Contact Urticaria and Contact Urticaria Syndrome
Contact urticaria, contact urticaria syndrome (CUS), protein contact dermatitis (PCD), and oral allergy syndrome (OAS) are diseases which are precipitated by immediate contact skin and mucous membrane reactions. They may be the result of a specific immune
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Contact Urticaria and Contact Urticaria Syndrome Hans F. Merk
Contact urticaria, contact urticaria syndrome (CUS), protein contact dermatitis (PCD), and oral allergy syndrome (OAS) are diseases which are precipitated by immediate contact skin and mucous membrane reactions. They may be the result of a specific immune reaction after sensitization to a high or low molecular weight compound (ICoU), or they are mediated by a nonimmunological reaction which needs no prior sensitization (NICoU). Compounds in numerous environmental materials which can come in contact with the skin are able to induce contact urticaria such as animal dander, plants, foods and flavorings, enzymes, cosmetics including fragrances and preservatives, medications, disinfectants, and metals [1, 2]. Clinically contact urticaria is characterized by a typical triple response—wheal, flare, and itching—of the skin at the site of contact to the eliciting agent. It appears within 30 min after the contact and disappears completely within hours without residual signs and symptoms. The triple response precipitates alone or together with an immediately induced eczema, which can also result, if the exposure to the antigen persists.
H.F. Merk Department of Dermatology & Allergology, RWTH Aachen University, Aachen, Germany Dohlenfeld 8, 45479 Muelheim an der Ruhr, Auf’m Hennekamp 50, Düsseldorf D-40225, Germany e-mail: [email protected] © Springer International Publishing Switzerland 2018 J. Krutmann, H.F. Merk (eds.), Environment and Skin, https://doi.org/10.1007/978-3-319-43102-4_6
Most compounds which induce these reactions belong to cosmetics, plants, vegetables, and food. Contact urticaria has been first described by Fisher and has been recognized as a syndrome by Johnson and Maibach subsequently [3]. Small molecular weight as well as high molecular weight compounds can induce a contact urticaria. In particular, nonimmunological urticaria (NICoU) is mainly mediated by numerous small molecular compounds [4]. Examples include dimethyl sulfoxide, benzoic acid, cinnamic acid, cinnamic aldehyde, eugenol, methyl niconate, and sorbic acid. Among fragrances, cinnamic aldehyde, cinnamic alcohol, isoeugenol, hydroxycitronellal, and geraniol can induce NICoU [5, 6, 7]. The mechanism of the NICoU is not well understood. There are at least three possible pathways or concepts to explain these reactions: nonspecific histamine release, modulation of the metabolism of arachidonic acid, and activation of cutaneous nerves including mediators such as substance P [8]. However antihistamines such as terfenadine do not inhibit most of the nonimmunological urticarial reactions, whereas nonsteroidal anti-inflammatory drugs (NSAIDS) can inhibit them after oral or topical application [9]. Interestingly UV light is capable to inhibit this reaction [4]. Although nonimmunological contact urticaria is more common than immunological contact 51
H.F. Merk
52 Fig. 6.1 Basophil activation test (BAT) in a hairdresser with contact urticaria, eczema, and asthma after exposure t
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