title: Exacerbating factors of itch in atopic dermatitis.
abstract: Atopic dermatitis (AD) displays different clinical symptoms, progress, and response to treatment during early infancy and after childhood. After the childhood period, itch appears first, followed by formation of well-circumscribed plaque or polymorphous dermatoses at the same site. When accompanied with dermatitis and dry skin, treatment of skin lesions should be prioritized. When itch appears first, disease history, such as causes and time of appearance of itch should be obtained by history taking. In many cases, itch increases in the evening when the sympathetic nerve activity decreased. Treatment is provided considering that hypersensitivity to various external stimulations can cause itch. Heat and sweating are thought to especially exacerbate itch. Factors causing itch, such as cytokines and chemical messengers, also induce itch mainly by stimulating the nerve. Scratching further aggravates dermatitis. Skin hypersensibility, where other non-itch senses, such as pain and heat, are felt as itch, sometimes occurs in AD. Abnormal elongation of the sensory nerve into the epidermis, as well as sensitizing of the peripheral/central nerve, are possible causes of hypersensitivity, leading to itch. To control itch induced by environmental factors such as heat, treatment for dermatitis is given priority. In the background of itch exacerbated by sweating, attention should be given to the negative impact of sweat on skin homeostasis due to 1) leaving excess sweat on the skin, and 2) heat retention due to insufficient sweating. Excess sweat on the skin should be properly wiped off, and dermatitis should be controlled so that appropriate amount of sweat can be produced. Not only stimulation from the skin surface, but also visual and auditory stimulation can induce new itch. This "contagious itch" can be notably observed in patients with AD. This article reviews and introduces causes of aggravation of itch and information regarding how to cope with such causes.
authors.affiliation: Department of Dermatology, Course of Integrated Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan. Electronic address: h-murota@derma.med.osaka-u.ac.jp.
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Murota
authors.affiliation: Department of Dermatology, Course of Integrated Medicine, Graduate School of Medicine, Osaka University, Osaka, Japan.
authors.forename: Ichiro
authors.initials: I
authors.lastname: Katayama
mesh_terms: D016207:Cytokines / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D004817:Epidermis / Q000294:innervation / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D011537:Pruritus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D013564:Sympathetic Nervous System / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
chemical_list: D016207:Cytokines
keywords: Atopic dermatitis; Exacerbating factors; Itch; Life rhythm; Pruritus