Distinct immune inflammatory markers and proteomic signatures underlying psoriasis with pruritus

Pruritus is a common and burdensome symptom in patients with psoriasis, yet its underlying systemic mechanisms are not sufficiently defined. To characterize systemic immune-inflammatory profiles and serum proteomic differences associated with pruritus in patients with psoriasis and identify potential biomarkers linked to pruritus. Serum immune-inflammatory markers from 267 psoriasis patients were analyzed. Proteomic profiling was performed by mass spectrometry in pruritic psoriasis ( n = 8), non-pruritic psoriasis ( n = 5), and healthy controls ( n = 3). Pruritic psoriasis patients tended to be younger with shorter disease duration, while other clinical characteristics were comparable. Total IgE tended to be higher in pruritic psoriasis, particularly in moderate-to-severe cases. The eosinophil-to-lymphocyte ratio (ELR) was significantly elevated in pruritic psoriasis, whereas other inflammatory indices did not differ. Proteomic analysis revealed distinct clustering of pruritic psoriasis from non-pruritic psoriasis and healthy controls, with enrichment of complement activation, coagulation, and fibrinolysis. Compared with non-pruritic psoriasis, pruritic psoriasis additionally showed upregulation of actin cytoskeletal organization, wound healing proteins, and transient receptor potential melastatin 2 (TRPM2). Pruritic psoriasis is characterized by elevated ELR and distinct proteomic signatures involving complement activation, coagulation, tissue remodeling, and TRPM2 upregulation, implicating these pathways in the mechanisms underlying psoriatic pruritus.