Rheumatoid arthritis

Rheumatoid arthritis: lack of biomarkers a barrier to early management


The lack of biomarkers for the immune dysregulation that underlies rheumatoid arthritis is hampering further advances in the management of the disease, an international expert says.

Professor John Isaacs told the APLAR-ARA meeting that rheumatologists are good at diagnosing the disease by measuring CRP and imaging but that these are consequences of the disease not early indicators.

While a treat-to-target approach and tight control over the last 20 years had really improved outcomes, clinicians willneed to be intervening earlier in order to potentially reverse the disease process, he said.

Professor Isaacs, Professor of Clinical Rheumatology at Newcastle University in the UK, said we are currently only aiming for clinical remission.

“In some patients we only need to get them back to clinical remission, that is, no symptoms. For some their imaging will improve but we can’t at the moment get them back to immunological remission.”

However he was very confident that there would be opportunities to ‘nudge’ the immune system back into balance.

He mentioned peptide therapy might be a strategy in this very early phase of disease he called the breach of tolerance.

“If we are trying to switch off disease, we know from animal models that the immune mechanisms take several months to develop. Whatever you treat you patient with, the important thing is to treat early. This window of opportunity is really critical.”

A precision medicine approach would be ideal, said Professor Isaacs.

“At the moment we use methotrexate because it’s cheap, it’s effective, and if patients can tolerate it, some patients do really well. About 50% of patients achieve remission and perhaps implicit in what I’ve said is that if we went earlier, you might improve on that 50%, but I don’t think we know that.”

“There is obviously still an unmet need there. So I think going back to precision medicine, if we could subdivide out patients at the start, we would do better still. The best we could possibly do would be to stratify people AND treat them early.”

“People have been saying for years, shouldn’t we be using anti-TNF right from the start? The argument against that is every strong drug has its side effects so maybe you’d be over-treating a few patients, but I think if we had those biomarkers, you could make a really strong case for using anti-TNF in some, maybe an anti-IL-6 in others, maybe a B-cell therapy in others.”

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