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Understanding the importance of early detection and multidisciplinary care in PSO and PsA

PsA=psoriatic arthritis; PSO=psoriasis.

PSO and PsA are closely related conditions that fall under the umbrella of psoriatic disease.1 PSO is a chronic immune-mediated inflammatory skin condition characterized by scaly skin lesions.2

PsA is a chronic inflammatory disease of the skin and musculoskeletal system, characterized by joint pain and other musculoskeletal manifestations.1,3 PsA can begin to develop years before a diagnosis in some cases, with skin symptoms often preceding joint symptoms.4,5

Because PsA has the potential to cause irreversible joint damage and impact quality of life, understanding the relationship between PSO and PsA is important for early and effective management of PsA and improved patient outcomes.5,6

Understanding the link between PSO and PsA

Up to 40%
of patients with PSO
will develop PsA9

Cumulative prevalence of PsA in PSO patients increases over time7,8

The annual incidence rate of PsA among patients with PSO ranges from 1.69 to 5.49 per 100 person years, with cumulative prevalence increasing over time.3,7

The timing of PsA onset varies among patients. In most cases (70%), PsA is diagnosed 9–10 years after a diagnosis of PSO. However, in 20% of cases, PsA may be diagnosed simultaneously with PSO. Less than 10% of PsA cases are diagnosed without the presence of PSO.1

Go deeper: Examine the clinical features of PsA

PSO and PsA share common genetic and immunological factors

PSO and PsA share common genetic factors that underlie susceptibility to psoriatic disease.2

Both PSO and PsA are immune-mediated inflammatory diseases.10 The inflammatory processes in the skin and joints involve similar pathways, including the overactivation of T cells and increased production of pro-inflammatory cytokines such as TNF-α, IL-17, and IL-23.2

IL=interleukin; TNF=tumor necrosis factor.

Shared inflammatory pathways of PSO and PsA

PSO and PsA share underlying inflammatory processes that contribute to the pathobiology of both conditions.2,11 Several cytokines have been implicated in PSO and other inflammatory diseases, including IL-17, IL-23, and TNF.11,12

Explore the role of key cytokines in driving inflammation in PSO and PsA:

IL-17

The IL-17 family of cytokines consists of six structurally related signaling molecules (IL-17A, IL-17B, IL-17C, IL-17D, IL-17E, and IL-17F) that play important roles in the immune system.13 In PSO and PsA, IL-17A and IL-17F are key inflammatory mediators.14 They cooperate with other inflammatory mediators, including TNF, to amplify inflammatory responses.14

As pleiotropic effector cytokines, both IL-17A and IL-17F promote joint and skin inflammation.11 In PsA, skin lesions and inflamed synovia have similar patterns of IL-17A and IL-17F expression and upregulation.15 IL-17F is found at higher levels in lesional skin of patients with PSO, while IL-17A has been shown to have a more potent pro-inflammatory effect.10

IL-17

IL-23

IL-23 expression is increased in both psoriatic skin lesions, as well as the synovia of inflamed joints of patients with PsA.16,17

IL-23 plays a pro-inflammatory role by driving the differentiation of naive T cells towards Th17, and stimulating Th17 cells to produce pathogenic cytokines such as IL-17 and IL-22.16,17

The downstream inflammation triggered by the IL-23/IL-17 axis contributes to skin and joint pathology, and may also lead to structural damage, including bone erosion and pathologic bone formation, which are hallmark features of PsA.16-18

IL-23

TNF

Elevated levels of TNF can be found in psoriatic synovium and skin plaques, as well as entheses, joint, and spine involvement.19,20 TNF plays a central pro-inflammatory role in psoriatic disease, but its function is increasingly understood as synergistic rather than isolated.21,22

In PsA, IL-17 and TNF together amplify inflammatory cytokine expression more potently than either alone.23

In PSO, the therapeutic response to TNF inhibitors may be mediated not solely by direct TNF suppression, but also through downstream effects on IL-17 pathway gene expression.22,23

TNF

A closer look at characterization, screening, and treatment of PSO

Comorbidities and disease burden

Due to chronic inflammation, PSO poses an increased risk of cardiovascular comorbidities.25 In addition, PSO is associated with an increased risk of mental health issues and IBD.25

PSO and its associated comorbidities pose a psychological, social, and financial burden to patients.26 These comorbidities, along with patient preferences and varying insurance coverage, may complicate treatment decisions.26

Risk factors for PsA development

The severity of PSO plays a significant role in the progression to PsA, with extensive body surface involvement, and earlier age of PSO diagnosis associated with a higher risk of PsA.5

Specific PSO characteristics, such as nail involvement and PSO in certain locations (scalp, intergluteal, and perianal areas), are also linked to increased PsA risk.4,5

Additionally, certain comorbidities, such as uveitis and type 2 diabetes, are also associated with increased risk of PsA.1,4

Clinical progression of PSO to PsA

A three-stage scheme for progression from at risk of PsA to frank PsA. Onset may be variable and could occur quickly in some subjects, for example, after trauma or following infection with a reactive arthritis type onset. Although visuals imply directionality and inevitable progression, some subjects may have spontaneous resolution of PsA, and subjects with arthralgia may regress. Strategies in at-risk people (for example, weight loss in obesity) may lead to reduction of risk. This scheme recognizes the importance of enthesitis in pathophysiology, but for trials of interception suggests the use of synovitis development as an outcome measure since this was by far the most common manifestation of early disease from the accompanying systematic literature reviews.27

*Role of immunogenetics awaits definition.

©Zabotti A, De Marco G, Gossec L, et al. EULAR points to consider for the definition of clinical and imaging features suspicious for progression from psoriasis to psoriatic arthritis. Ann Rheum Dis. 2023;82(9):1162-1170. doi:10.1136/ard-2023-224148. Licensed under CC BY 4.0.

Identifying PSO patients at risk of PsA

Research suggests that clinicians should suspect PsA in patients with PSO and at least one extra-articular manifestation.28 While there is no diagnostic test for PsA, several domain-specific screening tools may help identify PsA in patients with PSO, including4,6,11:

Psoriatic Arthritis Screening and Evaluation (PASE)29,30MORE

  • Validated 15-item tool assessing both symptoms and functional impact via Likert scale
  • Can take 5–6 minutes to complete
  • For use in dermatology and rheumatology clinicsLESS

Psoriasis Epidemiology Screening Tool (PEST)29,31MORE

  • Validated 5-item yes/no tool with a joint diagram
  • For use in community settings or hospital clinicsLESS

Toronto Psoriatic Arthritis Screen (ToPAS)6,29,32MORE

  • Validated 12-item tool including questions and visuals
  • For use in dermatology, rheumatology, PsA, and family medicine clinics
  • Includes questions about psoriatic skin involvementLESS

Early Arthritis for Psoriatic Patients (EARP)29,33MORE

  • Validated 10-item yes/no questionnaire
  • Can take less than 5 minutes
  • For use in dermatology clinics
  • May be slightly more accurate than PEST, PASE, or ToPASLESS

Psoriatic arthritis UnclutteRed screening Evaluation (PURE-4)34MORE

  • Validated 4-item yes/no questionnaire with items including dactylitis, inflammatory heel pain, bilateral buttock pain, and peripheral joint pain/swelling in patients aged <50
  • For use in dermatology clinics
  • Promising sensitivity and specificity in an early validation studyLESS

Imaging modalities, such as ultrasound, MRI, and PET-CT, may be used to identify asymptomatic patients with PSO who will develop PsA, as they can detect sub-clinical synovial-entheseal abnormalities.4

Screening tools such as these may help facilitate timely referral to a rheumatologist for early treatment of PsA.6

Read about disease outcome measures in PsA

Differentiating features of PsA, beyond joint pain

Joint pain often presents as an initial symptom of PsA in patients with PSO.11 Other extra-articular inflammatory features that can provide diagnostic clues for PsA include:

Enthesitis
A characteristic feature of PsA, which may be one of its earliest signs, involves inflammation at entheseal sites where tendons and ligaments insert into bone35
Dactylitis
Inflammation that causes swelling of the fingers or toes, which can occur in up to 50% of people with PsA35
Nail symptoms
Pitting, onycholysis, and hyperkeratosis can precede joint symptoms of PsA4,35

Impact of PSO on quality of life in patients with PsA

People with skin involvement in PsA may experience diminished quality of life compared to patients with only joint involvement.36 Along with physical limitations caused by joint involvement, skin involvement reduces quality of life through emotional distress and discomfort.35 Greater skin involvement is also associated with fatigue, pain, loss of function, and impaired ability to work or complete daily activities.37

Because of this impact on quality of life, it is important to measure patient experience alongside clinical parameters during patient assessments.38 One measurement tool is the Psoriasis Symptoms and Impacts Measure (P-SIM), which was developed to capture patients’ experience of the impacts of PSO with a daily 14-item electronic diary and may be useful in assessing treatment outcomes.39

Management considerations for PSO

Treatment options for PSO vary based on a variety of factors, including comorbidities, patient preference, and disease severity.26

PSO disease severity can be classified by extent of skin involvement
  • <3%–5%
    Mild PSO <3%–5% of body surface area25
  • 3%–10%
    Moderate PSO 3%–10% of body surface area25
  • ≥10%
    Severe PSO ≥10% of body surface area25

Mild-to-moderate PSO may be adequately treated with topical medications or phototherapy.40 Moderate-to-severe disease may be treated with biologics, either alone or alongside other topical or systemic medications.40

Consider the value of a multidisciplinary approach to treating PSO and PsA

While many PsA patients are managed by rheumatologists alone, the patient burden of skin disease highlights the importance of multidisciplinary management.36

Dermatologists play a key role in identifying early signs of PsA. Monitoring for signs of joint or arthritic involvement in patients with PSO, along with knowledge of PsA screening, diagnosis, and treatment, can help dermatologists proactively address PSO progression to clinical PsA.35

Dermatologists should consider early referral of suspected PsA to a rheumatologist where possible, especially if PsA manifestations do not respond to treatment.35 This multidisciplinary approach ensures comprehensive management of both skin and joint symptoms and can improve treatment outcomes for both skin and musculoskeletal symptoms.41

Early detection of signs of PsA is crucial, as a greater than 6-month delay in diagnosis can contribute to poor outcomes.4

Pathway to earlier treatment of PsA in patients with PSO4

©Pennington SR, FitzGerald O. Early origins of psoriatic arthritis: clinical, genetic and molecular biomarkers of progression from psoriasis to psoriatic arthritis. Front Med (Lausanne). 2021;8:723944. doi:10.3389/fmed.2021.723944. Licensed under CC BY 4.0.

GRAPPA recommendations for patients with PsA42

Does not include all possible domains of PsA in GRAPPA treatment schema; other domains include peripheral arthritis, axial disease, IBD, and uveitis. Bold text indicates a strong recommendation, standard text a conditional recommendation. Asterisks indicate a conditional recommendation based on data from abstracts only. bDMARD=biologic DMARD; csDMARD=conventional synthetic DMARD; CTLA4-Ig=CTLA4–immunoglobulin fusion protein; GC=glucocorticoid; JAKi=Janus kinase inhibitor; PDE4i=phosphodiesterase 4 inhibitor; phototx=phototherapy; TNFi=TNF inhibitor.

©Coates LC, Soriano ER, Corp N, et al. Group for Research and Assessment of Psoriasis and Psoriatic Arthritis (GRAPPA): updated treatment recommendations for psoriatic arthritis 2021 [published correction appears in Nat Rev Rheumatol. December 2022;18(12):734. doi: 10.1038/s41584-022-00861-w]. Nat Rev Rheumatol. 2022;18(8):465-479. doi:10.1038/s41584-022-00798-0. Licensed under CC BY 4.0.

The choice of biologic should be tailored to individual patient needs such as comorbidities and affected domains.42 Read full GRAPPA recommendations

LECTURE SERIES WITH DR. SAAKSHI KHATTRI

Comprehensive care for PSO requires collaboration between dermatologists and rheumatologists3,36

“When I have a patient in my practice who I’m seeing for psoriasis, I’m always acutely aware of psoriatic arthritis, just given the data that says many psoriasis patients will develop PsA.35

“Frequently, there’s a delay in diagnosing PsA, and even 6 months of delay in diagnosis can result in irreversible joint damage.4 So, in the dermatology space, when I have a psoriasis patient, I’m always thinking PsA in the back of my head.”

Watch Dr. Khattri’s lecture on clinical manifestations of PsA.

TAKE YOUR SEATS IN THE PATHOBIOLOGY LEARNING THEATRE

Uncover how IL-17A and IL-17F work in tandem to drive inflammation in SpA

Explore more manifestations of inflammation in new special exhibits

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of cytokines in controlling
inflammation

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uveitis as a manifestation
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