Basal cell carcinomas (BCC) are known to co-exist with other cutaneous lesions, but the collision of BCC with malignant melanoma is rare. We report on the case of an 82-year-old woman with a translucent papule set on a beige-brown plaque on the right side of the nose. Histologic examination showed lesions of lentigo maligna melanoma (LMM) in situ and invasive melanoma involving nests of BCC that invaded the dermis. Immunohistochemical studies with S100 protein, HMB-45, and Melan-A antibodies showed the melanocytic component in the epidermis and dense clusters of ''atypical'' melanocytes in the dermal nests of BCC. On examination of the biopsy specimen, melanoma was still in situ because it was limited to the nests of BCC and not detectable between dermal collagen bundles. However, the re-excision of the lesion showed residual BCC and invasive LMM, level II, measuring 0.2 mm in thickness. The diagnosis, pathogenesis, and prognosis of this collision tumor are discussed.B asal cell carcinoma (BCC) is the most frequent primary skin carcinoma. Its association with another tumor at the same site has been reported, but collision with melanoma is rare. A case associating BCC and lentigo maligna melanoma (LMM) is herein described. The difficulties of the diagnosis of such tumor, its pathogenesis and its prognosis will be discussed. CASE REPORTAn 82-year-old woman consulted for a translucent papule set on a beige-brown plaque on the right side of the nose ( Fig. 1). At first, the clinical diagnosis was BCC. The translucent papule was biopsied.The formalin-fixed tissue was embedded in paraffin and sliced in 5 m-thick sections. In addition to our routine trichromic hematoxylin-eosin-saffron stain, an immunohistochemical study was performed using antibodies against cytokeratins AE 1/3, S-100 protein, HMB-45, and Melan-A. We used the avidin-biotin-peroxidase complex for staining, after heat-induced epitope retrieval.Histologic examination revealed an atrophic epidermis and an infiltrating trabecular tumor (Fig. 2). It showed an atypical melanocytic proliferation within the epidermal basal cell layer. More melanocytes were present, and were focally contiguous. They were evident in hair follicles as well (Fig. 3). The melanocytes showed pale cytoplasm, and hyperchromatic irregular nuclei. The underlying dermis was infiltrated by a proliferation of basophilic cells forming nests, cords, and solid nodules. Deposits of melanin pigment were scattered throughout the tumor. The stroma was fibrous and retraction clefts were present at the periphery of the tumoral nests (Fig. 4). The histologic features of the dermal component were typical of a BCC.The CK AE1/3 antibody showed positive staining in most basaloid cells in the dermis (Fig. 5). Staining with S-100 protein, HMB-45, and Melan-A not only highlighted the intra-epidermal atypical melanocyte proliferation, but also positively marked a number of cells in the dermal epithelial nests (Fig. 6). Within the epithelial component, the Melan-A positive cells were densely clustered and not...

Introduction Stevens-Johnson syndrome and toxic epidermal necrolysis are severe cutaneous drug eruptions characterized by epidermal detachment. Pembrolizumab is a monoclonal antibody that binds to the programmed death-1 receptor, and it has been associated with numerous cutaneous adverse side-effects, including Stevens-Johnson syndrome. Case report We describe a 63-year-old male with metastatic lung adenocarcinoma who developed a rapidly progressing maculopapular rash three days after a first dose of pembrolizumab. On day 16, the rash affected more than 80% of body surface area with detachment of large sheets of necrolytic epidermis in 30–40% of body surface area. However, the patient only presented with mild mucosal involvement. Histopathologic examination of a skin biopsy showed a subepidermal blister with overlying prominent full thickness epidermal keratinocytic necrosis and a superficial perivascular infiltrate of lymphocytes. A toxic epidermal necrolysis secondary to pembrolizumab was then diagnosed. Management and outcome: In addition to supportive cares, the patient received corticosteroids and cyclosporine. The patient responded rapidly to the immunosuppressant therapy, and nearly complete re-epithelialization was achieved 24 days after the start of the reaction. Discussion In our review of the literature, 15 other cases of Stevens-Johnson syndrome/toxic epidermal necrolysis were reported with programmed death-1/programmed cell death ligand-1 inhibitors. To our knowledge, this is the first case of toxic epidermal necrolysis secondary to pembrolizumab published in the literature. The American Society of Clinical Oncology guidelines suggest that cyclosporine, in addition to corticosteroids, be initiated when toxic epidermal necrolysis is suspected. Clinicians should be aware of this rare dermatological emergency with the increasing use of pembrolizumab in oncology.

We present a case of a 64-year-old man who presented with a rapidly growing tumor in the left buttock and intergluteal cleft area, which was affected by hidradenitis suppurativa. The patient was on tumor necrosis factor-alpha inhibitors for hidradenitis suppurativa for 2 years prior to the development of the mass. Initial biopsy of the mass showed a well-differentiated squamous cell carcinoma with spindle cells and positive epithelial immunomarkers. Subsequent excisional biopsy of the tumor showed an infiltrating poorly differentiated squamous cell carcinoma composed of islands of atypical sarcomatoid spindle cells. Squamous cell carcinoma arising in hidradenitis suppurativa is a rare complication which may occur secondary to chronic inflammation and epidermal hyperproliferation in hidradenitis suppurativa–affected areas.

This is a 40-year-old woman with sideroblastic anemia with B cell immunodeficiency, periodic fevers, and developmental delay syndrome, who has genital and extragenital lichen sclerosus on the abdomen and the upper back that have become erythematous and painful during febrile episodes. This report summarizes the published cases of sideroblastic anemia with B cell immunodeficiency, periodic fevers, and developmental delay and highlights associated mucocutaneous features.