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arabinoside/отёк
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Страница 1 от 27 полученные результаты
Ara-C lung: noncardiogenic pulmonary edema complicating cytosine arabinoside therapy of leukemia.
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Unexplained fatal pulmonary edema observed at autopsy in leukemic patients treated with cytosine arabinoside (Ara-C) suggested a possible role of the drug in causing increased alveolar capillary permeability. We reviewed clinical and pathologic features of the 181 patients with leukemia who were
Non-cardiogenic pulmonary edema complicating intermediate and high-dose Ara C treatment for relapsed acute leukemia.
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Infection, hemorrhage and adult respiratory distress syndrome (ARDS) are pulmonary complications occurring after remission induction therapy for acute leukemia. The aim of this study was to analyze the incidence of these causes by serial roentgenogram, clinical, microbiological and laboratory tests
Enhancement of axonal growth into a spinal lesion by topical application of triethanolamine and cytosine arabinoside.
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We have demonstrated that a brief compression lesion of the rat spinal cord produces axotomy with minimal necrosis or scarring and that axons grow into such a lesion along longitudinally oriented capillaries and similarly oriented cordons of ependymal cells and astrocytes. Inasmuch as extensive,
Feasibility study of intraarterial vs intravenous cisplatin, BCNU, and teniposide combined with systemic cisplatin, teniposide, cytosine arabinoside, glycerol and mannitol in the treatment of primary and metastatic brain tumors.
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Sixteen patients with intracerebral tumors received intraarterial cisplatin, teniposide, and BCNU combined with intravenous cisplatin, teniposide, and cytosine arabinoside. Oral glycerol and intravenous mannitol were given along with the intravenous chemotherapy in an attempt to increase drug
[Early adenine arabinoside therapy in herpes simplex encephalitis (HSE)].
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Five patients with HSE were treated with adenine arabinoside and one additional patient with cytosine arabinoside. The diagnosis of HSE was confirmed in retrospect by the rising CF titers and the Enzyme-Linked Immunosorbent Assay (ELISA) levels in CSF (Table 2). Brain biopsy was not performed. The
Fatal pulmonary failure complicating high-dose cytosine arabinoside therapy in acute leukemia.
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One hundred three relapsed leukemia patients were treated with high-dose cytosine arabinoside (Ara-C); 3 g/m2 intravenously over 2 hours every 6 to 12 hours for a total of nine to 12 doses or 3 g/m2 intravenously over 2 hours for two doses 12 hours apart followed by a continuous infusion of 1.5 g/m2
Pulmonary insufficiency complicating therapy with high dose cytosine arabinoside in five pediatric patients with relapsed acute myelogenous leukemia.
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BACKGROUND
The occurrence of fatal or nearly fatal pulmonary insufficiency in 5 of 22 pediatric patients with relapsed acute myelogenous leukemia (AML) treated with high dose cytosine arabinoside (Ara-C) at St. Jude Children's Research Hospital, Memphis, Tennessee, and institutions affiliated with
Continuous infusion high-dose cytosine arabinoside in refractory childhood leukemia.
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Ten pediatric patients with refractory leukemia received continuous infusion high-dose cytosine arabinoside (ara-C) according to one of two escalating dosage schedules: (1) a 500-mg/m2 rapid infusion loading dose followed by 3.5 g/m2 per day continuous infusion daily for four consecutive days, or
Unexpected high incidence of severe toxicities associated with alpha interferon, low-dose cytosine arabinoside and all-trans retinoic acid in patients with chronic myelogenous leukemia.
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Preclinical data have shown that all-trans retinoic acid (ATRA) with interferon-alpha (IFN-alpha) can exert significant suppressive effects on Philadelphia-chromosome (Ph)-positive cells. The aim of this study combining IFN-alpha, low-dose cytosine arabinoside (ara-C) and ATRA was to increase the
Phase II-study for treatment of refractory acute leukemia with intermediate-dose cytosine arabinoside and amsacrine.
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25 consecutive leukemia patients (21 AML, 4 ALL) with either primary resistance (n = 22) or resistant relapse (n = 3) of all FAB-subtypes were treated with 1 or 2 cycles of ID-ara C (1 g/m2 i.v. q 12h days 1-6) and AMSA (120 mg/m2 i.v. days 5-7). Patients reaching CR received 1 cycle of intensive
Phase-II study of treatment of refractory acute leukemia with intermediate-dose cytosine arabinoside and amsacrine.
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Twenty-five consecutive leukemia patients (21 AML, 4 ALL) with either primary resistance (n = 22) or resistant relapse (n = 3) of all FAB subtypes were treated with 1 or 2 cycles of ID-ara C (1 g/m2 i.v. q 12 h, days 1-6) and AMSA (120 mg/m2 i.v., days 5-7). Patients reaching CR received 1 cycle of
Prolonged high dose ARA-C infusions in acute leukemia.
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High doses of cytosine arabinoside (ara-C) were administered by continuous infusion to 24 patients with acute leukemia in relapse or blast phase of chronic myelogenous leukemia (CML). Ara-C was infused at a dose rate of 250 mg/M2/hr for 36 to 72 hr. The major toxicities were myelosuppression,
Fatal pulmonary toxicity resulting from treatment with gemcitabine.
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BACKGROUND
Pulmonary toxicity reported with gemcitabine is usually mild and self-limiting. The authors report a series of three patients who had life-threatening pulmonary toxicity after receiving gemcitabine.
METHODS
The three patients presented to two major teaching hospitals with significant
[PET-MR in patients with glioblastoma multiforme].
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Glioblastoma multiforme (GBM) is the most common and most aggressive primary tumor of the brain. In recent years newer therapeutic approaches have been developed. To allow for an optimized treatment planning it is important to precisely delineate necrotic tissue, edema and vital tumor tissue and to
Gemcitabine-induced systemic capillary leak syndrome.
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Systemic capillary leak syndrome (SCLS) is a rare disorder with a high mortality rate, characterized by rapidly developing edema, weight gain and hypotension, hemoconcentration and hypoproteinemia. This syndrome is caused by sudden, reversible capillary hyperpermeability with a rapid extravasation
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