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  • Chronic inflammatory arthritis associated with skin and nail psoriasis.
  • Symmetric polyarthritis or asymmetric oligoarthritis of peripheral joints (frequently with distal interphalangeal [DIP] joint involvement).
  • Spondylitis and enthesitis may occur.
  • Current or past history of psoriasis; family history of psoriasis.
  • Dactylitis and characteristic nail dystrophy.
  • Absence of rheumatoid factor.
  • Radiographic findings of erosions, osteolytic destruction of the interphalangeal joints, and juxta-articular new bone formation.

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Psoriatic arthritis is a chronic inflammatory arthritis associated with skin and nail psoriasis. It is one of the spondyloarthropathies, a group of inflammatory arthritides, characterized by arthritis of the axial skeleton (ie, the sacroiliac joints and spine), asymmetric oligoarthritis or symmetric polyarthritis of peripheral joints, enthesitis (inflammation at the insertion sites of tendons to bone), and the absence of rheumatoid factor. Unlike rheumatoid arthritis, psoriatic arthritis has a predilection for the DIP joints.

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Psoriatic arthritis develops in approximately 20–30% (range 6–42%) of adults with psoriasis. The overall prevalence of psoriatic arthritis in the general population has been estimated to be 0.04–0.1%, but this may be an underestimate. In the United States, the incidence of psoriatic arthritis has been reported to be approximately 6–7 per 100,000 per annum. The mean age of disease onset ranges from 30 to 55 years, with men and women equally affected.

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The etiology of psoriatic arthritis is unknown. Genetic susceptibility studies indicate associations with major histocompatibility alleles HLA-B27, HLA-B7, HLA-B13, HLA-B17, HLA-B57, and HLA–Cw*0602. Recent genome-wide association studies of patients with psoriasis and psoriatic arthritis have identified other susceptibility loci, including interleukin (IL)-23A, IL-23R, IL-12B, tumor necrosis factor-induced protein 3 (TNFIP3), TNFIP3 interacting protein 1 (TNIP1), IL-4, IL-13, and tumor necrosis factor receptor-associated factor 3-interacting protein 2 (TRAF3IP2). As in the pathogenesis of many other autoimmune disorders, an infectious trigger has been suspected. Group A streptococcal infections have been implicated in guttate psoriasis, and ribosomal RNA from this species has been detected in peripheral blood and synovial fluid of psoriatic arthritis patients. In addition, HIV is strongly associated with the development of psoriasis and psoriatic arthritis. Physical trauma (Koebner phenomenon) has also been implicated.

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Psoriatic arthritis typically develops after or coincident with the onset of psoriasis. In 15–20% of cases, however, arthritis precedes the onset of psoriasis by as much as 2 years. An asymmetric oligoarthritis was once believed to be the usual clinical presentation of psoriatic arthritis, but recent evidence supports that symmetric polyarthritis is the most frequent presentation. Widespread destructive arthritis (arthritis mutilans) and mostly DIP joint involvement are observed less frequently but are more specific to psoriatic arthritis. The pace of joint destruction may occur over a period of months.

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There may be a direct correlation between the severity of arthritis at the time of presentation and the subsequent disease course. Polyarthritis in the presence of elevated acute phase reactants, radiographic evidence of joint erosions, and inadequate response to initial pharmacotherapy predicts a more severe disease course. As seen in rheumatoid arthritis, ...

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