Psoriatic arthritis


  • Psoriatic arthritis (PsA) affects up to 1%1,2 of the population. The proportion of patients with skin psoriasis who develop PsA is uncertain, with estimates ranging from 6% to 42%,1,3,4 usually within 5–10 years of cutaneous disease onset1
  • Patients with psoriasis or PsA, or both, generally have reduced health-related quality of life, productivity and functionality1
  • Approximately two-thirds of patients with PsA develop joint damage;5 joint erosions develop within 2 years of PsA symptom onset in approximately 50% of patients4
  • The presence of PsA and psoriasis adds approximately US $23,000/year (approximately €20,000) to the total medical costs versus patients without PsA and psoriasis6

Differences between PsA and rheumatoid arthritis

Despite apparent similarities between PsA and rheumatoid arthritis, there are important differences between them7

 Psoriatic arthritisRheumatoid arthritis
  • DIP joint and axial arthritis
  • Often asymmetrical
  • Enthesitis common
  • MCP and wrist joints
  • Predominantly symmetrical
  • HLA Cw6 and B27
  • IL23 receptor
  • HLA DRB1
  • Absence of circulating autoantibodies
  • Distinct vascular pathology
  • T-lymphocyte predominance
  • Early expression of vascular growth factors
  • Circulating autoantibodies RF/ACPA
  • T-lymphocyte and B-lymphocyte infliltrate
  • Late expression of vascular growth factors
Response to therapy
  • DMARDs, e.g. MTX
  • TNF inhibitors
  • Abatacept
  • Ustekinumab
  • Secukinumab
  • DMARDs, e.g. MTX
  • TNF inhibitors
  • Abatacept
  • Rituximab
  • Tocilizumab

ACPA, anti-citrullinated protein antibody; DIP, distal interphalangeal; DMARDs, disease modifying anti-rheumatic drugs; HLA, human leukocyte antigen; MCP, metacarpophalangeal; MTX, methotrexate; RF; rheumatoid factor; TNF, tumor necrosis factor.

Adapted from Veale and Fearon.7

Burden of psa

PsA: Under-diagnosis and under-treatment

  • PsA may be underdiagnosed,8 and if untreated it can lead to severe disability and comorbidities9
  • An international survey (712 PsA patients) found that more than half of patients (59%) reported that they were receiving no treatment or receiving topical therapy only, and were not receiving any systemic medication for their joint disease10

Multinational Assessment of Psoriasis and Psoriatic Arthritis (MAPP) survey: Affected joint count and self-perceived severity10

Adapted from Kavanaugh et al.10 A total of 712 patients with PsA were included. *Including only patients with PsA who reported joint pain (n=628).


MAPP survey: Impact of PsA on physical function1

Adapted from Kavanaugh et al.10 Shown are the proportions of patients who responded ‘with much difficulty’ or ‘unable to do’.

MAPP survey: Impact of PsA on work productivity1

Adapted from Kavanaugh et al.10 Shown for ‘Missed work in past 12 months’ is the proportion of patients who responded with ‘yes’; all other responses represent the proportion of patients reporting ‘a lot’ or ‘some’ impact of PsA.


Treatment options in PsA

  • Still widely used for PsA treatment, especially in mild disease
  • Can relieve musculoskeletal symptoms, but have no efficacy on skin lesions
  • Milder/less toxic than DMARDs
  • Local injections of steroids can be used as adjunctive therapy for peripheral arthritis and enthesitis
  • Systemic steroids can lead to flares of skin psoriasis, so should be used with caution
Conventional DMARDs
  • Patients with active disease despite NSAID therapy should receive DMARDs
  • They are ineffective in axial disease, and little evidence of efficacy in enthesitis

Methotrexate (MTX)

  • MTX is recommended in guidelines as the first choice DMARD, either as monotherapy or in combination


  • May improve peripheral arthritis and functional outcomes
  • No evidence that it can inhibit progression of joint damage


  • May improve joint and skin symptoms in PsA
  • The combination of leflunomide and MTX is associated with elevated liver function tests and so should be monitored carefully

Cyclosporine and tacrolimus

  • May be effective for the treatment of peripheral arthritis, axial involvement and skin lesions
  • Adverse events include renal toxicity and hypertension, which requires careful monitoring

TNF inhibitors

  • Can improve signs and symptoms of inflammation in both peripheral and axial joints as well as in peri-articular tissues such as enthuses
  • Can also improve functional status, quality of life, and skin and nail manifestations of PsA
  • Can slow the progression of damage in peripheral joints
  • Options include etanercept, infliximab, adalimumab, golimumab, and certolizumab pegol

IL-12/23 inhibitor (ustekinumab)

  • Evidence of efficacy in PsA in terms of ACR20 and ACR50 responses, and evidence of slowed radiographic progression

IL-17 inhibitor (secukinumab)

Small molecular weight inhibitors

Phosphodiesterase inhibitor (apremilast)

  • Downregulates the inflammatory response
  • Has been shown to be effective in PsA, improving signs, symptoms and physical function

DMARDs, disease-modifying anti-rheumatic drugs; NSAID, non-steroidal anti-inflammatory drug. Adapted from Kang and Kavanaugh.11


Grappa guidelines

The Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) guidelines place equal emphasis on the dermatological and rheumatological aspects of PsA.

Adapted from Ritchlin et al.12

EULAR guidelines

Unlike GRAPPA, the EULAR guidelines put the primary emphasis on the musculoskeletal aspects of the disease.13

EULAR treatment guidelines13

Adapted from Gossec et al.13 CsA, ciclosporin A; csDMARD, conventional systemic disease-modifying anti-rheumatic drug; LEF, leflunomide; SSZ, sulphasalazine; TNF, tumour necrosis factor.


Additional information

You can find additional information about PsA by following these links:

NHS Choices:

National Psoriasis Association:

Psoriasis and Psoriatic Arthritis Alliance:

1. Mease PJ, and Armstrong AW. Drugs. 2014;74:423–41.
2. Gladman DD, et al. Ann Rheum Dis. 2005;64(Suppl 2):ii14–ii17.
3. Gottlieb A et al. J American Acad Dermatol. 2008;58(5):851-864.
4. Boehncke WH, et al. Am J Clin Dermatol. 2013;14:377–388.
5. Coates LC, et al. BMC Musculoskelet Disord. 2013; 21:14.
6. Feldman SR et al. Arthritis Care Res (Hoboken). 2015;67:708–717.
7. Veale DJ, Fearon U. RMD Open. 2015;1:e000025.
8. Lenman M, Abraham S. Br J Gen Pract. 2014;64:424–425.
9. Lloyd P, et al. Arthritis. 2012;176298
10. Kavanaugh A, et al. Rheumatol Ther. 2016;3:91–102.
11. Kang EU, and Kavanaugh A. Ther Adv Chronic Dis. 2015;6:194–203.
12. Ritchlin CT, et al. Ann Rheum Dis. 2009;68:1387–1394.
13. Gossec L, et al. Ann Rheum Dis. 2016;75:499–510.

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