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Over the past 10 years, there has been increasing evidence on the benefit of treating RA patients to a target, and adjusting therapy until the target is met. With the ongoing evolution of advanced therapeutics, we are truly able to target clinical remission, with stringent clinical criteria, that we would have never considered in the past.
In a packed room today during a session titled "Fifty Shades of Remission," there was a healthy debate on how we define clinical remission and whether clinical remission is enough. Should radiology, namely ultrasound, be included in our definition of remission? Should we be adjusting therapy based on biomarkers?
Until now, the most widely accepted criteria for clinical remission are the ACR-EULAR remission criteria of 2011, which are not perfect. One criticism is that these criteria do not include imaging modalities such as ultrasound and MRI, which should be part of a treat-to-target (T2T) strategy. There is some evidence that up to 60% of RA patients who are classified as being in clinical remission can still have residual synovitis on US. Does this subclinical disease result in silent radiographic progression? Does this predict increase in clinical flares? At this time, we don't have good answers, particularly in established disease.
Two studies including US in a T2T strategy in early RA (TaSER and ARCTIC) showed that adding US leads to more intensive treatment (with added costs and potential toxicity) but not improved outcomes (both clinical or radiographic). Based on this, I'm not convinced that adding US to routine clinical assessment is needed to define remission in RA but I suspect that this story will keep evolving over time.
What are the other issues with the EULAR-ACR clinical remission criteria for RA? They are largely influenced by the 28 joint count, and we know that joint counts have poor accuracy for detecting synovitis. Moreover, when considering only 28 joints, synovitis in non-included joints could be missed. Finally, to be classified as being in "remission," patients need to have a global VAS 1/10. This begs the question – Is there a composite biomarker that helps us define remission? Can we measure something that reflects what is happening biologically in the joint?
The MBDA score (multi-biomarker disease activity score) is probably the best evaluated biomarker in RA. It has been shown to correlate well with CRP and with clinical outcome measures such as DAS28-CRP, CDAI, and SDAI in patients treated with TNF inhibitors. However, in patients treated with baricitinib, it correlated poorly with measured joint counts and patient reported outcomes. In a sub-analysis of the AMPLE study, there was a difference in MBDA score between groups treated with adalimumab compared to those treated with abatacept, but no difference in clinical outcomes. This suggests that MBDA is likely no better than CRP, and seems to be influenced by cytokine inhibition.
At the end of the session, I think most would agree that T2T should continue to be aimed at clinical remission. Ideally, in the coming years, there will be a biomarker available that will be accurate, reliable, independent of mechanism of treatment, and cost-effective.
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About the Author
Dr. Shahin Jamal
Dr. Jamal is a Clinical Associate Professor at the University of British Columbia and an active staff physician at Vancouver Coastal Health. Her interests include diagnosis and prognosis of early inflammatory arthritis, and timely assessment and access to care for patients with rheumatoid arthritis.
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