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An 87-year-old woman was admitted to our hospital (day 0) because of acute disorientation caused by multiple acute intracerebral hemorrhages. T2*-weighted magnetic resonance imaging (MRI) at admission revealed multiple subcortical old microbleeds indicative of cerebral amyloid angiopathy. Microbleeds in the right cerebellar hemisphere and acute spotty ischemia in the left cerebellum were also identified. The patient had been afebrile, and blood examinations on day 7 were within normal limits of inflammatory findings without antibiotics. On day 11, she developed a high fever and blood culture was performed. Her fever resolved within 2 days of antibiotic administration, although subsequent findings revealed her blood culture was positive for Staphylococcus aureus . Echocardiogram revealed bacterial vegetation in the mitral valve and moderate mitral regurgitation, with a diagnosis of infectious endocarditis (IE). Follow-up MRI demonstrated multiple spotty acute infarctions and an increased number of microbleeds. The patient may have been infected via peripheral infusions administered during the first few days after admission. However, considering the coexistence of acute hemorrhagic and ischemic lesions on MRI, as well as the acute lesions in the cerebellum, it is possible that IE was already latent on admission, and that the multiple brain hemorrhages might have been caused by IE rather than by cerebral amyloid angiopathy., (© 2024 Published by Elsevier Inc. on behalf of University of Washington.)

Two multiple myeloma (MM) patients developed venous thromboembolism (VTE) while being treated with lenalidomide and low-dose dexamethasone. Aspirin is recommended for VTE prophylaxis when using lenalidomide/dexamethasone for MM patients with a standard risk of VTE. Despite aspirin administration, however, these two patients experienced VTE. Following VTE development, warfarin and then a Factor Xa inhibitor, edoxaban, were administered. The edoxaban treatment, especially, resulted in favorable and effective control of VTE. Considering these observations, Factor Xa inhibitors may in future become a preferred option for prevention and treatment of VTE when managing MM patients.

Three patients with chronic myeloid leukemia (CML) in blastic transformation were treated with G-CSF plus middle dose cytosine arabinoside (Ara-C). G-CSF was administered (150 mg, s.c. or 300 mg, d.i.v./day) 24 hr prior to Ara-C (2-3 g/body, 6 hour d.i.v. for 2-5 days) and continued until the peripheral neutrophil count rose above 1,000/microlitre. As a supplement, VP-16 (80 mg/m2, for 2 days) was administered as warranted to control the growth of blastic cells. All 3 patients survived for more than 12 months with a favorable performance status. Normal karyotypes were detected in 2 of the patients after chemotherapy. One of those patients in paticular demonstrated normal bone marrow findings with the almost complete disappearance of the Ph-positive clone. In vitro cultures of peroxidase-negative CML blastic cells revealed that G-CSF stimulated the induction of blastic cells into the cell cycle and that blastic cell apoptosis was more pronounced in cells cultured with G-CSF plus Ara-C than with G-CSF or Ara-C alone. G-CSF plus middle dose Ara-C therapy appears to be a strong candidate for the treatment of CML in blastic transformation with a poor prognosis.

A 44 year-old man was admitted to our hospital in October, 1992 with epistaxis. Fifteen months before admission, thrombocytopenia had been pointed out, but he had no bleeding episode. At admission, neither hepatosplenomegaly nor lymph node swelling was observed. Hematological findings were as follows; WBC 10,000/microliter, Hb 14.0 g/dl, PLT 5,000/microliter, including giant platelets. Platelet associated IgG (PAIgG) was 471 ng/10(7) cells. Bone marrow aspiration revealed normocellularity with moderate increase in the number of mature megakaryocytes, but no dysplastic changes were seen. Biochemical and radiological examinations disclosed neither malignant diseases nor autoimmune diseases. Based on the diagnosis of idiopathic thrombocytopenic purpura, danazol therapy (300 mg/day) was started in November, 1992. After initiation of treatment, the platelet count changed cyclically every 4 weeks. To elecuidate the mechanism of this phenomenon, we periodically evaluated the patient's immunological background. T lymphocyte counts and subset proportions remained almost the same through out the course, whereas NK cell counts and NK activity coincided with the change of the platelet count. These results suggest that in this case NK cells may play a role in the cyclic fluctuation of platelet count by regulating the immune system.

A skin ulcer of the lateral malleous developed in a 61-year-old man receiving hydroxyurea for essential thrombocythemia. In the past, skin ulcers have been reported in patients with chronic myeloproliferative diseases, including essential thrombocythemia, who had been treated with hydroxyurea. In the current case, vasculitis or thrombi in vessels of the biopsied specimen of the lower leg were not observed, and the patient required skin-graft operation. Accordingly, we concluded that the skin ulcer might be due to the administration of hydroxyurea. Thus, the dose of hydroxyurea was decreased.

A 22-year-old female was admitted on June 19, 1993 with pancytopenia. Aplastic anemia was diagnosed and she was treated with anti-thymocyte globulin. After one month, she started to feel abdominal pain. Her platelet count was 1.3 x 10(4)/microliters at that time. Computed tomography revealed vast accumulation of blood in the abdomen and pelvis. A total of 1,000 ml blood was obtained from the right ovarium and she underwent right partial oophorectomy. Although ovarian bleeding is rarely reported in aplastic anemia, we should always keep in mind this possibility when abdominal pain occurs in a female patient.

A 54-year-old man was admitted with fatigue. The peripheral blood count showed leukocytosis (9, 600/microliters), including 76% granular lymphocytes (GLs), which expressed CD2, 3, 8, 16 and HLA-DR, and anemia (hemoglobin 8.1 g/dl). He was diagnosed as having T cell type-granular lymphocyte proliferative disorder with anemia. Bone marrow examination revealed the involvement of 4.6% of GL and erythroblastopenia. A clonogenic assay of bone marrow cells revealed the decrease in erythroid colony formation in both CFU-E and BFU-E, but the number of erythroid colonies increased when CD8-positive cells were depleted from bone marrow cells and the number of erythroid colonies decreased again when CD8-positive GLs were added. The supernatant of cultured CD8-positive GLs had no inhibitory effect on CFU-E and BFU-E colony formation. These suggested that CD8-positive GLs suppressed the erythroid colony formation in this case. Treatment with 6,000 U/body of recombinant human erythropoietin (rh-Epo) subcutaneously three times a week was started and increased dose of 12,000 U/body of rh-Epo led to an increase in the hemoglobin level to 10.5 g/dl two months later. He has been treated with rh-Epo only.

We statistically analyzed the hematologic findings of patients with refractory anemia (RA) to identify parameters associated with a poor prognosis. We first separated the RA patients into two groups: one group with disease progression and one without. The patients with disease progression were predominantly male and had a significantly higher percentage of bone marrow (BM) blasts at the time of diagnosis (3.06 +/- 1.29% vs. 1.44 +/- 1.38%, P < 0.005). This finding was confirmed when the patients were separated into the two groups; those who survived and those who expired (BM blasts: 2.68 +/- 1.59% vs. 1.37 +/- 1.27%, P < 0.005). The survival probabilities were calculated depending on whether or not the RA patients had > or = 3% BM blasts. The RA patients with > or = 3% BM blasts had a significantly worse prognosis (P < 0.01) than the patients with < 3% BM blasts. Notably, the RA patients with > or = 3% BM blasts did not show any significant differences in the incidence of disease progression, mortality rate, or survival probability, when compared with the patients with RA with an excess of blasts (RAEB). The present findings indicate that RA patients are heterogeneous with regard to prognosis, and the RA patients with > or = 3% BM blasts might have a poorer prognosis than those with fewer BM blasts. Thus we propose a general approach in predicting the prognosis of RA patients: those with complex chromosomal changes will expire shortly. Secondly, when the patients do not have any complex changes, the prognosis might be linked to the percentage of BM-blasts at the MDS diagnosis.

A 69-year-old woman was examined due to abnormal pulmonary shadows on her chest roentgenogram. Although small lymphocyte proliferation was revealed in specimens by transbronchial lung biopsy (TBLB), immunoglobulin light chain restriction could not be seen. We attempted to verify the B-cell clonality by broncho-alveolar lavage (BAL) and a new sensitive method called kappa-lambda imaging (KLI), which was available for the detection of monoclonal B cells. Therefore, B-cell monoclonality was found. Thus, the patient was diagnosed as having primary pulmonary lymphoma (PPL). PPL may be differentiated from benign lymphoproliferative disorders such as pseudolymphoma and lymphocytic interstitial pneumonia by KLI of BAL-derived lymphocytes.

A 56-year-old male was admitted to our hospital with lymphocytosis (16.4 x 10(9)/l; 79% lymphocytes including 50% small lymphocytes), generalized lymphadenopathy, massive splenomegaly, and heavily infiltrated bone marrow. Immunophenotype analysis of the neoplastic cells in the bone marrow revealed that they were B cells (CD20 + CD19 + Ia1 + sIgM+) positive for CD10. By contrast, the cells in the lymph node were CD20 + CD19 + Ia1 + sIgM+ but negative for CD10. The patient was tentatively diagnosed as having lymphosarcoma cell lymphoma, however, the final diagnosis was leukemic phase of intermediate lymphocytic lymphoma. We concluded that CD10+ neoplastic cells in the bone marrow and peripheral blood had differentiated to CD10- cells.

23 patients with myelodysplastic syndromes (MDS) and 8 normal controls were analyzed for dysmegakaryopoiesis (DMP) in the bone marrow by alkaline phosphatase anti-alkaline phosphatase (APAAP) technique and by conventional May-Giemsa staining. In the immunocytochemical study, monoclonal antibody (MoAb) against glycoprotein (GP) IIb/IIIa was utilized to demonstrate megakaryocytic cells. 91% (21/23) of MDS cases were detected as having DMP by APAAP method, while only 52% (12/23) were detectable by Giemsa stain. There were difficulties in recognizing small micromegakaryocytes (micro MKs), designated as type 1 atypical MKs, by Giemsa staining. Furthermore, megakaryoblasts (MKBs) were detectable only by APAAP technique. In 8 normal controls, no type 1 and type 3 atypical MKs (round shaped multinuclear MKs) were observed either by Giemsa staining or by the APAAP method, suggesting that they are a distinctive feature of MDS. These results indicate the necessity of immunocytochemical technique for accurate recognition of DMP in MDS.

A 74-year-old Japanese male with a 4-year history of refractory anemia with excess of blasts is reported here. Chromosome study revealed the bone marrow cells of this patient to contain a t(3;4)(q26;q21). Ultrastructural analysis of platelet peroxidase and immunocytochemical study using monoclonal antibody for platelet antigen revealed a large number of blasts in the bone marrow to be megakaryoblasts. Thus, this case was thought to be one of a myelodysplastic syndrome with excess of blasts including megakaryoblastic proliferation showing chromosome changes at 3q26 and 4q21. The relationship of the anomaly on the long arm of a chromosome #3, especially at band 3q26, to abnormal megakaryoblastic proliferation is discussed.

A 75-year-old man with gastric cancer metastatic to the liver was treated by combined administration of Tegafur (800 mg/body/day), 5-fluorouracil (300 mg/body/day) and Mitomycin C (hepatic arterial infusion of 20 mg/body and intravenous infusion of 8 mg/body). The total dose of Tegafur was 5.6 g, that of 5-FU was 11.4 g, and that of MMC was 36 mg for one month and a half. After therapy, primary and metastatic sites was completely disappeared. The patient has survived for 6 years 8 months in a state of complete response.