Psoriatic Arthritis (PsA)

Tina Arkee

Background

  • Chronic inflammatory arthritis associated with psoriasis (occurring in up to 20-30% of psoriasis patients)
  • Incidence: onset usually around 30-50y; men and women equally affected. Psoriasis usually precedes the development of arthritis
  • Etiology: multigenic autoimmune disease that involves inflammatory infiltrate (likely driven by CD8 T cells) to entheses, synovial tissue, and skin. Joint trauma may trigger arthritis flare (“deep” Koebner phenomenon)
  • Classified under seronegative arthritis, though up to 15% of patients will have serologic positivity (RF most common)

Presentation

  • Variable joint pattern involvement (may evolve over time):
    • DIP arthritis - asymmetric oligoarthritis (large joint involvement in addition to small joints)
    • symmetric polyarthritis (may look like RA)
    • axial arthritis (involves the spine and SI joints)
    • arthritis mutilans (severe destructive joint disease leading to osteolysis and shortening of digits)
  • Periarticular manifestations:
    • Enthesitis: inflammation of tendon and ligament insertion sites, including the Achilles tendon, patellar tendon, and spinous processes of vertebral bodies
    • Tenosynovitis: flexor tendons of hands and posterior tibial tendons often involved
    • Dactylitis: diffuse swelling of a single finger or toe (sausage digit). Acute dactylitis presents with a red, hot, tender, swollen digit, whereas chronically affected digits are often just swollen.
  • Extra-articular manifestations: nail changes (pitting, ridging, onycholysis), psoriasis plaque, chronic bilateral uveitis, conjunctivitis
  • Comorbidities: Decreased bone mineral density, psychiatric disease (depression, anxiety), hyperuricemia, increased risk of CVD/metabolic syndrome/DM/fatty liver

Evaluation

  • Laboratory data: CBC, BMP, uric acid, ESR, CRP; consider HIV testing
    • Autoimmune testing to rule out other conditions: ANA (shouldn’t have high titer positivity), RF (positive in 2-10%), anti-CCP
    • HLA-B27: present in 25-30% patients; identifies patients at risk for axial disease or acute anterior uveitis but does not diagnose them
  • Imaging
    • X-rays often show evidence of both bone erosion and new bone formation, such as the “pencil in cup” deformity (often involves the DIP), osteolysis leading to digital shortening, bone spurs at entheses, periosteal reactions (new bone formation around eroded sites), and ankylosis (fusion of adjacent joints).
    • MRI changes can be more sensitive in detecting articular and soft tissue inflammation and sacroiliitis; however, these do not always correlate with clinical symptoms
  • CASPAR classification criteria for diagnosis are >90% sensitive and specific for PsA (≥3 points = diagnostic)
    • Autoimmune testing to rule out other conditions: ANA (shouldn’t have high titer positivity), RF (positive in 2-10%), anti-CCP
    • Current psoriasis (2), a personal history of psoriasis (1), or family history of psoriasis (1)
    • Psoriatic nail findings observed on physical exam (1)
    • Negative test for RF (1)
    • Current dactylitis or a history of dactylitis documented by a rheumatologist (1)
    • Xray evidence of juxta-articular new bone formation in the affected hand or foot (1)

Management

  • Non-pharmacologic strategies: PT/OT, exercise, weight loss, nutritionist referral for metabolic syndrome, dermatology referral for comanagement
  • Treatment is dependent on pattern of involvement, skin disease, severity, and comorbidities
    • Mild: NSAIDs (e.g. naproxen 375-500mg BID)
    • Moderate or resistant to NSAIDs: conventional DMARDS (e.g. MTX 15-25mg q weekly or leflunomide 20mg QD) or occasionally apremilast (PDE4 inhibitor) if avoiding biologics
    • Severe (many joints, erosive, functional limitation) or no response to above: biologic DMARD, usually TNF inhibitor (infliximab, adalimumab, etanercept); if no response, trial to another TNF inhibitor. If TNFi are contraindicated OR psoriasis is severe, try an anti-IL17a biologic (secukinumab, ixekizumab). Patients with concomitant IBD may benefit from anti-IL12/IL-23 agents (ustekizumab). Anti-IL17 biologics are contraindicated in patients w/IBD.
    • Refractory to two TNFi/IL-12/IL-23: consider the JAK inhibitor tofacitinib
  • Note: avoid oral glucocorticoids given risk of developing erythroderma or pustular psoriasis!
  • Skin and joint disease often do not correlate — evaluate independently
Last updated on