The prevalence of psoriasis is 1-2 per cent, while for psoriatic arthritis (PsA), it is about 0.3 per cent.1 A practice of 5,000 patients would expect to see 100 patients with psoriasis and 15 with PsA. Both are equally common in men and women, and have a peak age of onset between 20 and 40 years. The role of environmental factors, such as infection, in the aetiology is unclear. Familial aggregation has been demonstrated in PsA.
PATHOGENESIS AND PROGNOSIS
The T-cell plays a central part in the pathogenesis of psoriasis and PsA. Evidence for this includes the abundance of T-cells within psoriatic plaques and the involved synovium, the response to therapies that suppress lymphocyte function and the association of psoriasis and PsA with HIV infection.
Cytokines, such as tumour necrosis factor (TNF), are overexpressed in skin and synovium. However, because manifestations of skin and joint can occur independently, the pathogenesis is not identical.
The diagnosis of psoriasis is suggested by the presence of a rash comprising raised, well-marginated, erythematous plaques with silver scales. Nail changes, such as pitting, ridging, discoloration or onycholysis, are common and may be a useful clue to diagnosis. Psoriatic plaques occur most commonly on the scalp, extensor aspects of the limbs and hidden sites, such as the genital area and the umbilicus.
PsA is an inflammatory arthropathy characterised by morning stiffness and joint swelling. Whole digits may swell because of arthritis and tenosynovitis (dactylitis). Large and small joints may be involved and distribution is often asymmetrical.
Enthesitis, inflammatory lesions at the insertion of tendon into bone, are a hallmark of PsA. Sacroiliitis or spondylitis are uncommon, but are suggested by morning stiffness and pain in the low back or buttocks that improves with activity.
About 70 per cent of patients manifest psoriasis first, with the arthritic symptoms developing later. Of the remaining 30 per cent, about half present with symptoms in skin and joints, and the remainder initially with arthritic symptoms alone.
There is no specific test for PsA. Acute phase reactants, such as ESR or C-reactive protein, may be elevated and there may be anaemia of chronic disease. Rheumatoid factor is usually absent, but its presence does not exclude a diagnosis of PsA.
Characteristic radiographic features include asymmetry of involvement, osteolysis or pencilling of phalanges, proliferative erosions, tendon spurs and sacroiliitis.
Joint involvement varies from isolated monoarthritis to widespread, destructive arthritis. For some, symptoms are mild and change little over decades. For others, PsA is a progressive and disabling disease. Involvement of joints and skin means that for some, quality of life is poor.2 As in rheumatoid arthritis, there is an increased risk of premature mortality.
Topical treatments are the first step for psoriasis. Many are good at reducing scaling, but compliance can be problematic because frequent applications may be needed. UV irradiation is effective,3 but inconvenient.
Physiotherapy, occupational therapy and self-management education are important. NSAIDs offer good symptomatic relief, while intra-articular steroid injections may also be effective in monoarthritis. Any patient with suspected PsA should be referred to a rheumatologist. Early treatment with disease-modifying antirheumatic drugs (DMARDs) improves long-term outcome. Although evidence for the efficacy of DMARDs in PsA is not as strong as for rheumatoid arthritis, sulfasalazine, methotrexate, ciclosporin and leflunomide all appear effective.
In terms of newer drugs, the anti-TNF alpha drugs adalimumab, etanercept and infliximab are licensed for use in the treatment of active and progressive PsA that has not responded to DMARDs. NICE has produced guidance on etanercept and infliximab for PsA4 and on adalimumab in moderate-to-severe PsA.5 The British Society for Rheumatology has produced guidelines on the use of anti-TNF drugs in PsA.6
Biological therapies improve symptoms and decrease radiographic progression in PsA and are effective in psoriasis. NICE has produced guidance on etanercept and efalizumab in psoriasis7 and is reviewing infliximab for this indication.
The toxicity profiles of biological agents are better than those of conventional DMARDs and blood test monitoring is less important. However, one potential concern with anti-TNF drugs is reactivation of latent TB due to an immunosuppressant adverse effect. Finally, biological agents are costly, although there may be long-term savings.
- Dr John Berth-Jones is consultant dermatologist at the University Hospitals Coventry and Warwickshire NHS Trust; Dr Rebecca Neame is consultant dermatologist at the University Hospitals of Leicester NHS Trust.
1. Gladman DD, Antoni C, Mease P et al. Psoriatic arthritis: epidemiology, clinical features, course, and outcome. Ann Rheum Dis 2005;64 Suppl 2:ii14-17.
2. Sokoll KB, Helliwell PS. Comparison of disability and quality of life in rheumatoid and psoriatic arthritis. J Rheumatol 2001;28:1842-6.
3. Prins M, Krabbe PF, Swinkels QO et al. The effect of treatment on quality of life in psoriasis patients. Acta Derm Venereol 2005;85:304-10.
4. NICE. Etanercept and infliximab for the treatment of adults with psoriatic arthritis . Technology Appraisal 104. NICE, London, 2006.
5. NICE. Adalimumab for the treatment of psoriatic arthritis . Technology Appraisal 125. NICE, London, 2007.
6. Kyle S, Chandler D, Griffiths CE et al. Guideline for anti-TNF-alpha therapy in psoriatic arthritis. Rheumatology 2005;44:390-7.
7. NICE. Etanercept and efalizumab for the treatment of adults with psoriasis . Technology Appraisal 103. NICE, London, 2006.