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In lymph nodes, classical Hodgkin lymphoma can typically be distinguished from non-Hodgkin lymphoma (NHL) by the presence of Hodgkin and Reed-Sternberg cells that co-express CD30 and CD15. However, anaplastic large cell lymphoma (ALCL) and diffuse large B-cell lymphoma (DLBCL) can show identical features, and some cases of classical Hodgkin lymphoma lack CD15 expression, rendering them difficult to differentiate from CD30-positive NHL. The differential diagnosis of cutaneous Hodgkin lymphoma similarly includes ALCL and DLBCL, and, additionally, tumors of mycosis fungoides. Recent studies have shown that classical Hodgkin lymphoma is of B-cell origin in virtually all cases, and shows at least focal weak expression of the B-cell marker PAX5 and often focal weak expression and no expression of the B-cell markers Oct-2 and BOB.1, respectively. All three of these markers are almost invariably absent in T-cell lymphomas and are strongly expressed in B-cell lymphomas. We report a 40-year-old man with classical Hodgkin lymphoma who developed cutaneous nodules. A biopsy from one revealed Hodgkin/Reed-Sternberg cells with a similar immunophenotype to the diagnostic lymph node biopsy, namely CD30+/CD15+, diffusely but weakly PAX5+, focally weakly Oct-2+ and lacking BOB.1 expression, thereby confirming a diagnosis of cutaneous Hodgkin lymphoma. To our knowledge, this is the first report of the expression pattern of the combination of PAX5, Oct-2 and BOB.1 in the context of cutaneous involvement by Hodgkin lymphoma.

Leukemia cutis represents the cutaneous infiltration of neoplastic leukocytes or their precursors that results in clinically identifiable skin lesions. For patients with myelodysplastic syndrome, developing such a lesion may indicate impending leukemic transition. These patients are also often immunocompromised, putting them at risk for infection by opportunistic fungal pathogens such as Fusarium. We describe an 85-year-old man with myelodysplastic syndrome who presented with a reddish-purple nodule with a surrounding erythematous plaque on his shin. Histopathologic examination revealed a dense diffuse infiltrate of large atypical cells in the reticular dermis, with ulceration and necrosis. Immunohistochemical studies showed positive staining with CD15, CD68 and myeloperoxidase of constituent large cells. Concurrently, there were branching and septate hyphae with occasional macroconidia-like structures throughout the infiltrate. Cultures from this lesion grew Fusarium and Enterococcus, supporting the diagnosis: leukemia cutis with superinfection involving both Fusarium and Enterococcus. To our knowledge, this is a novel report of two separate infections occurring in a lesion of leukemia cutis. This case shows that in patients with a hematologic malignancy and skin lesions, a high index of suspicion for infection is necessary when reviewing both the clinical and histopathological data to avoid overlooking an important occult infectious agent.