Identification of a genetic variant for joint damage progression in autoantibody-positive rheumatoid arthritis

摘要

Rheumatoid arthritis (RA) is characterised by persistent joint inflammation and joint destruction. The severity of radiographic destruction can be measured objectively and reflects the cumulative burden of inflammation. Up-to-date treatment strategies have improved the outcome of patients with RA, though the chronic and destructive character of the disease is not prevented. Anticitrullinated peptide antibody (ACPA)-positive patients with RA in particular are characterised by progressive joint destruction.1 The severity is highly variable between ACPA-positive patients, some develop almost no joint destruction, whereas others have a severely progressive disease (see online supplementary figure 1). Current treatment is not individualised; we are neither able to identify the patients that will have the most severe disease course nor do we understand the processes underlying these interindividual differences. To improve this, risk factor studies are required.