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Granuloma annulare (GA) is a common, benign, often self-limiting granulomatous disease. The condition classically presents clinically with asymptomatic, flesh-colored to erythematous, nonscaling papules, often arranged in a ring or annular pattern. Histologically, GA is characterized by a perivascular lymphocytic infiltrate, the accumulation of macrophages in the dermis, and palisading of the macrophages around degenerated areas with altered collagen. A delayed-type cell-mediated hypersensitivity reaction is the favored hypothesis; however, the etiology and pathogenesis of GA is not fully understood. It has been associated with various systemic diseases, including diabetes mellitus and dyslipidemia, and has also been reported to develop after exposure to assorted triggers, often cutaneous trauma.1 Although uncommon, familial occurrences of GA have also been reported. Friedman and Winkelmann2 last reviewed familial GA in 1987, describing 11 families and 21 cases of GA with at least 2 immediate family members affected. These authors also suggested that the incidence of specific human leukocyte antigens (HLAs) (eg, HLA-B35) within some of these family members might indicate that genetically predisposed individuals could develop a cell-mediated immune reaction in response to an unknown antigen. In this report, we describe the cases of 2 patients, a father and his daughter, who presented with clinical and histologically confirmed GA. We also review all familial occurrences of GA since 1987.

Erythema multiforme (EM) is an immune-mediated reaction first described by von Hebra1 in 1860, presenting typically as acrofacial target lesions. The rash may be confined to the skin (EM minor), or it may involve ocular, oral, or genital mucosa with systemic symptoms (EM major). In most cases, only 1 outbreak of EM occurs in a lifetime; however, very rarely, repeated episodes of EM may occur, known as recurrent EM.2 Few cases of pediatric recurrent EM have been reported, with the etiology being identified in less than half of these cases.3 We report a pediatric case of recurrent EM resistant to conventional treatments in which a peculiar human leukocyte antigen (HLA) haplotype has been identified.

Trichophyton erinacei is a member of the Trichophyton mentagrophytes complex, a zoonotic dermatophyte that is very rarely isolated as a human pathogen. It often causes a localized itchy rash at the size of contact, such as the extremities, and is typically reported in the context of hedgehog exposure.1, 2, 3, 4, 5, 6, 7, 8 Epidemiologically, T erinacei was first recognized in New Zealand then in Europe, Africa, and Australia. Case reports existed in East Asia since the early 2000s in Japan,7 Korea,1 and Taiwan.5 We report the first case, to our knowledge, of T erinacei arising in Southeast Asia in the context of hedgehog exposure.

Approximately 25,000 allogeneic hematopoietic stem cell transplants (HSCTs) are performed annually. Cutaneous complications are common and include a spectrum of acute and chronic graft-versus-host disease (GVHD). Mechanisms implicated in the rare development of sarcoidosis after HSCT include specific pretransplant conditioning regimens, possible donor-to-recipient transmission, genetic predisposition of sarcoidosis, and post-HSCT immune dysregulation.

Atypical hydroa vacciniforme (HV) is a rare vesiculopapular eruption reported mainly in patients from Asia and Latin America1, 2, 3 and presents with similar but more severe cutaneous manifestations than classic HV. In addition, systemic findings may be present.1 Distinguishing between classic and atypical HV is essential, as the latter carries a worse prognosis and may progress to HV-like lymphoma.1, 2 Involvement of muscle resulting in a picture similar to dermatomyositis (DM) is a rarely reported presentation of atypical HV.4, 5 Herein, we present the first case, to our knowledge, of a 9-year-old Lebanese girl with atypical HV presenting with a picture of DM.