Actinic Prurigo
Actinic prurigo (AP) is a chronic idiopathic photodermatosis. It affects those living in populations such as North, Central, and South America. AP is most commonly seen in the mestizo (mixed indigenous Indian and European) populations. Human leukocyte ant
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Actinic Prurigo Prescilia Isedeh and Henry W. Lim
49.1
Contents 49.1
Introduction......................................................................
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49.2
Clinical Features ..............................................................
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49.3
Natural History and Prognosis .......................................
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49.4
Histopathological Features..............................................
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49.5
Diagnosis and Differential Diagnosis .............................
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49.6
Treatment .........................................................................
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References ....................................................................................
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Introduction
Actinic prurigo (AP) is a chronic idiopathic photodermatosis affecting those living in North, Central, and South America [1–4]. It is most commonly seen in the mestizo population, which refers to people of mixed Indian and European ancestry, who live in Central and South America [1]. Individuals living in these areas at high attitudes, particularly greater than 1,000 m above sea level, are more likely to develop AP [1, 3]. AP has been found to have a strong association with human leukocyte antigen (HLA) subtypes [1, 2, 5, 6]. The most prevalent HLA subtype is HLA DRB1*0407 followed by HLA DRB1*0401, found in at least 60–70 and 20 % of affected patients, respectively [1, 2, 5]. AP is caused by electromagnetic radiation, predominately ultraviolet (UV) A light [2]. It has been postulated that AP is a form of autoimmune disease associated with an antigen, such as an epidermal protein that is transformed by UV exposure [7]. Langerhans cells are thought to present the UV-induced antigen to the cellular immune system, thus inducing or augmenting the inflammatory response [8].
P. Isedeh, MD (*) Department of Dermatology, Henry Ford Medical Center, Henry Ford Hospital, 3031 West Grand Blvd., Suit 800, Detroit, MI 48202, USA e-mail: [email protected] H.W. Lim, MD Department of Dermatology, Henry Ford Medical Center, Henry Ford Hospital, 3031 West Grand Blvd., Suit 800, Detroit, MI 48202, USA e-mail: [email protected] D. Jackson-Richards, A.G. Pandya (eds.), Dermatology Atlas for Skin of Color, DOI 10.1007/978-3-642-54446-0_49, © Springer-Verlag Berlin Heidelberg 2014
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P. Isedeh and H.W. Lim
Clinical Features
AP is characterized by intensely pruritic papules, plaques, and nodules with secondary eczematization, lichenification, and excoriations, which often heal with pitted scarring and dyspigmentation (Figs. 49.1 and 49.2) [1–5]. Vesicles are not present unless there is a secondary infection [2]. The eruption occurs on sun-exposed areas such as the face, neck, extensor forearms, dorsal surfaces of the hands, and upper aspect of the chest [1–6]. Lesions can also occur in covered
areas, such as the back and buttocks, but these are often less severe [1, 2, 6]. Immediately after sun exposure, edema and erythema develops, which then subsides and slowly transitions to an eczematous phase and then a pruriginous phase
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