MRI not yet ready for disease monitoring in RA

Rheumatoid arthritis

By Tony James

1 Nov 2017

Changes in RA joint inflammation on MRI are only weakly correlated with changes in conventional disease activity scores, suggesting that MRI is not an appropriate tool to guide escalation of therapy, New Zealand researchers have concluded.

Professor Fiona McQueen, from the University of Auckland, and colleagues compared changes in MRI inflammation and DAS28CRP in 66 patients whose treatment was escalated to a conventional DMARD (cDMARD) combination or who had anti-TNF therapy added.

“There was no or minimal change in the median MRI inflammation score over four months, despite clinical improvement,” they said.

There was also no difference in the MRI inflammation response between those escalating to a different cDMARD regimen and those escalating to a cDMARD/anti-TNF regimen.

Treat-to-target regimens using clinical targets had been profoundly effective in limiting the progression of joint damage and disability in RA, Professor McQueen wrote.

However, there was little evidence that using more stringent imaging targets would be associated with better outcomes.

“Our study has indicated considerable disparity between clinical disease activity and MRI joint inflammation, and has emphasised that the goal of complete imaging resolution of inflammation is far off in the majority of real world patients,” she said.

MRI could provide detailed information about the disease process, including the level of inflammation affecting synovium, bone, tendons and tendon sheaths.

These new findings, from the first real-world study to assess links between MRI inflammation and clinical disease activity scores, showed the clinical implications are not straightforward.

“It was obvious that many patients improved clinically after treatment escalation, with only minor changes in their MRI inflammation scores. In some instances MRI inflammation worsened despite clinical improvement,” Professor McQueen said.

The research team proposed a number of possible explanations for the disparities.

A ‘ceiling effect’ for MRI inflammation could be one reason: a severely inflamed joint could have a very high score which remains high even when swelling and tenderness have subsided, or the four-month follow-up might be insufficient for MRI changes to abate.

In addition, DAS28CRP and MRI inflammation captured different aspects of the disease: MRI findings do not detect pain (manifest as joint tenderness), but do reveal osteitis which is not apparent clinically.

Finally, the MRI inflammation score is based only on changes in the dominant wrist while DAS28CRP assesses 28 joints.

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