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Psoriatic Arthritis

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(Redirected from Psoriasis)


Other Names

  • Psoriatic arthritis (PsA)
  • Psoriasis

Background

  • This page discusses Psoriatic Arthritis (PA) and focuses on the MSK manifestations of Psoriasis

History

  • Recognized as a separate disease by the American College of Rheumatology in 1964 (need citation)

Epidemiology

  • Incidence
    • Among patients with psoriasis, the incidence ranges fom 0.27 to 2.7 per 100 person years[1]
  • Prevalence
    • Meta-analysis: PA is seen in 3.8% of patients with psoriasis[2]
  • Demographic[3]
    • Highest among patients age 30 to 60
    • Affects men and women equally
    • The majority are white
    • Lower in Asia than in Europe and North America
  • Diagnosis
    • Significant delays in diagnosis for about half of patients[4]
    • Delays in diagnosis of 6 and 12 months have impact on long term joint health, functional disability[5]

Pathophysiology

Classic chronic plaque psoriasis of the extensor elbow
Illustration of the stages in the evolution of psoriasis to psoriatic arthritis[6]
  • General[7]
    • Seronegative spondyloarthropathy that presents with arthritis, rash with silvery plaques, uveitis and dysmorphic nails
    • About 10-15% of patients develop arthritis before psoriasis (psoriatic arthritis sine psoriasis)
    • Heterogenous disease with multiple musculoskeletal and dermatological manifestations
    • Early recognition, treatment lead to better outcomes
    • About half of cases in primary care and secondary clinics are unrecognized
    • Associated with significant metabolic comorbidities, cardiovascular risk
    • Traditional DMARDS have modest benefit, newer biologic agents are more effective
  • General characteristics
    • About 30-50% of patients have multiple joint involvement
    • Any joint can be involved
    • About 60-80% of patients have enthesitis
    • About 30% of patients have dactylitis
    • there is a phenotype which includes axial spondyloarthritis
    • About 80% have psoriasis, 60% have nail disease
    • Usually RF, CCP negative
    • Radiographs may show new bone formation
  • 5 patterns of arthritis
    • Asymmetric oligo/monoarticular arthritis affecting DIPJ, PIPJ, MCPJ
    • DIP-predominant arthritis
    • Arthritis mutilans
    • Symmetric, RF-negative polyarthritis
    • Psoriatic spondyloarthropathy

Etiology

  • General
    • Exact sequence of events leading to onset, progression not entirely understood
    • Triggered by complex interplay of genetic predisposition, environmental influences
    • Subsequently, immune response leads to entry, proliferation of immune cells at articular, periarticular and extra-articular sites
  • HLA associated genetic factors
    • Strong genetic contribution to the development of psoriasis and PA[8]
    • HLA-C*06:02 is found in ~60% of those with psoriasis, only 28% in PA[9]
    • 18% of of patients with PA are HLAB*27 positive
    • Other implicated HLA genes includes HLA-B*08, HLA-B*38, HLA-B*39
  • Non-HLA associated genetic factors
    • Implicated genes include IL12B and TRAF3IP2 which are involved in IL-17 signaling[10]
    • PTPN22 (which encodes a potent inhibitor of T cell activation) and RUNX3 (which is involved in CD8+ T lymphocyte differentiation)[11]
  • Environmental Factors
    • Musculoskeletal injury
      • Bone and joint trauma associated with increased risk of PA[12]
    • Obesity
      • Thought to be due to higher mechanical low at entheseal sites, increased stress
    • Infection
      • Association between streptococcal infection and guttate psoriasis is well established[13]
      • Increased risk in patients with HIV[14]
    • Evidence stress or anxiety, alcohol consumption or smoking is controversial

Risk Factors

Differential Diagnosis

Clinical Features

A, B, Infiltrated plaque lesions of psoriasis located on the extansor surfaces of the extremities at the initiation of secukinumab therapy. C, D, Residual plaques on the forearms and shins after dose escalation of secukinumab[16]
  • History
    • About 80% of patients have psoriasis/ psoriatic plaques, typically before PA develops
    • These can be hidden in the scalp, umbilicus and gluteal clef
    • Nails are involved in about 60% of patients
    • Patients often report morning stiffness greater than 30 minutes
    • Joint tenderness
    • Pain aggravated by rest and relieved by exercise
    • Symptoms have improved with NSAID or corticosteroid use
    • Joint erythema, warmth
    • Fatigue
    • Symptoms are often worse in hands
  • Physical Exam
    • Fully examine skin and nails for evidence of psoriasis
    • Rash: silvery plaques over the extensor surfaces (elbows and knees)
    • Hands: dactylitis (swelling), onychodystrophy (nail pitting), onycholysis (lifting of nail)
    • Joints may be swollen, with limited motion, deformity
    • Arthritis mutilans (opera glass hands or la main en lorgnette)

Evaluation

Polyarthropathy involving both the carpus and fingers. Marginal erosions are most apparent in the carpus. There is a pencil-in-cup deformity of the fifth finger. No soft tissue calcification. [17]
Differentiating rheumatoid arthritis from psoriatic arthritis[7]

Diagnosis

  • General
    • Factors: patient history, physical examination, laboratory findings, imaging results
    • Goal: make an accurate and timely diagnosis to allow prompt therapy
  • Delay in diagnosis
    • Well described in the rheumatology literature
    • 2015 UK audit estimated a median delay of 29 weeks[18]
    • Delay associated with worsening physical function, increased chance of peripheral erosive disease[19]
  • Distinguishing from rheumatoid arthritis, osteoarthritis can be challenging
    • See Table 1 for some common differences

Radiographs

  • General
    • Uncommon in early disease, more prevalent with increasing disease duration
    • Several studies have found only 27% of patients had findings at presentation[20]
    • Limited diagnostic utility, none are specific and findings are often minimal
  • Classical Findings
    • Periosteal new bone formation at entheseal sites
    • Erosive changes
    • Bone resorption or osteolysis
    • Sacroiliitis, which is often asymmetrical
    • "Pencil-in-cup" deformity: results from a combination of new bone formation and osteolysis
  • Hands
    • Distal phalanx acrolysis
    • DIP arthritis
      • "Pencil-in-cup" deformity: simultaneous destruction of the head of the middle phalanx and expansion of the base of the distal phalanx
      • Different than DJD by presence of centripetal erosions which cause joint space widening
    • Small joint erosions or fusions (PIP, MCP, and wrist commonly involved)
    • Fluffy periostitis (caused by periosteal ossification)
    • Acroosteolysis (resorption of the distal phalanx tuft)
    • Flail digits
  • Spine (in patients with axial disease)
    • Sacroiliitis
    • Syndesmophytes
    • Paravertebral ossification
    • Destructive discovertebral lesions

Laboratory

  • General
    • Specific tests are lacking to confirm the diagnosis
    • Patients are typically seronegative
  • CCP
    • Usually negative
  • Rheumatoid Factor
    • Usually negative
  • ESR/CRP
    • Elevated in acute phase response
    • Somewhere between 33 and 89% of patients demonstrate elevated CRP at presentation[21]

Classification

CASPAR Criteria

  • Evidence of psoriasis
    • Current: Psoriatic skin or scalp disease present today as judged by a rheumatologist or dermatologist
    • Personal history: history of psoriasis obtained from patient, family doctor, dermatologist, rheumatologist
    • Family history: history of psoriasis in a first- or second-degree relative according to patient report
  • Psoriatic nail dystrophy
    • Typical psoriatic nail dystrophy including onycholysis, pitting and hyperkeratosis observed on current physical examination
  • Negative test for rheumatoid factor
    • By any method except latex but preferably by ELISA or nephelometry, according to the local laboratory reference range
  • Dactylitis
    • Current: Swelling of an entire digit
    • History: A history of dactylitis recorded by a rheumatologist
  • Radiological evidence of juxta-articular new bone formation
    • Ill-defined ossification near joint margins on plain radiographs of hand or foot
    • Excluding osteophyte formation

Management

Nonoperative

  • Multidisciplinary team
    • Patients require input from the multidisciplinary rheumatology team
    • Dermatology
    • Rheumatology
    • Nurses with experience in PA
    • Podiatrists, therapists with experience in PA
  • Monitoring
    • Perform a full 68/66 joint count
    • Assess key enthesis (achilles tendon, lateral epicondylitis)
    • Examination for dactylitis
    • Question for back pain, evaluate if necessary
  • Therapeutic end points
    • EULAR: "treatment should be aimed at reaching the target of remission or, alternatively, minimal/low disease activity, by regular monitoring and appropriate adjustment of therapy"[22]

Pharmacotherapy

  • General
    • Stepwise approach recommended by EULAR[22]
    • Start with NSAIDS, topical therapies
    • Escalate with DMARD, perhaps more than one, followed by biologic drugs
  • Corticosteroids
    • Used to settle inflammatory disease rapidly
    • Can be administered intramuscularly or intra-articularly
    • One study showed 41% of patients improved at 3 months following steroids, of those, 33% relapsed subsequently[23]
    • Oral steroids are not generally recommended for fear of "skin rebound" when they are withdrawn
  • Methotrexate
    • Commonly considered first line, although this is controversial
  • Sulfasalazine
    • Cochrane review: significant but small effect against placebo with no effect on enthesitis[24]
  • Leflunomide
    • Effective treatment for PsA and psoriasis[25]
    • Not commonly used in clinical practice
  • Tumor Necrosis Factor Inhibitors (TNF Inhibitors)
    • Includes adalimumab, certolizumab, etanercept, golimumab and infliximab
    • Recommended and commonly used when patients have failed 2 standard DMARDS and have 3 symptomatic joints[26]
  • Ustekinumab
    • IL-12/23 inhibitor that is used commonly for psoriasis
    • Shown to be effective for arthritis, skin, enthesitis and dactylitis.[27]
  • IL-17A Inhibitors
    • Monoclonal antibody to IL-17A, has excellent efficacy in psoriasis
    • Secukinumab: Superior to both etanercept[28] and ustekinumab[29]
    • Ixekizumab: good response to PA with similar efficacy to adalimumab[30]
    • Brodalumab: studies halted due to safety concerns
  • Apremilast
    • Phosphodiesterase-4 inhibitor
    • Efficacy seems lower than biologics, particularly for higher levels of response[31]
    • Safety profile is favorable, no blood monitoring, no hepatotoxicity

Operative

  • Indication
    • Advanced disease
  • Technique
    • Digit fusion
    • Arthroplasty

Rehab and Return to Play

Rehabilitation

  • Needs to be updated

Return to Play/ Work

  • Needs to be updated

Complications and Prognosis

The negative impact of psoriatic arthritis (PsA) on the quality of life (QoL) occurs through a complex interplay of physical, psychological and social domains. The Venn diagram lists the individual elements that impact QoL within each domain.[32]

Prognosis

  • Poor prognostic markers[33]
    • Increased number of joints involved (polyarthritis or five or more joints)
    • The presence of dactylitis
    • High levels of inflammatory markers (for example, CRP)
    • Baseline erosive disease
  • Progression[34]
    • In most cases, increased joint involvement over time with increasing disease duration
    • High proportion of patients with mono- or oligo-arthritis show progression to polyarthritis
  • Joint damage risk increases with[35]
    • Baseline joint damage
    • Elevate of acute phase labs (ESR/ CRP)
    • High number of actively inflamed joints
  • Impact on quality of life (QOL), functional ability
    • Significant impact on QOL
    • Complex interplay between psychological, physical and social domains
    • Similar to rheumatoid arthritis[36]

Complications

  • Overall mortality
    • Overall mortality among patients with PsA is not higher than in the general population[37]
  • Cardiovascular
    • Cardiovascular comorbidities have a higher prevalence in PA
    • Increased risk of myocardial infarction[38]
  • Skin
  • Ophthalmology
    • Uveitis
  • Gastrointestinal
    • Associated with crohns disease, ulcerative colitis
  • Psychiatric

See Also

References

  1. ↑ Alinaghi, F. et al. Prevalence of psoriatic arthritis in patients with psoriasis: a systematic review and meta-analysis of observational and clinical studies. J. Am. Acad. Dermatol. 80, 251–265 (2019).
  2. ↑ Scotti, L., Franchi, M., Marchesoni, A. & Corrao, G. Prevalence and incidence of psoriatic arthritis: a systematic review and meta-analysis. Semin. Arthritis Rheum. 48, 28–34 (2018).
  3. ↑ Ogdie, A. et al. Prevalence and treatment patterns of psoriatic arthritis in the UK. Rheumatology 52, 568–575 (2013).
  4. ↑ Coates LC. Savage L. Waxman R, et al. Comparison of screening questionnaires to identify psoriatic arthritis in a primary care population: a cross sectional study. Br J Dermatol. 2016;175:542–8.
  5. ↑ Tillett W. Jadon D. Shaddick G, et al. Smoking and delay to diagnosis are associated with poorer functional outcome in psoriatic arthritis. Ann Rheum Dis. 2013;72:1358–61.
  6. ↑ FitzGerald, Oliver, and Robert Winchester. "Psoriatic arthritis: from pathogenesis to therapy." Arthritis research & therapy 11.1 (2009): 1-9.
  7. ↑ 7.0 7.1 Coates, Laura C., and Philip S. Helliwell. "Psoriatic arthritis: state of the art review." Clinical Medicine 17.1 (2017): 65.
  8. ↑ O’Rielly, D. D. & Rahman, P. Genetic, epigenetic and pharmacogenetic aspects of psoriasis and psoriatic arthritis. Rheum. Dis. Clin. North Am. 41, 623–642 (2015).
  9. ↑ Winchester, R. et al. HLA associations reveal genetic heterogeneity in psoriatic arthritis and in the psoriasis phenotype. Arthritis Rheum. 64, 1134–1144 (2012). An important study of the HLA genetic associations in patients with psoriatic arthritis in comparison to those with psoriasis only.
  10. ↑ Bowes, J. et al. Dense genotyping of immune-related susceptibility loci reveals new insights into the genetics of psoriatic arthritis. Nat. Commun. 6, 7741 (2015).
  11. ↑ Apel, M. et al. Variants in RUNX3 contribute to susceptibility to psoriatic arthritis, exhibiting further common ground with ankylosing spondylitis. Arthritis Rheum. 65, 1224–1231 (2013).
  12. ↑ Thorarensen, S. M. et al. Physical trauma recorded in primary care is associated with the onset of psoriatic arthritis among patients with psoriasis. Ann. Rheum. Dis. 76, 521–525 (2017).
  13. ↑ Teng, Y. et al. Infection-provoked psoriasis: induced or aggravated (Review). Exp. Ther. Med. 21, 567 (2021).
  14. ↑ FitzGerald, O., Haroon, M., Giles, J. T. & Winchester, R. Concepts of pathogenesis in psoriatic arthritis: genotype determines clinical phenotype. Arthritis Res. Ther. 17, 115 (2015).
  15. ↑ O’Rielly, D. D., Jani, M., Rahman, P. & Elder, J. The genetics of psoriasis and psoriatic arthritis. J. Rheumatol. Suppl. 95, 46–50 (2019).
  16. ↑ Polat Ekinci, Algün, Kübra Nursel Bölük, and Goncagül Babuna Kobaner. "Secukinumab and acitretin as a combination therapy for three clinical forms of severe psoriasis in multi‐drug refractory patients: A case series of high efficacy and safety profile." Dermatologic therapy 34.1 (2021): e14704.
  17. ↑ Case courtesy of Henry Knipe, Radiopaedia.org, rID: 77947
  18. ↑ Holland, R. et al. Psoriatic arthritis is associated with diagnostic delay and worse outcome at three months when compared to rheumatoid arthritis: results from the UK National Audit for Inflammatory Arthritis [abstract FRI0514]. Ann. Rheum. Dis. 76, 685 (2017).
  19. ↑ Tillett, W. et al. Smoking and delay to diagnosis are associated with poorer functional outcome in psoriatic arthritis. Ann. Rheum. Dis. 72, 1358–1361 (2013).
  20. ↑ Coates, L. C. et al. Effect of tight control of inflammation in early psoriatic arthritis (TICOPA): a UK multicentre, open-label, randomised controlled trial. Lancet 386, 2589–2598 (2015).
  21. ↑ Bonifati, C. et al. The diagnosis of early psoriatic arthritis in an outpatient dermatological centre for psoriasis. J. Eur. Acad. Dermatol. Venereol. 26, 627–633 (2012).
  22. ↑ 22.0 22.1 Gossec L. Smolen JS. Ramiro S, et al. European League Against Rheumatism (EULAR) recommendations for the management of psoriatic arthritis with pharmacological therapies: 2015 update. Ann Rheum Dis. 2016;75:499–510.
  23. ↑ Eder L. Chandran V. Ueng J, et al. Predictors of response to intra-articular steroid injection in psoriatic arthritis. Rheumatology. 2010;49:1367–73
  24. ↑ Jones G. Crotty M. Brooks P. Interventions for psoriatic arthritis. Cochrane Database Syst Rev. 2000;(3):CD000212.
  25. ↑ Kaltwasser JP, Nash P, Gladman D, Rosen CF, Behrens F, Jones P, Wollenhaupt J, Falk FG, Mease P; Treatment of Psoriatic Arthritis Study Group. Efficacy and safety of leflunomide in the treatment of psoriatic arthritis and psoriasis: a multinational, double-blind, randomized, placebo-controlled clinical trial. Arthritis Rheum. 2004 Jun;50(6):1939-50. doi: 10.1002/art.20253. PMID: 15188371.
  26. ↑ National Institute for Health and Care Excellence Etanercept, infliximab and adalimumab for the treatment of psoriatic arthritis. NICE technology appraisal No 199. London:: NICE; 2010.
  27. ↑ McInnes IB. Kavanaugh A. Gottlieb AB, et al. Efficacy and safety of ustekinumab in patients with active psoriatic arthritis: 1 year results of the phase 3, multicentre, double-blind, placebo-controlled PSUMMIT 1 trial. Lancet. 2013;382:780–9.
  28. ↑ Langley RG. Elewski BE. Lebwohl M, et al. Secukinumab in plaque psoriasis–results of two phase 3 trials. N Engl J Med. 2014;371:326–38
  29. ↑ Thaci D. Blauvelt A. Reich K, et al. Secukinumab is superior to ustekinumab in clearing skin of subjects with moderate to severe plaque psoriasis: CLEAR, a randomized controlled trial. J Am Acad Dermatol. 2015;73:400–9.
  30. ↑ Mease PJ. van der Heijde D. Ritchlin CT, et al. A Randomized, double-blind, active- and placebo-controlled phase 3 study of efficacy and safety of ixekizumab, adalimumab, and placebo therapy in patients naïve to biologic disease modifying anti-rheumatic drugs with active psoriatic arthritis. Arthritis Rheumatol. 2015;67(Suppl S10) 977.
  31. ↑ Kavanaugh A. Mease PJ. Gomez-Reino JJ, et al. Treatment of psoriatic arthritis in a phase 3 randomised, placebo-controlled trial with apremilast, an oral phosphodiesterase 4 inhibitor. Ann Rheum Dis. 2014;73:1020–6.
  32. ↑ FitzGerald, Oliver, and Robert Winchester. "Psoriatic arthritis: from pathogenesis to therapy." Arthritis research & therapy 11.1 (2009): 1-9.
  33. ↑ Gladman, D. D. & Farewell, V. T. Progression in psoriatic arthritis: role of time varying clinical indicators. J. Rheumatol. 26, 2409–2413 (1999).
  34. ↑ Marsal, S. et al. Clinical, radiographic and HLA associations as markers for different patterns of psoriatic arthritis. Rheumatol 38, 332–337 (1999).
  35. ↑ Bond SJ. Farewell VT. Schentag CT, et al. Predictors for radiological damage in psoriatic arthritis: results from a single centre. Ann Rheum Dis. 2007;66:370–6
  36. ↑ Sokoll KB. Helliwell PS. Comparison of disability and quality of life in rheumatoid and psoriatic arthritis. J Rheumatol. 2001;28:1842–6
  37. ↑ Karmacharya, P., Chakradhar, R. & Ogdie, A. The epidemiology of psoriatic arthritis: a literature review. Best. Pract. Res Clin. Rheumatol. 75, 101692 (2021).
  38. ↑ Ogdie, A. & Weiss, P. The epidemiology of psoriatic arthritis. Rheum. Dis. Clin. North Am. 41, 545–568 (2015).
  39. ↑ Lukmanji, A., Basmadjian, R. B., Vallerand, I. A., Patten, S. B. & Tang, K. Risk of depression in patients with psoriatic disease: a systematic review and meta-analysis. J. Cutan. Med. Surg. 25, 257–270 (2020).
  40. ↑ Michelsen, B. et al. Do depression and anxiety reduce the likelihood of remission in rheumatoid arthritis and psoriatic arthritis? Data from the prospective multicentre NOR-DMARD study. Ann. Rheum. Dis. 76, 1906–1910 (2017).
Created by:
John Kiel on 19 January 2023 14:56:22
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19 January 2023 17:02:02
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