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Psoriatic arthritis (PsA) is a chronic inflammatory condition affecting about one-third of individuals with psoriasis. Defining axial involvement in PsA (axPsA) remains debated. While rheumatologists guide clinical practice, consensus on axPsA is still lacking. This paper explores historical and upcoming definitions from the Axial Involvement in Psoriatic Arthritis (AXIS) study, which aims to establish a validated axPsA definition. Epidemiological data reveal diverse axPsA prevalence rates, emphasizing its complex relationship with peripheral arthritis and enthesitis. Unique genetic, clinical, and radiological features differentiate axPsA from ankylosing spondylitis (AS), necessitating refined classification criteria. The recommendations from the Assessment of Spondylarthritis international Society (ASAS) provide valuable guidance due to the limited direct evidence. Emerging therapies, including interleukin-23 (IL-23) inhibitors or Janus kinase (JAK) inhibitors, are under investigation for axPsA. Currently, secukinumab, an interleukin-17 (IL-17) inhibitor, is an evidence-based option for axPsA management. However, given the variability in individual patient responses and disease manifestations, personalized, evidence-based treatment approaches remain essential for optimizing patient outcomes. In the final section, two real-life cases illustrate the challenges in managing axPsA, emphasizing the importance of tailored therapies. Achieving precision in defining axPsA remains a formidable task, making detailed criteria essential for effective strategies and improving patient outcomes.
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BACKGROUND: this is an exploratory study to evaluate calprotectin serum levels in patients with rheumatic immune-related adverse events (irAEs) induced by immune checkpoint inhibitor (ICI) treatment. METHODS: this is a retrospective observational study including patients with irAEs rheumatic syndromes. We compared the calprotectin levels to those in a control group of patients with RA and with a control group of healthy individuals. Additionally, we included a control group of patients treated with ICI but without irAEs to check calprotectin levels. We also analysed the performance of calprotectin for the identification of active rheumatic disease using receiver operating characteristic curves (ROC). RESULTS: 18 patients with rheumatic irAEs were compared to a control group of 128 RA patients and another group of 29 healthy donors. The mean calprotectin level in the irAE group was 5.15 µg/mL, which was higher than the levels in both the RA group (3.19 µg/mL) and the healthy group (3.81 µg/mL) (cut-off 2 µg/mL). Additionally, 8 oncology patients without irAEs were included. In this group, calprotectin levels were similar to those of the healthy controls. In patients with active inflammation, the calprotectin levels in the irAE group were significantly higher (8.43 µg/mL) compared to the RA group (3.94 µg/mL). ROC curve analysis showed that calprotectin had a very good discriminatory capacity to identify inflammatory activity in patients with rheumatic irAEs (AUC of 0.864). CONCLUSIONS: the results suggest that calprotectin may serve as a marker of inflammatory activity in patients with rheumatic irAEs induced by treatment with ICIs.
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OBJECTIVE: To study the differences between disease activity score 28 (DAS28) index and an ultrasound (US) approach using index echographic disease activity score (ECODAS). METHODS: This was a cross-sectional study in patients diagnosed with rheumatoid arthritis (RA). Demographic, clinical, and laboratory data were collected. We created a US index (ECODAS) evaluating the joints with synovitis using gray scale US (GSUS) and power Doppler US (PDUS) and calculated the formula of DAS28 index with both variables substituting tender joint for GSUS and swollen joint for PDUS (ECODAS1) and vice versa (ECODAS2). RESULTS: A total of 58 patients (65.5% women and 34.5% men) were included in the study. There was no significant difference between the 2 US indexes. We obtained a Pearson's correlation coefficient (Pearson's r) of 0.56 (p<0.00001) between DAS28 and ECODAS1 and of 0.57 (p<0.00001) between DAS28 and ECODAS2, respectively. However, for patients with a high disease activity [DAS28>5.1, tender joint count (TJC, high)], the correlation was poor (0.18) and ECODAS indexes were significantly lower (p=0.001). The correlation increased (0.86, p<0.001) when we excluded the tender joints and the joints with GS-positive synovitis in both the scores. CONCLUSION: US reduces the bias in the evaluation of patients with RA with a high value in DAS28 index. We found a clear difference between DAS and ECODAS when TJC was high. The results suggest that joint tenderness reported by the patient is not a good reflection of inflammation. More studies are needed to find a new combined clinical and sonographic index that would better assess the disease activity in patients with RA.