Overall, with the recent scientific discoveries describing a novel neuro-immune interaction associated with chronic pruritus, we can hypothesize that the availability of new immune-modulatory treatments for regulating peripheral sensory neurons to alter itch sensation appears promising. Given the different roles of IL-4/IL-13 to sensitize neurons to pruritogens, IL-31 acting as an acute pruritogen, and JAK as an intracellular signaling mechanism in neurons to transmit itch independent of inflammation, the next series of obvious clinical questions include the use of combination treatments to address these different aspects of itch sensation (Figure 1 and Table 1). Since most of the JAK studies have been off-label, stronger clinical trials that test the efficacy of these inhibitors with regard to chronic pruritus are warranted. With advances in understanding the pathogenesis of pruritus, including a central nervous system pathway for itch sensation, combined with concordant trials on drugs targeting receptors and their signaling pathways, we are poised to gain an even greater understanding of the underlying biologic mechanisms that may guide the development of new and more effective treatments for chronic pruritus.
Skin Therapy Letter. 2018;23(5):5-9. © 2018 SkinCareGuide.com