Recent advances in reactive arthritis

Abstract

Reactive arthritis (ReA), one of the spondyloarthropathies, is an infectious related disease that occurs in a genetically predisposed individual, characterized by an immune-mediated synovitis with intra-articular persistence of viable nonculturable bacteria and/or immunogenic bacterial antigens. ReA long term prognosis is not as good as it was earlier believed. Two-thirds of patients develop prolonged joint discomfort, low back pain, or enthesopathies after acute ReA, and 15% to 30% of them develop chronic symptoms. The therapeutic options for patients with the more severe forms of the disease have been rather limited. The efficacy of tumor necrosis factor antagonists in other spondyloarthritis suggested that anticytokine therapy could also be effective for ReA. This paper reviews the latest concepts in urogenital and postenteric human leukocyte antigen-B27-associated ReA.

Poncet’s disease in human immunodeficiency virus: a case report

“…This non-tuberculous reactive arthritis developing following a distant infection as seen following a primary pulmonary portal in our patient, has been described to preferentially affect young adults [12]. Large weight bearing joints disease is the typical presentation as was the case of bilateral knee and ankle joint involvement in our patient [11].…”

Post-infectious new daily persistent headache may respond to intravenous methylprednisolone

“…The course of ReA is comparable to that of NDPH: short or self-limiting form, continuous, and remitting form [22]. Although acute ReA may be associated with low TNF-α, chronic ReA shows high production of TNF-α (like NDPH) [23]. Therefore, we speculate a local immune reaction in the meninges for the generation of headache in our patients and a subset of NDPH.…”

Post-infectious headache: a reactive headache?

“…The course of ReA is comparable to that of NDPH: short or self-limiting form, continuous, and remitting form [20]. Although acute ReA may be associated with low TNF-α, chronic ReA shows high production of TNF-α (like NDPH) [21]. ReA is the persistence of pathogenic organisms or its products in the joint/synovium leading to local immune response.…”