Kotaro Matsui

Protective effects of platinum nanoparticles against UV‐light‐induced epidermal inflammation

Please cite this paper as: Protective effects of platinum nanoparticles against UV‐light‐induced epidermal inflammation. Experimental Dermatology 2010; 19: 1000–1006.

A case of giant vascular eccrine spiradenoma with unusual clinical features

Giant vascular eccrine spiradenoma (GVES) is a rare, highly vascular variant of eccrine spiradenoma (ES). To our knowledge, only five such cases have been previously reported in the literature. We report a Japanese patient with GVES on his right shoulder. A 76-year-old Japanese man presented with a tumour involving his right shoulder, which had been present for about 3 years and had gradually increased in size. On physical examination, a pale red pedunculated tumour measuring 50 · 34 · 26 mm was seen, which had erosive lesion on the surface (Fig. 1a). The patient had no pain and reported no other symptoms except bleeding from the lesion. There was no regional lymph-node involvement. The blood test results were almost within normal limits. Enhanced computed tomography showed some high-density nodules in the peripheral region of the tumour (Fig. 1b); in contrast, the central region of the tumour was low density and was not enhanced. The patient underwent total excision of the lesion. Histological examination of the excised tumour showed a prominent blood-filled vascular space and clearly delimited cords (Fig. 2a), showing two types of cell: cells with large pale nuclei in the centre and basaloid cells with small, dark nuclei at the periphery (Fig. 2b). Dilated vascular spaces containing red blood cells were present in the stroma. Immunohistochemically, the luminal large, pale epithelial cells were strongly positive for cytokeratin 19, carcinoembryonic antigen and epithelial membrane antigen, and the outer layer of small basaloid cells was negative. In addition, the cells lining the vascular space were positive for vimentin, CD31 and CD34. Mindbomb homologue (MIB)-1, an antibody against Ki67, was expressed on 3% of the tumour cells. These histological findings were diagnostic of GVES. ES is a benign, adnexal tumour originating from the eccrine sweat glands. It occurs commonly as a subcutaneous solitary nodule, or rarely as multiple lesions. The tumour usually measures < 10 to > 50 mm in diameter. Most of the lesions follow a benign clinical course, and gradually increase in size. In addition, malignant degeneration may also rarely occur. GVES is a rare variant of ES and was first described by Cotton et al. in 1986. Only five such cases have been previously reported in the literature. According to those reports, the lesions were dome-shaped tumours, measuring 20–50 mm in size with a marked degree of vascularity. However, our case was a unique pedunculated tumour, and the clinical features were different (a)

Bullous pemphigoid with IgG anti-LAD-1 antibodies

Bullous pemphigoid (BP) is an autoimmune subepidermal blistering disease that commonly presents with IgG autoantibodies to the NC16a domain of BP180 and/or BP230 [1]. The detection of other types of antibodies in BP patients has occasionally been reported [2, 3]. This report describes a BP patient in whom only IgG antibodies to the 120-kDa LAD-1 were detected.A 65-year-old Japanese female presented with pruritic blisters. The patient had no particular familial history; however, she had been treated [...]

Induction of Skin Lesions by Ultraviolet B Irradiation in a Case of Pemphigus Erythematosus

© 2014 The Authors. doi: 10.2340/00015555-1781 Journal Compilation

Squamous cell carcinoma arising from Darier's disease

Darier s disease (DD; OMIM 124000) is an autosomal dominant keratinization disorder characterized by the loss of adhesion between epidermal cells, thus resulting in abnormal keratinization. A mutation in the ATP2A2 gene, encoding the sarcoplasmic ⁄ endoplasmic reticulum Ca ATPase (SERCA)2, has previously been identified as the cause of this disease. Squamous cell carcinoma (SCC) arising from DD has not been commonly reported. We report a case of SCC developing in a patient with DD. A 62-year-old Japanese woman, who had been diagnosed as having DD, which had been treated with oral etretinate for the previous 25 years, presented with a 3-month history of a skin tumour on her head. On physical examination, a red erosive tumour measuring 20 · 20 mm in size was seen on the top right of the head. The tumour and its surrounding skin had the appearance of DD. The lesion was excised. Histological examination of the excised tumour found that the irregular tumour mass proliferated downward into the dermis (Fig. 1b). The invading tumour mass was composed of atypical squamous cells and mitotic cells. Acantholysis was also seen within the tumour nest, which is characteristic of DD (Fig. 1c). Immunohistochemically, most of the tumour cells were positive for p53 (Fig. 1d). In addition, MIB-1 was expressed in approximately 50% of all tumour cells. These histological findings indicated a diagnosis of SCC. After obtaining the patient s informed consent, ATP2A2 gene analysis was performed. A heterozygous missense mutation (p.T700A) at exon 15 was found (Fig. 2a). We did not find it in 100 healthy Japanese controls, indicating that it is a pathogenic mutation, not a neutral polymorphism. To our knowledge, this mutation has not been previously described. In this tumour, the cell-specific loss of wild-type ATP2A2 expression was not seen in the genomic DNA, which was isolated from the tumour cells by lasercapture microdissection (Fig. 2b). In addition, no missense mutation in either the H-ras or p53 gene was detected, and there was no evidence of human papilloma virus (HPV) in the tumour cells. SCC arising from DD seems to be rare, and only four such cases have been reported to date. Some of these cases suggested HPV infection to be the cause of carcinogenesis. Recently, heterozygous mutant (ATP2A2 ⁄ ) mice have been reported to develop SCCs on the fore stomach or on the skin, thereby suggesting that SERCA2 haploinsufficiency predisposes keratinocytes to develop neoplasia. Furthermore, loss of heterozygosity was not involved in the carcinogenesis, and the levels of p53 protein in the SCCs increased even though no mutations were found in the p53 gene. Our case is consistent with these reports. In addition, alterations in the ATP2A2 gene have also been reported to lead to the development of various human carcinomas, such as colon and lung cancer. Therefore, our case suggests that SERCA2 haploinsufficiency might cause SCC and thus, this may be a new model of skin carcinogenesis.

Giant cystic basal cell carcinoma mimicking epidermal cyst

Dear Editor, Basal cell carcinoma (BCC) is the most common malignant tumor composed of basaloid cells that arise from the basal cells of the epidermis or the epithelial structures of the adnexa. BCC has many different clinical and histological presentations. We herein report a case of cystic BCC which was clinically similar to epidermal cyst. A 91-year-old Japanese man presented with a 4-year history of a soft tumor involving his right cheek. It had recently rapidly increased in size. The physical examination revealed a cystic tumor measuring 5.0 cm · 5.0 cm, including a dark-brown lesion on the center of the surface and irregular telangiectasia on the peripheral area (Fig. 1a). No regional lymph node involvement was detectable. The blood test findings were almost completely normal. Magnetic

Unusual bullous pemphigoid without infiltration of inflammatory cells in the skin lesions

Bullous pemphigoid (BP) is an inflammatory subepidermal blistering disease associated with an autoimmune response to BP180 and/or BP230. The histopathological findings demonstrate subepidermal blisters with the infiltration of eosinophils and neutrophils [1]. This report describes a Japanese patient with BP, in whom only a few inflammatory cells were observed in the skin lesions.An 84-year-old Japanese female presented with tense blisters. She had no particular family history; however, she had been [...]

Coexistence of antilaminin-332-type mucous membrane pemphigoid, lamina lucida-type linear IgA bullous dermatosis and Sjögren syndrome

1 Mikeljevic J, Highet AS. Nicorandil-induced leg ulceration without mucosal involvement. Clin Exp Dermatol 2011; 36: 372–3. 2 McKenna DJ, Donnelly J, Armstrong DKB. Nicorandilinduced leg ulceration. Br J Dermatol 2007; 156: 394–6. 3 Patel GK, Harding KG. Nicorandil ulcer: moves beyond the mucosa. Ann Royal College Surgeons England 2010; 92: 451–2. 4 Heil M, Hubiche T, Beltran C et al. Isolated cutaneous inguinal ulcerations induced by nicorandil. J Eur Acad Dermatol Venereol 2008; 22: 1139–40. 5 Yap T, Philippou P, Perry M et al. Nicorandil-induced penile ulcerations: a case series. BJU Int 2011; 107: 268– 71. Coexistence of antilaminin-332-type mucous membrane pemphigoid, lamina lucida-type linear IgA bullous dermatosis and Sj€ ogren syndrome

Successful treatment with UVA rush hardening in a case of solar urticaria

Solar urticaria (SU) is a rare idiopathic photodermatosis. The symptoms are usually observed within ten minutes after exposure to sunlight. The action spectra are different among cases, ranging from ultraviolet B (UVB) to visible light [1]. SU is commonly treated with oral antihistamines, sunscreen, plasmapheresis and/or immunosuppressants. Phototherapy with various wavelengths of light and methods has also been performed to induce a tolerant state [2-4]. However, the symptoms of SU are frequently [...]