title: New evidence on the management of spondyloarthritis.
abstract: Non-steroidal anti-inflammatory drugs (NSAIDs) are the first-line treatment for patients with symptomatic axial spondyloarthritis (SpA), who seem to respond best if treated early in the course of disease. The effect of NSAIDs on radiographic disease progression is less clear. Conventional disease-modifying antirheumatic drugs (DMARDs) are not recommended in the treatment of axial SpA, either alone or in combination with TNF blockers. Patients with nonradiographic axial SpA (nr-axSpA) seem to respond as well to TNF blockers as do patients with radiographic axial SpA (ankylosing spondylitis (AS)). However, patients with nr-axSpA should, in addition to a high severity of symptoms, also have objective signs of inflammation, detectable by MRI or by C-reactive protein testing, to be treated with TNF blockers. Whether early TNF-blocker treatment can retard new bone formation needs clarification. In clinical trials, anti-IL-17 agents and TNF blockers showed similar efficacy in patients with AS. The potential of IL-23 blockade for treatment of axial SpA needs to be further investigated. Treatment options for peripheral SpA have been much less thoroughly investigated than those for axial SpA. However, some data indicate that TNF blockers are effective for treating peripheral arthritis, enthesitis and dactylitis, the typical manifestations of peripheral SpA.
authors.affiliation: Rheumatology, Medical Department I, Campus Benjamin Franklin, Charité Universitätsmedizin Berlin, Hindenburgdamm 30, 12203 Berlin, Germany.
authors.forename: Joachim
authors.initials: J
authors.lastname: Sieper
authors.affiliation: Rheumatology, Medical Department I, Campus Benjamin Franklin, Charité Universitätsmedizin Berlin, Hindenburgdamm 30, 12203 Berlin, Germany.
authors.forename: Denis
authors.initials: D
authors.lastname: Poddubnyy
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*; D050071:Bone Density Conservation Agents / Q000627:therapeutic use*; D002097:C-Reactive Protein / Q000276:immunology; D004164:Diphosphonates / Q000627:therapeutic use; D019468:Disease Management; D005938:Glucocorticoids / Q000627:therapeutic use*; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein / Q000627:therapeutic use; D008279:Magnetic Resonance Imaging; D011859:Radiography; D025241:Spondylarthritis / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000276:immunology; D013167:Spondylitis, Ankylosing / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D000069549:Ustekinumab / Q000627:therapeutic use
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D050071:Bone Density Conservation Agents; D004164:Diphosphonates; D005938:Glucocorticoids; D053590:Interleukin 1 Receptor Antagonist Protein; D014409:Tumor Necrosis Factor-alpha; D000069594:Abatacept; D002097:C-Reactive Protein; C555450:secukinumab; D000069549:Ustekinumab; C502936:tocilizumab