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Rheumatology clinic - psoriatic arthritis

Rheumatologists Dr Farrouq Mahmood and Dr Philp Helliwell discuss newly-presenting progressive joint pain

Case

A 27-year-old male presented to his GP with a two year history of gradually worsening joint pains that started in his right thumb. Over the past six months the pain spread to his other fingers and his feet. He complained of early morning stiffness lasting up to three hours. He complained of thoracic spinal pain but denied any lumbar pain. His blood tests showed a raised CRP 31 and a plasma viscosity of 1.86. He had no rash but there was a family history of psoriasis.

When he was examined by the specialist, he had evidence of seven swollen and tender joints in his hands and a swollen left knee. He had nail pitting in both thumbs and right Achilles tendon enthesitis.

He was rheumatoid factor and anti-CCP negative. X-rays of hands and feet showed no frank erosions. A diagnosis of psoriatic arthritis was made. He was referred for an assessment by physiotherapy and occupational therapy and to the rheumatology nurse in order to start disease modifying therapy.

The problem

Psoriatic arthritis (PsA) is a chronic, multisystem inflammatory disorder that mainly affects the skin and joints. It is part of the seronegative spondylarthroapthy group of rheumatic diseases which include Ankylosing Spondylitis and Reactive Arthritis. These conditions share similar clinical characteristics. If left untreated it can lead to disability and reduced quality of life. Diagnosis can be difficult1 and patients can experience severe, debilitating pain and loss of function in everyday activities. Joint pathology can precede onset of skin disease in up to 15% of cases, leading to uncertainty and delay of diagnosis. Some patients may never develop skin symptoms at all. At present there are no formal diagnostic criteria for PsA, although the CASPAR classification criteria are used to help classify and differentiate PsA from rheumatoid arthritis.2 Due to the varied clinical phenotypes and lack of skin signs in some cases, making a diagnosis of PsA can be very challenging. However there are several distinguishing features clinically and on imaging that, if present, can enable the clinician to consider it as a differential diagnosis in a patient presenting with inflammatory arthritis, especially if there is a family history of psoriasis.

Inflammatory articular disease (joint, spine, or entheseal)

With 3 or more points from the following:

1. Current psoriasis (scores 2 points)

Psoriatic skin or scalp disease present today as judged by a dermatologist

2. Personal history of psoriasis (if current psoriasis not present)

A history of psoriasis that may be obtained from patient, family doctor, dermatologist or rheumatologist

3. Family history of psoriasis (if personal history of psoriasis or current psoriasis is not present)

A history of psoriasis in a first or second degree relative according to patient report

4. Psoriatic nail dystrophy

Typical psoriatic nail dystrophy including onycholysis, pitting and hyperkeratosis observed on current physical examination

5. A negative test for rheumatoid factor

By any method except latex but preferably by ELISA or nephlemetry, according to the local laboratory reference range

6. Current dactylitis

Swelling of an entire digit

7. History of dactylitis (if current dactylitis is not present)

A history of dactylitis recorded by a rheumatologist

8. Radiological evidence of juxta-articular new bone formation

Ill-defined ossification near joint margins (but excluding osteophyte formation) on plain xrays of hand or foot

Table 1: CASPAR criteria

Features

Psoriatic arthritis typically presents with patients complaining of painful and swollen joints associated with stiffness. But it can have a varied pattern of clinical presentations.1 Psoriatic arthritis can present as an asymmetrical oligoarthritis, a rheumatoid like symmetrical polyarthritis, predominant distal interphalangeal disease or spondylitis.1

The type of joint swelling can differ between psoriatic arthritis and rheumatoid arthritis. Dactilitis is the swelling of an entire digit3,4 as opposed to a joint (see figure 1). It can manifest as a combination of synovitis, tenosynovitis and soft-tissue oedema. Enthesitis, inflammation at the point where tendons and ligaments attach to bone4, can be widespread but is most commonly seen at the heel (see figure 2). In severe cases, psoriatic arthritis can lead to shortening of digits, which is secondary to severe bone lysis. Arthritis mutilans is a severe phenotypic expression of psoriatic arthritis with extensive bony deformities.

There are several extra-articular features which can help distinguish psoriatic arthritis from other arthropathies. Nails can be affected, with nail pitting and onycholysis.4 Rheumatoid nodules are absent and rheumatoid factor is found only occasionally in PsA. Inflammatory markers at time of presentation can be normal or raised. Psoriatic arthritis is associated with dry, scaly skin plaques, commonly found over the elbows, knees and scalp, although it can occur all over the body. As discussed earlier some patients may not have any skin symptoms at time of presentation.

Radiographs of the hands and feet can be a useful investigation to confirm the type of arthritis a patient is suffering from. Erosions are typically the hallmark feature of joint inflammation. In psoriatic arthritis the erosions are more distal and asymmetrical5 whereas RA erosions are more MCP dominant and usually occur in a symmetrical pattern. Psoriatic arthritis may develop ‘pencil-in-cup’ deformities which results from periarticular erosions and bone resorption.5 Bone proliferation can give a ‘fuzzy’ appearance to bone margins in psoriatic arthritis. If a patient presents with inflammatory sounding low back pain, X-rays of the sacroiliac joints can show an asymmetrical sacroiliitis.

gig 1 dactylitis

 

Figure 1: Dactylitis 

fig 2 achilles enthesitis

 

Figure 2: Achilles enthesitis 

Diagnosis

Table 2 below summarises the differences between psoriatic arthritis and RA.

Clinical featuresRAPsoriatic arthritis

Joint involvement

Symmetrical, poly articular

Asymmetrical, oligo articular

Hand involvement

MCP/PIP joint predominant

DIP joint predominant

Skin involvement

Rare

Skin plaques present

Inflammatory markers

Raised

Normal or moderately raised

Nail changes

Absent

Pitting/onycholysis

Enthesitis

Usually absent

Present

Spinal disease

Rare

Present

Nodules

Present

Absent

Rheumatoid factor

Present

Usually absent or low titre

Anti-CCP

Present

Usually absent or low titre

Dactilitis

Absent

Present

Table 2

Management

Psoriatic arthritis should be managed with appropriate specialist input with prompt referral to rheumatology and, if there is skin involvement, with dermatology. According to the British Society of Rheumatology6 the aim should be to suppress inflammation in all domains of the disease – joints, skin, tendons and enthesis.

Management with NSAIDs and local/intra-articular steroid injections would be first-line treatment for patients with psoriatic arthritis while awaiting specialist review. Intramuscular corticosteroids can give effective systemic relief while awaiting the effect of systemic disease-modifying drugs. Patients should, however, be warned that it can cause a flare in skin disease. Caution should also be used if giving steroid treatment to a patient prior to initial consultation with a specialist as it can mask clinical signs needed for a diagnosis.

Disease modifying anti-rheumatic drugs (DMARDs) are used in systemic inflammatory conditions like psoriatic arthritis4,5 in order to suppress underlying inflammation and prevent further joint damage. These drugs should only be initiated by a specialist as patients need to be counselled on side-effects, blood monitoring regimes and family planning. While evidence is not as robust for use of DMARDs in psoriatic arthritis when compared with RA, there are reports of efficacy. Specialists may initiate treatment with methotrexate, sulphasalazine or leflunomide. Blood tests need close monitoring for neutropenia or hepatotoxicity. Drug toxicity secondary to renal failure can also occur. If patients suffer with an infection while being on DMARDs it is normally recommended that the drug is stopped while the patient recovers. Most rheumatology departments would have shared care guidelines that GPs could use to guide them in managing DMARD patients.

Biologic treatment with anti-TNF drugs has been an emerging therapeutic field that has revolutionised the treatment of inflammatory diseases in the past 20 years. Generally they are reserved for patients who have failed at least two conventional DMARDs.6 However, there are some patients who may have more severe disease with polyarticular involvement and raised inflammatory markers who would benefit from an earlier switch to biologics.6 This group of drugs target and block various immune pathways leading to suppression of inflammation. Data shows that they have good efficacy for both skin and joints but like DMARD therapy, patients need close monitoring for side effects and blood disorders. Reactivation of tuberculosis and risk of skin malignancy are some of the rare side effects associated with biologics.

Newer treatment options are being developed and show promising results. Other biologics, such as Ustekinumab and Secukinumab, and newer oral agents such as Apremilast have shown good efficacy in psoriatic arthritis7 and psoriasis, allowing specialists to have a broader range of therapeutic options available. These drugs block pro-inflammatory cytokines causing a down-regulation in the inflammatory cascade. It is likely that their use will become more widespread in future clinical practice.

Dr Farrouq Mahmood is a clinical research fellow in rheumatology at Bradford Teaching Hospitals

Dr Philip Helliwell is a consultant rheumatologist at Bradford Teaching Hospitals and senior lecturer in rheumatology at the University of Leeds

References

  1. Conaghan PG, Coates LC. Improving recognition of psoriatic arthritis. Practitioner. 2009 Dec;253(1724):15-8, 2-3.
  2. Taylor WJ, Gladman DD, Helliwell PS, Marchesoni A, Mease PJ, Mielants H. Classification citeria for psoriatic arthritis: Development of new criteria from a large international study. Arthritis and Rheumatism. 2006;54(8):2665-73.
  3. Healy PJ, Groves C, Chandramohan M, Helliwell PS. MRI changes in psoriatic dactylitis–extent of pathology, relationship to tenderness and correlation with clinical indices. Rheumatology (Oxford). 2008 Jan;47(1):92-5.
  4. Kerschbaumer A, Fenzl KH, Erlacher L, Aletaha D. An overview of psoriatic arthritis – epidemiology, clinical features, pathophysiology and novel treatment targets. Wiener Klinische Wochenschrift. 2016;128(21):791-795.
  5. Liu J-T, Yeh H-M, Liu S-Y, Chen K-T. Psoriatic arthritis: Epidemiology, diagnosis, and treatment. World Journal of Orthopedics. 2014;5(4):537-543. doi:10.5312/wjo.v5.i4.537.
  6. Coates LC, Tillett W, Chandler D, Helliwell PS, Korendowych E, Kyle S, McInnes IB, Oliver S, Ormerod A, Smith C, Symmons D, Waldron N, McHugh NJ; BSR Clinical Affairs Committee & Standards, Audit and Guidelines Working Group and the BHPR. The 2012 BSR and BHPR guideline for the treatment of psoriatic arthritis with biologics. Rheumatology (Oxford). 2013 Oct;52(10):1754-7. doi: 10.1093/rheumatology/ket187. Epub 2013 Jul 25.
  7. Lubrano E, Perrotta FM. Beyond TNF Inhibitors: New Pathways and Emerging Treatments for Psoriatic Arthritis. Drugs. 2016 Apr;76(6):663-73. doi: 10.1007/s40265-016-0557-4.

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