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in patients with severe psoriasis. Renal biopsy has to be discussed with the nephrologist. Management of IgAN include angiotensin blockade (if proteinuria > 0.5 g/d and/or blood pressure > 140/90 mmHg). Corticosteroids could be considered with urine protein > 1 g/d with preserved renal function.9 The exact role played by antiTNFa and ustekinumab in psoriasis-related IgAN is not yet established. Acknowledgments We wish to thank Dr. Helene Perrochia for providing the immunofluorescence pictures.

Nicolas Kluger, MD Departments of Dermatology, Allergology and Venereology Institute of Clinical Medicine University of Helsinki Skin and Allergies Hospital Helsinki Finland E-mail: [email protected] Nicolas Kluger, MD Aurelie Du-Thanh, MD Didier Bessis, MD Department of Dermatology H^ opital Saint-Eloi University of Montpellier I Montpellier France Marie-Francßoise Servel, MD Centre dhemodialyse St Guilhem Sete France Georges Mourad, MD Department of Nephrology and Transplantation H^ opital Lapeyronie University of Montpellier I Montpellier France Conflicts of interest: None. Financial source: None. References 1 Dervisoglu E, Akturk AS, Yildiz K, et al. The spectrum of renal abnormalities in patients with psoriasis. Int Urol Nephrol 2012; 44: 509–514. International Journal of Dermatology 2015, 54, e79–e93

2 Bagga A, Menon S, Hari P, et al. Nephrotic syndrome preceding psoriasis in child. Pediatr Nephrol 2007; 22: 1373–1376. 3 Wan J, Wang S, Haynes K, et al. Risk of moderate to advanced kidney disease in patients with psoriasis: population based cohort study. BMJ 2013; 347: f5961. 4 Donadio JV, Grande JP. IgA nephropathy. N Engl J Med 2002; 347: 738–748. 5 Wasilewska A, Zoch-Zwierz WM, Tenderenda E, et al. IgA nephropathy in a girl with psoriasis and seronegative arthritis. Pediatr Dermatol 2008; 25: 408–409. 6 Marocchi E, Spadaro A, Giannakakis K, et al. Infliximab in a patient with ankylosing spondylitis and secondary IgA nephropathy requiring haemodialysis. Clin Exp Rheumatol 2010; 28: 440. 7 Jacquet A, Francois H, Frangie C, et al. IgA nephropathy associated with ankylosing spondylitis is not controlled by infliximab therapy. Nephrol Dial Transplant 2009; 24: 3540–3542. 8 Sakellariou GT, Vounotrypidis P, Berberidis C. Infliximab treatment in two patients with psoriatic arthritis and secondary IgA nephropathy. Clin Rheumatol 2007; 26: 1132–1133. 9 Rosselli JL, Thacker SM, Karpinski JP, et al. Treatment of IgA nephropathy: an update. Ann Pharmacother 2011; 45: 1284–1296.

Eosinophilic annular erythema in a patient with metastatic prostate adenocarcinoma

Editor, Eosinophilic annular erythema (EAE) is a rare, relatively recently described figurate dermatitis of unknown origin.1–3 We report a patient with metastatic prostate adenocarcinoma who developed EAE. To our knowledge, only one case of EAE in association with internal malignancy has been documented in the literature.3 A 60-year-old man presented in November 2012 with a 3-month history of a mildly pruritic eruption on the trunk and upper limbs. Four years previously, he had been diagnosed with prostate adenocarcinoma (Gleason score 4 + 4 = 8) and had demonstrated a serum prostate specific antigen (PSA) value of 750.8 ng/ml. At the time of diagnosis, radiological examinations revealed bone metastases in the lumbar vertebrae and left sacroiliac joint. The patient had since been treated with oral antiandrogens, zoledronic acid, taxanes, and abiraterone. No cutaneous side effects were observed with these treatments. At the current presentation, dermatological examination revealed multiple, non-scaly, arciform, and annular plaques involving the lower back, chest, and arms. These lesions showed a slightly pigmented center and well-demarcated, elevated erythematous borders (Fig. 1). A skin biopsy was performed. Histopathological examination revealed a superficial to deep, dense dermal ª 2014 The International Society of Dermatology

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Figure 1 Multiple annular and arciform erythematous plaques involving the lower back are apparent in a 60-yearold man with a previous diagnosis of prostate adenocarcinoma

inflammatory infiltrate. The infiltrate was perivascular and interstitial and was composed of mononuclear cells and abundant eosinophils (Fig. 2). Some isolated flame figures were also identified. Laboratory investigations showed no blood eosinophilia. However, the cutaneous eruption was temporally associated with both a rising PSA level and radiographic evidence of the progression of metastatic bone disease. A diagnosis of EAE was made. The patient was treated with prednisone (20 mg/day) and topical clobetasol propionate. A significant improvement was obtained after 10 days, although some new lesions have continued to appear.

Figure 2 (a) Histopathology of a biopsy in the current patient showed a dermal inflammatory infiltrate with abundant eosinophils and edema. (b) The dense dermal infiltrate consisted of eosinophils with isolated flame figures (white arrow). (Hematoxylin and eosin stain; original magnification [a] 9100, [b] 9200) ª 2014 The International Society of Dermatology

(a)

In this patient, EAE was diagnosed on the basis of the clinical picture of figurate erythematous lesions and histopathological findings of a dense dermal lymphohistiocytic infiltrate with numerous eosinophils. Furthermore, some flame figures were also observed. The flame figures are composed of eosinophilic major protein deposited on collagen fibers and are characteristic of eosinophilic cellulitis (Wells syndrome).3 However, two recent studies have shown that flame figures may be seen in well-developed EAE lesions.2,3 In this context, some authors believe that EAE is a peculiar clinical variant in the spectrum of Wells syndrome presenting with an annular or figurate pattern.2–4 The optimal treatment of EAE is not yet standardized. Systemic steroids and antimalarials have been used with variable degrees of response.1,2,5 However, EAE can also be a self-limiting process, and thus not all cases may require treatment.6 The cause and pathogenesis of EAE remain obscure, although the entity may represent a hypersensitivity reaction to an as yet unidentified antigen.6 Several conditions have been reported in association with EAE. These include autoimmune thyroid disease,1 chronic borreliosis,1 chronic gastritis with Helicobacter pylori infection,2 diabetes mellitus,2 chronic hepatitis C virus infection,2 and chronic kidney disease.2 Furthermore, the coexistence of EAE and clear cell renal carcinoma was observed in one patient.3 In this respect, the current patient represents the second with internal malignancy and the first with prostatic neoplasia to be reported with EAE. In this patient, the possibility of a drug eruption was considered in the

(b)

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differential diagnosis, but the medication history did not support this diagnosis. Although the association of EAE and prostate adenocarcinoma may be coincidental, the correlation between the onset of the eruption and the progression of the neoplastic disease suggests that the tumor may have been the triggering factor for EAE in this case. In conclusion, an underlying malignancy should be considered in patients presenting with EAE.

Marcos A. Gonza´lez-Lo´pez, MD, PhD Marıa Lo´pez-Escobar, MD Hector Fernandez-Llaca, MD Department of Dermatology Marques de Valdecilla University Hospital University of Cantabria Santander Spain E-mail: [email protected] M. Carmen Gonza´lez-Vela, MD, PhD Department of Pathology Marques de Valdecilla University Hospital University of Cantabria Santander Spain Marta Lo´pez-Brea, MD Department of Oncology Marques de Valdecilla University Hospital University of Cantabria Santander Spain References 1 Kahofer P, Grabmaier E, Aberer E. Treatment of eosinophilic annular erythema with chloroquine. Acta Derm Venereol 2000; 80: 70–71. 2 El-Khalawany M, Al-Mutairi N, Sultan M, et al. Eosinophilic annular erythema is a peculiar subtype in the spectrum of Wells syndrome: a multicenter longterm follow-up study. J Eur Acad Dermatol Venereol 2013; 27: 973–979. 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 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. 5 Mebazaa A, Kenani N, Ghariani N, et al. Eosinophilic annular erythema responsive to chloroquin. Eur J Dermatol 2009; 19: 84–85. International Journal of Dermatology 2015, 54, e79–e93

6 Prajapati V, Cheung-Lee M, Schloss E, et al. Spontaneously resolving eosinophilic annular erythema. J Am Acad Dermatol 2012; 67: e75–e77.

Post-herpetic eosinophilic papules and plaques

Editor, Wolf’s post-herpetic isotopic response refers to the occurrence of a new, unrelated disorder on an area of skin previously infected by a herpes virus.1 We describe two patients in whom several pruritic papules and erythematous plaques, respectively, developed on healed skin following herpes zoster infection. Patient 1 was a 69-year-old man affected by herpes zoster infection on his right chest and back. He was treated with anti-viral tablets (valaciclovir hydrochloride 3000 mg/d for seven days). Having improved, the patient later complained of persistent pruritus on the same sites. Three months later, physical examination revealed several red papules scattered on the healed sites. A biopsy specimen showed dense inflammatory cellular infiltrates composed of lymphocytes, histiocytes, and prominent eosinophils in the upper to mid-dermis (Fig. 1a–c). Results of immunohistochemistry revealed localization of varicella zoster virus (VZV) antigen in the sweat glands (Fig. 1d) as well as CD4- and CD8-positive T cells in the dermis. Patient 2 was a 72-year-old man affected with herpes zoster infection on the right chest and back. He was treated with anti-viral agents. Six months later, he complained of itching at locations consistent with the healed sites of herpes zoster infection. Physical examination showed erythematous infiltrative plaques corresponding to the previously infected sites on the chest as well as the back (Fig. 1e). A biopsy specimen revealed dense cellular infiltrates composed of eosinophils, lymphocytes, and histiocytes, as well as extravasation of red blood cells in the upper dermis (Fig. 1f). Immunohistochemistry revealed localized VZV antigen in the sweat glands in the dermis. Laboratory examination showed an eosinophilia in the peripheral blood (11%). The patient was successfully treated with topical corticosteroids. Healed skin following herpes zoster infection is not normal skin and is occasionally apt to develop various conditions, such as granulomatous reactions, malignant tumors, dysimmune reactions, and infections.1 Several possible mechanisms, including those of viral, immunological, vascular, and neural etiologies, are proposed in this process. Our two patients developed papular eruptions and erythematous plaques, respectively, corresponding to the herpes-infected sites. One patient complained of post-herpetic itch after improvement of herpes zoster, whereas the other did not. Histological examination ª 2014 The International Society of Dermatology

Eosinophilic annular erythema in a patient with metastatic prostate adenocarcinoma.

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