12Psoriatic arthritis
Introduction
Psoriatic arthritis (PsA) is a heterogeneous chronic inflammatory spondyloarthritis that occurs in combination with psoriasis and is usually seronegative [1]. It was considered independent from rheumatoid arthritis (RA) after rheumatoid factor was discovered in 1948, and it was acknowledged as a distinct entity by the American Academy of Rheumatology in 1964 *[2], [3].
The prevalence of psoriasis in the general population varies from 2% to 3%, and it affects men and women equally *[4], [5]. The exact prevalence of PsA is unknown, varying between 20 and 420 cases per 100 000 individuals in the west and 1 case per 100 000 individuals in Japan. Given the lower prevalence of other forms of spondyloarthropathy in Japan, this difference may be related to ethnicity [6], [7].
The wide variability in prevalence reported in different populations reflects differences in investigated cohorts, which have ranged from communities to groups of hospitalised patients, and the existence of five different diagnostic criteria with considerable variations of sensitivity and specificity, including Moll and Wright, Bennet, Vasey and Espinoza, Fournié, and CASPAR [1], [8], [9], [10], [11], [12]. The prevalence of PsA amongst psoriasis patients varies between 6% and 42%.
Up to 20% of affected patients exhibit severely destructive and disfiguring forms of PsA [2]. Zhang and colleagues observed a higher frequency of PsA in obese or overweight patients (7.81%) compared to normal weight patients (5.17%, p < 0.01) [13].
Section snippets
Immunopathogenesis
Psoriasis is the most common T-cell-mediated disease in humans [14], but its pathogenesis has not yet been fully elucidated. Genetic, environmental and immunological factors have all been implicated. Approximately 20 chromosomal regions have been associated with psoriasis [15]. The antigen required to activate T cells, if any, is still unknown, although some studies suggest that streptococcal antigens may be involved. Structural similarities between streptococcal M protein and type I keratin
Clinical manifestations
The peak of PsA incidence occurs between 30 and 50 years of age. It is clinically characterised by oedema, pain, tenderness, and stiffness of the joints, ligaments and tendons (dactylitis and enthesitis). Enthesitis occurs most often in the plantar fascia, Achilles tendon, pelvis annexed ligaments, ribs and vertebral spine [23]. The association between synovitis and enthesitis of tendons and ligaments belonging to the same digit is called dactylitis, or ‘sausage-digit’, and it is observed in
Classification
PsA classification is a controversial subject. Although the Moll and Wright criteria are used frequently, in practice, the five subgroups on this scale exhibit frequent overlap, and the same patient might shift between subgroups over time [8], *[35].
- 1.
Asymmetric oligoarthritis: <5 asymmetrically affected joints.
- 2.
Symmetric polyarthritis: >5 symmetrically affected joints with pattern similar to RA.
- 3.
Distal arthritis: participation of distal interphalangeal joints.
- 4.
Mutilating arthritis: destructive form
Diagnostic criteria
In 2006, a study by The Classification of Psoriatic Arthritis (CASPAR) group established highly sensitive (91–100%) and specific (97–99%) set of criteria that allow diagnosis even in cases of PsA sine psoriasis, as well as in positive rheumatoid factor patients [12], [33] (Table 1).
Recently, an arthritis symptoms screening technique was developed to improve PsA detection by dermatologists. It consists of a questionnaire that can be self-administered by psoriasis patients (PASE). Scores equal to
Radiological findings
The radiological characteristics of peripheral PsA include asymmetric distribution, participation of distal interphalangeal joints, periostitis, bone density preservation, bone ankylosis and pencil-in-cup deformity. The most characteristic radiological finding of PsA is bone proliferation [9]. Findings for axial involvement include paravertebral ossification, syndesmophytes, interspinous or anterior ligament calcification, apophysis sclerosis and asymmetric sacroiliitis. Cervical intervertebral
Differential diagnosis
The main differential diagnoses of PsA are reactive arthritis (common signs include asymmetric arthritis, enthesitis, dactylitis and lumbar pain). Conjunctivitis and urethritis are not typical of PsA but are common in RA (symmetric polyarthritis in both). Distal interphalangeal joints are frequently affected in PsA, which does not occur in RA; furthermore, rheumatoid factor is negative, and skin lesions are present. Ankylosing spondylitis is another important differential diagnosis, which
Treatment
The goals of treatment for PsA are to provide relief from the signs and symptoms of the disease, prevent joint damage, improve patient quality of life and decrease mortality. As a rule, all PsA patients must be informed of the characteristics of the disease and given psychological counselling and physiotherapy.
Mild forms of the disease may respond to non-steroidal inflammatory agents, which are sometimes given in combination with intraarticular glucocorticoid injection [45]. Moderate to severe
Prognosis
PsA was at one time considered a benign form of arthritis, but it affects patient quality of life and causes significant functional impairment [62].
In one study, approximately 55% of patients with PsA who were followed up for more than 10 years exhibited five or more joint deformities. Another study found radiological signs of articular erosion in patients only 2 years after the onset of arthritis [63], [64].
It has been speculated that patients in whom five or more joints are involved at onset
Conflicts of interest
None.
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