BOTTOM LINE

Psoriatic arthritis (PsA) is prevalent in ~30% of patients with cutaneous psoriasis and can often present as oligo/polyarthritis with features of dactylitis, enthesitis, and tenosynovitis. Psoriatic arthritis can manifest with other features of spondyloarthritis like axial spondyloarthritis, uveitis, and inflammatory bowel disease. Common comorbidities include metabolic syndrome, metabolic dysfunction-associated fatty liver disease, and cardiovascular disease. CRP is less frequently elevated with disease activity (compared to rheumatoid arthritis) and there are no autoantibody associations. Treatment usually requires DMARD therapy for peripheral arthritis starting with methotrexate or leflunomide and advanced DMARDs (TNF, IL17i, JAKi, IL12/23i, PDE4i, or IL23i). Axial disease is treated with NSAIDs or advanced DMARDs (TNFi, IL17i, or JAKi).
[🕑 10 minute read]

EPIDEMIOLOGY

• Prevalence
  • ~1-2:1000 general population
    ~10-30% in the psoriasis population
• Annual Incidence (among patients with cutaneous psoriasis)
  • 0.27-2.7 per 100 person-years (depending on the study and outcome definition)
• Age:
  • Peak age at onset ~30-60 years
• Sex:
  • M=F, no difference in sex
  • Men: more often develop axial involvement and radiographic joint damage
  • Women: more likely to report functional limitation and impaired quality of life
• Ethnicity:
  • More common in Caucasians, lower prevalence in Asians, lowest in Africans
• Risk Factors
  •  Genetic:
    • Family history of skin psoriasis increases risk of PsA
      • OR 20.5 (95% CI, 2.49-169.10)
      • Recurrence risk ratio (λ) ~30-40 times higher if PsA in a first-degree relative
    • HLA associated:
      • HLA-B*27 (18% prevalent in PsA), HLA-B*08, HLA-B*38, HLA-B*39.
      • HLA-B*27: more prevalent in psoriasis patients who develop psoriatic arthritis; predicts shorter time between onset of skin psoriasis and onset of psoriatic arthritis.
      • HLA-C*06:02: more prevalent in psoriasis patients who do not develop psoriatic arthritis; predicts longer time between onset skin psoriasis and onset of psoriatic arthritis
    • Non-HLA associated:
      • Risk locus at chromosome 5q3, variants at IL12B, TRAF3IP2, IL23R, PTPN22
  • Environmental:
    • Musculoskeletal injury:
      History of major physical trauma or repetitive microtrauma at entheseal sites; thought to cause a “deep Koebner response” at the joint
    • Obesity:
      Repetitive entheseal microtrauma from mechanical load, pro-inflammatory mediators in fat tissue
    • Infection:
      May trigger PsA, for example streptococcal or HIV infection
  • Psoriasis characteristics:
    • Psoriatic nails (pitting, onycholysis)
    • Scalp and intergluteal/perianal psoriasis
    • Severe psoriasis
    • Uveitis

CLINICAL FEATURES

• Features of psoriatic arthritis can be thought of conceptually on the basis of
  • Joint presentation:
    Pattern of joints involved
  • Disease Domains:
    Involvement of peripheral joints, axial involvement, skin, nails, enthesitis, dactylitis
  • Associated Conditions:
    Inflammatory bowel disease (IBD) and Uveitis
  • Comorbidities:
    Including cardiovascular disease, metabolic syndrome, metabolic dysfunction-associated fatty liver disease, and depression.

—Joint Presentation

Moll and Wright Subtypes

Moll and Wright subtypes are no longer used, but may be referred to historically.
Patients can have >1 subtype, or a different subtype at different times

SUBTYPE	%	TYPICAL JOINTS
Polyarthritis “rheumatoid-like”	50-60	MCPs, PIPs, wrists
Asymmetric oligo-articular	15-20	DIP, PIPs, MCPs, MTPs, Joints, knees, hips, ankles
Arthritis mutilans	5	DIP, PIP. Destruction, telescoping digits, deformity
DIP Predominant	2-5	DIPs Frequently with psoriatic nails
Axial (spine) isolated	2-5	Sacroiliac, vertebral

Joint characteristics that distinguish PsA from RA

• Ray distribution
  • PsA can involve all joints within a single digit
• Asymmetric arthritis
  • PsA is more likely to involve multiple joints in the same digit rather than the same joint on the contralateral side
• Unique radiographic changes
  • PsA can cause simultaneous erosion, new bone formation (periostitis), ankylosis, arthritis mutilans on X-ray

Interval between onset of psoriasis (PsO) and psoriatic arthritis (PsA)

• PsO precedes PsA in ~80%
  • Precedes by years
  • Latency between PsO and PsA is shorter if patient is HLA-B*27+
• PsA precedes PsO in ~5-15%

—Disease Domains

• Peripheral arthritis:
  • Inflammatory arthritis involving peripheral joints
    
• Axial disease (25-70%):
  • Inflammatory arthritis of spine, SI joints, costochondral and sternoclavicular joints
  • PsA can be exclusively axial in 5% of patients
  • Features that distinguish between psoriatic spondyloarthritis from axial spondyloarthritis/”ankylosing spondylitis“.
    Psoriatic spondyloarthritis:
    • May have asymmetric sacroiliitis or spondyloarthritis without sacroiliitis
    • Vertebral syndesmophytes are more often large bulky “jug-handle” syndesmophytes rather than thin and “elegant” syndesmophytes of Axial Spondyloarthritis
    • Less frequently HLA-B*27 positive
    • Less likely to cause complete SI joint ankylosis and bridging syndesmophytes
      
• Enthesitis (30-50%):
  • Inflammation at insertion of tendon/ligament to bone
  • May be the first manifestation of PsA in a patient with cutaneous psoriasis
  • Can lead to new bone formation at entheses (enthesophyte/bone spur)
  • Examples: elbow epicondylitis, Achilles enthesitis, plantar fasciitis, patellar tendon, iliac crest, supraspinatus insertions, greater trochanters
    
• Dactylitis (40-50%):
  • Relatively uniform swelling of entire finger or toe (“sausage digit”)
  • Due to synovitis, osteitis, and flexor tenosynovitis
  • Often seen with polyarthritis subtype; may affect toes exclusively in two-thirds of patients
    
• Skin (Psoriasis, examples images):
  • Plaque psoriasis
    • Most common type of psoriasis; frequently affecting scalp, elbows, knees, gluteal cleft
    • Erythematous plaques with sharp margins and silvery scale
  • Pustular psoriasis
    • Acute widespread erythema, scaling, and superficial рսstսles.
    • Can sometimes be life-threatening.
    • Can sometimes be localized to palms and soles (palmoplantar pustular psoriasis)
  • Guttate psoriasis
    • Eruption of multiple small psoriatic papules and plaques on trunk and proximal extremities
    • Often triggered by strep infection
  • Erythrodermic psoriasis
    • Generalized erythema and scaling of almost entire body surface area
    • Dermatologic emergency and life threatening
  • Inverse psoriasis
    • psoriasis of folds, recesses, flexural surfaces (ears, axillae, groin, inframammary, navel, intergluteal cleft, penis, lips)
      
• Nail Psoriasis (85%):
  • Pitting, red spots, leukonychia, nail-plate crumbling, oil-drop discoloration, onycholysis, splinter hemorrhages, and subungual hyperkeratosis (example images)
  • Almost impossible to differentiate toe nail psoriasis vs fungal nail disease on physical exam.
    • Can assess for tinea elsewhere in the foot or do scrapings (Sensitivity 75%)

—Associated Conditions

• IBD (~3%):
  • Inflammatory bowel disease (Ulcerative colitis, Crohn’s colitis)
• Uveitis (~3%)
  • Usually anterior uveitis

—Comorbidities

• Obesity:
  • Decreases function, quality of life, response to DMARD therapy (especially skin response)
• Metabolic syndrome:
  • Hypertension, hyperlipidemia, type 2 diabetes
• Hepatic: 
  • MAFLD (metabolic dysfunction-associated fatty liver disease)
• Cardiovascular:
  • Accelerated atherosclerosis, myocardial infarction, peripheral vascular disease
• Psychiatric:
  • Depression, anxiety in 10-30% of patients

INVESTIGATIONS

Bloodwork

• CBC:
  • Hb: may be low due to underlying colitis, inflammation, NSAID use
• Chemistries:
  • ALT may be elevated if comorbid fatty liver
  • Creatinine: may be elevated due to NSAID use
• ESR, CRP:
  • Only elevated in ~40% of patients (less frequent compared to rheumatoid arthritis)
• HLA-B*27:
  • Indicates PsO patients at higher risk of developing PsA — especially with axial involvement
  • Positive in ~18% of PsA, but only ~6% of general North American Caucasian population
  • Predicts shorter latency between onset of skin psoriasis and onset of psoriatic arthritis.
• Serologies:
  • Not associated with rheumatoid factor, anti-CCP antibody, or ANA
    (i.e.: “seronegative” spondyloarthropathy)

Imaging: Peripheral joints

—X-RAYS

• Early:
  • Normal
• At diagnosis:
  • 27% of patients may have erosions (due to diagnostic delay) though in only a few joints
• Characteristic findings that distinguish psoriatic arthritis from rheumatoid and other arthritis on X-ray
  • “Fluffy” periostitis
  • New bone growth at site of enthesitis, bulky syndesmophytes
  • Ankylosis
  • Concurrent Erosions alongside New Bone Formation in the same joint
  • Erosions characeristics: marginal/nonmarginal, eccentric, DIP involvement, pencil-in-cup, located at entheses
  • Sacroiliac and spondylitis involvement
  • Polyarticular unidigit: MCP, PIP, and DIP in the same finger
  • Lack of juxta-articular osteoporosis (juxtra-articular osteoporosis is seen in early RA)

For further details regarding X-ray imaging of axial joints, please refer to axial spondyloarthritis (Axial Spondyloarthritis) chapter.

—ULTRASOUND

B-mode: shows structural abnormalities in soft tissue and bone

Doppler: superimposed Doppler detects abnormal vascularity, which suggests active inflammation

Ultrasound must be performed and interpreted by trained, experienced, and properly equipped rheumatologist-sonographer or other specialist in MSK sonography.

• Peripheral Joints, ultrasound
  • Inflammatory lesions
    • Synovial proliferation
    • Intra/extra-capsular Doppler vascularization
    • Peri-tendinitis, Tenosynovitis
    • Soft tissue edema
  • Structural lesions
    • Bony erosions, bony proliferation
• Peripheral entheses, ultrasound
  • Inflammatory lesions
    • Hypoechogenicity
    • Thickening
    • Doppler signal
    • Bursitis
  • Structural lesions
    • Bone erosion
    • Enthesophyte
    • Tendon calcification

—MAGNETIC RESONANCE IMAGING

STIR (short tau inversion recovery) or T2wFS (T2-weighted fat-suppression) sequences demonstrate water content, indicating bone marrow edema

T1w (T1-weighted) sequences demonstrate fat content, useful for assessing structural lesions corresponding to the bone marrow edema lesions

• Peripheral joints, MRI
  • Inflammatory lesions
    • Synovitis
    • Bone marrow edema
    • Periarticular inflammation
    • Tenosynovitis, Peri-tendonitis, Tendonitis, Tendinopathy
  • Structural lesions
    • Bony erosions, bony proliferation
• Peripheral entheses, MRI
  • Inflammatory lesions
    • Intra-tendon/fascia hypersignal
    • Peri-tendon/fascia hypersignal
    • Bone marrow edema
    • Bursitis adjacent to tendon
  • Structural lesions
    • Tendon/fascia thickening
    • Enthesophyte
    • Bony erosion

For further details regarding MRI imaging of axial joints, please refer to axial spondyloarthritis (Axial Spondyloarthritis) chapter.

DIAGNOSIS

Psoriatic arthritis should be suspected in a patient  presenting with inflammatory joint pain (morning stiffness, nocturnal joint pain, swelling) in the context of a personal or family history of psoriasis. Review should include a screen for spondyloarthritis features like dactylitis, enthesitis, nail changes, IBD and uveitis. Exam should reveal joint swelling and psoriasis. Supportive investigations may include inflammatory markers (like CRP), HLA-B*27 genotyping, and baseline X-rays. MSK ultrasound and MRI, in some cases, may be helpful to support diagnosis, identify active disease, and differentiate other causes of pain.

DIFFERENTIAL DIAGNOSIS

• Rheumatoid arthritis, seronegative:  
  • Unlike RA, PsA can manifest DIP involvement, dactylitis, enthesitis, asymmetric joint swelling and skin psoriasis.
• Reactive arthritis:
  • Reactive arthritis has antecedent mucosal infection, more often HLA-B*27 positive
• Enteropathic arthritis:
  • Enteropathic arthritis typically has more significant colonic disease, which can be confirmed on endoscopic biopsy. Enteropathic arthritis is less likely to have nail and DIP disease

Some consider reactive arthritis, Enteropathic (IBD-related) arthritis, and psoriatic arthritis together as a spectrum of “peripheral spondyloarthritis”.

• Axial spondyloarthritis (“Ankylosing spondylitis“):
  • Psoriatic axial spondyloarthritis more often has asymmetrical sacroiliitis, larger asymmetric syndesmophytes, more frequent cervical spine and less frequent lumbar spine disease:
• Gout
  • Psoriasis is associated with hyperuricemia (related to increased skin cell turnover)
  • Both gout and PsA can co-exist in the same patient
  • PsA is more likely to have upper extremity disease, enthesitis, dactylitis, and axial disease
  • Gout can be confirmed with monosodium urate crystals on synovial fluid analysis or may be identified with imaging (double contour sign on ultrasound or MSU deposits on dual-energy CT)
• CPPD
  • CPPD (Calcium pyrophosphate deposition disease) can mimic many types of inflammatory arthritis
  • Calcification of the triangular fibrocartilage complex, knee menisci, symphysis pubis, glenoid and acetabular labra are clues to support underlying CPPD.
  • CPPD can be confirmed with calcium pyrophosphate crystals on synovial fluid analysis
• Osteoarthritis:
  • May present with local inflammation and swelling in a degenerated joint, but synovial fluid typically has lower cell counts and patients lack features like psoriasis, nail disease, enthesitis or dactylitis.

CLASSIFICATION CRITERIA

Classification criteria are not meant as diagnostic criteria to diagnose disease in a single specific patient. Classification criteria are a standardized way of recruiting a well-defined homogenous population of patients in research studies in order to ensure comparability across studies of a heterogenous disease.

Criteria	Point
Skin psoriasis · Currently, OR · Previously present by history, OR · A family history of psoriasis	· 2 · 1 · 1
Nail dystrophy	· 1
Dactylitis	· 1
Negative RF	· 1
Juxta-articular bone formation on radiographs (not osteophytes)	· 1

DISEASE MEASURES

Various disease measures exist, no broad consensus yet on which measures to adopt.
Below are some measures that may be used day-to-day in rheumatology clinic.

—COMPOSITE DISEASE MEASURES

MDA (Minimal Disease Activity): Binary value, yes or no.

• 5 of 7:
  • TJC ≤1/68, SJC ≤1/66, PASI≤1 or BSA ≤3, enthesitis ≤1, PtGA ≤2/10, pain VAS ≤1.5/10, HAQ ≤0.5

DAPSA (Disease Activity in PSoriatic Arthritis)

• Sum of: SJ66 + TJ68 + PtGA (out of 10) + pain VAS (out of 10) + CRP
  • DAPSA-LDA = ≤14
  • DAPSA-REM = ≤4

MDA evaluates more disease domains than DAPSA

—ENTHESITIS

LEI: Leeds Enthesitis Index

• 6 sites of Enthesitis: lateral epicondyle, medial femoral condyles, Achilles tendon

SPARCC and MASES

• Two other enthesitis indices. Have more enthesitis points to measure.
• SPARCC was based on the most frequent sites identified on Doppler ultrasound in imaging studies.
• LEI is more often used in clinical trials as it is easier to perform but is not as sensitive as the SPARCC index.
• MASES is more focused on axial disease and does not include many peripheral sites.

—PSORIASIS

BSA: body surface area

• 1% BSA: area of patient’s palm
• Mild: <3% BSA
• Moderate 3-10% BSA
• Severe: >10% BSA

PASI is another measure of psoriasis, but more cumbersome for rheumatologists
BSA*PtGA is strongly correlated with PASI

—AXIAL

See Ankylosing Spondylitis chapter for axial disease measures (ASDAS, BASDAI)

TREATMENT

Non-pharmacologic

• Patient Education
• Regular exercise; as needed physiotherapy, occupational therapy
• Weight loss, Smoking cessation

Pharmacologic

—Goal: remission or low disease activity (via disease score, ex: MDA or DAPSA)

One can take a molecular and clinical view when considering psoriatic arthritis treatment.

Molecular view	“Hierarchy of cytokines”: certain cytokines have more importance for disease pathogenesis in certain tissues
Clinical view	“Disease domains”: psoriatic arthritis disease can affect different organs in characteristic ways

Choice of treatment may consider:
Which disease domain is most active?
Which cytokine is most important?

—ACUTE

• Steroids:
  • Intra-articular glucocorticoid may be considered for peripheral arthritis or cautious short term oral systemic steroids.
  • Not for axial disease.
  • Glucocorticoid injections may be considered for some enthesitis sites (lateral epicondyle, greater trochanter) but should be avoided in others (Achilles).

—MAINTENANCE

Peripheral arthritis

• Initial therapy
  • Mono/oligoarticular mild disease (minimal swelling/functional limitation, no structural damage, normal CRP, no dactylitis nor nail disease):
    • NSAIDs max 4 weeks, caution with cardiovascular/renal risk.
      If no better after ≤4 weeks, quickly move onto csDMARDs.
    • Intra-articular glucocorticoid injections may be considered for oligoarticular disease. If not effective or recurrence, addition of csDMARDs should be considered.
  • Polyarthritis, significant mono/oligoarticular disease:
    • Methotrexate 20-25mg/week;
      May also consider other csDMARDs as mono or combination therapy (sulfasalazine, leflunomide)

If not improved/at-target by 3-6 months, move onto subsequent therapy

• Subsequent therapy
  • bDMARD (TNFi, IL-17i, or IL-23i. IL-12/23i may be considered but are less effective for joints and skin compared to IL17i and IL23i
    or
    tsDMARD (JAK inhibitor)
  • If significant skin psoriasis:
    • Consider favouring IL-17i or IL23i over TNFi or tsDMARD
  • If inappropriate for b/ts-DMARD or mild/moderate disease
    • PDE4 inhibitor (apremilast) may be considered

Axial arthritis

• Initial therapy:
  • NSAIDs as needed, use with caution, consider cardiovascular and renal risk
  • Oral steroids are not used to treat axial disease

Expect peak response in 2-4 weeks. If inadequate efficacy with 2 different NSAIDs, move onto subsequent therapy

• Subsequent therapy
  • bDMARD (TNFi or IL17i) or
    tsDMARD (JAK inhibitor)
  • IL23i or IL12/23i do not appear effective for axial disease

Unequivocal enthesitis, dactylitis

• Initial Therapy:
  • NSAIDs, glucocorticoid injections
  • Physiotherapy for enthesitis
• Subsequent Therapy: Methotrexate; TNF, IL17i, IL12/23i, IL23i, JAKi, PDE4i

—OTHER DOMAINS, ASSOCIATED CONDITIONS, COMORBIDITIES

• Psoriasis
  • Mild local disease:
    • Topical: steroids, calcineurin inhibitor, PDE4i
  • Widespread, resistant disease:
    • Phototherapy, methotrexate, cyclosporin, PDE4i, tsDMARD, bDMARDs.
    • Consider favouring IL17i, IL12/23i, IL23i if significant skin disease
• Nail Disease:
  • bDMARDs (TNFi, IL17i, IL12/23i, IL23i)
• IBD:
  • bDMARDs (TNFi monoclonal antibody, not etanercept), IL12/23i, IL23i, JAKi
  • Methotrexate, sulfasalazine
• Uveitis:
  • TNFi (adalimumab, infliximab, certolizumab; not etanercept), cyclosporin, methotrexate
• Cardiovascular:
  • Routine screening of traditional modifiable cardiovascular risk factors.

In patients with sustained remission, cautious tapering of DMARDs may be considered

TNFi	Adalimumab , certolizumab, etanercept, golimumab, infliximab
IL-17i	Bimikizumab, ixekizumab, secukinimuab
IL-23i	Guselkumab, risankizumab, tildrakizumab
IL12/23i	Ustekinumab
PDE4i	Apremilast

Evaluating Treatment Response

• Treat-to-Target approach:
  • Goal of low-disease activity or remission, utilizing a disease activity score (ex: MDA or DAPSA)
• Regular-interval clinical evaluation (history, exam) with disease activity score
  • Ex: q1-3 months when active disease, then q6+ months when stable
  • Consider adding CRP with clinical evaluation, particularly if measuring DAPSA
  • Review all PsA disease domains for activity
  • Screen for associated conditions and comorbidities

PROGNOSIS

• Poor prognostic factors:
  • High BMI
  • Higher joint count at initial presentation
  • Higher CRP at initial presentation
  • Failed previous advanced DMARDs
  • Sex
    • Men: more often develop axial involvement and radiographic joint damage
    • Women: more likely to report functional limitation and impaired quality of life.
• Mortality
  • Increased prevalence of cardiovascular disease
  • Some studies have shown increased mortality
    • Driven by excess comorbidity; possibly higher mortality in younger and female patients

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