Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.5.1.1 (asparaginase)
 2,695 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.
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PMID:Electrolyte and acid-base disturbances in the management of leukemia. 26 90

A combination of eight cytotoxic drugs, administered simultaneously, has been used in 86 cases of acute leukemia. The regimen, designated TRAMPCOL, incorporated thioguanine, rubidomycin, (daunorubicin), cytosine arabinoside, methotrexate, prednisolone, cyclophosphamide, vincristine, and usually L-asparaginase. Treatment was administered in five-day pulses with treatment-free intervals varying from nine to 23 days. Subjective and objective toxic effects were not more severe than those seen with two- and four-drug regimens previously employed. Substantial clinical and hematologic improvement occurred in 8/19 patients with chronic granulocytic leukemia (CGL) in acute transformation. Complete clinical and hematologic remission (CR) was achieved in 3/7 patients with untreated acute myeloid leukemia (AML), 5/19 patients with AML who had failed to achieve CR with other therapy, and 4/18 patients with AML in relapse after CR obtained with regimens other than TRAMPCOL. CR occurred in 15/17 patients with acute lymphocytic leukemia (ALL), most of whom had had multiple previous relapses. CR was not achieved in four patients with AML superimposed on pre-existing myeloproliferative disorders. The TRAMPCOL regimen merits further evaluation in CGL after acute transformation, as a primary treatment for AML, and as therapy for ALL 1) in relapse, 2) in adults, 3) in children with adverse prognostic features, and 4) in T-cell ALL.
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PMID:Multiple-drug chemotherapy for acute leukemia The TRAMPCOL regimen: results in 86 patients. 26 3

L-asparaginase from Escherichia coli--Crasnitin was used in 14 children with acute leukemia unresponsive to conventional treatment: 11 acute lymphoblastic leukemias, 1 acute myeloblastic leukemia, 2 other forms of leukemia. The remission induction was obtained in 70% of applications. Median of remission duration was 90 days. Serious side effects were observed. The validity of L-asparaginase in therapy of advanced childhood ALL is stressed.
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PMID:L-asparaginase in treatment of acute leukemia in children. 27 52

The capacity of 1-asparaginase in two separate schedules (consecutive and intermittent), along with vincristine and prednisone to produce multiple responses, was evaluated in previously treated children with acute leukemia in relapse. The response rates varied inversely with previous 1-asparaginase exposure. A history of prior resistance to prednisone and vincristine appeared to reduce the response rate. Hypersensitivity reactions occurred in 14%.
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PMID:Repeated use of L-asparaginase in multi-drug therapy of childhood leukemia. 27 34

Of 41 adults with a diagnosis of acute leukemia that were randomized for induction therapy in combination with methotrexate, 6-MP, vincristine and prednisone (POMP) versus a combination of cytosine arabinoside, cytoxan, vincristine and prednisone (COAP), 23 (56%) patients achieved a complete remission. During remission, patients received consolidation therapy with the three courses of remission induction regimen that they had not received initially. They then received daunomycin (three courses) and L-asparaginase and were then maintained for two years with their induction therapy. The median duration of survival for all patients was 40 weeks; the median duration of survival of those patients that responded to chemotherapy was 80 weeks. There was no significant difference between the two induction regimens with regard to complete remission more than four and one half years from diagnosis and two and one half years from discontinuation of all therapy.
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PMID:A study of intermittent alternating drug program reinduction therapy on the frequency and duration of response in adult acute leukemia. 97 15

At least two chemotherapeutic agents, prednisone and L-asparaginase, have been demonstrated to produce pancreatic injury. Early diagnosis of pancreatitis is frequently not possible, as symptoms are vague, physical findings may be minimal, and laboratory studies are frequently inconclusive until the injury is severe. Abdominal echography, as a monitor of pancreatic size, has proven to be helpful in the diagnosis of subclinical and early pancreatic injury of 14 of 19 selected children receiving prednisone and/or L-asparaginase therapy for acute leukemia or non-Hodgkin's lymphoma at the M.D. Anderson Hospital and Tumor Institute. Employment of this new diagnostic method permits prompt withdrawal of the causative agent(s), thus preventing further insult.
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PMID:Early detection of chemotherapy-related pancreatic enlargement in children using abdominal sonography: a preliminary report. 99 Oct 74

Cytosine arabinoside (CA) was utilized in efforts to synchronize leukemic cells in DNA synthesis for treatment with vincristine, prednisone, and L-asparaginase in children with acute leukemia in relapse. The results did not indicate any therapeutic advantage for patients treated with this combination compared to those treated without any attempt at CA synchronization.
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PMID:Study of cytosine arabinoside (NSC-63878) synchronization plus vincristine (NSC-67574), prednisone (NSC-10023), and L-asparaginase (NSC-109229) for remission induction in advanced acute leukemia in children. 99 Nov 48

Six regimens utilizing L-asparaginase in doses of 6,000 IU/M2, 2,000 IU/M2, and 500 IU/M2 in two separate schedules (consecutive and intermittent) along with vincristine and prednisone yielded remarkably similar response rates, approximating 70%, in 306 previously treated children with acute leukemia in relapse. The addition of daunorubicin to one regimen did not alter the response rate. Hypersensitivity reactions occurred in 5% and hyperglycemia in 7%. Lower doses of L-asparaginase significantly reduced the hypersensitivity rate but no such pattern was noted for hyperglycemia. A history of prior resistance to prednisone and vincristine significantly reduced the response rate.
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PMID:Evaluation of dose and schedule of L-asparaginase in multidrug therapy of childhood leukemia. 100 82

Over 20 cytoenzymochemical tests were carried out in 152 patients with different types of acute leukemia to estimate the effects of some antiblastic drugs such as L-asparaginase, Purinethol, Methotrexate, Endoxan, Vinchristine, Cytosine Arabinoside a.o. The patients selected for the study were carefully examined before treatment at different moments during and/or at the end of the treatment. The effects of these drugs on the blast cells were mild when the cellular populations had a low rate of nucleic acid synthesis, high glycogenic score and high amounts of lipids or an important oxidative enzymatic activity. The enzymatic prediction tests: the acid phosphate deviation test and the succinic dehydrogenase inhibition test including the variant suggested by some of the authors - the latic dehydrogenase inhibition test - gave satisfactory results only in certain cases of acute leukemia.
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PMID:Cytoenzymochemical effects of some antiblastic drugs and prediction of response to chemotherapy in acute leukemias. 105 33

14 children with acute lymphoblastic leukemia and 6 with lymphosarcoma were treated in 13 cures with 300-500 IU/kg bodyweight/day of L-asparaginase and in 11 cures with 501-760 IU/kg/day. An increase of all fractions of immunoglobulins with maximal values at the end of the cures was observed in the group treated with low doses. In the children receiving the high doses of this drug, an increase was observed only in the first 3 or 4 days of therapy and a decrease occurred at the end of the cure. Decreased IgM levels at the end of therapy were noted in children with acute leukemia. Anti-asparaginase antibodies occurred only in 3 children with anaphylactic shock.
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PMID:Immunological aspects of L-asparaginase treatment in children with lymphoproliferative disease. 106 Jun 5


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