2023-06-13 13:07:48
The pathologic processes that eventually lead to the development of rheumatoid arthritis (RA) begin long before the disease can be classified as RA. The various phases of RA begin with genetic disposition and environmental toxins and lead via systemic autoimmunity to the onset of symptoms and unclassifiable arthritis, finally to full-blown rheumatoid arthritis. From the onset of symptoms, the autoimmune processes characteristic of RA are fully developed, even if the clinic does not yet meet the classification criteria of RA.1,2
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It has long been hoped that an intervention prior to classification might prevent or at least delay the development of RA. So far, however, this approach has encountered several limitations. Above all, it was unclear in which affected persons full progression to RA actually occurs. “While genetic and epidemiological factors have traditionally been used to describe the risk of developing RA, in recent years the definition of high-risk status has improved. This was achieved by including autoantibodies and symptom complexes such as inflammatory joint pain in the prediction models,” says Prof. Dr. Andrew Cope from the Center for Rheumatic Diseases at King’s College London.
In this way, it was possible to define groups of people with a very high risk of progression. In some cohorts, the risk of progression to RA was greater than 50 percent, Cope said. This knowledge now makes it possible to design studies that examine strategies to prevent or delay the development of RA. Cope presented the results of the Arthritis Prevention In the Pre-clinical Phase of RA with Abatacept (APIPPRA) study at EULAR 2023.3 The randomized, double-blind, placebo-controlled phase IIB study enrolled ACPA and rheumatoid factor positive subjects or subjects with high ACPA titres and arthralgia. Subjects were stratified by gender, nicotine status, and country and treated with placebo or abatacept for 52 weeks. Abatacept is a fusion protein of the Fc portion of human IgG1 and the extracellular domain of human CTLA-4. Through the CTLA-4 domain, abatacept can bind to CD80 and CD86 of antigen presenting cells (APCs), thereby preventing T cell costimulation by an APC.
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