l asparaginase/hemorrhage

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A syndrome of thrombosis and hemorrhage complicating L-asparaginase therapy for childhood acute lymphoblastic leukemia.

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L-Asparaginase therapy for childhood acute lymphoblastic leukemia causes deficiencies of plasma hemostatic proteins, especially antithrombin, plasminogen, and fibrinogen. Severe thromboses and hemorrhages occurred in 18 children receiving vincristine, prednisone, and asparaginase therapy for ALL.

L-asparaginase induced intracranial haemorrhage in acute lymphoblastic leukemia.

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A 20-year-old national serviceman with acute lymphoblastic leukaemia, developed a large left parieto-occipital haemorrhage 7 days after completion of induction chemotherapy. Severe hypofibrinogenemia had been noted while he was receiving L-asparaginase. The haemorrhage could not be attributed to

Neurosurgical management of L-asparaginase induced haemorrhagic stroke.

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The authors describe a case of L-asparaginase induced intracranial thrombosis and subsequent haemorrhage in a newly diagnosed 30-year-old man with acute lymphoblastic leukaemia who was successfully managed by surgical intervention. At presentation, he had a Glasgow Coma Score of 7/15, was aphasic

Intracranial hemorrhage and focal seizures secondary to use of L-asparaginase during induction therapy of acute lymphocytic leukemia.

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L-Asparaginase is commonly used for induction therapy of acute lymphocytic leukemia of childhood. Severe clinical bleeding secondary to clotting dysfunction has not been previously reported. We observed intracranial hemorrhagic infarcts with focal seizures and hemiparesis associated with clotting

Successful treatment of acute lymphoblastic leukemia with L-asparaginase-induced intracranial hemorrhage to activated recombinant factor VIIa in a child.

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L-Asparaginase, a major component of therapy in children with acute lymphoblastic leukemia, has been shown to induce coagulopathy by inhibiting synthesis of clot-forming and clot-inhibitory proteins. The authors report the successful use of recombinant factor VIIa in a 15-year-old girl with acute

Intracranial bleeding during therapy with L-asparaginase in childhood acute lymphocytic leukemia.

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Two patients developed clinical features of intracranial bleeding--which were confirmed by computerized axial tomograms--during their induction therapy for acute lymphocytic leukemia. Coagulation studies showed clotting abnormalities including severe hypofibrinogenemia. These findings most probably

Successful management with octreotide of a child with L-asparaginase induced hemorrhagic pancreatitis.

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BACKGROUND Octreotide is a synthetic somatostatin analogue which has been suggested for use in the management of acute pancreatitis. While studies have looked at octreotide use in the setting of pancreatitis due to chronic alcohol use or trauma, little is known of its role in management of drug

Sequelae of thrombotic or hemorrhagic complications following L-asparaginase therapy for childhood lymphoblastic leukemia.

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Thirty-four cases of childhood lymphoblastic leukemia that were complicated by CNS and peripheral thrombosis or hemorrhage associated with L-asparaginase (L-asp) therapy were reviewed to determine the effect of the events on the subsequent clinical status. There was no predilection for any site in

Hemorrhagic complications of L-asparaginase therapy.

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Thrombosis and hemorrhage during L-asparaginase therapy.

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Acute haemorrhagic pancreatitis following L-asparaginase therapy in acute lymphoblastic leukaemia --a case report.

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[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)

Changes in hemostatic and fibrinolytic proteins in patients receiving L-asparaginase therapy.

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Hemostatic changes were evaluated in ten patients with acute lymphoblastic leukemia and lymphoma who received chemotherapy with L-asparaginase, vincristine, and prednisolone for 1 week. Following treatment, prothrombin time and activated partial thromboplastin time were significantly prolonged,

L-asparaginase-induced coagulopathy in children with acute lymphoblastic leukaemia.

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Haemostatic changes induced with vincristine (VCR), prednisone (PDN) and L-asparaginase (L-ase) in 53 children with ALL were prospectively evaluated. Relative to pretreatment values, mean FG concentration diminished significantly in the first week with a minimal level in the third week and PT was

Factor VIII/von Willebrand factor abnormalities during L-asparaginase treatment in patients with acute lymphoblastic leukemia.

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Factor VIII/von Willebrand factor (VIII/vWf) related properties were studied in 10 patients affected by acute lymphoblastic leukemia during L-asparaginase-vincristine-prednisone treatment. These properties remained within the normal range during the period of observation without any difference from

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