Spondyloarthritis (SpA) can be split into axial (ax) and peripheral SpA, according to the predominant clinical presentation. Major progresses have been made over the last decade defining optimal treatment for axial SpA while there are still only limted data how to treat peripheral SpA optimally, with the exception of psoriatic arthritis (PsA). The term axSpA covers both patients with non-radiographic axial SpA (nr-axSpA) and patients with radiographic axSpA (=ankylosing spondylitis, AS). A correct diagnosis is an important first step for developing a treatment strategy because non-inflammatory causes of chronic back pain, such as degenerative spine disease, will not respond to anti-inflammatory therapies. There are only two types of drugs which are highly effective in the treatment of axSpA: NSAIDs and TNF-blockers, glucocorticoids might work if given in a high dosis. Most treatment data are available for AS, but more recent studies indicate that the response to these drugs is similar in patients with nr-axSpA. NSAIDs are, together with physical therapy, the first line of treatment and a full dosis of an NSAID should be given if demanded by the symptoms. If patients are treated in the first three years of their disease remission rates up to 35% can be expected if treated with an NSAID. If NSAIDs fail TNF-blocker therapy would be the next step. Currently there are five TNF-blockers approved for the treatment of AS and two for the treatment of nr-axSpA. Elevated CRP, active inflammation on MRI and/or short disease duration are the best predictors for a good response to TNF-blocker therapy. Even if treated early with a TNF-blocker a TNF-blocker free remission can only be reached in up to 20%. However a dose reduction (or prolongation of the injection interval) is probably possible in a substantial proportion of patients. If TNF-blocker therapy fails a switch to another one would be the first option, especially in case of a secondary failure. There are currently no other approved (biologic) therapies for axSpA. However, therapies targeting the cytokines IL-23 (ustekinumab) or IL-17 (secukinumab) are currently the most promising. How to prevent best new bone formation and, in this context, with lonterm disability is currently still under debate. This can probably be achieved by early and/or longterm therapy with a TNF-blocker or by treatment with NSAIDs. Whether and how a combination of these two treatments should be used and which subgroup of patients benfits most from stopping progression of structural damage is a major focus of ongoing research. Only a few studies addressed so far the treatment of peripheral SpA, indicating that TNF-blockers but also some of the conventional DMARDs might work here. Studies performed so far in PsA investigated nearly exclusively patients with polyarthritic PsA, a manifestation not typically for peripheral SpA.
Disclosure of Interest None declared