e98
Correspondence
2 Mebazaa A, Kenani N, Ghariani N, et al. Eosinophilic annular erythema responsive to chloroquin. Eur J Dermatol 2009; 19: 84–85. 3 Rongioletti F, Fausti V, Kempf W, et al. Eosinophilic annular erythema: an expression of the clinical and pathological polymorphism of Wells syndrome. J Am Acad Dermatol 2011; 65: e135–e137. 4 El-Khalawany M, Al-Mutairi N, Sultan M, et al. Eosinophilic annular erythema is a peculiar subtype in the spectrum of Wells syndrome: a multicentre longterm follow-up study. J Eur Acad Dermatol Venereol 2013; 27: 973–979. 5 Howes R, Girgis L, Kossard S. Eosinophilic annular erythema: a subset of Wells syndrome or a distinct entity? Australas J Dermatol 2008; 49: 159–163. 6 Sempau L, Larralde M, Luna PC, et al. Eosinophilic annular erythema. Dermatol Online J 2012; 18: 8. 7 Marks R. Eosinophilic cellulitis – a response to treatment with dapsone: case report. Australas J Dermatol 1980; 21: 10–12. 8 Zhu YI, Stiller MJ. Dapsone and sulfones in dermatology: overview and update. J Am Acad Dermatol 2001; 45: 420–434. 9 Moon S-H, Shin M-K. Bullous eosinophilic cellulitis in a child treated with dapsone. Pediatr Dermatol 2013; 30: e46–e47.
Localized lymphomatoid papulosis
A 63-year-old woman presented with a 2-month history of multiple asymptomatic cutaneous lesions on the abdomen. She was otherwise healthy and was not taking any medication. Dermatological examination revealed a crop of 2–4 mm, erythematous papules confined to the left side of the abdomen; some lesions were covered with crusts (Fig. 1). No other cutaneous or mucosal lesions were noted. There was no lymphadenopathy or hepatosplenomegaly. Routine laboratory studies were normal. A skin biopsy showed a dermal infiltrate containing anaplastic lymphoid cells with pleomorphic vesicular nuclei and abundant cytoplasm (Fig. 2). These cells are mixed with neutrophils, eosinophils, lymphocytes, and histiocytes. Immunohistochemical staining was performed using EnVision+ method (DAKO, Glostrup, Denmark). The atypical lymphoid cells were immunoreactive for CD45, CD4, and CD30 (Fig. 2) but negative for CD15, CD20, CD8, perforin, granzyme B, and T-cell receptor-gamma and -betaF1. A T-cell receptor gene rearrangement was not detected. A diagnosis of localized lymphomatoid papulosis (LyP) type A was made. Treatment with topical clobetasol led to a complete resolution of skin lesions. However, new lesions continued to appear, limited to the affected area, which healed spontaneously. After 18 months of follow-up, no recurrence or associated disease have been detected. International Journal of Dermatology 2015, 54, e94–e108
(a)
(b)
Figure 1 (a) A crop of erythematous papules confined to the left abdomen. (b) Close-up view of the lesions.
LyP is currently classified within the spectrum of CD30+ lymphoproliferative disorders according to the WHO-EORTC classification for cutaneous lymphomas.1 Clinically, it consists of red–brown papules and/or nodules that may develop necrosis and crusting and heal spontaneously, sometimes with scarring.1,2 The individual lesions resolve within weeks or months, while the disease may recur for decades. Histopathologically, LyP has traditionally been classified into three subtypes: type A (histiocytic), type B (mycosis fungoides-like), and type C (anaplastic large cell lymphoma-like).1–3 Recently, a further variant simulating histologically an aggressive epidermotropic CD8-positive T-cell lymphoma has been described, which was named LyP type D.3 More recently, an angioinvasive CD30+ CD8+ variant of LyP that simulates aggressive angiocentric T-cell lymphomas has been reported (LyP type E).4 The lesions of LyP usually occur in a generalized distribution, with multiple lesions over the trunk and extremities. However, in a small subset of patients, the eruption is limited to a single anatomic region (localized or regional LyP).5 To date,
Correspondence
2 Mebazaa A, Kenani N, Ghariani N, et al. Eosinophilic annular erythema responsive to chloroquin. Eur J Dermatol 2009; 19: 84–85. 3 Rongioletti F, Fausti V, Kempf W, et al. Eosinophilic annular erythema: an expression of the clinical and pathological polymorphism of Wells syndrome. J Am Acad Dermatol 2011; 65: e135–e137. 4 El-Khalawany M, Al-Mutairi N, Sultan M, et al. Eosinophilic annular erythema is a peculiar subtype in the spectrum of Wells syndrome: a multicentre longterm follow-up study. J Eur Acad Dermatol Venereol 2013; 27: 973–979. 5 Howes R, Girgis L, Kossard S. Eosinophilic annular erythema: a subset of Wells syndrome or a distinct entity? Australas J Dermatol 2008; 49: 159–163. 6 Sempau L, Larralde M, Luna PC, et al. Eosinophilic annular erythema. Dermatol Online J 2012; 18: 8. 7 Marks R. Eosinophilic cellulitis – a response to treatment with dapsone: case report. Australas J Dermatol 1980; 21: 10–12. 8 Zhu YI, Stiller MJ. Dapsone and sulfones in dermatology: overview and update. J Am Acad Dermatol 2001; 45: 420–434. 9 Moon S-H, Shin M-K. Bullous eosinophilic cellulitis in a child treated with dapsone. Pediatr Dermatol 2013; 30: e46–e47.
Localized lymphomatoid papulosis
A 63-year-old woman presented with a 2-month history of multiple asymptomatic cutaneous lesions on the abdomen. She was otherwise healthy and was not taking any medication. Dermatological examination revealed a crop of 2–4 mm, erythematous papules confined to the left side of the abdomen; some lesions were covered with crusts (Fig. 1). No other cutaneous or mucosal lesions were noted. There was no lymphadenopathy or hepatosplenomegaly. Routine laboratory studies were normal. A skin biopsy showed a dermal infiltrate containing anaplastic lymphoid cells with pleomorphic vesicular nuclei and abundant cytoplasm (Fig. 2). These cells are mixed with neutrophils, eosinophils, lymphocytes, and histiocytes. Immunohistochemical staining was performed using EnVision+ method (DAKO, Glostrup, Denmark). The atypical lymphoid cells were immunoreactive for CD45, CD4, and CD30 (Fig. 2) but negative for CD15, CD20, CD8, perforin, granzyme B, and T-cell receptor-gamma and -betaF1. A T-cell receptor gene rearrangement was not detected. A diagnosis of localized lymphomatoid papulosis (LyP) type A was made. Treatment with topical clobetasol led to a complete resolution of skin lesions. However, new lesions continued to appear, limited to the affected area, which healed spontaneously. After 18 months of follow-up, no recurrence or associated disease have been detected. International Journal of Dermatology 2015, 54, e94–e108
(a)
(b)
Figure 1 (a) A crop of erythematous papules confined to the left abdomen. (b) Close-up view of the lesions.
LyP is currently classified within the spectrum of CD30+ lymphoproliferative disorders according to the WHO-EORTC classification for cutaneous lymphomas.1 Clinically, it consists of red–brown papules and/or nodules that may develop necrosis and crusting and heal spontaneously, sometimes with scarring.1,2 The individual lesions resolve within weeks or months, while the disease may recur for decades. Histopathologically, LyP has traditionally been classified into three subtypes: type A (histiocytic), type B (mycosis fungoides-like), and type C (anaplastic large cell lymphoma-like).1–3 Recently, a further variant simulating histologically an aggressive epidermotropic CD8-positive T-cell lymphoma has been described, which was named LyP type D.3 More recently, an angioinvasive CD30+ CD8+ variant of LyP that simulates aggressive angiocentric T-cell lymphomas has been reported (LyP type E).4 The lesions of LyP usually occur in a generalized distribution, with multiple lesions over the trunk and extremities. However, in a small subset of patients, the eruption is limited to a single anatomic region (localized or regional LyP).5 To date,
