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Latent dystrophic subcutaneous calcification in patients with chronic venous insufficiency.

Dystrophic calcification in the skin occurs in association with a variety of disorders. To determine the association between subcutaneous calcification and chronic venous insufficiency, X-ray examinations were performed in 20 patients with chronic venous insufficiency and in 20 control subjects to detect latent calcification in their lower legs. Of the 20 patients, 13 (65%) had subcutaneous calcification, and the prevalence appeared to increase with disease duration, while only 4 control subjects (20%) had minimal calcification. Two types of calcification were identified based on their radiographic features: punctate and trabecular/reticular types. Patients with trabecular/reticular calcification had longer disease duration and more severe clinical scores than patients with punctate calcification. None of the control subjects had trabecular/reticular types of calcification. The identification of the presence and progression of latent calcification in the lower legs is useful, and may be necessary for the long-term management of chronic venous insufficiency, since calcification of skin tissues impedes wound healing and can be a risk factor for refractory ulcers.

Drug-induced hypersensitivity syndrome by ethambutol: A case report

induced by levetiracetam. Seizure 2012; 21: 823–825. 3 Naranjo CA, Busto U, Sellers EM et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther 1981; 30: 239–245. 4 Bunnell K, Pucci F. Levetiracetam-induced neutropenia following traumatic brain injury. Brain Inj 2015; 29(1): 115–117. 5 Bonastre MT, Munoz SP, Boza FM, Padro JG. Neutropenia secondary to exposure to levetiracetam. Tumori 2015; 101: e145–e146.

Dermoscopic features of lymphocytoma cutis: A case report of a representative dermoscopic feature

1 Happle R. Mosaicism in Human Skin: Understanding Nevi, Nevoid Skin Disorders, and Cutaneous Neoplasia. Berlin: Springer, 2014. 2 Mabuchi T, Akasaka E, Kondoh A et al. Seborrheic keratosis that follows Blaschko’s lines. J Dermatol 2008; 35: 301–303. 3 Rogers M. Epidermal nevi and the epidermal nevus syndromes: a review of 233 cases. Pediatr Dermatol 1992; 9: 342–344. 4 Hafner C, van Oers JM, Vogt T et al. Mozaicism of activating FGFR3 mutations in human skin causes epidermal nevi. J Clin Invest 2006; 116: 2201–2207. 5 Hafner C, Haltmann A, van Oers JM et al. FGFR3 mutations in seborrheic keratoses are already present in flat lesions and associated with age and localization. Mod Pathol 2007; 20: 895–903.

Histiocytoid Sweet syndrome: a novel association with relapsing polychondritis

1 Akiyama M. ABCA12 mutations and autosomal recessive congenital ichthyosis: a review of genotype/phenotype correlations and of pathogenetic concepts. Hum Mutat 2010; 31:1090–6. 2 Shibata A, Ogawa Y, Sugiura K et al. High survival rate of harlequin ichthyosis in Japan. J Am Acad Dermatol 2014; 70:387–8. 3 Thomas AC, Cullup T, Norgett EE et al. ABCA12 is the major harlequin ichthyosis gene. J Invest Dermatol 2006; 126:2408–13. 4 Rajpopat S, Moss C, Mellerio J et al. Harlequin ichthyosis: a review of clinical and molecular findings in 45 cases. Arch Dermatol 2011; 147:681–6. 5 G€ urkan H, Fischer J, Ulusal S et al. A novel mutation in the ABCA12 gene in a Turkish case of harlequin ichthyosis. Clin Dysmorphol 2015; 24:115–17. 6 Koochek A, Choate KA, Milstone LM. Harlequin ichthyosis: neonatal management and identification of a new ABCA12 mutation. Pediatr Dermatol 2014; 31:e63–4.

Bullous eosinophilic annular erythema

Dear Editor, Eosinophilic annular erythema (EAE) is a rare dermatosis characterized by annular erythematous plaques with a dense tissue eosinophilia. EAE is usually devoid of bullae, hypereosinophilia and flame figures histopathologically in addition to annular erythematous plaques. The disease entity of EAE and Wells syndrome (WS) is still debatable. However, no case of EAE with bullous lesions has been reported to date. Here, we present a case of EAE with bullous lesions. A 69-year-old woman presented with multiple annular erythematous plaques on her trunk and limbs. The patient had a past history of asthma, hypertension, uterine fibroids and

Extraocular sebaceous carcinoma in association with a clonal seborrheic keratosis: Dermoscopic features

Dear Editor, The clinical diagnosis of extraocular sebaceous carcinoma is challenging due to the lack of specific clinical manifestations of this neoplasm. However, previous reports of extraocular sebaceous carcinomas using dermoscopy have been limited. Here, we present a case of an extraocular sebaceous carcinoma in association with a clonal seborrheic keratosis and we describe its dermoscopic features. A 75-year-old woman presented with a tumor in a black plaque on her abdomen. The patient had a history of burn injury on her abdomen 30 years prior. Her burn scar had gradually become black and then developed a tumor with bleeding 3 months earlier. Physical examination revealed a 20 mm 9 12 mm black keratotic plaque with an elevated tumor in the center of her abdomen infraumbilically (Fig. 1a). Dermoscopic examination revealed that this lesion had two components: polymorphous vessels with homogenous yellow backgrounds in the center and blue-gray globules at the periphery (Fig. 1b). The polymorphous vessels were composed of linear irregular vessels, glomerular vessels and hairpin-like vessels (Fig. 1c). At the periphery, similar findings with bluegray structures of various size and shape were observed.

Phakomatosis pigmentovascularis type IIb: A case with Klippel–Trenáunay syndrome and extensive dermal melanocytosis as nevus of Ota, nevus of Ito and ectopic Mongolian spots

Dear Editor, Phakomatosis pigmentovascularis (PPV) has several variants due to different combinations of pigmentary lesions and vascular lesions. PPV type IIb is characterized by capillary malformation and dermal melanocytosis with or without nevus anemicus. Here, we present a case of PPV type IIb in association with Klippel–Tr enaunay syndrome. Our case is rare in terms of its extensive dermal melanocytosis. A 53-year-old man presented with a diffuse bluish gray pigmentation on his left cheek, right back and shoulder, and diffuse red-purple aggregated patches on his upper and lower limbs (Fig. 1a,b). There was no familial history of PPV or other

Histiocytoid Sweet syndrome with ophthalmologic involvements: A novel association with uveitis

Dear Editor, Histiocytoid Sweet syndrome (HSS) is histologically characterized by a predominant inflammatory infiltrate of mononuclear histiocytoid cells, and M2-like macrophages have been speculated to participate in the pathogenesis of HSS. Here, we present a novel case of HSS associated with uveitis. A 70-year-old man presented with multiple erythematous plaques on his trunk and upper limbs. The patient had initially developed erythematous plaques 10 years prior. He was diagnosed with uveitis and serous retinal detachment 1 year before, and methylprednisolone pulse therapy had been performed. He also had slight anemia and was diagnosed with myelodysplastic syndromes from a bone marrow biopsy. Physical examination revealed multiple erythematous plaques on his trunk and limbs (Fig. 1a), some of which were annular and indurated (Fig. 1b,c). Ophthalmologic examinations in addition to magnetic resonance imaging revealed conjunctivitis, uveitis and serous retinal detachment in his right eye (Fig. 1d). Histopathological examination showed a moderate perivascular and periadnexal inflammatory infiltrate in the dermis (Fig. 1e). The interface change was slight (Fig. 1f). Nuclear debris was intermingled with an inflammatory infiltrate of histiocytoid mononuclear cells and neutrophils (Fig. 1g). Immunohistochemical examination showed positive reactions for phosphoglucomutase-1 (PG-M1), lysozyme, kinesin-like protein 1 (KP-1) and (a) (b)

A case of subungual melanoma with bone invasion: destructive local invasion and multiple skin metastases

to abnormal adhesion and migration of keratinocytes. Br J Dermatol 2008; 159: 1192–1196. 7 Fassihi H, Wessagowit V, Jones C et al. Neonatal diagnosis of Kindler syndrome. J Dermatol Sci 2005; 39: 183–185. 8 Burch JM, Fassihi H, Jones CA, Mengshol SC, Fitzpatrick JE, McGrath JA. Kindler syndrome: a new mutation and new diagnostic possibilities. Arch Dermatol 2006; 142: 620–624. 9 Techanukul T, Sethuraman G, Zlotogorski A et al. Novel and recurrent FERMT1 gene mutations in Kindler syndrome. Acta Derm Venereol 2011; 91: 267–270. 10 Penagos H, Jaen M, Sancho MT et al. Kindler syndrome in native Americans from Panama: report of 26 cases. Arch Dermatol 2004; 140: 939–944. 11 Ussar S, Moser M, Widmaier M et al. Loss of Kindlin-1 causes skin atrophy and lethal neonatal intestinal epithelial dysfunction. PLoS Genet 2008; 4: e1000289. 12 Sadler E, Klausegger A, Muss W et al. Novel KIND1 gene mutation in Kindler syndrome with severe gastrointestinal tract involvement. Arch Dermatol 2006; 142: 1619–1624.

Peripheral arterial bypass surgery for intractable wounds caused by limited cutaneous systemic sclerosis.

asymptomatic) and calcification of the large arteries (Fig. 1i,j). Eosinophilic granulomatosis with polyangiitis was excluded as a differential diagnosis because there was no history of asthma or allergic rhinitis, no eosinophilia and very little eosinophilic infiltration of the biopsy specimen. Therefore, we diagnosed microscopic polyangiitis (MPA) presenting with multiple punched-out ulcers and interstitial pneumonia. Pulse corticosteroid therapy with methylprednisolone (1000 mg/day for 3 days) followed by oral prednisolone (60 mg/day) was effective for MPA, resulting in the gradual improvement of the leg ulcers and pneumonia with decreased serum myeloperoxidase ANCA level to 2.9 U/mL. During the clinical course, cytomegalovirus enterocolitis, invasive pulmonary aspergillosis and leg phlegmon developed and were treated with ganciclovir, voriconazole, and tazobactam with vancomycin, respectively. Microscopic polyangiitis is part of ANCA-associated necrotizing vasculitis (AAV). Myeloperoxidase ANCA is detected in 50–75% of MPA patients and infection can be a trigger of MPA, although no antecedent infection was found in this case. AAV is associated with interstitial lung disease (ILD), but the pathogenesis of ILD in AAV remains poorly understood. There are three hypotheses: (i) alveolar hemorrhage due to pulmonary capillaritis; (ii) an anti-myeloperoxidase-directed autoimmune response; or (iii) production of ANCA by ILD as a result of neutrophil destruction. Palpable purpura is the most common skin manifestation, occurring in 30–40% of patients with MPA. Other skin manifestations include livedo reticularis and nodules, because MPA usually affects small blood vessels. Deep skin ulcers caused by MPA, which are rare but previously reported, can occur when necrotizing vasculitis affects the deeper vessels at the dermis. Although abnormal blood vessel calcification was not detected with von Kossa staining, we speculate that the punched-out ulcers might have developed due to necrotizing vasculitis at the dermosubcutaneous junction from angiopathy caused by diabetes and/or hemodialysis.