Psoriasis arthropathica, also known as psoriatic arthritis (PsA), is a chronic, progressive inflammatory disease with high clinical heterogeneity. Epidemiological data indicate that the global prevalence of PsA among patients with psoriasis is approximately 17.58%, whereas the prevalence among Chinese patients with psoriasis is approximately 10.4%.1,2 The etiology and pathogenesis of PsA have not yet been fully elucidated; however, chronic progressive inflammation is thought to be driven by a complex interplay of genetic predisposition, environmental triggers, and immune dysregulation. Domestic and international recommendations for PsA diagnosis and management have been continuously updated.3–5 Jointly initiated by the “China Dermatologist Association and the Chinese Dermatovenerology Society of Integrative Medicine”, and developed in accordance with the methodology and procedures for evidence-based clinical practice guidelines, the “Guideline for the Diagnosis and Treatment of Arthropathic Psoriasis (Psoriatic Arthritis) (2026 Edition)” has been formulated based on available current evidence and clinicians’ practical experience. This guideline covers disease classification and diagnosis, assessment of disease activity and severity, therapeutic strategies, comorbidity management, and treatment considerations in special populations, thereby enhancing the overall standard care for PsA and improving patient outcomes in China. This guideline has been registered on the International Practice Guidelines Registry Platform (http://www.guidelines-registry.org; No. PREPARE-2023C304). Questions, Recommendations, and Evidence Grade Through a systematic literature search and review, supplemented by input from selected clinical experts, the secretariat identified 14 key clinical questions. The Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach was applied to grade the evidence and the strength of recommendations Supplementary Table 1, https://links.lww.com/CM9/C912. Recommendations considered essential for clinical practice but not suitable for formal evidence grading were labeled as good practice statements (GPS), with consensus agreement rates reported where applicable Supplementary Materials, https://links.lww.com/CM9/C912. Clinical question 1: How can clinicians diagnose PsA early? Recommendation 1 It is recommended that all patients with psoriasis can be proactively questioned about the presence of musculoskeletal and joint pain (Grade 1B); routine use of the Early Arthritis for Psoriatic Patients (EARP) questionnaire or the Psoriasis Epidemiology Screening Tool (PEST) is suggested for early PsA screening (Grade 2C); nail involvement, obesity, severe cutaneous involvement of psoriasis, and a family history of PsA are risk factors for the development of PsA in patients with psoriasis (Grade 2C). The application of high-frequency ultrasonography for screening peripheral arthritis and enthesitis is helpful for the early diagnosis of PsA (Grade 2B). Clinical question 2: Is musculoskeletal joint pain in patients with psoriasis alone sufficient for diagnosing PsA? Recommendation 2 Musculoskeletal joint pain in patients with psoriasis does not necessarily establish a diagnosis of PsA. clinicians should obtain a detailed medical history, perform physical examination and appropriate investigations, and exclude other osteoarticular or soft-tissue rheumatic disorders (GPS, agreement: 100%). Clinical question 3: Is the use of the Classification Criteria for Psoriatic Arthritis (CASPAR) recommended for the diagnosis of PsA? Recommendation 3 The use of the CASPAR classification criteria is recommended for the diagnosis of PsA; however, clinicians should be aware that this criterion carries a certain risk of misdiagnosis and missed diagnosis (GPS, agreement: 100%). Clinical question 4: How should disease activity in PsA be assessed? Recommendation 4 Assessment of disease activity in peripheral arthritis is recommended using the 66/68 swollen joint counts (SJC66) and tender joint counts (TJC68) (GPS, agreement: 96.6%); for patients with axial involvement, the Ankylosing Spondylitis Disease Activity Score (ASDAS) is recommended for evaluation (Grade 2C). Comprehensive assessment of PsA disease activity is recommended using the disease activity index for psoriatic arthritis (DAPSA) or minimal disease activity (MDA) (Grade 2C). Clinical question 5: Which imaging modalities should be used to evaluate PsA? Recommendation 5 Ultrasound or MRI is recommended for the assessment of active lesions in PsA, whereas radiography or CT is recommended for the evaluation of structural damage (GPS, agreement: 86.2%). Clinical question 6: What are the treatment principles and targets for PsA? Recommendation 6 Treatment of PsA should follow an individualized approach and be based on shared decision-making between the patient and the physician. Multidisciplinary collaboration, including dermatologists and rheumatologists, is encouraged to optimize therapeutic strategies. Management of PsA should adhere to a treat-to-target (T2T) strategy, with the goal of achieving remission or minimal disease activity (MDA) (GPS, agreement: 100%). Clinical question 7: How should therapeutic agents be selected based on different clinical manifestations of PsA? Recommendation 7.1 For the treatment of PsA with peripheral arthritis, nonsteroidal anti-inflammatory drug (NSAID) (Grade 1B), conventional synthetic disease-modifying antirheumatic drug (csDMARD) methotrexate (MTX), sulfasalazine, leflunomide (Grade 1B), biologics tumor necrosis factor-alpha (TNF-α) inhibitors, interleukin (IL)-17 inhibitors, IL-12/23 inhibitors or IL-23 inhibitors (Grade 1B), as well as small-molecule targeted agents Janus kinase (JAK) inhibitors (Grade 1B), tyrosine kinase 2 (TYK2) inhibitors (Grade 1B), or phosphodiesterase 4 (PDE4) inhibitors (Grade 2B) are recommended. For patients with monoarticular involvement, intra-articular corticosteroid injection may be considered; however, systemic glucocorticoid therapy is not recommended (Grade 2B). Recommendation 7.2 For axial involvement, NSAID (Grade 1B), biologics (TNF-α inhibitors and IL-17 inhibitors) (Grade 1B), as well as JAK inhibitors (Grade 2B) are recommended. Recommendation 7.3 For enthesitis, NSAID (Grade 1B), MTX (Grade 1B), biologics (TNF-α inhibitors, IL-17 inhibitors, IL-12/23 inhibitors, or IL-23 inhibitors) (Grade 1B), as well as small-molecule targeted agents JAK inhibitors (Grade 1B), TYK2 inhibitors (Grade 1B), or PDE-4 inhibitors (Grade 2B), are recommended. Recommendation 7.4 For dactylitis, NSAID (Grade 1B), MTX (Grade 1B), biologics (TNF-α inhibitors, IL-17 inhibitors, IL-12/23 inhibitors, or IL-23 inhibitors) (Grade 1B), as well as small-molecule targeted agents JAK inhibitors (Grade 1B), TYK2 inhibitors (Grade 1B), or PDE-4 inhibitors (Grade 2B) are recommended. Recommendation 7.5 For mild skin involvement, topical therapy or phototherapy is recommended (GPS, agreement: 100%); for moderate-to-severe skin involvement, MTX (Grade 1B), biologics (preferably IL-17 inhibitors and IL-23 inhibitors) (Grade 1A), and small-molecule targeted agents JAK inhibitors (Grade 1B), TYK2 inhibitors (Grade 1B), or PDE-4 inhibitors (Grade 2B) are recommended.The treatment algorithm corresponding to different clinical manifestations of PsA is provided in Supplementary file, https://links.lww.com/CM9/C912. Clinical question 8: Can TNF-α inhibitors be combined with MTX for the treatment of PsA? Recommendation 8 When using TNF-α inhibitors, combination therapy with MTX may be considered, as it may help reduce the secondary failure rate of TNF-α inhibitors (Grade 2C). Clinical question 9: What are the recommended approaches to switching targeted therapies in patients with PsA? Recommendation 9 After primary failure to biologics, switching to a biologic agent with a different mechanism of action or to a JAK inhibitor is recommended. After secondary failure to biologics, switching to a biologic agent with a similar mechanism of action but a different structure, a biologic with a different mechanism of action, or to a JAK inhibitor is recommended (GPS, agreement: 82.7%). Clinical question 10: Can treatment for PsA be tapered or discontinued? Recommendation 10 For patients with clinical remission sustained for ≥6 months, cautious tapering may be considered under close monitoring (by extending dosing intervals or reducing the single dose); however, complete discontinuation is not recommended (GPS, agreement: 93.1%). Clinical question 11: Which phytomedicines can be used to treat PsA? Recommendation 11 Tripterygium wilfordii glycosides have indications and timing of use in the treatment of PsA similar to those of MTX and may be used as monotherapy or in combination with MTX; however, potential reproductive toxicity should be carefully considered. Total glucosides of peony may be used as an adjunctive therapy in PsA (Grade 2C). Clinical question 12: How should comorbidities in PsA be screened and managed? Recommendation 12 PsA is frequently associated with comorbidities; therefore, multidisciplinary collaboration and regular comorbidity screening are recommended. PsA patients with comorbidities should undergo comprehensive disease assessment and integrated management (GPS, agreement: 100%). Clinical question 13: How should targeted therapies be selected for PsA patients with comorbidities? Recommendation 13.1 For PsA patients with a history of uveitis, TNF-α inhibitors (excluding etanercept) should be preferentially selected (Grade 1B). Recommendation 13.2 For PsA patients with concomitant inflammatory bowel disease (IBD), IL-17 inhibitors should be avoided; TNF-α inhibitors (excluding etanercept), IL-12/23 inhibitors, IL-23 inhibitors, and JAK inhibitors (among which upadacitinib is indicated for ulcerative colitis and Crohn’s disease, whereas tofacitinib is indicated only for ulcerative colitis) are recommended (Grade 1B). Recommendation 13.3 For patients with PsA and severe or advanced congestive heart failure, TNF-α inhibitors are not recommended (Grade 1B). In patients at risk of arterial or venous thromboembolism, JAK inhibitors are not recommended (Grade 2C). Clinical question 14: How should treatment be selected for special populations with PsA? Recommendation 14.1 For PsA patients during pregnancy and lactation, certolizumab pegol is recommended as the preferred biologic agent (Grade 1B); MTX, leflunomide, and small-molecule targeted agents are contraindicated (GPS, agreement: 92%). Recommendation 14.2 For juvenile psoriatic arthritis (JPsA), priority should be given to PsA therapeutic agents with pediatric indications (Grade 1C). Recommendation 14.3 For PsA patients who are hepatitis B surface antigen (HBsAg)-positive, csDMARD, biologics, or JAK inhibitors are contraindicated before initiation of HBV therapy (Grade 1B). For PsA patients who are HBsAg-negative but hepatitis B core antibody (HBcAb)-positive, HBV-DNA quantification should be assessed before systemic therapy (GPS, agreement: 100%). Recommendation 14.4 For PsA patients with active tuberculosis, csDMARD, biologics, JAK inhibitors, and TYK2 inhibitors are contraindicated. For PsA patients with latent or inactive tuberculosis, MTX, IL-17 inhibitors, IL-23 inhibitors, or PDE-4 inhibitors are recommended (GPS, agreement: 86.2%). Recommendation 14.5 For PsA patients with concomitant active systemic fungal infection, antifungal therapy should be initiated first, and systemic treatment for PsA should be started only after the infection is controlled. Among biologic agents, IL-17 inhibitors should be avoided; IL-12/23 inhibitors or IL-23 inhibitors are recommended, and TNF-α inhibitors should be used with caution (Grade 2C). Recommendation 14.6 For PsA patients with malignancy (excluding non‑melanoma skin cancer) in remission for ≥5 years, MTX may be considered; TNF‑α inhibitors, IL‑12/23 inhibitors, IL‑23 inhibitors, or IL‑17 inhibitors may be used with caution if necessary. If biologics are not suitable, PDE-4 inhibitors may be considered, while JAK inhibitors and TYK2 inhibitors should be used with caution (GPS, agreement: 100%). Guideline development group Guideline development group in Supplementary materials, https://links.lww.com/CM9/C912. Funding This work was sponsored by grants from the National Key Research and Development Program of China (Grant No. 2023YFC2508106), the National Natural Science Foundation of China (Grant No. 82430101 and 82273510), the Innovation Program of the Shanghai Municipal Education Commission (Grant No. 2025GDZKZD06), Shanghai Dermatology Research Center (Grant No. 2023ZZ02017), and the Shanghai Hospital Clinical Diagnosis and Treatment Technology Promotion and Optimization Management Project (Grant No. SHDC22024246). Conflicts of interest None.
Shi et al. (Mon,) studied this question.