Rheuminating on the International Congress on Spondyloarthropathies

By Dr Irwin Lim, Rheumatologist

Gent, Belgium plays host to this congress held every 2 years. Almost 500 delegates attend to discuss and share their work and thoughts about spondyloarthritis.

Spondyloarthritis with its most prominent subgroups of ankylosing spondylitis and psoriatic arthritis, remains a relatively poorly characterised rheumatic disease.

The advances in this field have been huge in the last decade and this meeting promises much for the future.

I had the good fortune to attend. As a frontline rheumatologist, a clinician rather than a researcher, I thought it worthwhile giving you my take on the progress reported:

1) Many new genes which increase susceptibility to Ankylosing Spondylitis (AS) have been identified including the ERAP1 and ERAP2 polymorphisms. The hope would be that we could one day test a prospective patient's DNA against a panel of genetic variants to better assess risk of developing AS.

2) While the genetic contribution of HLAB27 positivity to development of spondyloarthritis/AS has been known for decades, how this happens exactly is still to be worked out. New buzzwords/phrases I learned this meeting included "HLAB27 misfolding", "ER stress" and "Unfolded Protein Response".

3) The importance of the microorganism layer in our gut, the microbiome, was highlighted (100 trillion microorganisms per human with >1000species). Gastrointestinal inflammation is a common feature in Spondyloarthritis. Disturbance of this microbiome combined with an abnormal T-cell immune response is likely to have some role in development of disease.

4) Cytokines (proteins which help promote the inflammatory response) increasingly thought to be key to the disease are IL23 & IL17. The good news for those patients who don't respond or who respond only partially to TNF-alpha inhibitor therapy is that medications to help block these cytokines are being trialed.

5) A key recent finding of a distinct class of immune cells, cells which seem very sensitive to stimulation by IL23, situated at the Enthesis, seems to add weight to the theory that Spondyloarthritis is primarily a problem of excessive inflammation at the enthesis organ (enthesitis). Think Achilles' tendon insertions, or heel pain, or where spinal ligaments attach to vertebrae.

6) MRI has a clear role to aid diagnosis of spondyloarthritis, especially in the absence of characteristic damage on Xrays of the sacroiliac joints. Technical issues and the need for further validation remain, before we can answer questions about how to best use MRI serially to monitor or provide a target-to-treat approach.

7) A distinct feature of Spondyloarthritis is excessive bone formation. It's now been shown that the levels of proteins called Sclerostin & DKK-1 are reduced. Normally, these proteins help in balancing bone turnover. As they reduce, bone formation is increased.

The meeting was made more memorable as I got to meet 3 fellow twitter activists in the flesh. All 3 work to enhance the lives of those with spondyloarthritis:

• Debbie Cook, director of the dynamic UK-based National AS Society,
• Raj Sengupta, rheumatologist at the Royal National Hospital for Rheumatic Diseases at Bath, UK,
• Philip Robinson (@philipcrobinson), rheumatologist & PhD candidate at the Diamantina Institute, Queensland, Australia.

I left humbled by the depth and breadth of scientific endeavour.

Patients with spondyloarthritis should carry hope for major advances in understanding, management & outcomes.