Central sensitization in psoriatic arthritis: prevalence, clinical correlates, and association with therapeutic refractoriness in an unselected cohort excluding fibromyalgia

Abstract

Background: Central sensitization (CS) contributes to persistent pain in psoriatic arthritis (PsA), yet its prevalence, independent predictors, and association with therapeutic refractoriness remain incompletely characterized across disease phenotypes. Objectives: To evaluate CS prevalence and clinical correlates in unselected PsA patients excluding fibromyalgia, with emphasis on predictors, multidimensional pain phenotypes, and the association between CS and therapeutic refractoriness. Design: Cross-sectional observational study. Methods: A total of 228 consecutive PsA patients were recruited from April to November 2025 at a single tertiary center. Patients with fibromyalgia (2016 modified ACR criteria, systematically screened) were excluded. CS was assessed using the Central Sensitization Inventory (CSI ⩾40). Disease activity, functionality, pain phenotypes (PAIN DETECT questionnaire (PDQ)), sleep quality (Pittsburgh Sleep Quality Index), depression and anxiety (Hospital Anxiety and Depression Scale), and physical activity (International Physical Activity Questionnaire) and therapeutic refractoriness were systematically measured. Binary and linear regression analyses identified independent predictors of CS. Results: CS was present in 35.1% of patients. CS was associated with higher disease activity indices (Clinical Disease Activity Index for Psoriatic Arthritis: 14 vs 9.8, p = 0.001; Ankylosing Spondylitis Disease Activity Score with C-reactive protein: 4.8 vs 1.8, p = 0.007), greater functional disability (Health Assessment Questionnaire—Disability Index: 0.8 vs 0.2, p = 0.001), increased neuropathic pain (55.6% vs 8.2%, p = 0.001), and notably higher prevalence of therapeutic refractoriness (61.5% vs 6.8%, p = 0.003). Independent predictors of CS presence were depression severity (HADS-D: odds ratio (OR) = 1.32, p = 0.01), poor sleep quality (Pittsburgh Sleep Quality Index: OR = 1.21, p = 0.001), and PDQ (OR = 1.07, p = 0.03). Depression, sleep quality, and fatigue explained 47% of CS variance in linear regression. Conclusion: Approximately one-third of unselected PsA patients experience CS, which independently contributes to therapeutic refractoriness despite inflammatory control. Psychosocial factors—particularly sleep dysfunction and depression—emerge as robust predictors of CS. These findings support systematic CS screening in PsA patients with inadequate symptomatic response and highlight the need for integrated biopsychosocial interventions addressing both inflammatory and non-inflammatory pain mechanisms.