Diagnosing allergic rhinitis in children relies heavily on clinical symptoms and skin-prick tests, but objective blood markers that capture underlying systemic inflammation have remained elusive. Two circulating proteins — endocan and eosinophil-derived neurotoxin — now show promise as high-accuracy diagnostic tools, potentially sharpening the precision of pediatric allergy assessment beyond conventional cell counts.
This prospective case-control study enrolled 85 children with allergic rhinitis and 67 healthy controls, measuring serum endocan (a proteoglycan released by activated vascular endothelium) and eosinophil-derived neurotoxin (EDN, a ribonuclease secreted during eosinophil degranulation) via sandwich ELISA. Both markers were significantly elevated in the allergic rhinitis group. ROC curve analysis yielded AUCs of 0.931 for endocan and 0.929 for EDN — meaningfully higher than absolute eosinophil counts (AUC 0.871). The two biomarkers were strongly intercorrelated (r = 0.88), and both tracked with total IgE and eosinophil levels. Notably, neither correlated with disease severity scores, symptom control ratings, or specific allergen sensitization profiles.
The high AUC values place endocan and EDN among the better-performing single biomarkers in pediatric allergy research, comparable to performance benchmarks seen with exhaled nitric oxide in asthma diagnostics. The strong intercorrelation between the two proteins is mechanistically coherent: activated eosinophils degranulate and release EDN, while endothelial cells respond to the resulting inflammatory milieu by shedding endocan — capturing two nodes of the same inflammatory cascade. However, several limitations temper enthusiasm. The case-control design cannot establish whether elevated levels precede diagnosis or merely mirror acute disease state. The absence of any correlation with severity is a notable gap that limits clinical utility beyond initial diagnosis. The cohort is also relatively modest in size, and external validation across diverse ethnic populations and atopic phenotypes is needed before these markers could inform routine clinical workflows. This work is best characterized as confirmatory and hypothesis-generating rather than practice-changing.