psoriatic arthritis

**Definition/Epidemiology:** Chronic inflammatory arthritis associated with psoriasis, classified as a seronegative spondyloarthropathy (with ankylosing spondylitis, reactive arthritis, and IBD-associated arthritis). Affects ~20-30% of patients with psoriasis; onset typically age 30-50; men and women affected about equally. Arthritis usually follows skin disease by about 10 years, but can precede it in ~15% of patients. Risk factors for developing PsA among psoriasis patients: nail disease (pitting, onycholysis), scalp/intergluteal psoriasis, and obesity.

**Pathophysiology:** Genetic predisposition (HLA-B27, HLA-B38, HLA-B39, HLA-Cw6 for psoriasis) plus environmental triggers (trauma/Koebner-like mechanical stress, infection) lead to dysregulated innate and adaptive immunity. The IL-23/IL-17 axis is central: IL-23 drives Th17 cell and ILC3 activation, producing IL-17, IL-22, and TNF-α. This causes synovitis, enthesitis (the primary site of inflammation), and both bone erosion (osteoclast activation) and new bone formation (periostitis, pathologic proliferation). This is why therapeutic targets are TNF-α, IL-17, and IL-23.

**Clinical patterns (Moll and Wright):** 1. Asymmetric oligoarthritis (≤4 joints), the most common pattern in many series 2. Symmetric polyarthritis, which resembles RA but is RF-negative 3. DIP-predominant, the classic pattern, strongly associated with nail disease 4. Spondylitis/axial disease (sacroiliitis, often asymmetric; HLA-B27 associated) 5. Arthritis mutilans, the most severe and destructive form with osteolysis and telescoping digits ("opera-glass hand")

**Key features:** - Dactylitis ("sausage digit"), a diffuse swelling of the whole digit from flexor tenosynovitis plus joint synovitis - Enthesitis (Achilles tendon, plantar fascia insertion) - Nail changes: pitting, onycholysis, ridging, and oil-drop discoloration - Skin: well-demarcated erythematous plaques with silvery scale on extensor surfaces - Uveitis/iritis (anterior uveitis), which can occur like in other spondyloarthropathies - Asymmetric, often involving both small and large joints; morning stiffness that improves with activity (inflammatory pattern)

**Diagnosis:** - Clinical diagnosis supported by CASPAR criteria: inflammatory articular disease plus ≥3 points from current psoriasis (2 points), nail dystrophy, negative RF, dactylitis, and radiographic juxta-articular new bone formation - Labs: elevated ESR/CRP possible, RF and anti-CCP typically negative (low titers can occur in a minority); HLA-B27 positive in axial disease; uric acid may be mildly elevated in extensive psoriasis (can confuse with gout) - Imaging: Erosions with adjacent bone proliferation, "pencil-in-cup" deformity (tapering of proximal phalanx with cup-shaped erosion of the distal bone), DIP involvement, periostitis, asymmetric sacroiliitis, and non-marginal asymmetric syndesmophytes; notably, joint-space narrowing with bony ankylosis can occur, and periarticular osteopenia is typically absent (unlike RA)

**Differential diagnosis:** Rheumatoid arthritis (symmetric, MCP/PIP, RF/anti-CCP positive, periarticular osteopenia, no new bone formation), osteoarthritis (DIP involvement with Heberden nodes, no inflammation or nail changes), gout, reactive arthritis (keratoderma blennorrhagicum and circinate balanitis resemble psoriasis), and ankylosing spondylitis (symmetric sacroiliitis, marginal syndesmophytes).

**Management:** - Mild peripheral/enthesitis: NSAIDs, local steroid injection - Peripheral arthritis with erosive/persistent disease: csDMARDs (methotrexate, sulfasalazine, leflunomide) - Moderate-severe disease or axial/enthesitis/dactylitis: biologics — TNF inhibitors (etanercept, adalimumab, infliximab, golimumab, certolizumab), IL-17 inhibitors (secukinumab, ixekizumab), IL-12/23 inhibitor (ustekinumab), IL-23 inhibitors (guselkumab, risankizumab), also abatacept (CTLA4-Ig); oral small molecules: apremilast (PDE4 inhibitor) and JAK inhibitors (tofacitinib, upadacitinib) - Note: Methotrexate helps skin and peripheral joints but is not effective for axial disease. Systemic glucocorticoids are generally avoided because of risk of pustular psoriasis flare upon withdrawal. Antimalarials (hydroxychloroquine) may exacerbate psoriasis. Before biologics, screen for latent TB (and hepatitis B). - IL-17 inhibitors can worsen IBD, so use caution/avoid in patients with Crohn disease/ulcerative colitis; TNF inhibitors are preferred in patients with IBD or uveitis (monoclonal antibodies).

**Complications/Associations:** Increased cardiovascular disease and metabolic syndrome (obesity, diabetes, hypertension, dyslipidemia), NAFLD, depression, osteoporosis, uveitis, and progressive joint destruction with disability if untreated.

**High-yield board pearls:** - "Pencil-in-cup" + DIP + nail pitting + sausage digit = PsA - Seronegative (RF-/anti-CCP-), asymmetric, HLA-B27 associated for axial disease - Enthesitis is the hallmark pathologic lesion - TNF inhibitors, IL-17, and IL-23 blockade are the main biologic options