Evolving understanding on the aetiology of thermally provoked itch

Abstract

Background and objectives: Itch is one of the major symptoms in dermatology clinics, and severely impairs the quality of life. Itch is frequently produced by environmental stimuli, especially heat or warmth. Changes of temperature on the skin surface and noxious heat stimuli augment and develop itch, respectively. Thermally provoked itch is sometimes intractable with existing treatments.

Data bases and data treatment: Recent researches, linking heat sensation and itch, were searched in MEDLINE literature database through PubMed.

Results: Recent studies of the transient receptor potential cation channel subfamily vanilloid type 1 (TRPV1), the calcitonin gene-related peptide (CGRP) and the vesicular glutamate transporter 2 (VGLUT2), which link noxious heat and itch, contribute to a much better understanding of the thermally evoked itch process. From a clinical perspective, a warm sensation is a major provocative factor for subjects with atopic dermatitis. The accumulation of artemin (also known as enovin or neublastin) in the dermis of lesional skin can possibly provide a pathological mechanism for warmth-provoked itch.

Conclusions: This mini-review describes recent results of both basic and clinical research related to thermally provoked itch.

Figure 1

Expression and function of artemin (ARTN) in skin. A: Human skin specimens derived from atopic dermatitis, nummular eczema and healthy skin were immunohistologically stained with artemin antibody (green). The dotted line indicates the junction of the epidermis and dermis (magnification, ×200). B: Response to noxious heat stimuli were measured with the tail flick test. Grey and black bars show wild‐type and GFRα3 knockout mice, respectively, *p < 0.05, unpaired t‐test. C: The effect of exogenously administered artemin on thermal hyperalgesia (Hargreaves test) (n = 5). ***p < 0.001, unpaired t‐test. These figures were reprinted from ref (Murota et al., 2012), with permission.