LAUSR

Sir, The sudden development of multiple melanocytic nevi over weeks to months is an uncommon phenomenon known in the literature as eruptive melanocytic nevi (EMN), and it has been associated with a number of conditions, such as immunodeficiency, immunosuppression, medications and severe blistering skin disease. A man in his 50s with a history of cutaneous lupus for the last 10 years came to the Dermatology department with multiple purplered annular and infiltrated plaques as well as several erosions and bullous lesions of gradual onset on his back, chest, extremities and face affecting less than 10% of the body surface. Oral mucosa, soles and palms were not involved. The patient had hypertension and ischemic cardiomyopathy for the last five years and was in treatment with statins, acetylsalicylic acid, losartan and ivabradine. He also reported fatigue and weakness, but no other systemic symptoms. Autoimmune serology proved positive for antinuclear antibodies with a titer of 1/320, speckled pattern and positive anti-Ro. The rest of the laboratory tests including blood cell count, liver function, plasma creatinine, 24-hour urine proteinuria measurement, cryoglobulins, anti-skin antibodies, and antineutrophil-cytoplasmic antibodies were all negative or normal. Dermatopathology study showed an intense lymphocytic infiltrate with lichenoid and deep perivascular pattern, vacuolization of the basal stratum, mucin deposits and thinning of the epidermis with many dyskeratotic keratinocytes and Civatte bodies (Figure 1) as well as a negative direct immunofluorescence, being compatible with toxic epidermal necrolysis (TEN)like lupus. Treatments with hydroxychloroquine, rituximab, mycophenolate mofetil and cyclosporine were prescribed but discontinued because of absence of response. We started treatment with intravenous methylprednisolone at a dose of 125mg every day for five consecutive days and intravenous cyclophosphamide at a dose of 500mg every two weeks up to a total of six cycles with excellent response from the first dose to complete re-epithelialization and persistence of residual injuries after three weeks. In the following months, physical examination revealed the appearance of multiple pigmented macules on the trunk where he previously had erosions (Figure 2(a)). By dermoscopy, we observed a brown-stained core with a typical pigment network (Figure 2(b)). Dermatopathology study of these pigmented lesions was consistent with junctional nevus (Figure 2(c)). The diagnosis was EMN in a patient with TEN-like lupus. EMN, defined as the sudden development of multiple melanocytic nevi over weeks to months, has been associated with a number of conditions, such as immunodeficiency, immunosuppression, medications and severe blistering skin disease as in epidermolysis bullosa, erythema multiforme, Stevens-Johnson syndrome, TEN and pemphigoid. Less frequently EMN have been reported in primary adrenal insufficiency, trauma, cutaneous mastocytosis and Langerhans cell histiocytosis. To our knowledge, this is the first case described of a patient with TEN-like cutaneous lupus who developed EMN. This uncommon clinical expression of cutaneous lupus is explained from a histopathological point of view by an intense lichenoid lymphocytic infiltrate that can lead to epidermal necrosis and apoptosis of keratinocytes and development of blisters and erosions on the skin. This condition differs from bullous lupus erythematosus, in which histopathological evaluation reveals a neutrophilic infiltrate and direct immunofluorescence microscopy demonstrates immunoglobulin G (with or without immunoglobulin A and immunoglobulin M) deposits at the basement membrane zone. The development of EMN in TEN-like lupus could be explained by cytokines and other growth factors that are released by damaged keratinocytes and inflammatory cells during blister formation and epidermal regeneration and might be responsible for the proliferation and migration of melanocytes, and melanogenesis. Recently, Perry et al. defined the term Eruptive nevi associated with medications (ENAMs) as the development in association with medication use of Correspondence to: Cristina Collantes Rodrı́guez, Department of Dermatology, Hospital Universitario Puerta del Mar, Ana de Viya 21, Cádiz, 11009, Spain. Email: [email protected] Received 2 August 2017; accepted 6 December 2017