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l-asparaginase-induced biochemical toxicities in young adults with acute lymphoblastic leukaemia and T-lymphoblastic lymphoma.
Pathology
December 2021
Department of Haematology, PathWest Laboratory Medicine, Fiona Stanley Hospital, Perth, WA, Australia. Electronic address:
Investigation of protective effect of L-carnitine on L-asparaginase-induced acute pancreatic injury in male Balb/c mice.
Dig Dis Sci
May 2015
Department of Biology, Faculty of Science, Kafkas University, 36100, Kars, Turkey,
Introduction: The present analysis deals with the biochemical and histopathological effects of L-carnitine in mice with L-asparaginase (ASNase)-induced experimental acute pancreatic injury (API).
Methods: A total of 32 male Balb/c mice were divided into four groups as follows. Group I (control) was injected with single saline via the intraperitoneal route.
L-asparaginase induced hyperlipidaemia in acute lymphoblastic leukaemia.
J Pak Med Assoc
March 2013
Department of Pediatric Haematology, Oncology, Babol University of Medical Sciences, Babol, Iran.
Objective: To evaluate hyperlipidaemia in patients with acute lymphoblastic leukaemia (ALL) receiving L-asparaginase.
Methods: A case-control study carried out between October 2007 and October 2010 with 77 patients undergoing chemotherapy at a teaching children's hospital in Babol, Iran. Patients were treated with anti-leukaemic agents according to the protocols for standard-risk and high-risk ALL.
Increased endogenous thrombin generation in children with acute lymphoblastic leukemia: risk of thrombotic complications in L'Asparaginase-induced antithrombin III deficiency.
Blood
January 1994
Department of Paediatrics, McMaster University, Hamilton, Ontario, Canada.
Pediatric patients with acute lymphoblastic leukemia (ALL) are at an increased risk of thromboembolic events. Potential responsible mechanisms include the disease process itself, treatment with chemotherapeutic agents (particularly L-Asparaginase [ASP]), or a combination of the disease and treatment. We studied thrombin regulation in 26 consecutive children with ALL and 14 healthy age-matched controls by: (1) plasma concentrations of prothrombin; (2) plasma inhibition of 125I-alpha-thrombin; and (3) four biochemical markers of in vivo thrombin activation (thrombin complexed to its inhibitor antithrombin III [ATIII; TAT], prothrombin fragment 1.
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