Chronic Pruritus: A Review of Neurophysiology and Associated Immune Neuromodulatory Treatments

Jay M. Patel, BSc; Harry Dao Jr., MD, FAAD

Disclosures

Skin Therapy Letter. 2018;23(5):5-9. 

In This Article

Abstract and Introduction

Abstract

Chronic pruritus remains a difficult condition to treat with many non-specific therapeutic options. Recent scientific discoveries have elucidated the physiology associated with pruritus. Combined with clinical and experimental trials with immune-modulatory agents, chronic pruritus now has novel treatment options with known mechanisms of action. This review goes over recent scientific progress in understanding the molecular mechanisms governing pruritus, the cross-talk between the immune and nervous systems that regulate itch, and central nervous pathways and projections affected by itch. In light of these recent discoveries, we briefly discuss a growing body of data from relevant clinical trials investigating immunomodulatory drugs targeting specific interleukin receptors (IL-4/13/31) and intracellular signaling (e.g, Janus kinase) pathways. We focus on the physiological processes that control this complex physical and emotional experience, as well as the role of newer drugs used to treat chronic itch.

Introduction

Chronic pruritus (CP) is a debilitating condition defined as itch lasting longer than 6 weeks.[1] Causes of CP include both dermatologic and non-dermatologic diseases leading to involvement of the entire body (generalized) or specific areas (localized).[1] Treatment methods are often trial-error based in order to determine an optimal regimen to reduce symptoms. Generally, CP can be divided into broad categories of origin: dermatologic (e.g., atopic dermatitis and psoriasis), systemic (e.g., chronic kidney disease and cholestasis), neuropathic (e.g., post-herpetic itch), or psychogenic (e.g., obsessive-compulsive disorder and drug use).[2] Importantly, non-dermatologic causes can also present with skin findings due to the itch-scratch cycles and, therefore, can be masked by dermatitis. While CP is often a feature of inflammatory skin diseases, it can also stem from idiopathic causes, which are not marked by inflammatory processes.[3] Thus, the mechanisms of CP are multifaceted and numerous activating mediators of itch are known, including histamine and substance P.[4] Ultimately, the physiology of itch sensation results in the activation of peripheral sensory neurons.

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