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Serum varicella-zoster (VZ) antibody titers were determined by a simple, indirect immunofluorescent antibody technique in 50 children with leukemia or non-Hodgkin's lymphoma. Sixteen children had initial antibody titers that were not detectable at a serum dilution of 1:8 and were considered to be susceptible to varicella. Thirty-one patients had initial serum VZ antibody titers of 1:16 or greater, while three had levels of 1:8. The serum antibody titer was 1:8 or greater in 16 children with a history of varicella. Seven episodes of localized herpes zoster were observed in children whose VZ titer was 1:8 or greater prior to onset. Two nonfatal infections with primary varicella developed in children with leukemia in remission whose initial titers were less than 1:8 and were associated with a convalescent rise in VZ antibody to levels greater than 1:16. Three susceptible children received zoster immune plasma or zoster immune globulin for varicella exposure, causing a transient rise in serum VZ titer. The assessment of serum VZ titer by this immunofluorescent antibody technique combined with the prior varicella history is useful in defining the population of children with leukemia and non-Hodgkin's lymphoma who are susceptible to primary varicella.

The clinical and histopathological findings in 26 children with non-Hodgkin's lymphoma without initial marrow involvement are reviewed. A marked male predominance similar to that observed in previous series was noted. Biopsy material was classified according to the recommendations of Rappaport in 22 cases. All have diffuse lymphomas, and 16 of 22 patients had involvement of the mediastinum as part of their initial presentation. Of these 12, 5 developed lymphomatous involvement of the central nervous system prior to the development of leukemic transformation of the bone marrow. This observation suggests that prophylactic therapy against CNS relapse be considered for children with mediastinal non-Hodgkin's lymphoma, even in the absence of initial marrow involvement.

Two children who presented initially with a lymphoid malignancy were noted to develop recurrences with myeloid features late in the course of their disease. In both cases, evidence of lymphoid differentiation was present in the myelogenous cells that were Ph1 chromosome negative. The first patient had acute myelogenous leukemia and developed a recurrence with morphologic features of acute myelogenous leukemia. Terminal transferase was present in the myelogenous blasts. The second patient initially had a diffuse lymphoblastic non-Hodgkin lymphoma. During the course of her illness she developed a myeloproliferative disorder characterized by basophilic meningitis, splenomegaly, and hypereosinophilia. Lymphocyte T-cell (E-rosette) markers were present on the eosinophils. These observations lend further support to the hypothesis of varying lymphoid and myeloid differentiation in certain cases of leukemia.