Case report Anetoderma due to secondary syphilis: Report of two cases and discussion of the histopathological findings John V Veasey 1 , Rute F Lellis 2 , Rene ˆ L Porto 3 and Gladys MA Mattei 4 Abstract Anetoderma is a rare benign condition of diverse etiology whose characteristic is the diminution or absence of the dermal elastic fibers. Classified as primary and secondary, the latter associated with tumors, inflammatory, and infectious diseases. Although the etiology of the lesions is well described in literature, the pathogenesis is still poorly determined. Anetoderma in syphilis is rare, and occurs even in the most uncommon cutaneous manifestations of the disease, such as the nodular form. In order to better understand the changes that lead to elastolysis, we propose a better correlation with the histopathological findings of the lesions that precede it. We present two cases of anetoderma secondary to syphilis, whose clinical aspects resembled the pattern of their initial secondary syphilis rash. Keywords Bacterial disease, syphilis, anetoderma Date received: 21 February 2016; accepted: 9 May 2017 Background We are currently facing a worldwide epidemic of syph- ilis. 1 Clinical manifestations rarely seen have occurred, leading the dermatologist to confront unusual clinical conditions in daily practice. 2 Generally, the lesions of secondary syphilis evolve without scarring. The evolu- tion of lesions with anetoderma, a rare cutaneous dis- ease characterized by loss of elastic fibers, has been poorly reported. This loss may be explained by defect- ive synthesis, increased activity of elastolytic enzymes, or autoimmune-mediated destruction of fibers. 3,4 Primary anetoderma represents the appearance of well-defined cutaneous lesions in previously normal areas of skin. Previously classified clinically as Jadassohn–Pellizzari anetoderma, in which the areas of atrophy are preceded by inflammatory lesions (ery- thematous or urticarial lesions), and Schweninger– Buzzi anetoderma, when lesions arise ‘de novo,’ without any preceding eruption. 3,4 This classification has been abandoned, for there is no concordance between the clinical and pathological findings in these two groups: perivascular infiltration of inflammatory cells is present in all anetoderma lesions no matter the clinical appear- ance. 3 In both of these idiopathic cases, it is necessary to investigate diseases such as systemic lupus erythema- tosus, antiphospholipid antibody syndrome, and auto- immune thyroiditis. Secondary anetoderma involves lesions that arise in areas of current or previous derma- toses, the most common being acne and varicella, although also occurs in syphilis, leprosy, sarcoidosis, and tuberculosis, with a clinical appearance similar to the preceding dermatosis. 4,5 Some diseases such as HIV have been associated with both primary and secondary anetoderma, for there is some evidence that implicates HIV infection in the dysregulation of matrix proteins that degrades elastin. 5,6 1 Dermatology Clinic of Santa Casa, de Sa ˜o Paulo Hospital, Sa ˜o Paulo, Brazil 2 Pathology Laboratory of Santa Casa, de Sa ˜o Paulo Hospital, Sa ˜o Paulo, Brazil 3 Medical Clinic, Department of Santa Casa, de Sa ˜o Paulo Hospital, Sa ˜o Paulo, Brazil 4 Private Practice in Sa ˜o Paulo, Sa ˜o Paulo, Brazil Corresponding author: John V Veasey, Rua Dr Cesario Mota Jr, 112 Edificio Conde de Lara – 5 andar Vila Buarque, Sao Paulo CEP 01221-020, SP, Brazil. Email: johnveasey@uol.com.br International Journal of STD & AIDS 0(0) 1–5 ! The Author(s) 2017 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0956462417713586 journals.sagepub.com/home/std