AI Article Synopsis

  • Itch, a major symptom of atopic dermatitis, is linked to Janus kinase 1 signaling in skin sensory neurons, which is targeted by the selective inhibitor abrocitinib.
  • The study analyzed data from three clinical trials involving 942 patients to evaluate how quickly and effectively abrocitinib relieves itch and whether this relief is separate from overall disease improvement.
  • Results indicated that abrocitinib significantly reduced itch within two weeks, leading to better sleep and quality of life, and the effect on itch was found to be somewhat independent of the overall severity of the disease.

Article Abstract

Background: Itch, the most bothersome symptom in atopic dermatitis, is largely mediated by pruritogenic cytokines via Janus kinase 1 signaling in cutaneous sensory neurons.

Objectives: The aims of the study were to assess the magnitude and rapidity of itch relief with the Janus kinase 1 selective inhibitor abrocitinib and to evaluate the extent to which the effect of abrocitinib on itch relief is independent of overall disease improvement.

Methods: Pooled data from 1 phase 2b (NCT02780167) and 2 phase 3 (NCT03349060, NCT03575871) double-blind, randomized, placebo-controlled monotherapy trials in moderate to severe atopic dermatitis (N = 942) were analyzed.

Results: Abrocitinib produced significant and clinically meaningful itch relief versus placebo from week 2 through week 12 (end of treatment) that was associated with marked sleep and quality-of-life improvements. Mean percentage reductions in itch scores 24 hours after the first dose were greater for both abrocitinib doses (200 and 100 mg) versus placebo. Itch improvement occurred regardless of baseline itch severity, sex, race, body mass index, or Investigator Global Assessment response, suggesting that abrocitinib-associated itch relief is at least partially independent of overall disease improvement.

Conclusions: Abrocitinib showed a rapid and profound antipruritic effect, partially independent of improvement in overall disease.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8560158PMC
http://dx.doi.org/10.1097/DER.0000000000000770DOI Listing

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