Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A poor-risk population of children with primary malignant central nervous system (CNS) tumors, other than gliomas, can be identified by their young age, by the presence of disease dissemination at diagnosis, and possibly by subtotal resection of the primary tumor. These children require at least neuraxis radiation therapy and possibly chemotherapy for disease control. Unfortunately, once neuraxis radiation is administered, tolerance of subsequent chemotherapy is limited. The authors have explored a multimodal treatment approach in 14 poor-risk patients initially consisting of a modified Phase II chemotherapy trial followed by neuraxis radiation. The diagnoses were medulloblastoma (5), pineoblastoma (3), cerebral primitive neuroectodermal tumor (3), germinoma (2), and choroid plexus carcinoma (1). Eleven patients had disseminated CNS disease, and two had bone marrow involvement at diagnosis. Nine patients received 2 courses of intravenous cyclophosphamide (80 mg/kg) alone over 8 weeks, and five others received three daily doses of intrathecal Ara-C (50 mg/m2) and oral hydroxyurea (40 mg/kg) with each course of cyclophosphamide. There were four complete responses (two dysgerminomas, one pineoblastoma, and one primitive neuroectodermal tumor), one partial response (medulloblastoma), and three mixed responses (two medulloblastomas, one pineoblastoma) to chemotherapy alone, for a response rate of 57%. Twelve patients subsequently tolerated the planned dose of neuraxis radiation. The median survival of all patients was 11 months, and seven of eight deaths were related to recurrent disease. The hematologic toxicity was appreciable, and one death resulted from gram-negative septicemia. Through the use of this type of Phase II trial, valuable information can be obtained on the response rates to specific chemotherapy agents administered prior to radiation. Although cyclophosphamide alone was an active agent in this context, these treatment regimens did not have an important affect on survival.
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PMID:Preradiation chemotherapy for newly diagnosed childhood brain tumors. A modified Phase II trial. 662 14

We report three cases of fulminant sepsis due to viridans streptococci in leukemic children treated with high-dose cytosine arabinoside (Ara-C). The major predisposing factors to this occurrence are the presence of oropharingeal mucositis, which is the entry of streptococci into the bloodstream, and the use of antibiotic prophylactic regimens against gram-negative bacteria. In order to avoid fatal events during viridans streptococci sepsis, specific measures such as penicillin prophylaxis or early antibiotic treatment are needed. We suggest that the prompt empiric use of a glycopeptide antibiotic in addition to the conventional association of a beta-lactam plus an aminoglycoside may significantly decrease the mortality rate due to fulminant streptococci sepsis while the patient is severely neutropenic. In this regard, our current policy considers the addition of an anti-gram-positive antibiotic to the first-choice fever treatment in neutropenic patients who have received high-dose Ara-C.
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PMID:High-dose cytosine arabinoside and viridans streptococcus sepsis in children with leukemia. 757 91

Thirty-four adults with AML were treated with conventional remission induction chemotherapy consisting of Ara-C and daunorubicin. The median age was 55 years. Thirty (88%) patients showing complete remission (CR) were treated with four courses of intensive consolidation chemotherapy: course 1 with 7 days Ara-C and 4 days of mitoxantrone; course 2 and 7 days Ara-C, 5 days of etoposide, vincristine day 10 and vinblastine day 12 (A-Triple-V); course 3 with 7 days Ara-C and 3 days of aclacinomycin; course 4 with 7 days Ara-C and 3 days of daunorubicin. Then patients were observed without further therapy until relapse. The median duration of relapse-free survival for patients < 60 years of age was 13 months, with 49% patients projected to continue first CR at 52 months. In contrast, only 19% of patients 60 years or older were projected to be in CR at 22 months. Most patients experienced significant side effects including fever, liver dysfunction, pneumonia and septicemia during consolidation therapies. Short-term intensive consolidation therapy appeared to be efficacious for patients < 60 years of age. The results in older individuals were worse than expected, and the use of G-CSF was suggested to improve this problem.
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PMID:[Short-term intensive consolidation chemotherapy in the treatment of acute nonlymphocytic leukemia]. 831 94

A 75-year-old female was admitted to our hospital because of fever and hypotension. The peripheral blood showed 400 leukocytes/microliters with 13,000/microliters platelets. Bone marrow puncture revealed that NCC stood at 14,000 with 50.0% blasts. The surface characters of the blasts were CD13+, CD33+, and HLA-DR+, and blood culture tests were positive. Coagulation tests revealed DIC. Based on the foregoing results, hypoplastic leukemia was diagnosed accompanied by sepsis and DIC, and was placed on the concomitant administration of a combination of low dose Ara-C and M-CSF. After 14 days of Ara-C administration and 26 days of M-CSF, her clinical symptoms improved, with the peripheral blood showing a WBC of 2,800/microliters and platelet count of 111,000/microliters. The percentage of myeloblasts decreased to 7.0%. After the administration of Ara-C was suspended for 2 weeks, another course of low dose Ara-C plus M-CSF administration was carried out and the patient achieved full remission. M-CSF stimulates not only the production of monocytes but increases the number of neutrophils and platelets through monocytes. It is also expected that tumoricidal activity may be realized by the activation of monocytes. In this patients, the concomitant administration of M-CSF and low dose Ara-C was remarkably effective in treating hypoplastic leukemia with severe complication. This result suggests that M-CSF will be useful for the treatment of leukemia.
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PMID:[Hypoplastic leukemia which achieved remission with administration of M-CSF along with low dose ara-C]. 831 38

Gram-negative sepsis/septic shock in the newborn continues to be a major medical problem, causing high mortality. Hyperglycemia followed by hypoglycemia is a common symptom in endotoxic shock. However, the mechanism of newborn glucoregulatory response to endotoxin has not been well understood. Paradoxically, monocyte-phagocytes can contribute to shock by overwhelming secretion of cytokines and also host defense by detoxifying endotoxin. Since monocyte-phagocyte function is immature in the newborn, this study was performed to evaluate Kupffer cell's role in liver glycogenolysis during endotoxic shock. Endotoxin (LPS) induced hyperglycemia in 10-day-old rats, and increased net glucose output in the isolated perfused liver. 1) Cytarabine decreased Kupffer cell function (decreased hepatic colloid carbon uptake) and blunted LPS-increased liver net glucose output in the Cytarabine + LPS-treated group (104 +/- 4 vs. 146 +/- 3 micrograms/min/g wet liver in the LPS-treated group: P < .001). 2) Indomethacin (IND) suppressed LPS-induced liver net glucose output in the LPS + IND-treated group (133 +/- 5 vs. 146 +/- 3 micrograms/min/g wet liver, P < .05). Thus, prostaglandins were suggested to contribute to glycogenolysis in the 10-day-old rat liver. 3) Phorbol 12-myristate 13-acetate (PMA) increased liver net glucose output (166 +/- 4 micrograms/min/g wet liver), and H-7, a protein kinase C inhibitor, blunted PMA-induced liver glucose output (140 +/- 2 micrograms/min/g wet liver, P < .05). H-7 enhanced LPS-induced liver net glucose output (196 +/- 9 micrograms/min/g wet liver, P < .01). Therefore, protein kinase C may not be the dominant cell signaling system for LPS stimulation in suckling rat Kupffer cells.
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PMID:Lipopolysaccharide alters suckling rat liver glycogenolysis. 832 90

From July 1987 to July 1991, 12 children underwent AMBT following high-dose cytarabine (HD Ara-C) plus 14.4 Gy hyperfractionated total body irradiation (hyfr-TBI) for early isolated extramedullary relapse of ALL, while in first BM remission. No patient received intrathecal prophylaxis following AMBT. One patient died on day +5 due to sepsis and three patients, two of them transplanted in second and third CNS relapse, respectively, died from BM relapse occurring 1.5, 4 and 5 months after AMBT. Eight of the 12 survive disease-free with a median follow-up of 24 months (range 14-62 months). The toxicity of HD Ara-C plus hyfr-TBI was acceptable and well controlled with supportive therapy. These results suggest that ABMT following HD Ara-C plus hyfr-TBI may eradicate leukemia from extramedullary sites of ALL relapse.
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PMID:ABMT for early isolated extramedullary relapse of childhood ALL. 837 35

A 27-year-old male with acute lymphoblastic leukemia (L2) received allogeneic bone marrow transplantation on June, 7 1990. He was conditioned with cyclophosphamide, Ara-C and total body irradiation. GVHD prophylaxis consisted of cyclosporin and short term methotrexate. He was diagnosed as having hemolytic uremic syndrome (HUS) on the basis of microangiopathic hemolytic anemia, thrombocytopenia and renal dysfunction on day 224. Cyclosporin was discontinued and FFP was transfused and plasma exchange was performed. He died of heart failure and sepsis on day 582. Autopsy confirmed the findings of HUS.
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PMID:[An autopsy case report of hemolytic uremic syndrome after allogeneic bone marrow transplantation]. 849 23

High-dose cytarabine alone or in combination with mitoxantrone has been shown to be active against refractory non-Hodgkin's lymphoma in therapeutic trials. We administered these two drugs to 16 patients with advanced and refractory non-Hodgkin's lymphoma. Cytarabine was administered at 3 g/m2 as a 2-h intravenous infusion every 12 h on days 1-4 (8 doses) and mitoxantrone at 6 mg/m2/day as a 1-h intravenous infusion on days 1-5. The clinical efficacy and toxicity were assessed according to the WHO criteria. Five patients (31%, 95% CI: 8-54%) attained complete remission and two had partial remission. In three of the five complete remission patients, the remission lasted for > 4 months. The remaining two patients had complete remission for only 1.3 months. Myelosuppression with subsequent infection was the major toxicity of this regimen. Severe leukopenia (WBC < 1000/microliter) lasted for an average of 20 days and thrombocytopenia (< 25000/microliter) 18 days. Five patients (31%) died of treatment-related complications: neutropenia-associated sepsis in three, pneumonia in one and electrolyte imbalance in one. Nonmyeloid toxicities included alopecia in 100% (19% Gr.2, 75% Gr.3), stomatitis in 88% (13% Gr.2, 31% Gr.3), hepatotoxicity in 38% (6% Gr.2, 6% Gr.3), dermatitis in 31% (19% Gr.2), CNS toxicity in 25% (6% Gr.2, 6% Gr.3), infection in 38% (13% Gr.3, 19% Gr.4) and chemical conjunctivitis in 6% (Gr.2). We conclude that a proportion of refractory non-Hodgkin's lymphoma cases will respond to high-dose cytarabine+mitoxantrone, but that the treatment seems too toxic to be acceptable as salvage therapy for refractory non-Hodgkin's lymphoma.
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PMID:High-dose cytarabine and mitoxantrone as salvage therapy for refractory non-Hodgkin's lymphoma. 925 69

The purpose of this study is to determine the efficacy of low dose cytosine arabinoside (LD Ara-C) as an alternative treatment to conventional cytotoxic induction chemotherapy in childhood acute promyelocytic leukemia (APL). Four children with APL in poor medical condition prior to chemotherapy were treated with LD Ara-C (10 mg/m2/12 h) for 3 weeks. In three patients, the second course was administered after a resting period of two weeks. Subsequent conventional cytotoxic induction chemotherapy was applied in patients who did not enter complete remission (CR). After induction of CR, maintenance chemotherapy with a conventional monthly multi-drug regimen was applied. CR in one patient and partial remission (PR) in two patients were obtained after two courses of LD Ara-C. Patients who did not enter CR after LD Ara-C entered on subsequent conventional chemotherapy. There were no major complications such as intracranial hemorrhage and sepsis; myelosuppression was not as severe as in conventional chemotherapy; there was clinical and laboratory improvement in coagulopathy. We concluded that LD Ara-C may be an alternative treatment to the conventional chemotherapy in children with APL, especially in whom conventional cytotoxic induction chemotherapy is thought to increase the risk of serious complications and early fatality during induction chemotherapy.
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PMID:Clinical trial of low dose cytosine arabinoside in the treatment of acute promyelocytic leukemia. 928 28

Mitoxantrone (M) is a synthetic aminoanthraquinone with anti-leukemic activity in patients with daunorubicin (D) resistant acute leukemia. The Cancer and Leukemia Group B (CALGB) has undertaken a limited access pilot study in which M, 12 mg/m2, over 30 min, daily for 3 days, and cytosine arabinoside (Ara-C), 100 mg/m2/day by constant infusion for 7 days were used for the induction of newly diagnosed patients with AML. Responding patients were consolidated with daunorubicin, 45 mg/m2/day for 3 days, and 7 days of Ara-C. After a second consolidation identical to induction, no further therapy was given. Twenty-nine patients with a median age of 50 years (range 18-72) were entered in the study; 18 were males and 11 females. Twenty-four (83%) patients achieved CR, 1 patient achieved a PR, and 4 died in induction from leukemia-related causes. Two patients died in CR from consolidation-related neutropenic sepsis and two additional patients died in CR. Of 24 patients, 7 remain disease-free at a median follow-up interval of 8 years. The regimen is active and well tolerated. The duration of disease-free survival in responding patients is consistent with that seen in similar regimens using intensification chemotherapy without prolonged maintenance.
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PMID:Sequential mitoxantrone, daunorubicin, and cytosine arabinoside for patients with newly diagnosed acute myelocytic leukemia. 939 81


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