Abstract
Itch is the main chief complaint in patients visiting dermatologic clinics and has the ability to deeply impair life quality. Itch results from activation of cutaneous nerve endings by noxious stimuli such as inflammatory mediators, neurotransmitters and neuropeptides, causing itch signal transduction from peripheral skin, through the spinal cord and thalamus, to the brain cortex. Primarily noninflammatory diseases, such as uremic pruritus, cause itch through certain pruritogens in the skin. In inflammatory skin diseases, atopic dermatitis (AD) is the prototypic disease causing intensive itch by aberrant skin inflammation and epidermal barrier disruption. Recent understanding of disease susceptibility, severity markers, and mechanisms have helped to develop targeted therapy for itch in AD, including monoclonal antibodies against IL-4, IL-13, thymic stromal lymphopoietin (TSLP), IgE and IL-31. Promising effects have been observed in some of them. In this review, we summarized targeted therapies for inflammatory itch in AD and for managing abnormal itch transductions in other common itching skin diseases.
Highlights
Itch is an unpleasant sensation that elicits the desire to scratch in order to remove noxious stimuli [1]
We summarize the current knowledge about the pathophysiological mechanisms of inflammatory and noninflammatory itch
It is noteworthy that patients with chronic and intractable itch without attributable causes should be evaluated for occult systemic diseases such as thyroid disease, polycythemia vera, Hodgkin disease, and human immunodeficiency virus (HIV) infection [16]
Summary
Itch is an unpleasant sensation that elicits the desire to scratch in order to remove noxious stimuli [1]. The signal is relayed from the synapse to the contralateral spinothalamic tract thalamus, and radiated to the neurons located in the sensory brain cortex [2] Anything interfering in this pathway could result in abnormal itch perception. In the CNS, several molecules attribute to itch perception and propagation, including gastrin-releasing peptides (GRP), opioid receptors, neuropeptides, and neurotransmitters. An itch-specific population of MrgprA3-expressing neurons in the dorsal root ganglion was identified, along with multiple synapses with nearby neurons expressing gastrin-releasing peptide receptors (GRPRs, see below). Specific ablation of these neurons diminished the pruritogen-induced scratching responses but not pain responses. The clinical effectiveness and significances of the potential targeting treatments on itch are updated
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