When considering the evidence, it appears that rather than it being a discrete clinical entity with a unique cause, rheumatoid arthritis (RA) is likely a syndrome that represents a common endpoint for a number of different causative agents.
Although published in 2009 in Open Access Rheumatology Research and Reviews, it remains a poignant review of the search for the origins of rheumatoid arthritis. Led by Alan P. Hudson, Ph.D., of Wayne State University, Detroit, Dr. Hudson and colleagues present a review of the evidence for rheumatoid arthritis looking at causative theories from environmental factors to genetic predisposition. They goal was to demonstrate that rheumatoid arthritis is a common endpoint as a result of many possible origins.
“RA as a common clinical endpoint for differing initiating factors and pathogenic mechanisms is supported by the many different clinical manifestations that encompass the diagnosis of RA,” the authors wrote.
The first know description of rheumatoid arthritis dates back to the early eighteen hundreds. With millions of sufferers worldwide, rheumatoid arthritis imposes a heavy burden on patients leading to functional disability and loss of productivity.
Rheumatoid arthritis is a chronic progressive disease most often presenting as symmetrical pain and swelling in the small joints of the hands and feet. While systemic features can accompany joint inflammation the primary goal is to treat quickly and aggressively in an attempt to prevent long-term joint damage.
One reason it is difficult to pinpoint a single cause in early rheumatoid arthritis is that the clinical picture in the early stages is extremely diverse and heterogeneous leading to missed diagnoses and delays in treatment.
EPIDEMIOLOGY AND PATHOGENESIS
Rheumatoid arthritis strikes as many as one percent of North Americans and puts patients at higher risk for death compared to the general population. Women are far more likely to develop rheumatoid arthritis then men and this fact has long been investigated in an effort to determine its significance.
Even after extensive investigation the pathogenesis of rheumatoid arthritis remains unclear although inflammation leading to joint damage possibly as a result of autoantibody and immune complex interaction is the leading theory.
The diagnostic utility of anti-citrullinated protein antibody assays and the presence of T-cell and B-cell abnormalities lend support for autoimmunity as a key pathogenic feature in rheumatoid arthritis.
AUTOIMMUNITY: A CLOSER LOOK
While it is known that autoimmunity is involved in the pathogenesis of rheumatoid arthritis it is unclear if a loss of tolerance to self-tissue is causative or merely a feature of the larger syndrome. In any case, proliferation of inflammatory immune cells in the joints is a primary characteristic of rheumatoid arthritis.
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