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S Kuriya

Publications and source records attributed to S Kuriya.

At least 19 recordsLinked to original sources
PubMed1998

[Hemophagocytic syndrome due to miliary tuberculosis in the course of aplastic anemia].

We report a 63 year-old female with aplastic anemia (AA) who was complicated with hemophagocytic syndrome induced by systemic miliary tuberculosis. Two years before admission to our hospital, she was diagnosed as AA and had been treated with granulocyte colony-stimulating factor, erythropoietin and methenolone acetate. In May, 1996, She was transferred to our hospital because of high fever and exacervation of pancytopenia. She showed severe pancytopenia, and an increase in macrophages showing remarkable erythrophagocytosis and decrease in hemopoietic cells in the bone marrow. In initial examination, high titer of IgM antibody to herpes simplex virus type I was identified and methylprednisolone pulse therapy was started under the diagnosis of virus associated hemophagocytic syndrome. Ten days later, however, she died for intestinal hemorrhage followed by multiorgan failure. In autopsy, multiple epitheloid cell granulomas with acid-fast bacilli were found in bone marrow, lungs, liver, spleen and kidneys.

Anemia, Aplastic↗
PubMed1998

In vitro and in vivo effects of KT6352, a derivative of indolocarbazole compounds, on murine megakaryocytopoiesis.

We investigated the in vitro and in vivo effects of KT6352, a derivative of indolocarbazole compound, on murine megakaryocytopoiesis. When serum-free megakaryocyte (Meg) colony assay was performed with 100 U/mL of recombinant mouse interleukin-3 (rmIL-3), the addition of 1x10(-11)M to 1x10(-9)M of KT6352 increased the number of Meg colonies. An additional increase of Meg colonies by KT6352 was observed in the serum-free culture containing rmIL-3 plus recombinant mouse interleukin-6 or rmIL-3 plus recombinant mouse stem cell factor. KT6352 did not stimulate Meg colony formation without rmIL-3. When KT6352 was administered intraperitoneally to normal BALB/c male mice at a dose of 10 mg/kg daily for 5 consecutive days, a 2.1-fold increase in the platelet count was observed on day 14, and the prolonged thrombocytopoiesis was detectable from 9 to 27 days after KT6352 administration. A marked increase in the white blood cell count was also observed from 5 to 14 days after KT6352 treatment. Before the gradual increase of platelet counts, 8 days after KT6352 administration, a marked increase in the number of colony-forming units of megakaryocytes (CFU-Megs) in bone marrow and spleen was observed, and a substantial increase in the number of splenic CFU-Megs was observed 14 and 23 days after KT6352 administration. Bone marrow Meg ploidy analysis by two-color flow cytometry showed a shift in the modal ploidy class from 16 to 32 and an increase in the frequency of 64 cells in KT6352-treated mice. These results suggest a possible therapeutic benefit of KT6352 in the management of thrombocytopenia.

Animals↗
PubMed1997

[Early establishment of bone marrow hypoplasia by antileukemic chemotherapy with concurrent rhG-CSF in a case of acute myelogenous leukemia complicated with intestinal perforation].

We report a case of 53-year-old man with acute myelogenous leukemia (M2) showing a karyotype of t(7;11) (p15;p15), del(10) (q11;q12), who was complicated with perforation of a duodenal ulcer during the antileukemic chemotherapy using behenoyl ara-C, daunorubicin, 6-mercaptopurine and prednisolone. As his bone marrow still showed high cell density and leukemic proliferation at the time of intestinal perforation, the therapeutic regimen was changed to a combination of behenoyl are-C and mitoxantrone, and daily rhG-CSF was concurrently administered for the purpose of early establishment of bone marrow hypoplasia. On the 8th day after the therapeutic regimen had been changed, his bone marrow became nearly aplastic, and complete remission was obtained on the 24th day. This case may indicate that the concurrent administration of cell-cycle specific antileukemic drugs and rhG-CSF is available for AML patients with emergent need of leukemic cell reduction.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1996

A combination chemotherapy with low doses of cytarabine and etoposide for high risk myelodysplastic syndromes and their leukemic stage. A pilot study.

BACKGROUND: Even now, no definitely effective therapy is inducted to high risk myelodysplastic syndromes (MDS) and their leukemic stage (MDS-AML) except bone marrow transplantation. METHODS: Ten patients with high risk MDS and 6 with MDS-AML were treated with daily low doses of cytarabine (10 mg/m2/12h, infused over 2h) etoposide (50 mg/m2/day, infused over 2h). RESULTS: Fourteen of these patients were finally evaluated among whom 6 with high risk MDS and 3 with MDS-AML (64.3%) had complete remission, and 2 with high risk MDS (14.3%) achieved partial remission after this chemotherapy for 9 to 21 days. Three of 11 responders were resistant to the prior chemotherapies with single and low dose cytotoxic agents including cytarabine, etoposide, or aclarubicin. Although all of the patients who could be assessed developed severe marrow hypoplasia after chemotherapy, the nonhematologic side effects were mild enough to be tolerated. CONCLUSIONS: This combination chemotherapy must be effective and useful in high risk MDS and MDS-AML not only without prior chemotherapy but in cases which have been resistant to single and low dose oncostatic agent.

Adult↗
PubMed1996

Recombinant human interferon alpha-2b (rh IFN alpha-2b) therapy for steroid resistant idiopathic thrombocytopenic purpura (ITP).

The efficacy of recombinant human interferon alpha-2b (rh IFN alpha-2b) in the treatment of steroid resistant idiopathic thrombocytopenic purpura (ITP) was studied in 50 cases. Forty-one patients treated with rh IFN alpha-2b three times a week, six of 18 (33.3%) in the low dose group (150 x 10(4)IU: 3 MIU) and four of 20 (20.0%) in the high dose group (300 x 10(4)IU: 3 MIU) responded with platelet counts increasing to above 50 x 10(9)/L. Because of the exacerbation of thrombocytopenia and nasal bleeding, treatment was discontinued within 2 weeks in three patients out of 41 cases. On the other hand, six of nine patients (66.7%) treated with 3 MIU of IFN alpha-2b once a week for 8 weeks showed satisfactory response. Treatment with either administration schedule did not result in sustaining platelet counts above 50 x 10(9)/L for a long time after treatment. The results indicate that once a week administration schedule of rh IFN alpha-2b is more efficacious for platelet counts increasing for short period in patients who failed to respond to steroid and other medications than other schedules. The maintenance of this treatment schedule will allow sustained increased platelet levels, resulting in relief of bleeding tendency, while also being cost effective in comparison with other IFN treatment schedules and achieving better patient compliance without flu-like symptoms.

Adolescent↗
PubMed1996

Recombinant human c-Mpl ligand is not a direct stimulator of proplatelet formation in mature human megakaryocytes.

To evaluate the effect of the c-Mpl ligand on platelet production by megakaryocytes, we investigated proplatelet formation in isolated human megakaryocytes cultured in serum-free medium, with or without the c-Mpl ligand, interleukin-6 and erythropoietin. When interleukin-6 was added to the culture medium, the percentage of megakaryocytes displaying proplatelets was approximately 1.5-fold the control value; whereas, in the presence of the c-Mpl ligand, the percentage of megakaryocytes displaying proplatelets decreased in a dose-dependent manner and did not increase compared to control values at any dose tested. However, the viability of megakaryocytes after a 4 d culture in the presence of the c-Mpl ligand was significantly higher than that of the cells cultured without it. The c-Mpl ligand did not stimulate the proplatelet formation in megakaryocytes in vitro.

Blood Platelets↗
PubMed1996

[Interleukin-3 therapy in patients with aplastic anemia refractory to prior therapies].

A therapeutic trial of interleukin-3 (IL-3) was carried out in four patients with aplastic anemia refractory to the prior therapies. Daily subcutaneous doses of 2.5, 5.0 or 7.5 micrograms/kg was given for 7 or 14 days. In a patient who had co- and immediate boost-administration of granulocyte colony-stimulating factor (G-CSF) and/or erythropoietin (Epo) and another who had sequential administration of G-CSF and Epo two weeks after IL-3, definite hematological response was obtained during the course after IL-3. In one patient, moderate to severe side effects consisting of facial edema, conjunctival bleeding, chills and fever, were observed after two days' administration of IL-3. Co- or sequential administration of other hemopoietic factor(s) may be essential in IL-3 therapy for aplastic anemia.

Adult↗
PubMed1995

Ceroid pigment deposition in circulating blood monocytes and T lymphocytes in Hermansky-Pudlak syndrome: an ultrastructural study.

An electron microscopic study of peripheral leukocytes obtained from a 39 year old woman with Hermansky-Pudlak syndrome was performed. Ceroid pigment granules were found within the lysosomes in 3.5% of monocytes and 5.4% of lymphocytes. Infrequently, pigment granules were also found in the parallel tubular arrays of lymphocytes. The lymphocytes containing ceroid pigment granules were confirmed to be T cells by immunoelectron microscopy. It was speculated that intralysosomal accumulation of ceroid pigment granules in Hermansky-Pudlak syndrome may be due to lysosomal dysfunction.

Adult↗
PubMed1995

[Initiation of hematopoietic recovery by recombinant human granulocyte-macrophage colony-stimulating factor in a case of severe aplastic anemia induced by gold salt].

A 65-year-old female with severe aplastic anemia induced by gold salt, whose hematopoietic recovery was initiated by rhGM-CSF therapy, was reported. The patient has been given a total of 500 mg of gold-sodium thiomalate for treatment of her rheumatoid arthritis. Two months after the final administration of it, she was admitted to our hospital with complaints of palpitation and shortness of breath. The hemogulobin was 5.9 g/dl, the platelet count was 0.5 x 10(4)/microliter, and the leukocyte count was 800/microliters with 19% neutrophils. Her bone marrow showed aplasia, and both of Ham and sugar-water tests were positive. Three times of bolus-methylprednisolone treatment, with or without methenolone acetate, resulted in no definite improvement of peripheral pancytopenia and marrow aplasia. Subsequent subcutaneous rhGM-CSF, 300 micrograms daily for 28 days with oral prednisolone 5 mg and methenolone acetate 40 mg daily, initiated hematopoietic recovery of all three cell lineages in both peripheral blood and bone marrow. The same doses of prednisolone and methenolone acetate were continued after rhGM-CSF administration, and three months later peripheral cytopenia and positive Ham and sugar-water tests disappeared completely.

Aged↗
PubMed1995

[Response-oriented salvage chemotherapy with mitoxantrone, etoposide and enocitabine for previously treated acute myeloid leukemia. Tohoku Leukemia Study Group].

Twenty-two patients with previously treated acute myeloid leukemia (AML) received salvage chemotherapy with mitoxantrone, 5 mg/m2/d on days 1 to 3, etoposide, 70 mg/m2/d on days 1 to 5, and enocitabine, 170 mg/m2/d on days 1 to 7 (BHAC-ME). Additional mitoxantrone, etoposide (both for up to 2 days) and enocitabine (for up to 7 days) were given if the bone marrow obtained on day 8 was not severely hypoplastic. Mitoxantrone and etoposide had been previously administered in 14 and 15 patients, respectively. Seven patients had primary resistance; 14 patients had first relapse (4 early and 10 late): and 2 patients had second relapse. Overall, seven patients (31%) achieved a complete remission; 7/14 with first relapse, and 0/8 with primary resistance or second relapse. Four patients, 3 with primary resistance and 1 with first relapse, died of infectious complication in aplasia. First relapse patients who had been previously treated both with mitoxantrone and etoposide, had a lower CR rate than the other first relapse patients [2/8 (25%) vs 5/6 (86%)], although patient characteristics such as duration of first CR, initial karyotype, and performance status, were similar between the two groups. We conclude that response-oriented BHAC-ME regimen is still active in first relapse AML patients unless they have received both mitoxantrone and etoposide previously.

Acute Disease↗
PubMed1994

[Aplastic anemia].

Explore the source record for details and available documents.

Anemia, Aplastic↗
PubMed1994

Interleukin-6 and erythropoietin act as direct potentiators and inducers of in vitro cytoplasmic process formation on purified mouse megakaryocytes.

Mouse megakaryocytes were purified using a rabbit antimouse platelet serum, and magnetic beads were conjugated with an antirabbit IgG antibody. The purified cells were 95.8 +/- 1.2% megakaryocytes, and the recovery and viability of the megakaryocytes were 70 +/- 18.4%, and 80 +/- 13.4%, respectively. The effects of recombinant erythropoietin (Epo), interleukin-6 (IL-6), and IL-1 beta on these purified megakaryocytes were studied. Epo and IL-6 significantly increased DNA synthesis in these cells, but IL-1 beta did not. Similarly, both Epo and IL-6, but not IL-1 beta, increased the acetylcholinesterase (AchE) activity in the megakaryocytes. Epo and IL-6 stimulated the megakaryocytes to form cytoplasmic processes, which are considered to represent in vitro proplatelet formation. This process formation was inhibited by the addition of colchicine to the cultures. It was concluded that Epo and IL-6 are not only direct potentiators of megakaryocytes, but also inducers of in vitro cytoplasmic process formation on megakaryocytes.

Acetylcholinesterase↗
PubMed1993

A novel megakaryocyte potentiator produced by MC-1 human lung cancer cell line.

The hematopoietic stimulating activity of a human lung cancer cell line, MC-1, was investigated. The protein fraction (MC-1 protein) was prepared from the serum-free culture supernatant of MC-1 cells using hydroxyapatite and concanavalin A-agarose columns. In serum-containing cultures, MC-1 protein stimulated colony formation by megakaryocyte colony-forming units (CFU), erythroid burst-forming units and granulocyte/macrophage (GM) CFU. The stimulating effect was strongest for megakaryocyte CFU. The factor having megakaryocyte colony-stimulating activity was shown to be a protein whose molecular weight was determined to be 23,000 daltons by gel filtration. By various analyses, this protein was shown to be molecularly different from the heretofore-identified cytokines that may affect megakaryocytopoiesis, i.e., interleukin-1 (IL-1), IL-2, IL-3, IL-6, IL-7, IL-11, granulocyte colony-stimulating factor (CSF), macrophage CSF, GM-CSF, leukemia inhibitory factor, stem cell factor and tumor necrosis factor. Under serum-free conditions, MC-1 protein augmented murine megakaryocyte colony formation in the presence of murine IL-3 and increased the acetylcholinesterase activity of purified murine megakaryocytes. It was also shown that MC-1 protein stimulated human megakaryocyte colony formation. It was concluded that MC-1 cells produce a megakaryocyte potentiator which is molecularly different from any heretofore-identified cytokines.

Animals↗
PubMed1993

[Indications of G-CSF in patients with drug-induced agranulocytosis].

Bone marrow findings at the onset of disease were analyzed in five patients with drug-induced agranulocytosis to detect simple indices for a determination of the indications G-CSF therapy. Two patients showed severe marrow hypoplasia, extremely low ME ratio and complete absence of myelocytes or more mature neutrophils in their bone marrow. In these cases, the periods for recovery to 500 or more peripheral neutrophils per microliter were 5 and 9 days in a G-CSF-treated patient and a non-treated patient, respectively. On the other hand, the bone marrow of other three patients revealed normal or slightly high cellularity, moderately low ME ratio and appearance of myelocytes and more mature neutrophils. In the latter cases, the periods for recovery to 500 or more peripheral neutrophils were 3 days in all cases, regardless of whether G-CSF was administered or not. These findings suggest that G-CSF should be administered to drug-induced agranulocytic patients with severe marrow hypoplasia, extremely low ME ratio and absence of marrow neutrophilic cells.

Adult↗