
doi: 10.1111/jdv.12741
pmid: 25199646
AbstractReactive arthritis (ReA) is an immune‐mediated seronegative arthritis that belongs to the group of spondyloarthropathies and develops after a gastrointestinal or genitourinary system infection. The condition is considered to be characterized by a triad of symptoms (conjunctivitis, arthritis and urethritis) although a constellation of other manifestations may also be present. ReA is characterized by psoriasiform dermatological manifestations that may resemble those of pustular psoriasis and, similar to guttate psoriasis, is a post‐infectious entity. Also, the articular manifestations of the disorder are similar to those of psoriatic arthritis and both conditions show a correlation with HLA‐B27. These facts have led several authors to suggest that there is a connection between ReA and psoriasis, listing ReA among the disorders related to psoriasis. However, the pathogenetic mechanism behind the condition is complex and poorly understood. Bacterial antigenicity, the type of host response (i.e. Th1/Th2 imbalance) and various genetic factors (i.e. HLA‐B27 etc.) play an important role in the development of the disorder. It is unknown whether all the aforementioned factors are part of a mechanism that could be similar to, or share basic aspects with known psoriasis pathogenesis mechanisms.
Prohibitins, Humans, Arthritis, Reactive
Prohibitins, Humans, Arthritis, Reactive
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