PSORIATIC ARTHRITIS

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Psoriatic arthritis (PsA) is an inflammatory arthritis associated with psoriasis. It has been reported in 7% to 42% of patients with psoriasis.22 Since the prevalence of psoriasis is thought to be 1% to 3% of the population, PsA may occur in almost 1% of the population. Indeed the estimate for the prevalence of PsA in the United States is 0.67, 45 although recent figures from Olmstead county question this frequency.72 PsA was recognized as a distinct entity with the discovery of the rheumatoid factor, and the realization that while 80% of patients with rheumatoid arthritis (RA) were rheumatoid factor positive, patients with PsA were usually seronegative. Since psoriasis is a common condition and arthritis, particularly osteoarthritis, is quite prevalent, it is conceivable that psoriasis and some unrelated form of arthritis may occur in the same patient. Indeed, some patients with psoriasis do present with a coincidental RA, or osteoarthritis. Cats7 has argued that psoriasis is just a measure of disease expression in certain patients with peripheral arthritis and spondyloarthropathy. However, epidemiologic studies have confirmed that PsA is a unique entity, as psoriasis was increased among patients with arthritis, and arthritis was increased among patients with psoriasis.55

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CLINICAL FEATURES OF PSORIATIC ARTHRITIS

With the recognition of PsA as an entity separate from RA, it was noted that there were several features which distinguished this form of arthritis associated with psoriasis. Whereas rheumatoid arthritis tends to affect women more often than men, with a 3:1 ratio, PsA has no gender preference and most studies demonstrate a ratio closer to one (Table 1). PsA also tends to be less symmetric in its distribution than RA. Several patterns of PsA were recognized by Wright and Moll.81 These include:

PSORIATIC SPONDYLOARTHROPATHY

In their initial studies Wright and Moll81 identified spondyloarthropathy as a specific pattern of PsA. They defined that group as predominantly spondyloarthropathy. However, it has become clear that the presence of isolated spondyloarthropathy in PsA is unusual and, in most cases, it occurs with peripheral arthritis. Once peripheral arthritis is noted, it is difficult to consider the arthritis as predominantly spondyloarthritis, since the patient would tend to complain more about what is

EXTRA-ARTICULAR FEATURES OF PSORIATIC ARTHRITIS

The most common extra-articular feature in patients with PsA is, by definition, the psoriatic skin lesions. The skin lesions, however, do help make the correct articular diagnosis. The majority of patients with PsA have psoriasis vulgaris, with much lower frequency of guttate psoriasis, pustular psoriasis, or flexural psoriasis. About 80% of the patients with PsA will have nail lesions, including nail pits and onycholysis. In a study comparing patients with PsA to patients with uncomplicated

RADIOLOGICAL FEATURES OF PSORIATIC ARTHRITIS

The peripheral arthritis of PsA has several unique radiologic features. In addition to the distribution noted clinically, including the presence of distal interphalangeal (DIP) joint disease and the tendency to asymmetry, the specific radiologic features of PsA include: lack of juxta-articular osteopenia; the presence of pencil-in-cup change; ankylosis; periosteal reaction; and spur formation. The erosions noted in PsA are often not marginal, as they are in RA, but are paramarginal.

PSORIATIC SPONDYLOARTHROPATHY COMPARED TO

OTHER SERONEGATIVE SPONDYLOARTHROPATHIES

Since spondyloarthropathy occurs frequently in patients with PsA, and the disease shares many of the extra-articular features common to the seronegative spondyloarthropathies, PsA is classified among this group of conditions.50, 81 The spondyloarthropathy of PsA can be distinguished clinically from that of classic ankylosing spondylitis by the lower level of pain and less restriction of spinal movement.29 Both Reiter's disease and idiopathic ankylosing

CLASSIFICATION OF PSORIATIC ARTHRITIS

There are no valid classification criteria for PsA.21 Most investigators have used the definition of an inflammatory arthritis associated with psoriasis, usually seronegative for rheumatoid factor, to include patients in their studies. Once included, patients were classified according to the clinical patterns described above. The European Spondyloarthropathy Study Group (ESSG) proposed preliminary criteria for the classification of spondyloarthropathy which are not particularly helpful for PsA,

COURSE OF PSORIATIC ARTHRITIS

Despite the fact that arthritis mutilans was recognized as a distinct pattern of PsA, the disease was initially thought to be a benign form of arthritis, as the presence of arthritis mutilans was described in only 5% of the patients.44, 62, 80 However, more recent studies demonstrated that the disease may be as severe as RA.20, 24, 41, 71 Patients with PsA are less tender than patients with RA, a fact that may explain the misconception that it was a mild disease.4 In addition, the effusions

PROGNOSIS OF PSORIATIC ARTHRITIS

The development of deformities among patients with PsA may be related to the degree of inflammatory activity at presentation. Gladman et al30 demonstrated that patients who presented with five or more swollen joints were at an increased risk for progression of joint deformities compared to patients who did not have such active inflammation. Patients who had been given high levels of medications were also at greater risk for disease progression. While inflammatory activity did not remain in a

ETIOPATHOGENESIS OF PSORIATIC ARTHRITIS

The exact cause or pathogenesis of PsA is unknown. Several factors have been considered to be important. These include genetic, immunologic, and environmental factors.1

GENETIC FACTORS

Most studies document a familial predisposition to both psoriasis and PsA. With the discovery of the HLA system in humans it has become clear that there are genes on the short arm of chromosome 6 which confer susceptibility to PsA. The HLA antigens B13, B17, B38, B39, B27, Cw6, DR4, and DR7 have been implicated.1, 12, 22 Recently, molecular DNA techniques were applied to identify alleles of the HLA-C locus previously poorly detected using serologic techniques.14, 33 The HLA-Cw*0602 allele was

IMMUNOLOGIC FACTORS

The clinical and pathologic features of both psoriasis and PsA support the role of immunologic factors in the pathogenesis of these conditions. The inflammatory nature of the disease, the cellular infiltrates seen both in skin and joint lesions, and the deposition of immunoglobulins in the epidermis as well as the synovial membrane, all support an immune mechanism.18, 57 Autoantibodies (such as antinuclear antibodies), rheumatoid factor, and antibodies against skin antigens, as well as immune

ENVIRONMENTAL FACTORS INFECTION

Both viral and bacterial infections have been proposed as causative agents in PsA.1 Unlike Reiter's disease and ankylosing spondylitis where it has been suggested that gut bacteria may operate through the HLA-B27 molecule, in PsA it has been the streptococcus which has been incriminated and the relation to HLA-B27 is not as clear, since no more than 50% of the patients with PsA carry this antigen. Some investigators believe that guttate psoriasis is initiated by an infectious agent.73 Support

TRAUMA

The role of trauma has been questioned, particularly because of the well-described Koebner's phenomenon among patients with psoriasis. Although there are case reports suggesting a possible role for trauma in the development of PsA in some patients, 1, 66 and there is a retrospective study supporting the role of trauma, 68 there are no prospective studies which can be relied upon to explore the role of trauma in the development of PsA.

MANAGEMENT OF PSORIATIC ARTHRITIS

The management of patients with PsA requires attention to both skin and joint manifestations. It begins with patient education regarding the inflammatory and chronic nature of his or her disease, and the patient's understanding of the risk of progression of joint deformity and damage. Drug therapy will depend on the extent of the skin and joint manifestations.3, 22 In patients whose skin disease is severe, but the joint manifestations are mild, the latter may require only intermittent use of

References (81)

  • D. Buskila et al.

    Patients with rheumatoid arthritis are more tender than those with psoriatic arthritis

    J Rheumatol

    (1992)
  • BywatersE.G.L. et al.

    Paravertebral ossification in psoriatic arthritis

    Ann Rheum Dis

    (1965)
  • A. Cats

    Psoriasis and arthritis

    Cutis

    (1990)
  • B.L. Coulton et al.

    Outcome in patients hospitalized for psoriatic arthritis

    Clin Rheumatol

    (1989)
  • D.O. Clegg et al.

    Comparison of sulfasalazine and placebo in the treatment of psoriatic arthritis

    Arthritis Rheum

    (1996)
  • DougadosM. et al.

    The European Spondyloarthropathy Study Group preliminary criteria for the classification of spondyloarthropathy

    Arthritis Rheum

    (1991)
  • DougadosM. et al.

    Sulfasalazine in the treatment of spondyloarthropathy. A randomized, multicenter, double-blind, placebo-controlled study

    Arthritis Rheum

    (1995)
  • C.N. Ellis et al.

    Cyclosporin for plaque-type psoriasis. Results of a multidose, double-blind trial

    N Engl J Med

    (1991)
  • C. Enerback et al.

    Evidence that HLA-Cw6 determines early onset of psoriasis, obtained using sequence specific primers (PCR-SSP)

    Acta Derm Venereol

    (1997)
  • L.R. Espinoza et al.

    Psoriatic arthritis: Clinical response and side effects of methotrexate therapy

    J Rheumatol

    (1992)
  • L.R. Espinoza et al.

    Fibroblast function in psoriatic arthritis. I. Alteration of cell kinetics and growth factor responses

    J Rheumatol

    (1994)
  • L.R. Espinoza et al.

    Fibroblast function in psoriatic arthritis. II. Increased expression of beta platelet derived growth factor receptors and increased production of growth factor and cytokines

    J Rheumatol

    (1994)
  • D.D. Gladman

    Immunologic factors in the pathogenesis of psoriatic arthritis

  • D.D. Gladman

    Toward unravelling the mystery of psoriatic arthritis

    Arthritis Rheum

    (1993)
  • D.D. Gladman

    Psoriatic arthritis

  • D.D. Gladman et al.

    HLA antigens in psoriatic arthritis

    J Rheumatol

    (1986)
  • D.D. Gladman et al.

    Psoriatic arthritis—Clinical and laboratory analysis of 220 patients

    QJM

    (1987)
  • D.D. Gladman et al.

    Reliability of measurements of active and damaged joints in psoriatic arthritis

    J Rheumatol

    (1990)
  • D.D. Gladman et al.

    Longitudinal study of clinical and radiological progression in psoriatic arthritis

    J Rheumatol

    (1990)
  • D.D. Gladman et al.

    Chloroquine therapy in psoriatic arthritis

    J Rheumatol

    (1992)
  • D.D. Gladman et al.

    Psoriatic spondyloarthropathy in men and women: A clinical, radiographic, and HLA study

    Clin Invest Med

    (1992)
  • D.D. Gladman et al.

    Differences in the expression of spondyloarthropathy: A comparison between ankylosing spondylitis and psoriatic arthritis. Genetic and gender effects

    Clin Invest Med

    (1993)
  • D.D. Gladman et al.

    Clinical indicators of progression in psoriatic arthritis (PSA): Multivariate relative risk model

    J Rheumatol

    (1995)
  • D.D. Gladman et al.

    The role of HLA antigens as indicators of progression in psoriatic arthritis (PSA): Multivariate relative risk model

    Arthritis Rheum

    (1995)
  • D.D. Gladman et al.

    HLA antigens and progression in psoriatic arthritis

    J Rheumatol

    (1998)
  • D.D. Gladman et al.

    HLA C-locus alleles in psoriatic arthritis

    Hum Immunol

    (1997)
  • D.D. Gladman et al.

    Mortality studies in psoriatic arthritis. Results from a single centre. II. Prognostic factors for death

    Arthritis Rheum

    (1998)
  • M.W. Greaves et al.

    Treatment of psoriasis

    N Engl J Med

    (1995)
  • A.K. Gupta et al.

    Cyclosporin in the treatment of psoriatic arthritis

    Arch Dermatol

    (1989)
  • A.K. Gupta et al.

    Sulfasalazine therapy for psoriatic arthritis: A double blind, placebo controlled trial

    J Rheumatol

    (1995)
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    Address reprint requests to: Dr. Dafna Gladman, Centre for Prognosis Studies in the Rheumatic Diseases, The Toronto Hospital, Western Division, 399 Bathurst Street, Suite 1-318, Toronto, Ontario, M5T 2S8, Canada

    This work is supported by The Medical Research Council of Canada and The Canadian Arthritis Society.

    *

    From the University of Toronto, Division of Rheumatology; Centre for Prognosis Studies in the Rheumatic Diseases; and the Psoriatic Arthritis Program, the Toronto Hospital, Toronto, Ontario, Canada

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