Clinical symptoms in rheumatoid arthritis are associated with specific autoantibodies


The presence of different autoantibodies associated with rheumatoid arthritis should be evaluated separately to provide a better picture of prognosis and support for treatment decisions. This is shown in a new study from IGP, published in the recognised journal Annals of the Rheumatic Diseases.

Rheumatoid arthritis (RA) is a chronic inflammatory disease that mainly affects the joints. There are two main subtypes of RA, based on the presence or absence of certain autoantibodies. One group consists of patients that have any of the autoantibodies rheumatoid factor (RF) and/or antibodies against citrullinated peptides (ACPA). Patients that lack autoantibodies, which are in minority, belong to the second group.

Patients with antibodies have a worse prognosis that those without any of the antibodies, and patients that have both RF and ACPA have a particularly bad prognosis. The researchers in the current study examined the presence of RF and ACPA separately, and found that their individual occurrence in newly diagnosed RA patients could be associated with different clinical symptoms.

“We studied 1600 Swedish patients with early RA and found that patients with ACPA appear to have a lower number of swollen and tender joints at diagnosis. RF on the other hand was associated with a higher degree of inflammation as measured in blood samples, but only in patients who were also ACPA positive,” says Eleftheria Pertsinidou, doctoral student at IGP and first author of the paper.

“Previous studies have often equalised the presence of RF and ACPA, and compared them with combined scores of disease activity. Both the number of inflamed joints and inflammation measured in blood samples are included in the disease activity score for RA called DAS28. When we evaluated the effect of RF and ACPA separately, and compared with individual components of DAS28, we detected a pattern that was not evident when antibodies or clinical symptoms were studied collectively,” says Johan Rönnelid, who led the study.

Laboratory experiments by other research groups have indicated a potential mechanism for how ACPA and RF interact and thereby stimulate inflammation in RA. The clinical data in the new study support this hypothesis and suggest that ACPA are the main antibodies that drive inflammation. RF affects the inflammation in patients that also have ACPA, but does not seem to drive inflammation on its own.

“The presence or absence of RF and ACPA are also relevant for the choice of pharmaceutical treatment of RA patients. We anticipate that our strategy, where RF and ACPA are assessed individually and DAS28 components are also evaluated separately, can improve the precision in algorithms for treatment decisions in early RA,” says Johan Rönnelid.

More information:

Article in Annals of the Rheumatic Diseases

Johan Rönnelid’s research

Last modified: 2022-01-26