TITLE:
Reactive Arthritis: From Clinical Features to Pathogenesis
AUTHORS:
Ethelina Cargnelutti, María Silvia Di Genaro
KEYWORDS:
Reactive Arthritis; HLA-B27; Spondyloarthritis; Yersinia-Induced ReA; Therapy
JOURNAL NAME:
International Journal of Clinical Medicine,
Vol.4 No.12B,
December
27,
2013
ABSTRACT: Reactive arthritis (ReA) is a sterile
synovitis which occurs after
a gastrointestinal or urogenital infection. ReA belongs to Spondyloarthritis
(SpA), a group of diseases that share several clinical and radiological
features including familiar clustering, absence of rheumatoid factor and association
with HLA-B27. Clinically, ReA is characterized by an asymmetric arthritis predominantly affecting
the lower limbs, often associated with urethritis, conjunctivitis and other extraarticular symptoms. The ReA prevalence
depends on the incidence of causative pathogens. The ReA diagnosis is based on
clinical features and serological tests to evidence previous infection.
Different treatment including antibiotics, disease modifying antirheumatic drugs
(DMARs) and biologic agents has been recommended. Even though knowing that infections trigger the joint
inflammation, the ReA pathogenesis remains to be poorly understood. Several animal
models and in vitro studies have been used to elucidate the mechanisms involved
in ReA development. In this sense, HLA-B27 transgenic rat or mice have been
used to explain the role of this molecule in SpA aetiopathogenesis. Moreover, the infectious model of Yersinia-induced ReA in rodents has shed some lights on the relationship
between host genetic susceptibility to infection and abnormal immune response
in ReA development. Understanding the immune mediators triggering ReA will
contribute to find a specific treatment for this arthritis. In this review, we focus on clinical features, epidemiology,
treatment, and the different attempts to understand the pathogenesis of ReA.