Psoriatic arthritis

Inflammatory arthritis associated with psoriasis. Typically seronegative and can involve peripheral joints (often DIP joints of fingers/toes, with nail pitting) as well as spine or sacroiliac joints in some cases. May present with dactylitis (sausage digits) and enthesitis. Radiographically can show "pencil-in-cup" erosions in severe chronic disease.

• Occurs in up to ~30% of psoriasis patients, often years after skin disease. It bridges dermatology and rheumatology, making it a favorite for exam questions (e.g., a patient with skin plaques developing joint pain). PsA can cause significant joint damage (including deforming arthritis mutilans) if untreated. Recognizing the link between skin and joint findings is key.

• Patient with known psoriasis (often long-standing skin plaques or nail changes) who develops joint pain/stiffness. Patterns vary: can mimic RA (symmetric polyarthritis), or present as asymmetric oligoarthritis, or classic DIP joint arthritis (especially of fingers/toes).
• Dactylitis (diffuse swelling of an entire finger or toe) is a hallmark finding, due to inflammation of flexor tendon sheaths and joints – gives the "sausage digit." Enthesitis (e.g., Achilles tendon insertion pain) can also occur.
• Nail involvement is common: nail pitting, onycholysis (nail separating), and nail ridges correlate with PsA severity. In fact, nail changes + DIP arthritis is a strong clue for psoriatic arthritis (RA rarely affects DIPs).
• Skin: Often the patient will have active psoriatic skin lesions (scaly erythematous plaques on extensor surfaces, scalp, etc.), but sometimes arthritis precedes obvious skin flares. Severity of skin disease does not always match joint severity (someone with mild psoriasis might still get severe arthritis).
• Axial involvement: A subset have spondylitis and sacroiliitis akin to AS (particularly those who are HLA-B27 positive). These patients may have back pain similar to AS, but usually also have peripheral joint or skin manifestations that lead to the PsA diagnosis.

1. Always examine the skin and nails in patients with unexplained arthritis. Hidden psoriasis (scalp, behind ears, gluteal cleft) or subtle nail pitting might tip you off to PsA.
2. Labs: No definitive test. RF and anti-CCP are usually negative (helps distinguish from RA, though a small percentage of PsA patients can have low-positive RF). Uric acid may be elevated in severe psoriasis due to high skin turnover (don't confuse with gout in exam scenarios).
3. Imaging: Look for the classic pencil-in-cup deformity on hand X-ray (from erosion of one end of the bone and reactive proliferation on the other). Also, juxta-articular new bone formation and ankylosis (joint fusion) can occur in chronic PsA. Unlike RA, which causes osteopenia, PsA can have bone proliferation.
4. Differentiate from RA: PsA often involves DIPs (RA almost never does) and is more likely asymmetric. Also, PsA has the extra features (dactylitis, nail pitting, skin lesions). If a patient has RA-like arthritis but also psoriasis (or a family history of it), consider PsA.
5. Assess for ocular involvement (conjunctivitis or uveitis can occur in PsA, though less commonly than in AS) and for other comorbidities (PsA patients have higher risk of metabolic syndrome).

1. NSAIDs can help milder cases for symptomatic relief of joint pain and stiffness.
2. Methotrexate is commonly used in moderate to severe PsA, especially if there is significant skin involvement (helps both psoriasis and arthritis). It's a first-line DMARD for PsA (note: unlike in RA, methotrexate alone often doesn't prevent progressive joint damage in PsA, but it helps symptoms).
3. Sulfasalazine or leflunomide are additional traditional DMARD options for peripheral arthritis. (Sulfasalazine can be useful if concomitant IBD as well.)
4. Biologics: If inadequate response to methotrexate or severe disease, use TNF inhibitors (etanercept, adalimumab, etc.) or newer agents: IL-17 inhibitors (secukinumab, ixekizumab) and IL-12/23 inhibitor (ustekinumab) are approved for PsA and can help both skin and joints. PDE4 inhibitor apremilast is an oral option for moderate PsA. JAK inhibitors (tofacitinib) are also approved for PsA.
5. Avoid systemic corticosteroids if possible – tapering off steroids can sometimes trigger a severe flare of psoriasis (pustular psoriasis). If needed, use lowest effective dose and plan to transition to steroid-sparing therapy. Local steroid injections can be beneficial for isolated inflamed joints or enthesitis.

• Psoriasis + DIP joint arthritis = psoriatic arthritis (until proven otherwise).
• Nail pitting is a strong clue; nails are essentially skin, so nail changes link the skin and joint disease.
• Dactylitis (sausage digit) is a buzzword for PsA (also seen in reactive arthritis); RA does not cause full-digit swelling.
• "Pencil-in-cup" erosion on X-ray (phalangeal deformity) is classically PsA, reflecting destructive changes and bone resorption.

• Spinal involvement: If a PsA patient develops severe back pain or neurologic symptoms, evaluate for atlantoaxial subluxation or spinal fracture (PsA with long-standing axial involvement can have some of the same risks as AS).
• Psoriasis patient on systemic steroids who stops them abruptly → watch for pustular psoriasis flare (a dangerous generalized rash).
• Psoriatic arthritis can progress to arthritis mutilans (severe deformity with telescoping digits) if untreated – aggressive therapy is warranted when joint damage is progressing.

1. Psoriasis patient with joint pain → screen for PsA (ask about stiffness, examine joints, check nails).
2. If PsA suspected, evaluate extent: count involved joints, note if DIPs, look for dactylitis, enthesitis. Get baseline X-rays of affected hands/feet for erosions.
3. Labs: RF/CCP to rule out RA if pattern is polyarticular (seronegative helps point to PsA). Inflammatory markers (ESR/CRP) may be elevated. Document skin and nail findings.
4. Mild PsA → start with NSAIDs ± local steroid injections. If more active, start methotrexate (especially if skin also needs control).
5. Moderate-severe or inadequate response → add a biologic (TNF inhibitor or IL-17/IL-12/23 inhibitor depending on patient factors). Monitor disease activity in skin and joints (joint counts, functional status, skin lesion extent) each visit.

• 40-year-old patient with psoriasis has a swollen, painful index finger DIP joint and pitted nails → Psoriatic arthritis (likely DIP-predominant type).
• X-ray of a finger showing a tapered "pencil" distal phalanx and a cup-shaped erosion in the proximal phalanx → Psoriatic arthritis (arthritis mutilans).
• Patient with psoriasis presents with multiple tender, swollen finger joints (including DIPs) and a 'sausage' toe, RF is negative → Psoriatic arthritis.