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The inflammatory rheumatic diseases form a group of disorders that are highly variable in their phenotypic expression. However, they have in common the presence of localized and/or systemic inflammation, which results in characteristic musculoskeletal system and internal organ damage. Among these diseases, the specific clinical and pathologic features of each disorder likely reflect the initiating and propagating stimuli that determine the specific tissues targeted and the inflammatory effector mechanisms that predominate.

Although the spectrum of inflammatory rheumatic diseases is broad, some general principles provide a framework within which to discuss the pathophysiology of all. One of the most useful constructs is a kinetic one, which focuses on disease initiation, propagation, and flares. It is useful for discussing both acute and chronic diseases. Understanding the stimuli and mechanisms responsible for each of these phases among the different rheumatic diseases permits a deeper insight into these fascinating and complex syndromes.



The initiating force of acute diseases (eg, gout, immune complex vasculitis) is often clearly recognizable and can be endogenous (eg, crystal deposition) or exogenous (eg, new medication, systemic bacterial or viral infection) in origin. The disease is self-limited owing to the success of the inflammatory response in removing the offending initiating stimulus (eg, urate crystals in gout, bacterial antigen or drug in immune complex vasculitis) (Figure 24–1). Despite resolution of the acute episode, flares may occur upon re-exposure to the initiating stimulus.


Kinetics of acute and chronic inflammatory rheumatic diseases.


The initiating force in chronic diseases (eg, systemic lupus erythematosus [SLE], rheumatoid arthritis) is often remote and no longer recognizable once the unique disease phenotype becomes fully established and the diagnosis clear. Propagation of the disease typically occurs as a result of an autoimmune response that induces a self-amplifying cycle of damage. Autoimmune diseases are characteristically driven by “self-antigens” (eg, nucleosomes [composed of DNA and histones] in SLE) and can elicit both cellular and humoral immune responses. Conditions leading to the initiation of chronic autoimmune diseases occur rarely, but once a disease is established, flares are frequent. This circumstance probably reflects the abundant capacity of the immune system to “remember” previously encountered antigens and to respond to them with greater vigor when encountered again, even at lower concentrations (see Figure 24–1).

Different tissues are affected in various diseases (eg, specific synovial joints in gout and rheumatoid arthritis; skin, joints, kidneys, serosal surfaces, nervous system, and blood cell lines in SLE).


The nature of tissue damage and joint injury is determined in part by the inflammatory and immune effector functions that predominate. In addition, the pathologic features of the ...

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