Pain in autoimmune disorders

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Although often considered rare, there are over 80 known autoimmune diseases according to the Progress in Autoimmune Disease Research report by the National Institutes of Health's Autoimmune Diseases Coordinating Committee (ADCC, 2005). Each of these diseases has a unique autoantibody profile and primary clinical manifestations. Some examples of the more recognizable autoimmune disorders include multiple sclerosis, rheumatoid arthritis, type 1 diabetes, psoriasis, and irritable bowel syndrome. Although each disease varies in its presentation, the common underlying thread is the presence of autoantibodies and autoreactive T cells, which cause harm to the patient. These are thought to attack the various tissues and/or organs targeted in the individual disease. For example, autoantibodies against components of the myelin sheath cause the damage and clinical symptoms associated with multiple sclerosis. The main cause of most autoimmune diseases is not yet known, although many studies have linked these diseases to both genetic/epigenetic and environmental factors (Miller at el., 2012; Selmi et al., 2012; Aslani et al., 2016).
Given the variety of different diseases in this category, it is hard to determine the exact prevalence of autoimmune disorders. The first study examining prevalence was conducted in 1997 by Jacobson et al. and examined the prevalence of 30 autoimmune diseases. These authors estimated prevalence rates at ∼3.2%; however, this study examined only a small number of autoimmune diseases and is now out of date. Subsequent studies have tried to expand upon the work done by Jacobson et al. (1997) and have cited prevalence rates anywhere from 3% to 9.4%. (Cooper and Stroehla, 2003; Cooper et al., 2009; Hayter and Cook, 2012). One of the difficulties of assessing prevalence rates is the lack of data available, especially for those disorders that are rarer as many of the studies examining prevalence rates include only a small percentage of the 80 known autoimmune diseases, and the rates vary. In addition, for those rarer diseases, there is often a lack of information from which to determine whether the disorder should be considered “autoimmune” in nature, especially if the suspected autoantibody is as yet unknown. This means that the prevalence rates are most likely much higher than estimated in these studies.
Authors often also cite different prevalence rates for males and females, given that the incidence of autoimmune disorders is often higher among females (Hayter and Cook, 2012). For example, the most recent prevalence study cited a 2.7% prevalence for males and a 6.4% rate for females (Hayter and Cook, 2012). It is currently unknown why most autoimmune diseases affect women more than men, although recent work on immune activation suggests that women may have a more reactive population of T cells, making them more susceptible to certain autoimmune diseases (Dunn et al., 2007; Zhang et al., 2012). It is therefore not surprising that autoimmune disorders are considered one of the leading causes of death among young and middle‐aged women in the United States (Cooper and Stroehla, 2003). Given the chronic nature of most autoimmune diseases, they have a significant impact on the health‐care system and the quality of life of patients. This makes understanding their underlying biology and treatment imperative.
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