THE ANALYSIS OF THE THERAPEUTIC POTENTIAL OF USTEKINUMAB IN PSORIASIS VULGARIS TREATMENT.

The molecular mechanism of ustekinumab action involves an interruption of signaling pathways activated by IL-12/23. The aim of this paper was to evaluate the efficacy of the anti-IL12/23 therapy in 7 psoriatic patients by assessing changes in the values of PASI, DLQI, BSA indexes, and an analysis of changes in the mRNA expression profile of genes IL12A, IL12B, IL23A during three 40-week long observation periods. The clinical (PASI, DLQI, BSA indexes) and molecular (RTqPCR for IL12A, IL12B, IL23A) analyses were performed on the day of ustekinumab therapy initiation, 4 weeks post first administration, and every 12 weeks thereafter. The statistically significant differences were observed only during stage I for values of PASI (p=0.0134), DLQI (p=0.01299), BSA (p=0.0355). During the subsequent stages, we observed lower values of PASI, BSA indexes, which suggests that the lesions are less intensified than at the moment of the therapy commencing. The relationship between the selected genes was observed: IL23A>IL12A>IL12B. In conclusion, the aforementioned clinical and molecular analysis suggests the efficacy of ustekinumab therapy in patients with psoriasis vulgaris can be analyzed with the PASI, BSA, DLQI indexes, and changes in the expression of selected genes. The analysis of IL12A, IL12B, IL23A expression may serve as a valuable supplementation for the therapeutic methods currently used to evaluate the degree of disease progression and treatment efficacy. This article is protected by copyright. All rights reserved.