No abstract

Immune checkpoint inhibitors are increasingly being used in the treatment of various solid organ and hematologic malignancies. Dermatologic toxicities associated with programmed cell death protein-1 (PD-1) and programmed death ligand-1 (PD-L1) therapy have been widely reported in the literature. It is important for clinicians to be aware of these toxicities to ensure prompt recognition and treatment. Herein, we present the clinical, histopathologic, and immunofluorescence findings of 3 patients diagnosed with lichen planus pemphigoides (LPP) after treatment with anti-PD-1 inhibitors. We also reviewed the literature and summarize 7 previously reported cases of LPP associated with anti-PD-1 and anti-PD-L1 inhibitors. LPP was diagnosed at a median time of 24.4 weeks (range: 4-78 weeks) after initiation of immunotherapy. Clinical findings included papules, plaques, erosions, vesicles, and bullae on the trunk and extremities. Oral involvement was present in half the cases. Histopathologic features of immunotherapy-induced LPP included lichenoid or vacuolar interface dermatitis, the presence of eosinophils, and subepidermal bullae. Direct immunofluorescence demonstrated linear deposition of immunoglobulin G (IgG) or C3. Indirect immunofluorescence demonstrated linear IgG along basement membrane zone on monkey esophagus in 2 cases and linear IgG on the epidermal side of salt split skin in 3 cases. Serum anti-BP180 was elevated in all cases in which enzyme-linked immunosorbent assay was performed.

The term follicular keratosis of the chin was first coined in 1992 by Kanzaki et al. 1 who described keratotic papules on the chin, ascribed to chronic habitual trauma, in two unrelated Japanese boys. Follicular keratosis (FK) is a poorly understood disorder of often unclear pathogenesis, presenting as multiple hyperkeratotic follicular papules coalescing into plaques, typically on the chin or jawline. [1][2][3] In two separate case reports, histopathology has been described as cystic hair follicles containing keratotic material without a surrounding inflammatory cell infiltrate. 1,3 It has been proposed that FK occurs as a result of prolonged pressure or friction on the skin, as from patients resting their palm while reading, playing video games, or watching television. 1,3 However, in some cases, FK occurs without

Squamoid eccrine ductal carcinoma (SEDC) is a poorly documented but likely underrecognized sweat gland malignancy with significant risk for local recurrence and potential for metastasis and rare disease-related mortality. Histopathologically, the tumor demonstrates a biphasic differentiation pattern: superficially, the tumor has squamous differentiation [indistinguishable from welldifferentiated cutaneous squamous cell carcinoma (cSCC)], while the deeper aspect has a more infiltrative pattern with prominent ductal differentiation. Diagnosis of SEDC relies upon histopathologic examination alone. Its pathogenesis is poorly understood, and its genomic features have yet to be described. In this article, we characterize the genomic features in a case of SEDC through wholeexome sequencing, then compare its features with cSCC and other eccrine ductal carcinomas. Whole-exome sequencing revealed 30 mutations/Mb with 21 pathogenic or likely pathogenic mutations in total, identified across 14 different genes. The genomic abnormalities identified in this case of SEDC overlap considerably with those found in cSCC but not those of other sweat gland malignancies. The clinical and histopathologic features of SEDC previously reported and the genetic features determined from this case suggest that this tumor may arise initially as a well-differentiated cSCC that subsequently undergoes divergent differentiation focally to resemble a sweat gland malignancy. Genetic analyses of additional cases are warranted to clarify this consideration.