Influence of l-Asparaginase Escherichia Coli and Erwinia on Antithrombin III and Coagulation Factors During Induction Therapy of Acute Lymphoblastic Leukemia in Children

1997 ◽  
pp. 517-525
Author(s):  
A. Krauze ◽  
M. Jeleñska ◽  
M. Palester-Chlebowczyk ◽  
M. Ochocka
Keyword(s):  
Escherichia Coli ◽  
Acute Lymphoblastic Leukemia ◽  
Induction Therapy ◽  
Antithrombin Iii ◽  
Lymphoblastic Leukemia ◽  
Coagulation Factors ◽  
Leukemia In Children

scholarly journals PEG-asparaginase and native Escherichia coli L-asparaginase in acute lymphoblastic leukemia in children and adolescents: a systematic review

2020 ◽  
Vol 42 (1) ◽  
pp. 54-61 ◽  
Author(s):  
Camile Valle Medawar ◽  
Gabriela Bittencourt Gonzalez Mosegui ◽  
Cid Manso de Mello Vianna ◽  
Talita Martins Alves da Costa
Keyword(s):  
Escherichia Coli ◽  
Systematic Review ◽  
Acute Lymphoblastic Leukemia ◽  
Children And Adolescents ◽  
Lymphoblastic Leukemia ◽  
Leukemia In Children

scholarly journals Iatrogenic Coagulopathy and the Development of Posterior Reversible Encephalopathy Syndrome after L-asparaginase Chemotherapy

2016 ◽  
Vol 6 ◽  
pp. 7 ◽  
Author(s):  
Eugenia Rota ◽  
Daniele Vallisa ◽  
Nicola Morelli ◽  
Paola Scagnelli
Keyword(s):  
Escherichia Coli ◽  
Renal Failure ◽  
Posterior Reversible Encephalopathy Syndrome ◽  
Antithrombin Iii ◽  
Lymphoblastic Leukemia ◽  
Coagulation Factors ◽  
Immunosuppressive Drugs ◽  
Intrathecal Methotrexate ◽  
Posterior Reversible Encephalopathy ◽  
Reversible Encephalopathy

Posterior reversible encephalopathy syndrome (PRES) is a clinical and radiological syndrome mostly related to hypertension, eclampsia, renal failure, or to chemotherapy and/or immunosuppressive drugs. Although the PRES pathophysiology is multifactorial, hypertension and endothelial dysfunction are hypothesized to be the pivotal factors. Here we report a case of PRES in an adult patient after chemotherapy (Escherichia coliL-asparaginase [L-ASP], daunorubicin, vincristine, and intrathecal methotrexate) for acute lymphoblastic leukemia. The development of the PRES was strictly associated with an iatrogenic coagulopathy induced by L-ASP, which inhibits the biosynthesis of hepatic coagulation factors. The nadir of platelet count, antithrombin III (ATIII) and fibrinogen curve was coincident with the onset of the PRES neurological picture; subsequently, the normalization of the ATIII and fibrinogen levels seemed to parallel the good clinical evolution. This case seems to provide new insights into the PRES pathophysiological mechanisms.

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