Firstly described by Moulin et al. in 1992 in 5 patients [1], LAM is a distinct clinical entity characterized by acquired atrophic bandlike skin lesions that often show hyperpigmentation and always follow the lines of Blaschko. No preceding infl ammation is noted, but a transient infl ammatory stage is perhaps often unrecognized, and there is no induration or scleroderma. Usually the condition begins in childhood or adolescence, and there is no evidence of any long-term progression. Histopathologically, an irregular moderate hyperpigmentation of the lower part of the epidermis is found, along with a few perivascular lymphocytes in the dermis and slight thickening of the collagen bundles, as in our case [2]. The existence of LAM is controversial in its possible clinical overlap with linear scleroderma or morphea. Nevertheless, this latter is characterized by one or more linear streaks of progressive induration that can extend through the dermis, subcutaneous tissue, and muscle to the underlying bone, causing signifi cant deformities [3]. The lack of autoantibodies, such as ANA, found in 73% of adult patients with linear scleroderma and the chronic and unvaried course make this diagnosis unlikely in our patient, leading to the more compatible diagnosis of LAM [4]. The cause and pathogenesis of this disorder remain unclear

Zampetti, A., Antuzzi, D., Caldarola, G., Celleno, L., Amerio, P., Feliciani, C., Linear atrophoderma of Moulin, <<EUROPEAN JOURNAL OF DERMATOLOGY>>, 2008; 18 (1): 79-80. [doi:10.1684/ejd.2007.0316] [http://hdl.handle.net/10807/32079]

Linear atrophoderma of Moulin

Zampetti, Anna;Antuzzi, Daniela;Caldarola, Giacomo;Celleno, Leonardo;Amerio, Pierluigi;Feliciani, Claudio
2008

Abstract

Firstly described by Moulin et al. in 1992 in 5 patients [1], LAM is a distinct clinical entity characterized by acquired atrophic bandlike skin lesions that often show hyperpigmentation and always follow the lines of Blaschko. No preceding infl ammation is noted, but a transient infl ammatory stage is perhaps often unrecognized, and there is no induration or scleroderma. Usually the condition begins in childhood or adolescence, and there is no evidence of any long-term progression. Histopathologically, an irregular moderate hyperpigmentation of the lower part of the epidermis is found, along with a few perivascular lymphocytes in the dermis and slight thickening of the collagen bundles, as in our case [2]. The existence of LAM is controversial in its possible clinical overlap with linear scleroderma or morphea. Nevertheless, this latter is characterized by one or more linear streaks of progressive induration that can extend through the dermis, subcutaneous tissue, and muscle to the underlying bone, causing signifi cant deformities [3]. The lack of autoantibodies, such as ANA, found in 73% of adult patients with linear scleroderma and the chronic and unvaried course make this diagnosis unlikely in our patient, leading to the more compatible diagnosis of LAM [4]. The cause and pathogenesis of this disorder remain unclear
Inglese
Zampetti, A., Antuzzi, D., Caldarola, G., Celleno, L., Amerio, P., Feliciani, C., Linear atrophoderma of Moulin, <<EUROPEAN JOURNAL OF DERMATOLOGY>>, 2008; 18 (1): 79-80. [doi:10.1684/ejd.2007.0316] [http://hdl.handle.net/10807/32079]
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10807/32079
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