Thursday, June 8, 2023
In accordance with ACCME Standards for Commercial Support of Continuing Medical Education and the Health Science Center for
Continuing Medical Education Disclosure Policy for CME Activities, faculty members have been asked to disclose any relationship
they may have with commercial supporters of this CME activity or with companies providing drugs, medical equipment, etc, that
may have relevance to the content of their presentations. Such disclosure is intended to provide participants with sufficient
information to evaluate whether any given presentation has been influenced by the faculty's relationship(s) or financial interests
with said companies.
The following faculty have reported receiving something of value from the commercial supporter(s) of this activity or from
a corporate organization whose product(s) may have relevance to the content of their presentations:
Professor, Academic Section of Musculoskeletal Disease, University of Leeds; Clinical Director, Department of Rheumatology, Leeds Teaching Hospitals NHS Trust, Leeds, England
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The conventional view concerning the pathogenic mechanisms of RA has been that autoantibodies -- particularly rheumatoid factor (RF) and anticyclic citrullinated peptide (CCP) antibody -- appear to be of particular importance.[11] Nielen and colleagues[13] examined the relationship between these autoantibodies and the eventual diagnosis of RA symptoms by determining antibody concentrations in serial blood samples obtained for several years before the onset of RA symptoms. The proportion of patients with a positive test result for either antibody increased steadily in the years preceding the onset of symptoms. RF and anti-CCP antibody were not present in every patient, although they were more likely to appear in patients with more severe symptoms. These findings, and others,[14,15] suggest that an unidentified trigger stimulates the production of autoantibodies by B lymphocytes several years before the eventual onset of clinically evident RA. RF (or other autoantibody) immune complex deposition in the joint will eventually lead to joint destruction. Neutrophils and macrophages infiltrating the joint via chemotactic gradients bind to the immune complexes and/or to a fixed complement and are induced to degranulate, releasing destructive enzymes that damage the articular structures.[11]
