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Report of the 10th International Congress on Spondyloarthritides. Gent, Belgium 15-17 Sept, 2016

by Margaret Lewington

ABSTRACTS (some) of the lectures and posters are printed in :
“Clinical and Experimental RHEUMATOLOGY” Vol 34 no 4 2016 www.clinexprheumatol.org

Overview of the conference

The Gent SpA Congress has become the premier international research meeting focusing on all aspects of SpA. When looking at the program, even before the meeting commences, it is obvious that SpA research is blooming.

pic_Gent conference posterThe program for the meeting includes the latest advances in clinical and epidemiological research, genetics, immunology, bone biology and inflammation in the gut, skin and eye as well as in bone and joint. Internationally recognised specialists provide state of the art lectures about what is currently ‘hot’ in SpA research.
Australia was represented by Prof. Matthew Brown presenting in a Genetics debate and scientist Aimee Hanson, also from PAH, Brisbane, presenting an oral paper on further progress on the genetics front. “Interactions between HLA-B27 and specific KIR genes may contribute to AS by altering the inflammatory activity of NK cells”. Other attendees included Tony Kenna (scientist, Brisbane), with a poster and Rheumatologists Irwin Lim and Roberto Russo from Sydney and myself (physio, Brisbane). There was a smaller number of physio’s this year. I caught up with Liz from the UK again and also Saleema, from the Netherlands, who had a poster.

The meeting included 25 invited papers, 12 oral presentations and an amazing and overwhelming 162 posters – all to be digested in 3 days. This is exciting for health providers but also for health consumers – patients should be pleased to see that so many people are working at many levels on many different aspects to improve the understanding and management of SpA.

The city of Gent is a charming, vibrant and friendly city. If holidaying in the area, put it on your itinerary, you will not be disappointed.

Microbiology and SpA

I will attempt to give you a few points from the presentations, which I felt of most significance and interest to us.

The meeting commenced with microbiology and discussion of IL17/23. This area of basic science is developing and producing insights and explanations for inflammation, joint destruction, disease initiation and disease progression. The influence of IL23, IL17 and TNF and the resultant links with osteoproliferation, inflammation and bone loss are gradually becoming clearer, but not fully answered as yet. Some points were: Structural damage in axial and peripheral SpA is the result of a combination of destruction and new bone formation. Both TNF and IL17 play a central role in osteoclast-mediated bone destruction, and bone destruction is halted by TNFi as well as IL17 in PsA.  The exact mechanisms of new bone formation remain partially elusive, but increasing evidence indicates that IL17 can induce bone formation in specific conditions. Preliminary pre-clinical and clinical evidence suggests that IL17 blockade may block new bone formation in SpA.

Screening and public health

The second session commenced with a thought provoking talk on ‘public health advice’ in general and for us to be alert and thoughtful when considering ‘screening’, early diagnosis, over diagnosis, and early interventionist treatment. Dr Luc Bonneux, an epidemiologist and GP avoided rheumatology specifically, but addressed topics from sunscreens and cancer, cot death, breast and prostate cancer.  His message was that we should not assume all ‘public health advice’ is good or true, we should consider if ‘screening’ for any or all diseases is a good thing and we must be careful in the area of early and/or overdiagnosis. Be careful of Dr Power and consider VOMIT – Victims of Medical Investigative Technology. He who seeks shall find – hence if you screen enough people you will find more cases – but is this relevant, helpful and will it change treatment or outcome?

Treatment Targets

This led into discussion of what is our target of treatment. ASAS-EULAR recommendations include setting a target and treatment should be guided according to this. Phase one says there is good evidence for exercise – some patients do very well. Despite advances in SpA management, challenges remain – such as bringing the recommendations into clinical practice with a defined treatment target and strategies to reach it. Points included: Treat to target –T2T – as partial remission; NSAIDS as first treatment results in 35% of patients in partial remission; TNFi, in patients failing NSAIDS, result in 25% patients in partial remission: IL17, in patients failing NSAIDS, result in 20% of patients in partial remission. The risk benefit is generally favourable. Important remaining issues include: Only a limited number of effective drug classes available for the treatment of AxSpA; Is being in remission for a sustained time leading to better outcome?; Is this at the cost of adverse events?; Is the concept of T2T cost-effective?; Rational selection of bDMARDS based on the presentation of the disease (eg extra-articular manifestations); Tapering of bDMARDS in case of sustained remission and evaluate a T2T strategy. The big question continues – Will early diagnosis give better outcome in SpA? – currently not proven and is difficult to prove. The next talk continued and outlined ASAS partial remission criteria and ASDAS calculator, which can be found on the ASAS slides library. His summary was: Very important to define remission for the treating physician to get the patient free of symptoms; A T2T strategy might be effective; Remission predictor of drug free remission? No sufficient data yet; and remission relevant to avoid structural damage? – no sufficient data yet.

SpA and Pain

The final talk of the day discussed Fibromyalgia. It was retitled Central Sensitisation Syndrome (CSS). Fm is also known as CSS and presents as a syndrome of chronic widespread pain, fatigue, sleep disturbance and dyscognition. It is present as a concomitant illness in 10-30% of rheumatologic diseased patients. States of chronic pain and/or inflammation in AS and SpA are a setting in which CSS can arise, influenced by genetic as well as psychosocial factors. CS is characterized by dysregulation of nociceptive and anti-nociceptive neuro peptide function and neural signalling. Concomitant FM alters rheumatologic disease presentation, natural history, assessment and treatment outcomes including, potentially, ability to achieve ideal goals of treatment of remission or of low disease activity.  SpA patients with concomitant FM are more likely female, have a greater likelihood of enthesitis, and display worse disease activity measures than SpA patients without Fm, including BASDAI, BASFI, ASQoL, which are wholly patient reported outcome measures, and to a lesser extent ASDAS. SpA patients with Fm cycle through a greater number of treatment options in a shorter period of time. (My comments – This is important to consider, but not to judge too quickly. The females tended to have longer time to diagnosis and therefore appropriate treatment, so this may have had an influence. Also, although changes in the brain are detected, it is also seen that if pain is taken away – eg following a hip replacement – the brain changes also go away. Hence, we still need to treat the condition and not just the ‘brain’. This is something we need to look at more in all patients, but perhaps especially the non-responders or those who lose the effect of pharmaceuticals. It may also be relevant in the early role of adequate education and self-management instruction. Pain management is an area that physio’s and health professionals are good at treating in many conditions. It could be an area where we could intervene treating to address specific pain issues with musculoskeletal treatments and hence prevent the chronic pain state and/or treat the pain issues.)

Non-articular SpA

Day 2 gave updates on IBD, Psoriasis and Uveitis, followed by a session on Gut homeostasis, microbiota and arthritis. This area is exploding with developments, however, we are still a long way from diet being able to change an individual’s gut biome, but it is telling us a lot about the cause or development of inflammatory arthritis. It is also giving us some insights as to why some do and others don’t respond to different therapies which may lead to individualising biological therapy and therefore giving optimal care quickly. Some points that were made include – HLA B27 predisposes to AS by altering the gut microbiomes. 50% of SpA patients have microscopic (subclinical) bowel inflammation, 6% evolves to Crohn’s in 5 years and 20% over time. Emerging data implicates the human microbiome in the pathogenesis of SpA; Mucosal sites exposed to high load of bacterial antigens (gut) may represent the initial site of autoimmune generation in SpA and PsA perhaps in combination with host genotype.; Microbial metabolites as bioeffectors of immune response.; Pharmacomicrobiomics (how bugs modulate drugs) as novel precision medicine approach. Remission of gut inflammation was associated with disappearance of joint inflammation. Presence of gut inflammation is associated with accelerated need for biologics. Gut inflammation predispose to disease severity and extent in SpA.

Assessment

The day concluded with discussions on assessing disease activity, including questionnaires, clinical and radiological measures. Patient Reported Outcomes (PRO) were discussed. This is for patients to provide information concerning the impact of an intervention or therapy from their perspective. Aim to develop tools to measure the patient experience in clinical trials that would look at one or more aspects of a patient’s health status based on information gathered directly from the patient, without interpretation by physicians or others. Are PRO’s fit for purpose in axSpA?  Where do they fit with classification criteria, clinical diagnosis and treatment criteria? When comparing disease activity clinical measures and MRI, there is a disconnect. Both are helpful, but as yet we are not sure of the meaning of all MRI findings. We must treat the patients not the tests.

Basic Science

The final day was back to basic science and genetics, short oral papers and a session on mechanical stress, entheseal inflammation and bone formation. One oral paper was about MAIT cells. Recently, Mucosal Associated Invariant T (MAIT) cells have been implicated in autoimmune disease. MAIT cells – which are derived and responsive to bacterial antigens- are enriched in AS joints. MAIT cells may provide the missing link between genetic susceptibility (IL77-7R polymorphism), gut inflammation, and microbial triggers in AS. The next paper reported on 527 patients studied over 3 – 6 years. As patients have a 70% reduction in radiographic progression when exposed to both TNFi and high doses of NSAIDs – hence perhaps having a synergistic effect. The next paper was co-authored by Matt Brown. It concludes that healthy HLA B27 individual’s exhibit shared microbiota changes with AS, indicating a disrupted microbiota may be a primary event in AS pathogenesis rather than secondary to disease or its treatment. These findings support the hypothesis that HLA B27 operates to cause AS through interaction with the intestinal microbiome, and suggests that therapies targeting the microbiome may be effective in AS prevention and/or treatment.

In discussing the entheses, it was stated that the disc is an elaborate enthesis. Also, there are similarities between OA and SpA – as the enthesis becomes thickened with age – and sometimes it may be impossible to differentiate. There may be some evidence for Psoriasis therapy as potential PsA prevention. Finally, mechanical stress was discussed – with the question Does biomechanical stress at the cellular, tissue or organ level contribute to the onset or structural disease progression in SpA?  and hence – is strenuous exercise bad for patients with SpA? Exercise was considered to be a good thing – especially mobility and core strength, but we don’t know what the effect is on the bone in the spine.   Biomechanical cell or tissue stress likely contributes to onset of inflammation in the enthesis and inflammation-induced bone loss could be a trigger for entheseal ossification and progressive ankyloses. But, again, further research is needed. Thankfully, the research is continuing.