l asparaginase/nekrozė

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Avascular necrosis of bone after adult acute lymphocytic leukemia treatment with methotrexate, vincristine, L-asparaginase, and dexamethasone (MOAD).

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Four of 55 (7%) adult acute lymphocytic leukemia patients, age 27-58 years, who were treated with methotrexate, vincristine, L-asparaginase, and dexamethasone (MOAD) developed avascular necrosis (AVN) of one or both femoral heads 16-39 months after beginning treatment. All patients were treated with

Parathyroid necrosis and hypocalcemic tetany induced in rabbits by L-asparaginase.

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Fifty percent of New Zealand white rabbits became profoundly weak, had generalized seizures and died between 22 and 47 hours after an intravenous injection of 1000 IU/kg of L-asparaginase. The biochemical correlate of this syndrome is severe hypocalcemia associated with marked, single cell,

[Safety of polyethylene glycol conjugated L-asparaginase in patients with acute lymphoblastic leukemia and T cell non-Hodgkin lymphoma].

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OBJECTIVE To evaluate the safety of polyethylene glycol conjugated L-asparaginase (PEG-Asp) for patients with adult acute lymphoblastic leukemia (ALL) and T cell non-Hodgkin lymphoma (T-NHL). METHODS A retrospective analysis was conducted on the clinical data of 101 young patients (≤40 years old)

Bone marrow necrosis and thrombotic complications in childhood acute lymphoblastic leukemia.

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Two children with bone marrow necrosis at diagnosis or at relapse of acute lymphoblastic leukemia (ALL) had thrombotic complications 15 and 17 days after starting remission induction therapy including prednisone, vincristine, and L-asparaginase. The close temporal relationship of these two

Effects of Prednisolone, L-Asparaginase, Gemfibrozil, and Combinations of These Elements on Mice Lipid Profile, Liver, and Pancreas.

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The aim of this study is to determine the effects of L-asparaginase (L-ASP), corticosteroids (CSs), and antilipidemics, separately and in combination, on the lipid profiles and the liver and pancreas histology in mice. This study included 8 groups of 7 mice each. Before any drug administration,

Surgical pancreatic complications induced by L-asparaginase.

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Pancreatitis has been noted to be a potential complication in 2% to 16% of patients undergoing treatment with L-asparaginase for a variety of pediatric neoplasms, but rarely has surgical intervention been necessary. The authors present two fulminant cases of L-asparaginase-induced pancreatitis and

[Distal coronary thrombosis during L-asparaginase treatment for an acute lymphoblastic leukaemia].

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A 53-year-old man is treated by L-asparaginase for an acute lymphoblastic leukaemia. He received anti thrombin infusions. A systematic electrocardiogram showed an asymptomatic subepicardium ischemia without troponin elevation. Echocardiography and heart magnetic resonance imaging showed an apical

Acute pancreatitis in children with acute lymphoblastic leukemia treated with L-asparaginase.

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BACKGROUND L-asparaginase (L-asp) is used as part of the initial treatment in children with acute lymphoblastic leukemia (ALL), inducing remission in 83% to 95% of the treated patients. Major toxicity effects reported are hypersensitivity reactions and dysfunctions of the liver and pancreas. Acute

L-asparaginase-induced severe necrotizing pancreatitis successfully treated with percutaneous drainage.

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L-asparaginase is a key component of the antileukemic therapy in children with acute lymphoblastic leukemia (ALL). Pancreatitis has been noted to be a complication in 2-16% of patients undergoing treatment with L-asparaginase for a variety of pediatric neoplasms. Most cases of pancreatitis

Histopathological features of L-asparaginase-induced liver disease.

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We studied the histopathological changes of liver in four patients who developed hepatomegaly and abnormal liver chemistry tests 2 to 20 days following administration of L-asparaginase as a part of a combination chemotherapy regimen for treatment of acute lymphoblastic leukemia. The severity of the

L-Asparaginase Isolated from Phaseolus vulgaris Seeds Exhibited Potent Anti-Acute Lymphoblastic Leukemia Effects In-Vitro and Low Immunogenic Properties In-Vivo.

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Escherichia coli-derived L-asparaginases have been used in the treatment of acute lymphoblastic leukemia (ALL), however, clinical hypersensitivity reactions and silent inactivation due to antibodies against E. coli-asparaginase, lead to inactivation of these preparations in most cases.Therefore,

Adolescents with acute lymphoblastic leukemia: a new "age".

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Adolescents with acute lymphoblastic leukemia (ALL) have a higher incidence of T-cell immunophenotype, a higher incidence of Philadelphia chromosome positive ALL, a lower incidence of high hyperdiploidy and TEL-AML1 translocation, and a lower incidence of extramedullary bulk disease compared to

[Fulminant hepatitis cured by plasma exchange in a patient with acute leukemia--a case report].

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A 16-year-old male with acute myelogenous leukemia (M1) presented with fulminant hepatitis (massive hepatic necrosis). He achieved a complete remission with the administration of AdVP (doxorubicin, vincristine and prednisolone), and thereafter received consolidation or intensification therapy 5

Augmented Berlin-Frankfurt-Munster therapy abrogates the adverse prognostic significance of slow early response to induction chemotherapy for children and adolescents with acute lymphoblastic leukemia and unfavorable presenting features: a report from the Children's Cancer Group.

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OBJECTIVE Compared with previous Children's Cancer Group (CCG) acute lymphoblastic leukemia (ALL) trials, therapy based on the Berlin-Frankfurt-Munster (BFM) 76 trial has effected an improvement in event-free survival (EFS). In an attempt to improve EFS further, CCG investigators formulated an

Calcium and adenosine triphosphate control of cellular pathology: asparaginase-induced pancreatitis elicited via protease-activated receptor 2.

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Exocytotic secretion of digestive enzymes from pancreatic acinar cells is elicited by physiological cytosolic Ca(2+) signals, occurring as repetitive short-lasting spikes largely confined to the secretory granule region, that stimulate mitochondrial adenosine triphosphate (ATP) production. By

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