Psoriatic Arthritis

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Psoriatic arthritis (PsA) is inflammatory arthropathy affecting both large and small joints. PsA is seen in 1 in 5 patients with psoriasis and can occur either before, during or after the onset of psoriatic skin changes.1,2

The typical age of onset is 30-50 years old, with males and females equally affected.2

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There is a strong genetic association as the majority of patients with PsA have at least one first or second degree relative with psoriasis or psoriatic arthritis.3

PsA belongs to a group of seronegative inflammatory spondyloarthropathies where the human leukocyte antigen B27 (HLA-B27) is commonly implicated.4

As PsA is a seronegative arthropathy, blood tests for rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) are usually negative.


PsA results from an immune-mediated inflammatory response that affects the skin, joints, and periarticular structures. It tends to occur in patients with a genetic predisposition who are exposed to an environmental factor (e.g. joint trauma).

Risk factors

Risk factors for psoriatic arthritis include:

  • Personal history of psoriasis
  • First degree relative with psoriasis or psoriatic arthritis
  • History of joint trauma

Clinical features


Typical symptoms of psoriatic arthritis include:

  • Joint pain
  • Morning stiffness: greater than 30 minutes and improves over the course of the day
  • Constitutional symptoms: fatigue, malaise and low-grade fevers

The most common joints involved are the spine, sacroiliac joints (SIJ) and the small joints of the hands.

There are five recognised patterns of joint involvement:1

  • Asymmetric oligoarthritis: less than four joints affected in an asymmetrical pattern (most common)
  • Distal interphalangeal dominant: arthralgia of DIPs of fingers and toes with dystrophic nail changes
  • Symmetric polyarthritis: five or more joints affected in a symmetrical pattern
  • Spondylitis: inflammation of the spine including the neck, low back and SIJ
  • Arthritis mutilans: a rare and severe destructive arthropathy of the small joints in the hands and toes, coinciding with severe dactylitis

The Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) defines psoriatic arthritis by the following constellation of articular and extra-articular symptoms:5

  • Peripheral arthritis: joints of hands, feet, arms, leg
  • Axial disease: lower back and neck
  • Enthesitis: inflammation at the insertion of tendons and ligaments (most commonly the Achilles tendon)
  • Dactylitis: inflammation of whole digital fingers or toes
  • Skin psoriasis: plaques on extensor surfaces neck; dystrophic nail changes (hyperkeratosis, pitting, ridging)
  • Inflammatory bowel disease (IBD)

Clinical examination

Typical clinical findings of psoriatic arthritis on examination may include:6

  • Swelling of the affected joints
  • Tenderness of the affected joints
  • Reduced range of motion
  • Achilles tendonitis
  • Epicondylitis (enthesitis of the elbow)
  • Dactylitis
  • Lumbar spine flexion (by modified Schober test) (Figure 1)
The modified Schober test
Figure 1. The modified Schober test is used to assess lumbar spine flexion by measuring the distance between 2 points while the spine is in neutral alignment and while the spine is forward flexion.

Extra-articular manifestations

The following extra-articular manifestations are associated with seronegative spondyloarthropathies:

  • Mitral valve prolapse
  • Aortic root dilation
  • Aortic regurgitation
  • Uveitis
  • Urethritis

Differential diagnoses

Differential diagnoses to consider in the context of psoriatic arthritis include:

  • Rheumatoid arthritis (RA)
  • Reactive arthritis
  • Sarcoidosis
  • Ankylosing spondylitis
  • Calcium pyrophosphate deposition disease (CPPD)


Laboratory investigations

Relevant laboratory investigations include:

  • Rheumatoid factor (RF): a defining feature of PsA is seronegative blood tests, so RF positivity significantly lowers the likelihood of PsA
  • Anti-cyclic citrullinated peptide (anti-CCP): this finding is specific for rheumatoid arthritis, so positivity suggests RA rather than PsA
  • Inflammatory markers: erythrocyte sedimentation rate (ESR) and c-reactive protein (CRP) are non-specific markers that can indicate the degree of joint inflammation prognosis. They are less commonly elevated in PsA than RA.


Relevant imaging investigations include:

  • X-ray of affected joints: may show erosion of the small joints. Classic findings are erosions of the DIP with periarticular bone formation (osteophytes). In advanced disease, there may be โ€œpencil in cup deformityโ€ at the DIP
  • X-ray of the sacroiliac joints (SIJ): usually normal in the initial stages, but it is important to obtain a baseline radiograph for assessing disease progression
  • MRI of SIJ: looking for joint oedema (not routinely performed due to low specificity)


The diagnosis for PsA is a clinical diagnosis based on history and examination.

The CASPAR classification can be used to aid in the diagnosis, but it is intended for research, not clinical practice.7


Medical management

The goal of management is to control joint inflammation to prevent long-term erosive changes and disability.

Management options include:

  • Non-steroidal anti-inflammatory drugs (NSAIDs): control inflammation and relieve pain but can take weeks to see an effect. Consider selective COX-2 inhibitors like celecoxib for those who cannot tolerate non-selective NSAIDs
  • Intraarticular glucocorticoid injection: reduce arthralgia but can aggravate skin symptoms (not routinely done)
  • Disease-modifying antirheumatic drugs (DMARDs)

Typical DMARDs used in the management of psoriatic arthritis include:

  • Methotrexate (MTX): an antifolate drug that is effective at treating skin lesions and peripheral joint symptoms, but less effective for axial joint symptoms. Often used first-line when multiple peripheral joints are affected.8
  • Leflunomide
  • Sulfasalazine


Biologics are monoclonal antibodies that can target specific components of the immune response to control inflammation.

Biologics used in the management of psoriatic arthritis include:

  • Tumour necrosis factor-alpha (TNF-a) inhibitors: an effective therapy for those who do not respond to MTX or those with axial joint symptoms
  • Ustekinumab (Stelaraยฎ): blocks IL-12 and IL-23 which inhibits T cell activation in an alternate inflammatory pathway to TNF-a, so considered in those who do not respond to TNF-a inhibitors
  • Secukinumab (Cosentyxยฎ): blocks IL-17 in an which is another potential target for treatment affected for those who do not respond to initial therapy
  • Tofacitinib (Xeljanzยฎ): JAK inhibitors are a newer class of biologics that can be considered when the initial treatment options donโ€™t work
Pre-biologic screening tests

Patients need to be screened for underlying infections that may become reactivated when biologics are initiated.ย 

Pre-biologic assessment should include testing for:

  • Tuberculosis: chest X-ray and interferon-gamma release assay (IGRA) blood test
  • HIV: viral serology
  • Hepatitis B: viral serology
  • Hepatitis C: viral serology


Complications of psoriatic arthritis include:

  • Cardiovascular disease: PsA is associated with a higher prevalence of obesity and dyslipidaemia, so patients are at an increased risk for cardiovascular disease 9
  • Joint erosion: those with bilateral spondylitis may show rapid joint deterioration of the hip and need arthroplasty

Key points

  • PsA is a seronegative inflammatory spondyloarthropathy that affects a subset of patients with psoriasis. The timing of arthritis does not always coincide with the onset of skin lesions.
  • There are strong genetic links as many patients have a first or second-degree relative with psoriasis or PsA. The haplotype of HLA-B27 is common to many of the seronegative spondyloarthropathies.
  • There are multiple known patterns in PsA affecting small joints, large joints and the axial skeleton
  • Enthesitis and dactylitis are hallmark findings in PsA
  • Diagnosis of PsA is clinical, based on history and physical examination findings and can be aided by the CASPAR criteria
  • The initial management includes NSAIDs, but DMARDs like methotrexate prove to be an effective drug for those with peripheral disease. Those with axial symptoms often benefit from biologics like TNF-a inhibitors, with alternate inflammatory targets should these not be effective
  • In the long term, patients with PsA have an increased risk of metabolic syndromes and cardiovascular disease


Dr Grainne Murphy

Consultant Rheumatologist


Dr Chris Jefferies


  1. Alinaghi, F., Calov, M., Kristensen, L. E., Gladman, D. D., Coates, L. C., Jullien, D., Gottlieb, A. B., Gisondi, P., Wu, J. J., Thyssen, J. P., & Egeberg, A. (2019). Prevalence of psoriatic arthritis in patients with psoriasis: A systematic review and meta-analysis of observational and clinical studies. Journal of the American Academy of Dermatology, 80(1).ย 
  2. Gladman, D. D. (2005). Psoriatic arthritis: epidemiology, clinical features, course, and outcome. Annals of the Rheumatic Diseases, 64(suppl_2), ii14โ€“ii17.ย 
  3. Di Lernia, V., Ficarelli, E., Lallas, A., & Ricci, C. (2014). Familial aggregation of moderate to severe plaque psoriasis. Clinical and Experimental Dermatology, 39(7), 801โ€“805.ย 
  4. FitzGerald, O., Haroon, M., Giles, J. T., & Winchester, R. (2015). Concepts of pathogenesis in psoriatic arthritis: genotype determines clinical phenotype. Arthritis Research & Therapy, 17(1).ย 
  5. Coates, L. C., Kavanaugh, A., Mease, P. J., Soriano, E. R., Laura Acosta-Felquer, M., Armstrong, A. W., Bautista-Molano, W., Boehncke, W.-H., Campbell, W., Cauli, A., Espinoza, L. R., FitzGerald, O., Gladman, D. D., Gottlieb, A., Helliwell, P. S., Husni, M. E., Love, T. J., Lubrano, E., McHugh, N., โ€ฆ Ritchlin, C. T. (2016). Group for Research and Assessment of Psoriasis and Psoriatic Arthritis 2015 Treatment Recommendations for Psoriatic Arthritis. Arthritis & Rheumatology.ย 
  6. Korean Academy of Rehabilitation Medicine. Modified Schober Test assessing flexion at lumbar spine. Licence: [CC BY-NC 4.0]
  7. Taylor, W., Gladman, D., Helliwell, P., Marchesoni, A., Mease, P., & Mielants, H. (2006). Classification criteria for psoriatic arthritis: Development of new criteria from a large international study. Arthritis & Rheumatism, 54(8), 2665โ€“2673.ย 
  8. Black, R. L., O’Brien, W. M., Van Scott, E. J., Auerbach, R., Eisen, A. Z., & Bunim, J. J. (1964). Methotrexate Therapy in Psoriatic Arthritis. JAMA, 189(10).ย 
  9. Gladman, D. D., Ang, M., Su, L., Tom, B. D., Schentag, C. T., & Farewell, V. T. (2008). Cardiovascular morbidity in psoriatic arthritis. Annals of the Rheumatic Diseases, 68(7), 1131โ€“1135.ย 


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