What are the triggers and management options for psoriatic arthropathy?

Triggers and Management of Psoriatic Arthropathy

Triggers of Psoriatic Arthropathy

While the provided evidence focuses primarily on management rather than triggers, psoriatic arthritis develops in approximately 5-30% of patients with cutaneous psoriasis, with 85% developing skin disease before joint involvement. 1, 2

Key Clinical Triggers and Risk Factors

• Trauma and mechanical stress can precipitate joint involvement in susceptible individuals 1
• Infection may trigger disease flares, though specific pathogens are not consistently identified 1
• Stress and psychological factors can exacerbate both skin and joint manifestations 1
• Poor prognostic factors that predict more severe disease include: polyarticular involvement (≥5 actively inflamed joints), elevated acute phase reactants (ESR/CRP), existing structural damage, dactylitis, and nail involvement 3

Management Algorithm

Initial Assessment and Treatment Target

Treatment must aim for remission or, alternatively, low disease activity through regular monitoring and appropriate therapy adjustment. 3

• The primary goal is maximizing health-related quality of life through symptom control, prevention of structural damage, normalization of function, and social participation—with abrogation of inflammation as the critical component 3
• Rheumatologists should primarily manage musculoskeletal manifestations, with dermatologist collaboration when clinically relevant skin involvement exists 3

Step 1: First-Line Therapy for Mild Disease

NSAIDs should be used as initial therapy to relieve musculoskeletal signs and symptoms, though cardiovascular and gastrointestinal risks must be considered. 3

• NSAIDs provide symptomatic relief but have no demonstrated efficacy on skin lesions and do not modify disease progression 3, 1
• Local glucocorticoid injections may be considered as adjunctive therapy for persistent joint inflammation 3
• Systemic glucocorticoids should be used with caution at the lowest effective dose and are not recommended for long-term management 3

Step 2: Conventional Synthetic DMARDs (csDMARDs)

In patients with polyarthritis, a csDMARD should be initiated rapidly, with methotrexate strongly preferred when relevant skin involvement is present. 3

• For monoarthritis or oligoarthritis with poor prognostic factors (structural damage, elevated ESR/CRP, dactylitis, nail involvement), csDMARD should be considered 3
• Methotrexate is the first-choice csDMARD, particularly effective for both joint and skin manifestations 3, 4
• Alternative csDMARDs include leflunomide and sulfasalazine 3, 5
• Critical caveat: Methotrexate carries increased hepatotoxicity risk in PsA compared to other rheumatic conditions; transaminases require careful monitoring, especially with alcohol consumption, obesity, type II diabetes, or concurrent hepatotoxic drugs 3
• Important limitation: Traditional oral DMARDs have NOT been shown effective for axial manifestations of PsA and should not be considered adequate for axial disease 6

Step 3: Biological DMARDs (bDMARDs)

With inadequate response to at least one csDMARD, therapy with a bDMARD must be commenced; when relevant skin involvement exists, an IL-17 inhibitor or IL-12/23 inhibitor should be preferred. 3

TNF Inhibitors

• TNF inhibitors (etanercept, infliximab, adalimumab, golimumab, certolizumab) are effective for all disease domains and inhibit radiographic progression 5
• For predominantly axial disease with insufficient NSAID response, a TNF inhibitor should be considered according to current practice 3
• Etanercept 50 mg weekly is the standard dosing for rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis 7

IL-17 and IL-23 Pathway Inhibitors

• IL-17 inhibitors (secukinumab, ixekizumab, brodalumab) and IL-12/23 or IL-23 inhibitors (ustekinumab) are particularly effective when skin involvement is prominent 3, 5
• For axial disease with relevant skin involvement, IL-17 inhibitors may be preferred over TNF inhibitors 3, 6

Safety Considerations

• Critical warning: Patients on TNF inhibitors face increased risk of serious infections including tuberculosis reactivation, invasive fungal infections, and opportunistic infections 7
• Test for latent tuberculosis before initiating bDMARD therapy and periodically during treatment 7
• Lymphoma and other malignancies have been reported in patients treated with TNF-blockers 7

Step 4: Targeted Synthetic DMARDs (tsDMARDs)

With inadequate response to at least one csDMARD and at least one bDMARD, or when a bDMARD is not appropriate, a JAK inhibitor may be considered. 3

• JAK inhibitors (tofacitinib) represent an alternative when bDMARDs fail or are inappropriate 5
• Important safety note: Worldwide cautionary comments exist regarding JAK inhibitors following large RCT data in rheumatoid arthritis 3
• PDE4 inhibitors (apremilast) may be considered in patients with mild disease and inadequate csDMARD response when neither bDMARD nor JAK inhibitor is appropriate 3

Step 5: Switching Within or Between Classes

In patients who fail to respond adequately to or are intolerant of a bDMARD, switching to another bDMARD or tsDMARD should be considered, including one switch within a class. 3

Special Considerations for Enthesitis

For unequivocal enthesitis with insufficient response to NSAIDs or local glucocorticoid injections, therapy with a bDMARD should be considered. 3

Tapering in Sustained Remission

In patients achieving sustained remission, cautious tapering of DMARDs may be considered. 3

Comorbidity Management

When managing PsA, non-musculoskeletal manifestations (particularly skin, eye, gastrointestinal tract) and comorbidities (obesity, metabolic syndrome, cardiovascular disease, depression) must be taken into account. 3

• The choice of treatment should account for safety considerations regarding individual modes of action to optimize the benefit-risk profile 3
• Methotrexate, glucocorticoids, salicylates, NSAIDs, or analgesics may be continued during bDMARD treatment 7