Bronte Jeffrey1,2*, Logan Gardner6,7, Michelle Le1 , Julie Frost1 and Ming Wei Lin1,3,4,5
*Correspondence: Bronte Jeffrey 该Email地址已收到反垃圾邮件插件保护。要显示它您需要在浏览器中启用JavaScript。
1 Department of Clinical Immunology, Westmead Hospital, Sydney, Australia
2 St Vincent’s Clinical School, University of New South Wales, Sydney, Australia
3 Faculty of Medicine and Health, University of Sydney, Sydney, Australia
4 Department of Immunopathology, Westmead Hospital, Sydney, Australia
5 Centre for Immunology and Allergy Research, Westmead Institute of Medical Research, Sydney, Australia
6 Allergy, Asthma and Clinical Immunology, The Alfred Hospital, Melbourne, Australia
7 School of Public Health & Preventive Medicine, Monash University, Melbourne, Australia
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Background
Whilst contact anaphylaxis is rarely encountered in clini cal practice, its true incidence is uncertain as existing literature is limited to case reports. Contact anaphylaxis represents the severe end of the spectrum of immuno logical contact urticaria and is thought to be a Type I hypersensitivity reaction, whereby antigens absorbed through the dermal barrier bind with specific IgE mol ecules on pre-sensitized mast cells, resulting in mast cell degranulation with the release of histamine and other vasoactive substances, such as prostaglandins, leukotri enes and kinins [1]. This can result in clinical manifesta tions ranging from localised, milder symptoms (pruritis, paresthesia and localised wheal and flares) to more gen eralised urticaria or extracutaneous manifestations, including angioedema, bronchospasm, diarrhoea or severe anaphylaxis [2]. This has been best described in relation to grains and natural rubber latex [3]. Contrast ingly, non-immunological contact urticaria is more com mon and is the result of direct mast cell degranulation and release of localised vasogenic mediators, but rarely results in systemic symptoms [4]. This latter type of urti caria is typically not responsive to antihistamines and has been described in relation to numerous substances, including benzoic acid, sorbic acid and dimethyl sulfox ide [3, 4].
Case presentation
We present the case of a 69-year-old non-atopic male who developed anaphylaxis following the application of Redwin Moisturizer. The patient had suffered extensive
