The Euphorbiaceae family (commonly known as "spurge") is a large, diverse, and widely distributed family of plants that encompass around 300 genera and more than 8000 species. Their attractiveness and hearty nature have made them popular for both indoor ornamentation and outdoor landscaping. Despite their ubiquity, the potential to cause irritant contact dermatitis (ICD) is often overlooked in favor of more notorious causes of phytodermatitis, namely, Toxicodendron species and nettles. We examined case reports spanning 40 years and discovered that spurge-induced ICD tends to befall children and middle-aged adults who unwittingly encounter the plant through play or horticulture, respectively. Clinical presentation is pleomorphic. Erythema, edema, burning, vesicles, and pruritus of acute onset and rapid resolution are frequently observed. We present a classic case of ICD in a 12-year-old girl after exposure to Euphorbia myrsinites and review the literature on phytodermatitis caused by members of the Euphorbiaceae family.

Frontal fibrosing alopecia (FFA) is a primary lymphocytic cicatricial alopecia that is currently regarded as a variant of lichen planopilaris. FFA has historically been considered rare in black patients, in whom traction alopecia, central centrifugal cicatricial alopecia, and androgenetic alopecia are frequently assumed to be more common. We describe a case of FFA in a black woman that both clinically resembled androgenetic alopecia and lacked many of the physical exam and dermoscopic findings associated with FFA. In doing so, we highlight the need for physicians to have a high index of suspicion for FFA in any black patient who presents with frontotemporal alopecia.

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A young man in his late teens presented with numerous atrophic papules and plaques on his trunk and extremities that developed gradually over several years. Although most were asymptomatic, the patient was concerned about the ongoing appearance of new lesions and the associated pain that some lesions were causing. His medical history was significant for adenosine deaminase-deficient severe combined immunodeficiency (ADA-SCID), which had been managed since childhood with twice weekly intramuscular injections of pegademase bovine enzyme replacement, thrice weekly trimethoprim-sulfamethoxazole for Pneumocystis prophylaxis, and monthly infusions of intravenous immunoglobulin. Physical examination revealed 9smooth-surfaced,skin-coloredtohyperpigmented,0.5-to1.5-cmatrophicpapulesandplaques that exhibited the buttonhole sign on palpation (Figure , A). The multicentric lesions were located on the left knee, left thigh, bilateral chest, and back. Punch biopsies of lesions on his trunk andextremitiesweresentforhistopathologicalexaminationwithhematoxylin-eosin(H&E)staining (Figure , B and C), immunohistochemical (IHC) studies, and molecular evaluation with reverse transcription polymerase chain reaction.

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