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

A 13-year-old girl with preB-ALL was admitted because of headache during maintenance therapy including L-asparaginase. Magnetic resonance imaging revealed cerebral thrombosis. Coagulation studies showed decreased levels of fibrinogen, antithrombin-III and plasminogen. The patient was treated with antithrombin-III concentrates and fresh frozen plasma and recovered quickly. These findings suggest that coagulopathy induced by L-asparaginase is associated with the pathogenesis of cerebral thrombosis.
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PMID:[Cerebral thrombosis in a child with acute lymphocytic leukemia during L-asparaginase therapy]. 260 Oct 47

We report a child with acute lymphocytic leukaemia who developed simultaneous osteonecrosis of vertebrae and cerebral thrombosis during L-asparaginase therapy. Fibrinogen, antithrombin III and plasminogen were decreased. Fresh frozen plasma in addition to antithrombin III concentrates were used to replenish these haemostatic proteins. L-asparaginase induced coagulopathy may cause osteonecrosis.
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PMID:Osteonecrosis of vertebrae in a child with acute lymphocytic leukaemia during L-asparaginase therapy. 261 2

To determine if factor VIII-von Willebrand factor (vWF) complex is involved in the thrombosis associated with asparaginase-prednisone-vincristine induction therapy for acute lymphoblastic leukemia, plasma vWF was analyzed by sodium dodecyl sulfate-agarose gel electrophoresis and crossed immunoelectrophoresis. Five patients with cerebral thrombosis were studied; all had a decreased platelet count following the complication. Sequential studies of three patients disclosed changes in plasma vWF multimer pattern. One patient who was studied serially from 2 days before to 1 day after the event, had an increase in unusually large plasma vWF multimers that disappeared after the complication. The other two patients who were studied at presentation subsequently showed a decrease in plasma large vWF multimers, especially remarkable in the patient having the sharpest decrease in platelet count. No appreciable difference in vWF multimer pattern, when compared to normal pooled plasma, was found in the remaining two patients who were only studied at presentation, or in the seven controls who received the same treatment but did not develop thrombosis. Crossed immunoelectrophoretic analyses of two patients tested disclosed a right shift of immunoprecipitin line in one and a left shift in the other. Our findings suggest that the thrombotic complications resulted from platelet agglutination by plasma vWF.
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PMID:Involvement of von Willebrand factor in thrombosis following asparaginase-prednisone-vincristine therapy for leukemia. 311 Dec 51

Children with acute lymphoblastic leukemia (ALL), treated with L-asparaginase are at risk for cerebral thrombosis or hemorrhage because of coagulation protein deficiencies. The results and the importance of serial neuropsychological examinations after such complications in three children with ALL are presented. All patients showed marked aphasia and other cognitive deficits. Recovery was complete in two of three children.
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PMID:Cerebrovascular complications of L-asparaginase therapy in children with leukemia: aphasia and other neuropsychological deficits. 829 13