In New Zealand, psoriatic Arthritis is managed by rheumatologists. Psoriatic arthritis is a chronic immune-mediated inflammatory arthritis that develops in roughly 20-30% of people with psoriasis, producing painful, swollen, and progressively damaged joints alongside skin and nail disease. It affects approximately 0.05-0.25% of the general population and 0.5-1% of those of European descent, with peak onset between ages 30 and 50 and equal sex distribution.
Psoriatic arthritis (ICD-10: L40.50-L40.59) is a heterogeneous immune-mediated inflammatory arthritis classified within the seronegative spondyloarthritis family and clinically associated with psoriasis of the skin or nails. Pathogenesis involves dysregulated innate and adaptive immunity in genetically susceptible individuals: HLA-Cw0602 and HLA-B27 confer significant risk, and downstream pathways involving IL-23 / Th17, IL-17A, and TNF-alpha drive synovitis, enthesitis, and bone remodeling. The Moll and Wright classification originally described five clinical patterns: distal interphalangeal predominant, asymmetric oligoarticular, symmetric polyarticular (rheumatoid-like), arthritis mutilans, and predominant spondylitis. Most patients display overlapping features rather than pure patterns.
The key symptoms of Psoriatic Arthritis are: Joint pain, stiffness, swelling, and tenderness most marked in the morning and after rest, lasting more than 30 minutes (inflammatory pattern)., Asymmetric joint involvement, often beginning in a single knee, ankle, finger, or toe and spreading over weeks to months., Distal interphalangeal joint swelling adjacent to a nail with characteristic pitting or onycholysis — highly specific for PsA., Dactylitis (sausage digit): diffuse uniform swelling of an entire finger or toe with pain, warmth, and reduced movement, present at some point in 30-50% of patients., Enthesitis: pain and tenderness at tendon-bone insertions, classically the Achilles insertion, plantar fascia, lateral epicondyle, or iliac crest., Inflammatory back pain — pain and stiffness in the low back and buttocks that improves with movement and worsens with rest — in 25-50% with axial involvement., Nail changes: pitting, onycholysis (lifting of nail from nail bed), oil drop sign, subungual hyperkeratosis, splinter hemorrhages — present in 80-90% of PsA patients..
Diagnosis combines clinical pattern recognition with the CASPAR classification criteria. A patient with inflammatory joint, spine, or entheseal disease receives 1 CASPAR point each for current psoriasis (2 points), history of psoriasis, family history of psoriasis, current dactylitis (1 point), history of dactylitis, typical nail changes, juxta-articular new bone formation on radiographs, and negative rheumatoid factor and anti-CCP. Three or more points confirm PsA classification with 99% specificity. Clinical assessment captures the 68 tender and 66 swollen joint counts, dactylitis count, Leeds Enthesitis Index or MASES enthesitis score, BASDAI for axial symptoms, PsA-specific composite scores (DAPSA, MDA, PASDAS), psoriasis severity (PASI, BSA), and patient-reported outcomes (HAQ, fatigue, sleep). Laboratory work-up includes complete blood count, CRP, ESR (elevated in 40-50%, normal in mild disease), rheumatoid factor and anti-CCP (negative in 90-95%), HLA-B27 (positive in 25-40%, especially axial PsA), uric acid, kidney and liver function, vitamin D, and screening for hepatitis B and C, tuberculosis (QuantiFERON or PPD), and HIV before biologic therapy. Imaging includes hand and foot radiographs (juxta-articular new bone, fluffy periosteal reaction, erosions, pencil-in-cup deformities, ankylosis), sacroiliac and lumbar spine X-ray (sacroiliitis, syndesmophytes), and increasingly ultrasound and MRI for early disease — ultrasound detects subclinical synovitis, enthesitis, and tenosynovitis; MRI is the most sensitive modality for axial inflammation and early peripheral enthesitis. Cardiovascular risk assessment (lipid panel, blood pressure, fasting glucose), depression screening, and ophthalmology baseline are recommended at diagnosis.
Outlook has transformed since the introduction of biologic therapy. With timely treat-to-target therapy, 50-70% of patients achieve ACR20 response, 30-50% achieve ACR50, and 20-30% reach minimal disease activity or remission. Radiographic progression is substantially slowed with TNF inhibitors and other biologics. Without treatment, 40-60% develop structural joint damage within 2-3 years, and 20-40% of untreated patients develop irreversible deformity over 10 years. Predictors of more severe disease include polyarticular onset, dactylitis, elevated CRP, structural damage at presentation, and longer symptom duration before diagnosis. Comorbidities — cardiovascular disease (1.5-fold increase), metabolic syndrome (40-50% prevalence), depression (15-25%), uveitis (5-10%), inflammatory bowel disease (5-7%), and fatty liver — substantially affect overall survival and quality of life. Modern care reduces excess cardiovascular mortality, but adherence to lifestyle, vaccination, and comorbidity screening is essential. Life expectancy in well-managed PsA is approaching that of the general population.
Refer to a rheumatologist as soon as inflammatory joint, spine, or enthesis symptoms develop in a patient with psoriasis or family history. Early specialist referral and treat-to-target therapy reduce structural damage and disability. Concurrent dermatology, ophthalmology, gastroenterology, and cardiology input is needed for comorbidities.
Find specialists →NSAIDs and intra-articular steroid produce symptom relief in 24-72 hours. Conventional DMARDs (methotrexate) require 8-12 weeks for full effect. Biologics show meaningful improvement at 4-6 weeks with peak benefit by 12-24 weeks. Treat-to-target reassessment every 3-6 months guides escalation. Skin response often precedes joint response by 4-12 weeks with most biologics. Radiographic progression measurable on imaging at 6-12 months with appropriate therapy.
Combine moderate-intensity aerobic activity (30 minutes most days; cycling, swimming, walking) with resistance training (2-3 times weekly) and flexibility work. Patients with axial disease benefit from daily spinal mobility exercises and supervised hydrotherapy. Avoid high-impact activities during acute flares but resume promptly once active inflammation settles. Patients with hand involvement benefit from occupational therapy and joint-protection techniques. Exercise reduces pain, improves function, and addresses cardiovascular comorbidity.
Choose a rheumatologist with experience in PsA, ideally in a multidisciplinary clinic with dermatology. Ask about use of treat-to-target (DAPSA, MDA scores), familiarity with all biologic and oral targeted therapies, and pathway for fast-tracking patients with new dactylitis or severe disease. Continuity of care over years matters because disease evolves and therapy needs adjustment.
Medically reviewed by AIHealz Medical Editorial Board · May 13, 2026
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