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Abstract Background Calprotectin is a proinflammatory protein predominantly secreted by neutrophils and serves as a sensitive marker of inflammation, particularly in conditions involving neutrophil activation. While fecal calprotectin is widely used in gastrointestinal diseases, serum calprotectin is emerging as a valuable marker for systemic inflammatory conditions. This study aimed to compare serum calprotectin levels in children with systemic juvenile idiopathic arthritis (sJIA), polyarticular course juvenile idiopathic arthritis (pcJIA), systemic lupus erythematosus (cSLE), inflammatory bowel disease (IBD), and interleukin-1-mediated autoinflammatory diseases (AID) to evaluate its role as a diagnostic and discriminative marker of inflammation. Methods This prospective study included 145 children, categorized into six groups: 24 with sJIA, 62 with JIA, 18 with cSLE, 15 with IBD, 6 with AID, and 20 healthy controls. Serum calprotectin levels were measured using a turbidimetric assay (GCAL®, Gentian AS, Norway). Differences between patient groups and controls were analyzed using the Kruskal-Wallis test, followed by a post-hoc analysis. A p-value <0.05 was considered statistically significant. Results The median (range) serum calprotectin levels were as follows: sJIA: 3.02 (0.50–38.41) µg/ml. pcJIA: 1.19 (0.30–19.27) µg/ml, cSLE: 1.39 (0.31–6.29) µg/ml, IBD: 1.62 (0.40–5.80) µg/ml, AID: 1.26 (0.56–232.5) µg/ml, Controls: 1.00 (0.57–1.43) µg/ml. Both patients with active and non active disease were included in calculation of the median values. Serum calprotectin levels were further analyzed based on disease activity: sJIA (active): 21.56 (11.57–38.41) µg/ml, sJIA (remission): 0.98 (0.50–2.30) µg/ml, JIA (active): 3.18 (2.55–19.27) µg/ml, pcJIA (remission): 0.84 (0.30–1.45) µg/ml, cSLE (active): 5.43 (4.81–6.29) µg/ml, cSLE (remission): 1.29 (0.31–1.63) µg/ml. Patients with active disease in all three conditions (sJIA, pcJIA, cSLE) had significantly higher serum calprotectin levels compared to those in remission. Additionally, serum calprotectin levels in patients with active disease were significantly higher than in the control group, whereas levels in patients in remission did not differ from those in the control group. Conclusion Our pilot study suggests that serum calprotectin is a useful diagnostic marker of inflammation, particularly in distinguishing sJIA from other disorders. Additionally, it effectively differentiates patients with active disease from those in remission. Further studies are warranted to validate its clinical utility in pediatric inflammatory diseases.