Psoriatic arthritis

Introduction

  • 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 to 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 USD 23 000/year (approximately EUR 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 them.7

 Psoriatic arthritisRheumatoid arthritis
Clinical/anatomical
  • Distal interphalangeal joint and axial arthritis
  • Often asymmetrical
  • Enthesitis common
  • Metacarpophalangeal
    and wrist joints
  • Predominantly symmetrical
Genetic
  • HLA Cw6 and B27
  • IL-23 receptor
  • HLA DRB1
Pathogenesis
  • 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 infiltrate
  • Late expression of vascular growth factors
Response to therapy
  • DMARDs, e.g. MTX
  • Anti-TNF antibodies
  • Inhibitors of T-cell activation
  • Anti-IL-12/23
  • Anti-IL-17a
  • DMARDs, e.g. MTX
  • Anti-TNFs
  • Inhibitors of T-cell activation
  • Anti-CD20
  • Anti-IL-6R

ACPA, anti-citrullinated protein antibody; DMARD, disease-modifying anti-rheumatic drug; HLA, human leukocyte antigen; IL, interleukin; MTX, methotrexate; RF, rheumatoid factor; TNF, tumor necrosis factor.

Adapted from Veale and Fearon, 2015.7

Burden of PsA

PsA: Under-diagnosis and under-treatment

  • PsA is believed to be underdiagnosed;8 if untreated, it can lead to severe disability and comorbidities9
  • An international survey of 712 patients with PsA found that more than half of patients (59%) reported that they were receiving no treatment or receiving topical therapy but 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

A total of 712 patients with PsA were included. *Including only patients with PsA who reported joint pain (n=628).

Adapted from Kavanaugh et al, 2016.10

Impact

Many patients with PsA experience a considerable impairment in physical function. The impact of impaired physical function progressively increases with the number of affected joints or symptoms resembling enthesitis or dactylitis, as assessed by Health Assessment Questionnaire (HAQ-8 or modified HAQ). PsA also severely impacts patients’ work productivity.10 

MAPP survey: Impact of PsA on physical function10

The proportions of patients who responded ‘with much difficulty’ or ‘unable to do’ are shown.

Adapted from Kavanaugh et al, 2016.10 

MAPP survey: Impact of PsA on work productivity10

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.

Adapted from Kavanaugh et al, 2016.10 

Treatment

Treatment options in PsA

TreatmentComments
NSAIDs
  • Still widely used for PsA treatment, especially in very mild disease
  • Can relieve musculoskeletal symptoms, but have no efficacy on psoriasis skin lesions
  • Lower toxicity compared with DMARDs
Steroids
  • Local injections of steroids can be used as adjunctive therapy for peripheral arthritis and enthesitis
  • Systemic steroids, particularly high doses, should be used with caution because they have been associated with psoriasis flares 
Conventional DMARDs
  • Patients with active disease despite NSAID therapy should receive DMARDs
  • DMARDs are ineffective in axial disease, and there is little evidence that they are efficacious for treatment of enthesitis

MTX

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

Sulfasalazine

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

Leflunomide

  • May improve joint and skin symptoms in PsA
  • The combination of leflunomide and MTX is associated with elevated liver function test results 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 potentially associated with cyclosporine include renal toxicity and hypertension, and requiring monitoring during treatment 
Biologics

Anti-TNFs

  • Can improve signs and symptoms of inflammation in both peripheral and axial joints as well as in peri-articular tissues such as entheses
  • 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)

  • Evidence of improvement of joint symptoms and radiographic progression
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

Janus kinase inhibitor (tofacitinib)

  • Inhibits cytokine signaling (including IL-2, IL-12, IL-6, and many others)

ACR20/50, 20/50% improvement in American College of Rheumatology criteria; DMARD, disease-modifying anti-rheumatic drug; IL, interleukin; MTX, methotrexate; NSAID, non-steroidal anti-inflammatory drug; TNF, tumor necrosis factor.

Adapted from Kang and Kavanaugh, 2015.11

Guidelines

The Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA) guidelines

The GRAPPA guidelines place equal emphasis on the dermatological and rheumatological aspects of PsA.

DMARD, disease-modifying anti-rheumatic drug; IA, intra-articular; IL, interleukin; NSAID, non-steroidal anti-inflammatory drug; PDE, phosphodiesterase; TNF, tumor necrosis factor.

Text in italics indicates conditional recommendations for drugs that do not currently have regulatory approvals or for which recommendations are based on abstract data only. 

Adapted from Coates et al, 2016.12

EULAR guidelines

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

EULAR treatment guidelines13

CsA, ciclosporin A; (b-/cs-) DMARD, (biologic/conventional synthetic) disease-modifying anti-rheumatic drug; IL, interleukin; LEF, leflunomide; MTX, methotrexate; NSAID, non-steroidal anti-inflammatory drug; SSZ, sulphasalazine; TNF, tumor necrosis factor. 

Adapted from Gossec et al, 2016.13

Support

Additional information

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

NHS Choices:
http://www.nhs.uk/conditions/psoriatic-arthritis/Pages/Introduction.aspx

National Psoriasis Association:
https://www.psoriasis.org/psoriatic-arthritis

Psoriasis and Psoriatic Arthritis Alliance:
http://www.papaa.org/resources/about-psoriasis

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):851-64.

4. Boehncke WH, et al. Am J Clin Dermatol. 2013;14:377–88.

5. Coates LC, et al. BMC Musculoskelet Disord. 2013; 21:14.

6. Feldman SR et al. Arthritis Care Res (Hoboken). 2015;67:708–17.

7. Veale DJ, Fearon U. RMD Open. 2015;1:e000025.

8. Lenman M, Abraham S. Br J Gen Pract. 2014;64:424–25.

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. Coates LC, et al. Arthritis Rheumatol. 2016;68:1060 -71. 

13. Gossec L, et al. Ann Rheum Dis. 2016;75:499 -510.

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