Psoriatic Arthritis: Diagnosis and Management

Introduction

Psoriatic arthritis (PsA) is a chronic inflammatory arthritis that develops in a substantial minority - up to 30% - of people with psoriasis. Like ankylosing spondylitis, it belongs to the seronegative spondyloarthropathy family: rheumatoid factor and anti-CCP are typically negative, there is an association with HLA-B27 (particularly in axial disease), and enthesitis rather than pure synovitis is a defining feature.¹

It is examined heavily because its joint pattern deliberately overlaps with, yet differs from, rheumatoid arthritis, and recognising which is which - DIP involvement, dactylitis, nail changes, asymmetry - is exactly the kind of pattern-recognition question that comes up repeatedly.

Aetiology

As with psoriasis itself, PsA arises from a combination of genetic susceptibility (HLA-B27, HLA-Cw6 and others), immune dysregulation - particularly the IL-23/IL-17 axis, which is now the target of several effective biologic drugs - and environmental triggers, including physical trauma to a joint or entheseal site (the 'deep Koebner phenomenon').

Risk factors

• Psoriasis, particularly more extensive or severe skin disease and nail involvement
• Family history of psoriasis or psoriatic arthritis
• HLA-B27 and other HLA associations, particularly relevant to axial disease
• Obesity - both a risk factor for developing PsA and a predictor of poorer response to treatment
• Physical trauma to a joint or entheseal site, through the 'deep Koebner phenomenon'
• Smoking

Clinical features

PsA is classically divided into five patterns (Moll and Wright), though patients often show a mix and the pattern can evolve over time:

Distinguishing features

• Dactylitis - diffuse swelling of an entire digit ('sausage finger/toe') from combined synovitis, tenosynovitis and soft tissue oedema
• Enthesitis - Achilles tendon, plantar fascia, and other tendon insertions
• Nail changes - pitting, onycholysis (separation of the nail from the bed), subungual hyperkeratosis, and the 'oil drop sign' (a translucent yellow-brown discolouration under the nail plate). Nail disease correlates strongly with DIP joint involvement
• Asymmetry - in contrast to the symmetry typical of rheumatoid arthritis, though the symmetrical polyarthritis pattern is an exception
• Skin psoriasis - plaques on extensor surfaces, scalp, natal cleft and umbilicus; look in these hidden sites specifically
• Eye disease - conjunctivitis and, less commonly, anterior uveitis

Examination

• Look for asymmetrical joint swelling, dactylitis, and psoriatic plaques in visible and hidden sites (scalp, natal cleft, umbilicus, behind the ears)
• Feel the DIP joints and entheseal sites (Achilles insertion, plantar fascia origin, lateral epicondyle) for tenderness and swelling
• Nails - inspect closely for pitting, onycholysis, subungual hyperkeratosis and the oil drop sign, which can be subtle
• Spine and sacroiliac joints - assess range of movement and perform provocation tests if axial disease is suspected
• Function - grip strength and hand function can be significantly affected even with modest-looking joint swelling, because of concurrent tenosynovitis and dactylitis

Differential diagnosis

• Rheumatoid arthritis - symmetrical, spares the DIPs, seropositive in most
• Osteoarthritis - DIPs affected in both, but OA is non-inflammatory, bony rather than boggy, without dactylitis, nail pitting or a raised CRP
• Gout - can also cause DIP involvement and coexist with OA; aspirate if there is doubt
• Other seronegative spondyloarthropathies - reactive arthritis and enteropathic arthritis share the enthesitis/axial pattern but have their own triggers and associations

Investigations

• Rheumatoid factor and anti-CCP - typically negative (a small minority are RF positive, which does not exclude PsA)
• CRP/ESR - may be raised but are less reliably elevated than in rheumatoid arthritis, and normal inflammatory markers do not exclude active disease
• Plain radiographs - erosive change combined with new bone formation (periostitis), producing the classic 'pencil-in-cup' deformity at the DIP joint as the phalanx is whittled to a point while the base of the adjacent bone widens; also osteolysis in arthritis mutilans
• Ultrasound or MRI - more sensitive for detecting synovitis, tenosynovitis and enthesitis, and useful where the diagnosis is unclear clinically

Screening and classification

The PEST (Psoriasis Epidemiology Screening Tool) questionnaire is used in dermatology clinics to identify patients with psoriasis who may have undiagnosed arthritis, prompting referral to rheumatology. The CASPAR criteria are used to classify established psoriatic arthritis in research and specialist practice, requiring inflammatory joint disease plus a defined score across psoriasis, nail disease, a negative RF, dactylitis and radiographic new bone formation.²

Management

Management is tailored to which pattern predominates - peripheral, axial, enthesitis/dactylitis-predominant, or skin-and-joint disease together - and involves close working between rheumatology and dermatology.³

Mild peripheral disease

NSAIDs and intra-articular corticosteroid injection for mono- or oligoarthritis, alongside physiotherapy.

Conventional synthetic DMARDs

Methotrexate is generally first-line for peripheral arthritis, particularly attractive when significant skin disease coexists since it treats both. Leflunomide, sulfasalazine and ciclosporin are alternatives, chosen partly on the basis of predominant skin versus joint involvement.

Biologic and targeted synthetic therapy

For disease inadequately controlled on conventional DMARDs, biologic therapy is escalated to, with several classes now available that also treat the skin:

• Anti-TNF (adalimumab, etanercept, infliximab, certolizumab)
• Anti-IL-17 (secukinumab, ixekizumab) - effective for both skin and joint disease, including axial involvement
• Anti-IL-12/23 (ustekinumab) and anti-IL-23 (guselkumab, risankizumab)
• JAK inhibitors (tofacitinib, upadacitinib) - oral option where biologics are unsuitable
• Apremilast - an oral PDE4 inhibitor, an option for milder disease not requiring biologic therapy

Axial psoriatic disease is managed in the same stepwise way as ankylosing spondylitis: NSAIDs first, since conventional DMARDs do not work on the axial skeleton, then a biologic (anti-TNF or anti-IL-17) if needed.

Complications

Uncontrolled disease leads to progressive joint destruction, and in the most severe pattern, arthritis mutilans, to marked functional impairment from bone resorption and digit telescoping. Like the other spondyloarthropathies, PsA carries an increased risk of cardiovascular disease related to chronic inflammation, and metabolic syndrome is common in psoriasis more broadly. Psychological impact - depression and reduced quality of life from combined skin and joint disease - is significant and should be actively asked about.

Red flags

Prognosis

Course is variable: some patients have mild, self-limiting oligoarthritis, while others develop progressive, erosive, deforming disease, particularly with delayed treatment. As with rheumatoid arthritis, early DMARD therapy aiming for low disease activity or remission substantially reduces the risk of irreversible joint damage, and the expansion of biologic options has considerably improved outcomes for both skin and joint disease over the last two decades.