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Dermatology

What Drives PN Disease? Exploring the Complexity of PN Pathophysiology

Dr. Brian Kim discusses the numerous contributors to PN pathophysiology, including type 2 inflammation, neuronal dysfunction, and dermal fibrosis, emphasizing the unique and overlapping roles of IL 31, IL-4 and IL-13 in its pathology.

Brian Kim
MD
Brian Kim

Learning objectives

  • Recognize and elaborate on prurigo nodularis (PN) disease burden and classification
  • Describe the role of the molecules and processes that drive the complexities of PN disease
  • Review if emerging therapies can help address the heterogeneity of disease burden seen in PN patients

Description

Dr. Brian Kim presented the multifaceted contributions to PN disease, highlighting the roles of type 2 inflammation, neuronal dysfunction, and dermal fibrosis. He emphasized the cumulative effects of the repetitive itch-scratch cycle, a hallmark of PN, which can exacerbate disease severity. Dr. Kim explained the activation of cutaneous neurons which can release neuropeptides and subsequently promote a cycle of neuronal signaling, inflammation and pruritus. He further elucidated the involvement of specific cytokines, IL-31, IL-4 and IL-13, in PN pathogenesis. IL- 4 and IL-13 in particular contribute to neuronal sensitization, a process that heightens the sensitivity of neurons to itch stimuli, perpetuating the cycle of pruritus. To conclude, he underscored the need for continued research into PN pathophysiology to identify novel molecular targets for therapeutic interventions.

MAT-GLB-2305481 V2 11/2023

About this expert

Dermatology

Brian Kim

MD

Professor, Vice Chair of Research, and Site Chair of Mount Sinai West, Icahn School of Medicine, NY, US

See author’s profile
Brian Kim

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