Synergic Effect of Botulinum Toxin Type A and Triamcinolone Alleviates Scar Pruritus by Modulating Epidermal Hyperinnervation: A Preliminary Report.

[BACKGROUND] Patients often experience scar-related pruritus, which adversely affects quality of life. Triamcinolone acetonide (TAC) is widely used to treat pathologic scars, and botulinum toxin type A (BTX-A) reportedly improves scarring and associated discomfort.

[OBJECTIVES] The aim of this study was to investigate the clinical efficacy of combining TAC and BTX-A to reduce scar itch; potential mechanisms were investigated via an animal model.

[METHODS] For the clinical study, each scar on a patient was divided into 2 equal parts, with one part receiving TAC/BTX-A and the other TAC alone. Therapeutic interventions were administered over 3 sessions at 4-week intervals. Itch intensity was measured on a visual analog scale before each therapeutic intervention (V1, V2, V3) and 4 weeks after the last intervention (V4). For the animal model, rats were allocated into 5 groups: control, untreated burn, TAC, BTX-A, and TAC/BTX-A. We evaluated alloknesis in the right hind paw and analyzed possible molecular mechanisms.

[RESULTS] In humans, TAC/BTX-A significantly reduced scar itch compared with TAC alone at V4 (P = 0.04). In rats, post-burn itch was mitigated at 4 weeks after treatment with TAC, BTX-A, and TAC/BTX-A (P = 0.03, P = 0.0054, and P = 0.0053, respectively). TAC/BTX-A significantly decreased the density of intraepidermal nerve fibers post-burn relative to the untreated burn (P = 0.0008). TAC/BTX-A downregulated the expressions of nerve growth factor and protein transient receptor potential vanilloid subtype 1.

[CONCLUSIONS] TAC/BTX-A therapy exhibited enhanced and sustained clinical efficacy in relieving scar itch, possibly via modulating epidermal innervation and expression of transient receptor potential vanilloid subtype 1 .