[Bone marrow transplantation in a pediatric case of acute nonlymphocytic leukemia with hepatitis C].

An allogenic bone marrow transplantation (BMT) in an acute nonlymphocytic leukemia (ANLL) patient with post-transfusion hepatitis C is presented. A 13-year-old girl was admitted to our hospital on May 1988, and diagnosed as having ANLL M2 according to the FAB classification. During the induction and post-induction chemotherapy, 116 units of blood products were transfused to her as the supportive therapy until October 1988, when non-A non-B hepatitis developed. As the persistent liver dysfunction interfered with anti-leukemic chemotherapy on the protocol, allogeneic BMT from her HLA identical MLR nonreactive brother was done on July 1989. Preconditioning regimen consisted of busulfan and cyclophosphamide. GVHD prophylaxis consisted of cyclosporine A and short term methotrexate. After the BMT, her liver dysfunction once improved; her serum amino-transferase levels were normal for about 3 months. Soon after discontinuation of cyclosporine A, however, her liver function deteriorated again. The examination of hepatitis C virus antibody in her sera, which had been harvested sequentially and stored at -40 degrees C, on November 1989 revealed that she had been already seropositive at the time of BMT. The BMT-induced immunologic changes may have influenced the natural course of hepatitis C virus infection in the patient.

Morphometrical evaluation of acute leukemic cells by electron microscopy. Discrepancy between morphological characteristics in FAB classification and electron microscopic morphometry.

Leukemic cells from 39 patients with acute leukemia (20 lymphocytic and 19 myelogenous) were examined by transmission electron microscopy and the nucleus and cytoplasm were measured on the micrographs with a computer-controlled image analyzer. The ratios between the areas of the nucleus and whole cell profile (nucleus/cell ratio), heterochromatin and euchromatin, the nucleolus and nucleus, and the degree of irregularity of the nucleus were compared between the two major types of leukemia studied. Acute lymphocytic leukemia (ALL) cells had a relatively larger nucleus and relatively less cytoplasm than acute myelogenous leukemia (AML) cells, and a greater proportion of the area of the nucleus was occupied by heterochromatin in ALL cells than in AML cells. According to the FAB classification, L1 cells are characterized by narrow, and L2 cells by wide cytoplasm based on light microscopic observation of smeared cells, and we confirmed these features by morphometry of May-Giemsa-stained blood smears. However, by electron microscopy there was no difference in the nucleus/cell ratio between L1 and L2 cells, this constituting a discrepancy between the results obtained by electron and light microscopic morphometry. In addition there was no difference in the degree of nuclear irregularity between L1 and L2 cells. Among AML subtypes, significant differences were observed only in the nucleus/cell ratio between M3 and M1, M2 or M4 cells, and in the heterochromatin/euchromatin ratio between M5 and M1, M2 or M3 cells. In conclusion, electron microscopic morphometry revealed marked differences between ALL and AML, but the differences among their subtypes defined by the FAB classification based on nonmorphometric light microscopy were less evident by electron microscopic morphometry.

Giant mitochondria in acute lymphocytic leukemia.

Giant mitochondria were observed in 2 cases among 28 cases of ALL by electron microscopy. The cristae of the giant mitochondria in the leukemic cells were irregularly arranged, decreased in number, and formed concentric circles. Several morphological abnormalities were also observed in the normal mitochondria. Morphometric analysis of the mitochondria in the 2 patients disclosed that the sizes of mitochondria were well distributed from small to large and thus, the mitochondria could not be divided into different populations. Also, there were no clear differences in the distribution of shape between normal and giant mitochondria. These results suggest that the giant mitochondria were derived from normal mitochondria. Since they were observed before the initial treatment, they did not developed as a result of drug action.