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Classic EDS is inherited in an autosomal dominant manner and is caused by mutations in COL5A1 or COL5A2, which encode the alpha-1 and alpha-2 chains, respectively, of collagen type V.1 The disease is characterized by skin hyperextensibility, joint hypermobility and associated complications (luxations, pain, early osteoarthritis), and other clinical characteristics that are reviewed in a recent international consensus paper.1 Dermatologic manifestations of classic EDS include skin hyperextensibility and abnormal scarring, which results the formation of atrophic scars with a cigarette-paper-like appearance

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