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Rationale:Blastic plasmacytoid dendritic cell neoplasm (BPDCN), derived from precursors of plasmacytoid dendritic cells, is a rare and aggressive malignancy with frequent cutaneous involvement. Although cutaneous lesions are often chemosensitive, BPDCN portends a poor prognosis as most patients relapse after developing drug resistance.Patient concerns:We report a case of a 65-year-old man who presented with a rapidly enlarging hyperpigmented plaque on his shoulder with subsequent similarly appearing macules and plaques on his chest, back, and neck.Diagnosis:Skin biopsy revealed a dense adnexocentric dermal infiltrate of immature blastoid cells without epidermal involvement. The infiltrate was immunoreactive for CD4, CD56, CD123, and Bcl-2, but negative for CD3, CD8, CD30, MPO, EBER, and ISH. The patient was diagnosed with BPDCN based on these cell markers.Intervention:Bone marrow biopsy and radiologic work-up showed no evidence of extracutaneous involvement. The patient attained partial remission after undergoing 2 rounds of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP regimen) before autologous stem cell transplantation, however, he quickly relapsed and developed new cutaneous lesions.Outcomes:The patient was treated with venetoclax, a Bcl-2 inhibitor, and exhibits complete resolution of prior skin findings and continues to remain free of new cutaneous lesions 10 months posttreatment initiation with venetoclax.Lessons:Herein, we present a case that supports the use of venetoclax, a Bcl-2 inhibitor, in the off-label treatment of BPDCN with Bcl-2 overexpression. Only 1 prior case has reported the off-label use of venetoclax for the treatment of BPDCN. This case highlights a novel therapeutic option for BPDCN patients unresponsive to traditional treatment.

Spontaneous tumor regression, regression in the absence of therapeutic intervention, can be identified histologically in over 25% of primary cutaneous melanomas at initial diagnosis. A unique subset of T lymphocytes found in areas of regression can be histologically distinguished from tumor-infiltrating T lymphocytes (TIL) found in areas of tumor progression. We call this unique subset of T lymphocytes regression-associated T lymphocytes (RATs). The aim of this study is to determine the phenotype of lymphocytes and the density of specific cell types linked to immunosuppression in areas of tumor progression compared with areas of tumor regression. These specific cell types include T-regulatory cells (Tregs) and S100A9 cells. A total of 14 primary cutaneous melanomas with areas of progression and regression were used. Immunohistochemistry staining was used to identify CD4 cells, CD8 cells, Tregs, and S100A9 cells. Two independent observers manually counted three high-powered ×40 fields. There was no predominance of CD4 or CD8 T lymphocytes in either RATs or TIL. We identified a lower density of Tregs in RATs compared with TIL when using the FOXP3/CD4 Treg marker (P=0.04) and a marginal difference when using our second, confirmatory Treg marker, FOXP3/CD25 (P=0.11). We observed a lower density of S100A9 cells in RATs compared with TIL (P=0.002). There was an observable difference in the tumor microenvironments of RATs and TIL, with RATs having a significantly lower density of Tregs and S100A9 cells. We deduce that the absence of immunosuppression in areas of regression allows for a more robust immune response and thus effective eradication of tumor cells.

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Pembrolizumab-induced reactivation of bullous pemphigoidDear Editor,Pembrolizumab is a programmed cell death protein 1 (PD-1) inhibitor approved for use in several solid carcinomas. 1 It reverses T-cell suppression, causing immune stimulation. 2 Consequently, various immune-related adverse effects are described with its use, with skin toxicity accounting for up to 40% of adverse reactions. 2,3 Most cutaneous reactions are mild and do not necessitate drug discontinuation. These include mor-

Summary: Postoperative candida infection is a rarely reported complication in cutaneous surgery, although it may develop more often in particular clinical settings. We present a 59-year-old woman with a well-controlled human immunodeficiency virus infection. She developed a bright red eruption with satellite pustules 2 weeks after excision of recurrent lentigo maligna melanoma of the left lower eyelid and periocular region. Due to defect size and complexity of the reconstruction (glabellar transposition flap, Hughes flap, composite graft from upper contralateral eyelid, and full-thickness skin graft from ipsilateral retroauricular region), she was placed on prophylactic oral amoxicillin-clavulanic acid and topical bacitracin and polymyxin. Immediate postoperative course was unremarkable, and sutures were removed after 7 days. Three days later, she developed bright red erythema and pustules within the surgical site and complained of burning. Empirically she was switched to topical gentamicin and oral ciprofloxacin, and later to linezolid, due to inadequate response. Wound culture grew Candida albicans sensitive to fluconazole and voriconazole. After oral fluconazole and topical clotrimazole initiation, the patient rapidly improved. The graft remained viable and apart from small partial dehiscence on the cheek, the healing was unremarkable. Apart from the case presentation, we also discuss different factors associated with postoperative candida infection, including immunocompromised status, surgical procedure location, and postoperative antibiotic use. Early recognition and treatment of postoperative candida infections are crucial to prevent delayed healing and associated morbidity.

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We present a rare case of cutaneous cytomegalovirus (CMV) infection in a nonimmunocompromised patient. A 74-year-old woman with a history of diabetes presented with an ulcer on the right lateral tibia that occurred at the site of a nerve core biopsy. Subsequent biopsy of the ulcer edge showed granulation tissue with neutrophilic inflammation. The patient underwent extensive antibiotic treatment for possible infection with weekly wound care. However, the ulceration persisted and enlarged. A repeat biopsy 1 year later showed superficial and deep mixed inflammation with an associated vasculitis. On close examination, endothelial and eccrine ducts cells showed characteristic CMV viral cytopathic changes with positivity on CMV immunohistochemical stain. Although the patient was started on valganciclovir, the ulceration did not resolve with treatment and slightly enlarged. Treatment modalities included dapsone, prednisone, weekly wound care, wound vacuum, and eventually a skin graft of the ulcer site. This case highlights the presence of CMV infection in a cutaneous ulceration in a relatively immunocompetent patient, and the lack of response to treatment raises the question whether CMV was causative, partially contributory, or simply an innocent bystander.