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Review
. 2010 May;36(2):213-41.
doi: 10.1016/j.rdc.2010.02.001.

Preclinical rheumatoid arthritis: identification, evaluation, and future directions for investigation

Kevin D Deane  1 , Jill M Norris, V Michael Holers
Affiliations
Review

Preclinical rheumatoid arthritis: identification, evaluation, and future directions for investigation

Kevin D Deane et al. Rheum Dis Clin North Am. 2010 May.

Abstract

Rheumatoid arthritis (RA) likely develops in several phases, beginning with genetic risk, followed by asymptomatic autoimmunity, then finally, clinically apparent disease. Investigating the phases of disease that exist prior to the onset of symptoms (ie, the preclinical period of RA) will lead to understanding of the important relationships between genetic and environmental factors that may lead to disease, as well as allow for the development of predictive models for disease, and ultimately preventive strategies for RA.

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Figures

Figure 1*
Figure 1*. A model of rheumatoid arthritis (RA) development
Figure 1a: Based on RA-studies as well as prospective studies in other autoimmune disease (type 1 diabetes mellitus), RA may evolve through 3 phases of disease: Phase 1 = genetic risk, Phase 2 = asymptomatic autoimmunity (identified by presence of autoantibodies) and Phase 3 = clinically-apparent disease. Transition between phases may be caused by interactions between genetic and environmental factors, and/or changes in immune reactivity. Figure 1b: RA-related factors that can be measured during the pre-clinical phases of disease development._ *Figure adapted from Kolfenbach J et al. A prospective approach to investigating the natural history of preclinical rheumatoid arthritis (RA) using first-degree relatives of probands with RA. Arthritis Rheum. 2009 Dec 15;61(12):1735-4
Figure 1*
Figure 1*. A model of rheumatoid arthritis (RA) development
Figure 1a: Based on RA-studies as well as prospective studies in other autoimmune disease (type 1 diabetes mellitus), RA may evolve through 3 phases of disease: Phase 1 = genetic risk, Phase 2 = asymptomatic autoimmunity (identified by presence of autoantibodies) and Phase 3 = clinically-apparent disease. Transition between phases may be caused by interactions between genetic and environmental factors, and/or changes in immune reactivity. Figure 1b: RA-related factors that can be measured during the pre-clinical phases of disease development._ *Figure adapted from Kolfenbach J et al. A prospective approach to investigating the natural history of preclinical rheumatoid arthritis (RA) using first-degree relatives of probands with RA. Arthritis Rheum. 2009 Dec 15;61(12):1735-4
See this image and copyright information in PMC

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