| Research Abstract |
Histiocytic necrotizing lymphadenitis (HNL) was first reported in 1972 as a lymphadenitis with focal proliferation of retucular cells accompanying numerous nuclear debris by us. We gathered over 300 cases. The patients with HNL has characteristic clinical findings of an occurrence of adolescence in preference to female, localized lymphadenopathy on the neck, frequent leukopenia with a few atypical lymphocytes in peripheral blood and fever, occasional skin rashes, and natural healing within several months with rare recurrence. HNL represents distinctive histological features, such as focal, well circumscribed lesions with aggregation of large lymphocytes, immunoblasts, plasmacytoid monocytes, histiobytes with or without phagocytosis, and karyorrectic nuclear debris, mainly in the paracortex and/or cortex, an absence of significant numbers of neutrophils, eosinophils, and plasma cells, occasional prominent indiridual cell necrosis, eosinophilic fibrin deposits, foamy cells and necrotic foci. The cells in the affected areas consisted mainly of CD8+, CD15- cytotoxic T cells with proliferating activity and non-proliferating CD4, Ki-Mlp positive plasmacytoid monocytes and lysozyme and KP1 positive histiocytes. The same lesions were found in the skin and bone marrow also in some cases. The findings indicate HNL is not lymph node lesion, but generalized disease. A high incidence of tubuloreticular structures in lymphocytes, histiocytes, and vascular endothelial cells and increased production of interferon in the affected areas, the patterns of elevated serum levels of 2'5' oligoadenylate acetate synthetase in the early stage of disease suggested a viral nature of the lesion. We detected HHV-6 antigens with strong membranous reactions of clustering large lymphoid cells, but no difference of HHV-6 genomes in amounts between HNL and contral groups. The results postulate some role of HHV-6 in developing the lesion.
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