Abstract
PurposeThe etiology of several autoimmune disorders, including rheumatoid arthritis, remains unknown. While there are clear phases of disease progression, the mechanisms of transition between these phases are poorly understood. Additionally, treatment focuses on an alteration of the biological processes to prevent joint damage and functional decline. A goal is to potentially treat the disease during the preclinical phase to mitigate the disease process. Reactive arthritis is another rheumatologic condition known to be secondary to a distal infection. While prevention of infection would mitigate risk, serologic profiling patients with the disease may assist in the elucidation of potential disease risk factors. This study was initiated to enable an assessment of pre-disease biomarkers in patients newly diagnosed with rheumatoid arthritis and reactive arthritis. ParticipantsA retrospective cohort of 500 rheumatoid and 500 reactive arthritis cases with 500 matched controls was drawn from a population of active component US military personnel. Appropriate inclusion criteria limited subject selection. Additionally, 4 serum samples (3 pre-disease and 1 disease-associated) were obtained for each case and control. Findings to dateThe established cohort provides the framework for novel exploration of the host response through serum profiling and seroepidemiology prior to disease onset. Future plansThis study establishes the framework for the evaluation of novel serum biomarkers enabling the identification of signals prior to clinical disease that may enable disease prediction, elucidate disease pathogenesis and identify novel exposures leading to increased disease risk and/or disease severity.
Highlights
Rheumatoid Arthritis (RA) is a relatively common, chronic, systemic inflammatory disease of unknown aetiology that affects approximately 1% of the population worldwide [1,2,3]
There is increasing evidence that RA develops in phases and its underlying pathogenesis begins many years before clinical diagnosis [30]
With increased systemic and joint inflammation and anti-citrullinated protein antibodies (ACPAs) epitope spreading, undifferentiated/inflammatory arthritis (UA/IA) patients convert to clinically identifiable RA
Summary
Rheumatoid Arthritis (RA) is a relatively common, chronic, systemic inflammatory disease of unknown aetiology that affects approximately 1% of the population worldwide [1,2,3]. The incidence appears to be highest in Pima Indians (5.3%) and Chippewa Indians (6.8%), and lowest in people from China and Japan (0.2%–0.3%), suggesting the possibility that genetic factors contribute to RA [5,6]. These differences in regional RA prevalence may sug gest a role for environmental factors. It predominantly targets joints and can lead to significant long-term disability, secondary to cartilage and bone erosion. These long term effects are reflected in the work disability secondary to RA, which can be as high as 59%, with 90% of patients with RA retiring from work prematurely [7]
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