Journal of Rheumatology最新文献

Objective: Systemic sclerosis (SSc) gastrointestinal disease is heterogeneous in presentation, with individual symptoms lacking specificity for specific anatomical and functional abnormalities. We used factor analysis to investigate whether latent subgroups of SSc gastrointestinal symptoms can be detected.

Methods: Using SCTC UCLA Gastrointestinal 2.0 Questionnaire (GIT 2.0) data from 773 Australian Scleroderma Cohort Study participants, we performed a factor analysis of firstly, GIT 2.0 domains scores and then, individual GIT 2.0 question responses to identify latent factors. A subsequent cluster analysis was performed to explore whether clinically definable SSc phenotypes were associated with specific gastrointestinal symptoms.

Results: SSc gastrointestinal symptoms were highly correlated. Factor analysis of individual GIT 2.0 question responses revealed four latent factors within the dataset that could be clinically described as upper gastrointestinal tract symptoms, bloating, diarrhoea and incontinence, and constipation. Cluster analysis revealed two patient clusters, distinguished by disease duration and severity of gastrointestinal manifestations. Anti-centromere antibodies and pulmonary arterial hypertension were more common in participants with severe gastrointestinal disease.

Conclusion: Despite the high correlation between gastrointestinal manifestations, it is possible to detect subgroups of SSc gastrointestinal symptoms. Improved understanding of these subgroups of SSc gastrointestinal disease may advance the discovery of targeted interventions to improve the daily function and quality of life of those living with SSc.

Objective: The efficacy of nucleic acid-based vaccines against SARS-CoV-2 varies across individuals, partly due to genetic factors influencing neutralizing antibody production. In patients with systemic autoimmune diseases (SADs), this response may be further altered by immune dysregulation.

Methods: We conducted a genome-wide association study (GWAS) to identify genetic variants associated with postvaccination anti-SARS-CoV-2 IgG antibody levels and to assess whether these associations differ between patients with SAD and healthy individuals.

Results: The study included 165 participants (138 with SADs, 27 healthy controls), all of whom received nucleic acid-based vaccines. Antibody levels targeting the spike protein receptor-binding domain (RBD) and nucleocapsid were measured between 1 and 12 months after vaccination. GWAS results were metaanalyzed with data from a previously published GWAS with 1076 healthy individuals. We identified a novel association near RACGAP1 (rs706785; β_meta = -0.30, P _meta = 3.85 × 10^-8) and replicated a known association at HLA-DRB1 position 71 (β_meta = -0.23, P _meta = 1.94 × 10^-11). No significant interactions were observed between genotype and disease status.

Conclusion: This study highlights both MHC and non-MHC genetic contributions to SARS-CoV-2 vaccine responses and suggests these effects are consistent across patients with SADs and healthy individuals, supporting standard vaccination strategies for individuals with systemic autoimmune conditions.

Objective: To evaluate the validity of the 3-item visual analog scale (3VAS) and 4-item VAS (4VAS) and determine the minimal clinically important difference (MCID) and minimal detectable change (MDC) for each measure using data from 3 phase III randomized clinical trials of guselkumab in psoriatic arthritis (PsA).

Methods: Pooled data (1405 participants) from the DISCOVER-1, DISCOVER-2, and COSMOS studies were used. 3VAS/4VAS MCID and MDC were estimated using established formulas. Receiver-operating characteristic curve analysis was used to identify 3VAS/4VAS thresholds for low, moderate, and high disease activity. Criterion validity was assessed by correlating 3VAS/4VAS with other PsA measures. Mixed models evaluated the association between changes from baseline in 3VAS/4VAS at week 8 of guselkumab treatment with the total PsA-modified Sharp-van der Heijde (SvdH) score through week 100.

Results: 3VAS/4VAS showed moderate-to-strong correlation with all outcome measures assessed, with coefficients ranging from 0.56/0.62 for Health Assessment Questionnaire-Disability Index to 0.92/0.94 for patient global assessment. MCID was 0.9 for both 3VAS (range 0.7-1.3 depending on method used) and 4VAS (0.6-1.3); MDC was 3.1 and 3.0, respectively. 3VAS cutoffs for low, moderate, and high disease activity were 2.1, 3.3, and 4.8, respectively, and 2.1, 3.4, and 5.0 for 4VAS. Change in 4VAS at week 8 of guselkumab treatment significantly associated with change in SvdH score through week 100 (P = 0.04).

Conclusion: These analyses support the validity of 3VAS/4VAS as multidimensional measures of PsA disease activity. 4VAS may be preferred owing to its greater face validity and separate measurements of the 2 cardinal aspects of PsA (joint/skin disease) and pain.

Objective: This study aimed to retrospectively evaluate the provisional Paediatric Rheumatology International Trials Organisation (PRINTO) criteria in patients with juvenile idiopathic arthritis (JIA) classified according to the International League of Associations for Rheumatology (ILAR) criteria.

Methods: This retrospective cohort study was conducted at a single tertiary pediatric rheumatology center. A total of 310 patients with non-systemic JIA were classified according to both ILAR and provisional PRINTO criteria. Demographic, clinical, and laboratory features were recorded, and the distribution of JIA categories under both classification systems was analyzed.

Results: The mean age at study time was 169.8 ± 59.2 months. Using ILAR criteria, 136 patients (43.9%) were categorized as oligoarticular JIA, 73 (23.5%) as enthesitis-related arthritis, 34 (11.0%) as RF-negative polyarticular JIA, 12 (3.9%) as psoriatic arthritis, 7 (2.3%) as RF-positive polyarticular JIA, and 48 (15.5%) as undifferentiated JIA. The provisional PRINTO criteria classified 107 (34.5%) patients as early-onset antinuclear antibody-positive JIA, 93 (30.0%) as other JIA, 88 (28.4%) as enthesitis/spondylitis-related JIA, 17 (5.5%) as RF-positive JIA, and 5 (1.6%) as unclassified JIA. The other JIA category included 93 patients, consisting of oligoarticular JIA (54.8%), RF-negative polyarticular JIA (21.5%), undifferentiated JIA (11.8%), enthesitis-related arthritis (6.5%), and psoriatic arthritis (5.4%) under the ILAR classification system.

Conclusion: The provisional PRINTO criteria successfully reclassified a substantial proportion of previously undifferentiated JIA cases, improving diagnostic categorization by addressing some ILAR classification limitations. However, the high number of patients in the "other JIA" group highlights a potential limitation of the new system, warranting further investigation.

Objective: Secondary failure to biologic disease-modifying antirheumatic drugs (bDMARDs) is challenging and contributes to the complexity of managing psoriatic arthritis (PsA). We aimed to define the frequency and incidence of this phenomenon in PsA and identify the risk factors for its occurrence.

Methods: We retrieved data on patients with PsA from our single-center, specialized-care, prospective observational cohort who initiated and remained on bDMARDs for ≥ 1 year after clinic enrollment between 2000 and 2023. We defined response to therapy at the 1-year visit (baseline) as achievement of ≥ 40% reduction in the swollen joint count (SJC) and either ≥ 50% reduction in Psoriasis Area and Severity Index (PASI) or PASI ≤ 2. We defined secondary failure as the inability to maintain response criteria or as the clinician's judgment of loss of effectiveness. To examine factors associated with secondary failure, we fitted Cox regression models.

Results: Of 482 patients included in the study, 264 (54.8%) were responders at 1 year. Of these, 94 (35.6%) developed secondary failure at a median of 1.6 (IQR 0.7-3.8) years from response. In the multivariable model, higher SJC (hazard ratio [HR] 1.39, 95% CI 1.05-1.84) and PASI (HR 1.14, 95% CI 1.01-1.29) at baseline were associated with secondary failure. Tumor necrosis factor inhibitors (TNFi) vs other bDMARD use (HR 0.39, 95% CI 0.18-0.88), initiation as first-line bDMARD (HR 0.48, 95% CI 0.25-0.91), and treatment initiation during more recent calendar years (HR 0.34, 95% CI 0.12-0.98) were associated with less secondary failure.

Conclusion: Secondary failure to bDMARD is common in PsA and may be influenced by both disease- and therapy-related factors.