title: New treatment targets for axial spondyloarthritis.
abstract: Axial spondyloarthritis (axSpA) patients can be divided into those with structural damage in the SI joint visible on X-rays, termed radiographic axSpA or AS, and those in an earlier phase of the disease, without structural damage in the SI joint, termed non-radiographic axSpA. TNF-blockers have been shown to be highly effective in the treatment of active axSpA. Interestingly, conventional DMARDs and also non-TNF-blocker biologics targeting IL-1, IL-6 and T cells (abatacept) are not effective. Recent interest has focused on the cytokines IL-23 and IL-17 as potential treatment targets in axSpA. An open-label trial with ustekinumab showed a good efficacy in AS patients. Two placebo-controlled phase 3 trials with a mAb blocking IL-17, secukinumab, showed a good reduction in disease activity, similar to that shown for TNF blockers. Probably triggered by inflammation, new bone formation is another hallmark in AS and a potentially important treatment target. However, a previously reported inhibitory effect of NSAID treatment could not be confirmed in a recent NSAID trial.
authors.affiliation: Department of Medicine I, Rheumatology, Charité, Campus Benjamin Franklin, Berlin, Germany joachim.sieper@charite.de.
authors.forename: Joachim
authors.initials: J
authors.lastname: Sieper
mesh_terms: D000069594:Abatacept / Q000627:therapeutic use; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein / Q000627:therapeutic use; D020381:Interleukin-17 / Q000276:immunology; D053759:Interleukin-23 / Q000276:immunology; D058990:Molecular Targeted Therapy; D000069283:Rituximab / Q000627:therapeutic use*; D025242:Spondylarthropathies / Q000188:drug therapy / Q000276:immunology; D013167:Spondylitis, Ankylosing / Q000188:drug therapy* / Q000276:immunology; D013792:Thalidomide / Q000031:analogs & derivatives / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000276:immunology; D000069549:Ustekinumab / Q000627:therapeutic use*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D053590:Interleukin 1 Receptor Antagonist Protein; D020381:Interleukin-17; D053759:Interleukin-23; D014409:Tumor Necrosis Factor-alpha; D000069283:Rituximab; D013792:Thalidomide; D000069594:Abatacept; C555450:secukinumab; D000069549:Ustekinumab; C502936:tocilizumab; C505730:apremilast
keywords: IL-17–blockade; IL-23–blockade; ankylosing spondylitis; axial spondyloarthitis; biologics; small molecules