic use; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012219:Rheumatology / Q000639:trends; D013167:Spondylitis, Ankylosing / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D007140:Immunoglobulin Fab Fragments; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D011092:Polyethylene Glycols; C529000:golimumab; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept; D000068582:Certolizumab Pegol