45 1365-4632 International IJD Oxford, UK Journal of Dermatology Blackwell Publishing,Ltd, 2005 Publishing Ltd.
Immunopathologic study of erythema dyschromicum perstans (ashy dermatosis)
Vásquez-Ochoa et of Immunopathology al. ashy dermatosis
Luz A. Vásquez-Ochoa*†, MD, Diana M. Isaza-Guzmán‡¶, MSc, Beatriz Orozco-Mora*, MD, Rodrigo Restrepo-Molina*, MD, JudithTrujillo-Perez*, BLC, and Félix J. Tapia§, MPh
From the *Universidad Pontiﬁcia Bolivariana, Medellín, †Hospital Pablo Tobón Uribe, Medellín, ‡Instituto Colombiano de Medicina Tropical, Sabaneta, ¶Universidad de Antioquia, Medellín, Colombia, and §Instituto de Biomedicina, Universidad Central de Venezuela, Caracas, Venezuela Correspondence Luz Adriana Vasquez-Ochoa Diagonal 75 DD N°4–41 Bloque 54,Apt. 401 Medellín Colombia E-mail: firstname.lastname@example.org
Erythema dyschromicum perstans (EDP) is a pigmentary disease of unknown etiology in which damage to basal cells is thought to be mediated by adhesion molecules. The aim of this study was to characterize the histopathology and immunopathology of EDP. Forty-three patients from Medellín, Colombia, with the diagnosis of EDP wereevaluated. Skin biopsy specimens were obtained for histopathology and immunohistochemistry, using monoclonal antibodies directed against the following markers: CD4, CD8, CD56, CD1a, CD68, CLA, HLA–DR, ICAM-1 and LFA-1α. A dermal lymphocytic inﬁltrate was observed in all cases, with a perivascular location in 86%. Other histologic features included melanophages in all specimens, vacuolization of thebasement membrane zone (BMZ) 58% and exocytosis of lymphocytes (53.5%). The mean number of total leukocytes was 1510 cells mm−2 of tissue. There was a predominance of CD8+ T lymphocytes in the dermis and HLA–DR+, ICAM-1+ keratinocytes in the epidermis. Exocytosis of cutaneous lymphocyte antigen (CLA) + cells was observed in areas of BMZ damage, suggesting that response to antigenic stimulation mayplay a role in the development of EDP.
Introduction Erythema dyschromicum perstans (EDP), or ashy dermatosis, is an idiopathic dermal melanosis first described by Ramirez1–4 in 1957 in El Salvador; it typically occurs in the second decade of life, more often in women, and generally affects those with type IV skin.2,5–8 It has been described mainly in patients from tropical areas of Central andSouth America.5,9,11,12 Multiple factors, such as parasites, atopy, hypothyroidism and contact with chemical substances, have been implicated in the development of EDP, but the etiology remains obscure.5,16 It has been postulated that damage to melanocytes and basal layer keratinocytes1,17 results from an abnormal immune response to antigens.17,18 Opinions vary about whether EDP is an abortive formof lichen planus (LP) or a distinct entity.1,19–22 The characteristic clinical signs of EDP include gray macules with erythematous borders, which converge and cover variable percentages of the body surface. The most common histopathological findings are a dermal perivascular lymphocytic infiltrate with many melanophages, vacuolization of the basement membrane zone (BMZ), necrotic keratinocytes inthe basal layer, colloid bodies, exocytosis of lymphocytes, and incontinence of the pigment.5,17,19,21,23–26 It has been postulated that adhesion molecules such as leukocyte
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function-associated antigen (LFA-1β) and intercellular adhesion molecule-1 (ICAM-1), and molecules of the class II major histocompatibility complex (MHC-II/HLA–DR), may playa role in the development of abnormal melanocytes and BMZ damage.4,17,21,27–29 The presence of interleukin-2 (IL-2), interferon-gamma (IFN-γ), natural killer (NK) cells and cytotoxic T cells in lesions of EDP is evidence that the immune system participates in this disease.5,27,30,31 There have been no published studies from Colombia concerning the immunopathology of EDP. Hence, we examined the...