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K Muroi

Publications and source records attributed to K Muroi.

At least 73 records · Page 4Linked to original sources
PubMed1993

[Refractory bilateral pneumothoraces complicated with interstitial pneumonitis after bone marrow transplantation].

We report here a case of 33 year-old-man with refractory bilateral pneumothoraces during the treatment for interstitial pneumonitis 6 months after bone marrow transplantation (BMT). He was diagnosed as having acute myelogenous leukemia (AML) M1. He was treated with chemotherapy, and cerebral irradiation. BMT was performed in August 1989 from a sibling donor whose human leukocyte antigen was matched, ABO blood type mismatched. Preconditioning regimen was cyclophosphamide and total body irradiation (TBI). BMT was successful without major graft versus host disease. Thereafter he complained of respiratory symptom and was admitted on June 14 1990. Computed tomogram (CT) scan showed interstitial and alveolar shadows. We started the treatment against bacterial infection, Pneumocystis carinii, cytomegalovirus (CMV) and against interstitial pneumonitis with bolus dose of steroid. The transbronchial lung biopsy specimen revealed interstitial pneumonitis without typical CMV nor pneumocystis carinii pneumonia. Although a CT scan showed improvement of pneumonitis, bilateral pneumothoraces occurred. The adhesion therapy became successful after the reduction of steroid dosage. A pneumothorax rarely occurs after BMT. In this case it is speculated that TBI might be responsible for interstitial pneumonitis, and the steroid might have inhibited the adhesion therapy of pneumothorax.

Adult↗
PubMed1993

[Severe bleeding in a case of factor VIII inhibitor associated with intravascular lymphomatosis].

A 70-year-old man was admitted to Jichi Medical School Hospital on October 1, 1990, complaining of spontaneous severe hemorrhage in his extremities. He had prolonged APTT value and normal PT value. Factor VIII level was markedly diminished, and a high titer of factor VIII inhibitor was observed. He was diagnosed as having idiopathic factor VIII inhibitor because of no sign of underlying disorders. He received prednisolone and immunosuppressants, subsequently with plasma exchange and bolous factor VIII, resulting in disappearance of the inhibitor. He was admitted again in February 1991, because of the reappearance of factor VIII inhibitor. In June, furthermore, bone marrow smears showed infiltration of atypical B cells, although no evidence of organomegaly and adenopathy was observed. Therefore, he was suspected to have primary bone marrow lymphoma. He received CHOP therapy, but he died of multiorgan failure. Postmortem autopsy demonstrated multifocal intravascular lymphomatosis with marked intravascular involvement of the lung, liver, kidney, adrenal glands, spleen and bone marrow. Lymph nodes were not swollen, showing little evidence of intravascular lymphomatosis.

Aged↗
PubMed1992

Reactivity profiles of leukemic myeloblasts with monoclonal antibodies directed to sialosyl-Le(x) and other lacto-series type 2 chain antigens:absence of reactivity with normal hematopoietic progenitor cells.

We investigated the expression profiles of lacto-series type 2 antigens in hematopoietic cells and their progenitors, in comparison with leukemic leukocytes. Reactivity profiles of various anti-type 2 chain monoclonal antibodies (MoAbs) with leukemic blasts from 12 patients with acute myeloblastic leukemia (AML) and those from two patients with acute unclassified leukemia (AUL) show that anti-sialosyl-Le(x) MoAb SNH3 reacted strongly with greater than 95% of leukemic blast leukocyte populations from all patients (14 of 14). Another anti-sialosyl-Le(x) MoAb, FH6, showed less reactivity than SNH3 (12 of 14 patients), while anti-Le(y) MoAb AH6 showed reactivity with only 8 of 14 patients. On the other hand, none of the anti-type 2 chain MoAbs reacted with CD34+ normal adult bone marrow (BM) mononuclear cells obtained independently from three healthy volunteers. MoAb SNH3, but not FH6 or AH6, showed complement-mediated cytotoxicity to leukemic blasts from these patients, as well as to myelogenous leukemia cell line HL60. Colony-forming unit granulocyte-macrophage (CFU-GM), but not burst-forming unit-erythroid (BFU-E), was incompletely inhibited by treatment of normal BM mononuclear cells with SNH3 and complement. The absence of type 2 chain antigen expression in hematopoietic progenitor cells and in in vitro hematopoietic colonies (CFU-GM and BFU-E) strongly suggests that application of anti-carbohydrate MoAbs, particularly anti-sialosyl-Le(x) could be useful for elimination of leukemic myeloblasts infiltrating in BM, for purging of leukemic blasts in BM, and for facilitation of autologous BM transplantation.

Antibodies, Monoclonal↗
PubMed1992

[Acute undifferentiated leukemia from the viewpoints of diagnosis and therapy].

Myeloperoxidase (MPO)- and Sudan Black B-not more than 3%-positive, esterase staining-negative, lymphoid, megakaryocyte lineage and erythroid surface marker-negative and electron microscopic platelet peroxidase-negative acute leukemia (AL) was diagnosed as acute undifferentiated leukemia (AUL), and myeloid marker (CD13, CD33), electron microscopic MPO (EMMPO), and DNA analysis of immunoglobulin heavy chain and T cell receptor as well as chemotherapy and its reactivity were examined. Of 239 cases of AL, 10 (4.2%) were AUL, and of these 10 cases, 9 were CD13 or CD33-positive AML-MO (MO) cases. Of 9 cases examined for EMMPO, 4 (44%) were positive, and of 3 cases of MO subjected to DNA analysis, 1 and 1 showed rearrangements of immunoglobulin heavy chain and T cell receptor beta chain, respectively. Of 6 cases of MO on myeloid induction therapy, 1 and 1 showed complete remission (CR) and partial remission (PR), respectively, each having lymphoid genotype, and 4 showed no remission (NR), being 3 of them EMMPO-positive. Of 2 cases on lymphoid induction therapy, 1 and 1 showed CR and NR, respectively, the former being EMMPO-positive MO. BHAC-EM therapy with behenoyl cytosine arabinoside, VP-16 and mitoxantrone performed on 2 cases refractory to any one of both these myeloid and lymphoid induction therapies led to CR in all these 2 cases.

Adolescent↗
PubMed1992

[Burkitt's lymphoma with granulocytosis and a high level of C-reactive protein].

A case of Burkitt's lymphoma with granulocytosis including immature cells and a high level of C-reactive protein (CRP) is reported. The activity of interleukin-1 alpha (IL-1 alpha) was detected in the sera, although its activity was not detected in the supernate of the cultured lymphoblasts. The lymphoblasts stimulated production of IL-1 alpha from human umbilical endothelial cells. Therefore, the lymphoblasts infiltrating bone marrow may have stimulated production of IL-1 alpha from bone marrow stroma cells, and IL-1 alpha may have induced granulocytosis and a high level of CRP.

Aged↗
PubMed1991

Second relapse of acute promyelocytic leukemia (ANLL-M3) with t(15;17) and t(1;3)(p36;q21).

We describe herein a patient with acute promyelocytic leukemia (APL)-(ANLL-M3) whose bone marrow cells in the second relapse showed t(1;3)(p36;q21) together with t(15;17) (q22;q11-q12). Although a total of 21 patients with t(1;3) have been reported so far, among which three cases with de novo acute nonlymphocytic leukemia were included, our patient is the first case with APL. The hematologic findings in our case confirmed the previous observations that this anomaly is associated with relatively high platelet count and the multi-myeloid lineage involvement of leukemic cells. Our patient responded well to chemotherapy and achieved first and second remission with 42 months of total survival, contrary to our expectation that patients with this anomaly have a poor prognosis.

Chromosomes, Human, Pair 1↗
PubMed1991

Long-term bone marrow failure accompanied by skin pigmentation.

A rare case of long-term bone marrow failure with skin pigmentation is presented. The patient was a female with a long history of anemia and skin pigmentation since childhood, although she had no malformations nor chromosomal abnormalities. Hematological improvement has been maintained by the administration of prednisolone. This case may differ from other disorders known as congenital aplastic anemia.

Addison Disease↗
PubMed1991

[Multiple myeloma with hemolytic anemia and thrombocytopenia].

We report a 59 year old female patient who was diagnosed as having IgG kappa myeloma with hemolytic anemia and thrombocytopenia simultaneously. Although M-protein was suspected to contribute to the hemolysis, the IgG purified from the patient's serum did not bind to red blood cells. Therefore, massive non-specific binding of M-protein to blood cells might contribute to high levels of red blood cell-associated IgG and platelet-associated IgG in the patient.

Anemia, Hemolytic↗
PubMed1990

In vitro differentiation of leukemic cells to eosinophils in the presence of interleukin-5 in two cases of acute myeloid leukemia with the translocation (8;21)(q22;q22).

We demonstrated the significant eosinophilic growth of leukemic cells in the presence of interleukin-5 (IL-5) in 2 of 15 cases of acute myeloid leukemia. These two cases were M2 (FAB classification) with the translocation (8;21)(q22; q22). Bone marrow examination revealed the rather high percentages (6% and 9%) of atypical eosinophils in the total nucleated bone marrow cells in these two cases. In the remaining 13 cases, eosinophils were less than 2% in the nucleated bone marrow cells. In the methylcellulose culture system, 142 +/- 18 or 54 +/- 2 colonies were formed by 5 x 10(4) mononuclear cells in the presence of IL-5 in these two cases. These colonies mainly comprised mature eosinophils. Eosinophils were confirmed by Biebrich scarlet staining and electron microscopic examination using a specific lectin binding assay. The eosinophilic differentiation and proliferation of leukemic cells were also observed in the liquid culture system. It was shown that eosinophils observed in both systems were derived from leukemic cells using the chromosomal marker of leukemic cells, t(8;21). Leukemic cells also differentiated to neutrophils or both neutrophils and eosinophils in response to granulocyte colony-stimulating factor or interleukin-3, respectively, but did not respond noticeably to granulocyte-macrophage colony-stimulating factor. Although IL-5 acts on normal eosinophil committed precursors as a lineage-specific growth factor, at least some leukemic cells reacted to IL-5 and could proliferate and differentiate along eosinophilic pathway. Our findings suggest that atypical eosinophils observed in the bone marrow were derived from the leukemic clone in two cases of AML.

Cell Differentiation↗
PubMed1989

Medium pH determines the differentiation of human promyelocytic leukemia cells to basophils or eosinophils by culturing in a protein- and serum-free medium.

Cells containing large basophilic granules in the cytoplasm appeared after culturing human promyelocytic leukemia cells (HL-60) in a protein- and serum-free alkaline medium. These granules were stained with toluidine blue and alcian blue. Cells were morphologically and cytochemically similar to basophils. The existence of histamine in the cell lysates was detected in both uninduced and alkaline medium-induced HL-60 cells. After culturing HL-60 cells in a protein- and serum-free acidic medium, cells containing eosin-stained small granules (eosinophils) appeared. The differentiation of HL-60 cells to basophils or eosinophils may therefore depend on medium pH by culturing in a protein- and serum-free medium.

Basophils↗
PubMed1989

Effects of the in vivo administration of recombinant human granulocyte colony-stimulating factor following cytotoxic chemotherapy on granulocytic precursors in patients with malignant lymphoma.

We examined the effects of the in vivo administration of recombinant granulocyte colony-stimulating factor (rhG-CSF) on granulocytic precursors in the bone marrow of 4 patients with malignant lymphoma who received chemotherapy. Patients were treated with rhG-CSF at doses of 100-800 micrograms/m2/day intravenously for 14 days only in the first course of chemotherapy (G-CSF course) followed by the second course of chemotherapy without rhG-CSF which was used as a control course. In the G-CSF course, white blood cell counts (WBCs) demonstrated a biphasic response consisting of a first peak observed within a few days after the initiation of rhG-CSF administration, and a second peak observed on the last day of rhG-CSF injection or the day after. In the second peak, the incidence of granulocyte-macrophage colony-forming units (CFU-GM) in mononucleated bone marrow cells did not change significantly after treatment with rhG-CSF as compared with a control. However, since the number of nucleated cells in the bone marrow increased, the absolute number of CFU-GM in the bone marrow increased. The number of mature and immature granulocytes in the bone marrow increased. These findings suggest that G-CSF stimulates the proliferation and differentiation of granulocytic precursors in the bone marrow in granulocytopenic patients who received cytotoxic drugs and causes mature granulocytes to be released from the bone marrow.

Adult↗
PubMed1989

The effect of immunoadsorption therapy by a protein A column on patients with thrombocytopenia.

Immunoadsorption therapy employing protein A columns (PROSORBA columns) was used for the treatment of patients with naturally occurring or transfusion-induced immune thrombocytopenia purpura (ITP). Plasma from one unit of blood was perfused through the columns and returned to each patient. This procedure was performed once or twice weekly. In two cases of acute ITP, platelets markedly increased, and platelet-associated IgG (Pa-IgG) and circulating immune complexes (CIC) were decreased following the treatments. A transient increase in platelets was achieved in one patient with chronic ITP. Some improved response to platelet transfusions was noticed in one patient with aplastic anemia and platelet alloimmunization. Two mechanisms are suggested for the effect of protein A column therapy: one is the stimulation of the production of anti-idiotype antibody that neutralizes platelet auto-antibody and the other is activation of complement that induces solubilization and removal of CIC containing platelet autoantibodies. Immunoadsorption by protein A column is a useful therapy for some ITP cases, especially those that are acute.

Antibodies↗