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- W2048931718 abstract "<dm:abstracts xmlns:dm=http://www.elsevier.com/xml/dm/dtd><ce:abstract xmlns:ce=http://www.elsevier.com/xml/common/dtd view=all class=author id=aep-abstract-id8><ce:section-title>Publisher Summary</ce:section-title><ce:abstract-sec view=all id=aep-abstract-sec-id9><ce:simple-para id=fsabs033 view=all>Reactive arthritis is one of the spondyloarthritis family of clinical syndromes. With a calculated prevalence of 1.9%, spondylarthropathies are among the most frequent rheumatic diseases in the white population. The clinical features of reactive arthritis are those shared by other members of the spondyloarthritis family, though it is distinguished by a clear relationship with a precipitating infection. Nevertheless, the term reactive arthritis appropriately describes arthritis that is associated with demonstrable infection at a distant site without traditional evidence of sepsis at the affected joint(s). Reactive arthritis is still the most common type of inflammatory polyarthritis in young men. An HLAB27 genotype is a predisposing factor in over two thirds of the patients with reactive arthritis and autoimmune mechanisms versus autologous peptides have been shown. Therefore, based on the strength relationship with HLA-B27, reactive arthritis is considered a spondyloarthropathy. The syndrome most frequently follows genitourinary infection with Chlamydia trachomatis, but other organisms have also been implicated. A defective immune response against bacteria seems to characterize reactive arthritis patients, and reduced levels of Thl cytokines are observed in these patients. Because reactive arthritis is more frequent in male subjects, by considering that androgens are immunosuppressive, a possible favoring role of androgens on chronic infections can not be excluded.</ce:simple-para></ce:abstract-sec></ce:abstract></dm:abstracts>" @default.
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