Autoantibody loss doesn’t signal RA remission

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A study has confirmed that autoantibody seroconversion isn’t a biomarker for remission

It’s been hypothesised that the disappearance of autoantibodies may signal remission in patients with RA, but a study from The Netherlands has suggested that theory is incorrect.

The observational study examined data from around 100 patients with ACPA-positive or RF-positive rheumatoid arthritis over the course of a decade.

Patients were selected if they achieved DMARD-free remission around the five-year mark.

They were tested for their autoantibody levels at the time of remission and then followed-up for another four years to see whether their autoantibody levels changed over time.

In addition, the researchers also looked at around 20 patients with antibody-positive RA who had a flare one year (or more) after achieving drug-free remission, as well as 45 patients with persistent disease.

In all three groups, only a tiny proportion of patients had seroconverted to having no autoantibodies around the time of remission (between 13% and 6% of patients).

The proportion of seroconversions were similar in the patients with sustained remission, flares and persistent disease.

Over the four-year follow up, the RF levels dropped more in patients with remission than patients without remission, but the anti-CCP2 levels were the same across the different groups.

This study showed it was not common for the autoantibody status of patients with RA to change when they went into remission.

“This form of immunological remission may therefore not be a treatment target in patients with classified RA,” the authors said.

Professor Ranjeny Thomas, an autoimmune disease researcher at The University of Queensland, said it was not surprising that ACPA failed to disappear even as symptoms of RA subsided “as the immune processes that drove the development of ACPA in the first place, such as infection response, have not changed”.

“What it is telling us is that in drug-free remission, other immune processes are sustaining the regulation of signs, symptoms and inflammation,” she said.

“This includes things like regulatory cells and anti-inflammatory soluble factors (cytokines) that suppress the autoimmune process in the joint. Finding what these are in such patients is important as it will provide insight in how to leverage natural regulatory processes with new treatments.”

Dr Pravin Hissaria, a rheumatologist based in Adelaide, said it had been shown in multiple studies that autoantibody levels did not change significantly after treatment.

“The use of autoantibodies is currently restricted to diagnosis and prognosis of RA as it has been clearly shown that positive autoantibodies are associated with a more severe joint and extra-articular disease,” he said.

“This paper adds to the already known facts about the use of autoantibodies in RA. There is no role of serial testing of these autoantibodies in clinical situation as it is a wastage of health resources.”

Dr Hissaria said there could be other biomarkers that better reflect the disease activity and predict the patient’s response to expensive medications like biologicals.

But it would require a well-designed longitudinal cohort studies on several thousand patients to discover what these biomarkers were, he said.

Annals of the Rheumatic Diseases 2019, 14 August

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