Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 15-year-old boy diagnosed with acute lymphoblastic leukemia (ALL) in 1983. Induction therapy included L-asparaginase. After the second dose of L-asparaginase, he had a left sided focal seizure and computed tomography (CT) scan of the head showed a right frontal infarct. No further L-asparaginase was given. Complete remission was achieved and he successfully completed therapy in 1986. Eight months later he had an isolated bone marrow relapse. Reinduction therapy included L-asparaginase. After the fourth dose of L-asparaginase, he presented with severe headache and a CT scan showed a right temporal infarct. Repeat infarction on rechallenge with L-asparaginase has not been previously reported. Prophylactic therapy, such as fresh frozen plasma, should be considered before patients, with a previous cerebral insult, are rechallenged with L-asparaginase. However the effectiveness of such therapy has not been established.
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PMID:Recurrent cerebrovascular accident with L-asparaginase rechallenge. 143 23

The case histories of two patients with acute lymphocytic leukemia, who developed central nervous system complication during combined chemotherapy are described. The neurological picture could be characterized by symptoms of headache, mental deterioration, hemiparesis and seizures. Following L-asparaginase administration one patient had intracranial thrombosis with focal seizures and hemiparesis associated with clotting abnormalities, including severe hypofibrinogenemia and decreased antithrombin III activity. In the other patient, it was after intrathecal administration of Methotrexate when mental deterioration associated with the symptoms of progressive leukoencephalopathy occurred. It arises the possibility that with increasing complexity of combined chemotherapy the occurrence rate of neurological complications will also increase.
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PMID:[Neurologic complications during chemotherapy of children with acute lymphoid leukemia]. 157 51

42 dogs with non-Hodgkin's lymphoma (NHL) were randomized for treatment with either PEG-L-asparaginase 10 IU/kg intramuscularly (n = 22) or L-asparaginase 400 IU/kg intraperitoneally (n = 20). Another 20 dogs were treated with either PEG-L-asparaginase 30 IU/kg (n = 10) or L-asparaginase 400 IU/kg (n = 10). Each treatment protocol consisted of two asparaginase treatments followed by a 10-week period of induction chemotherapy and then maintenance on asparaginase until progression occurred. No significant differences were found between treatments in the response rates after 2 weeks of asparaginase therapy or in the time to relapse, the time to treatment failure or the remission period. The reaction to asparaginase after the initial 2 weeks was a prognostic factor for the total duration of remission under asparaginase maintenance therapy. No side-effects were noted in the dogs treated with PEG-L-asparaginase, whereas 14 (48%) of the L-asparaginase treated dogs had side-effects related to this drug, including anaphylactic shock (9), anorexia or vomiting (4), hypersensitivity-related oedema (3), seizures (1) and acute pancreatitis (1). No abnormalities in clotting times, fibrinogen levels or antithrombin-III levels were found in any of the 62 dogs. PEG-L-asparaginase has the same anti-tumour activity as native L-asparaginase in dogs with NHL, but lacks side-effects.
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PMID:Polyethylene glycol-L-asparaginase versus native L-asparaginase in canine non-Hodgkin's lymphoma. 214 33

In 79 children treated for acute lymphoblastic leukaemia according to protocol ALL-BFM 81, serial EEG examinations were performed before, during and after therapy. Diffuse changes of the background activity were observed in 64% of the children at the time of diagnosis. During induction and reinduction treatment with vincristine and L-asparaginase, and with some delay after CNS irradiation, a marked slowing developed in up to 65% of patients. Children who had not been irradiated showed transient disturbances during treatment with medium-dose-methotrexate. Reinduction induced more abnormal EEGs in the children who had been irradiated. At the end of maintenance therapy, only slight EEG changes were found. No differences between the irradiated and non-irradiated group were then seen. Children with CNS leukaemia or seizures differed from those with an uncomplicated treatment in that they more often showed focal and persistent disturbances. In 39 patients who stayed in first remission for at least 18 months after the termination of treatment, a follow up investigation was performed. From the EEG examination, including power spectral analysis, no differences were found between irradiated and non-irradiated patients. Slowing of the dominant frequency was seen in the patients with more severe leukaemia and in those whose EEG had been markedly abnormal at diagnosis. The visually evoked potentials were normal in all groups of patients. In the brainstem auditory evoked potential, a prolongation of the latency of wave I and a decrease of the I-V interval was found in irradiated patients. We conclude that the diffuse EEG changes frequently emerging during treatment are reversible. Persistent or lateralized changes can indicate a neurological complication.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prospective neurophysiological study in children treated for acute lymphoblastic leukaemia: serial EEG during treatment and long-term follow up with evoked potentials. 227 9

During a 4-year period, 26 children with systemic malignancies suffered cerebrovascular accidents. These occurred in 17 patients with lymphoreticular malignancy and nine patients with solid tumors. They were the presenting signs of malignancy in three patients and were the direct cause of death in six. Cerebrovascular accidents were directly related to disseminated intravascular coagulation in eight patients, to chemotherapy in eight patients, to metastatic tumor in three patients, to thrombocytopenia in three patients, and to fungal meningitis in one patient. All patients with disseminated intravascular coagulation had leukemia and at times, cerebrovascular thrombosis predated systemic or laboratory evidence of disseminated intravascular coagulation. This review indicates that four major syndromes are apparent in children with cancer: vascular thrombosis associated with disseminated intravascular coagulation, acute arterial or sagittal sinus thrombosis secondary to L-asparaginase in children with leukemia, acute neurologic dysfunction in patients with osteogenic sarcoma treated with high-dose methotrexate, and obtundation, seizures, and focal neurologic deficits in patients with neuroblastoma metastatic to the torcular region. Although elevated WBC counts and thrombocytopenia occur frequently in children with cancer, in themselves they uncommonly result in strokes. It is concluded that cerebrovascular accidents are a relatively frequent cause of acute neurologic compromise in children with cancer and that certain types of malignancies and their treatment predispose patients to this complication.
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PMID:Cerebrovascular accidents in children with cancer. 386 Jul 96

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, oxyphilic necrosis in the parathyroid glands. Although survivors remained clinically well, they also developed hypocalcemia and parathyroid necrosis but to a lesser degree. Rabbits given an equivolumetric amount of saline did not develop alterations in any of these parameters. L-Asparaginase, therefore, exerts a direct toxic effect on the parathyroid glands of rabbits. The implications of this finding for man are briefly discussed.
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PMID:Parathyroid necrosis and hypocalcemic tetany induced in rabbits by L-asparaginase. 505 53

Sudden cerebrovascular insults occurred during or immediately following remission induction therapy in 4 children with acute lymphoblastic leukemia. In 3, cerebral infarction was due to thrombosis. In the fourth, an intracerebral hematoma developed representing either frank hemorrhaging or a hemorrhagic infarction. None of the patients had central nervous system leukemia or extreme leukocytosis at the time of diagnosis. Symptoms were obtundation, hemiparesis, seizures, and headache. The induction chemotherapy included L-asparaginase which causes deficiencies of antithrombin, plasminogen, fibrinogen, and factors IX and XI. These hemostatic abnormalities may explain the thromboses and bleeding observed in these children.
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PMID:Thrombotic and hemorrhagic strokes complicating early therapy for childhood acute lymphoblastic leukemia. 693 53

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 abnormalities, including severe hypofibrinogenemia, probably the result of L-asparaginase administered during induction therapy of acute lymphocytic leukemia.
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PMID:Intracranial hemorrhage and focal seizures secondary to use of L-asparaginase during induction therapy of acute lymphocytic leukemia. 693 31

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. Thirteen children had intracranial thrombosis or hemorrhage, four had extremity thrombosis, and one had both an intracranial hemorrhage and an extremity thrombosis. These events occur characteristically in the third and fourth weeks of therapy during or just after a three-week course of L-asparaginase. Symptoms of headache, obtundation, hemiparesis, and seizure were common for the intracranial events: local pain, swelling, and discoloration were common for the extremity thromboses. These complications have been recognized in 1 to 2% of children undergoing induction therapy which includes asparaginase.
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PMID:A syndrome of thrombosis and hemorrhage complicating L-asparaginase therapy for childhood acute lymphoblastic leukemia. 695 21

We reviewed the records of 127 consecutive pediatric patients with acute lymphoblastic leukemia (ALL) to determine the incidence, timing, etiologies, and recurrence rate of seizures in this population. Patients with ALL and seizures were identified retrospectively by review of the records of all pediatric ALL patients who were diagnosed and treated during the years 1983 through March 1993 in a large tertiary-care hospital. Seventeen patients (13%) developed one or more seizures. In 16 patients, seizures occurred during antileukemic treatment, and in almost all of them seizures were related to intrathecal methotrexate (IT MTX) or subcutaneous L-asparaginase treatment. One patient who developed a seizure while not receiving chemotherapy had a history of cerebral infarctions. In 8 patients, (47%), the initial seizure episode was associated with a cerebral lesion. One or more seizures recurred in 6 patients. Four of these patients had an isolated recurrence, in 3 patients < or = 3 months and in 1 patient < or = 6 months after the initial event. Two patients (12%) with static encephalopathy and neurological deficits developed a chronic seizure disorder. There is a significant risk of acute symptomatic seizures in pediatric ALL patients. Most seizures in these patients occur during the acute treatment phase and are most frequently related to side effects of chemotherapy. The long-term recurrence risk is low; recurrence occurs most often in patients with evidence of cerebral structural lesions and neurological deficits. Long-term antiepileptic drug (AED) therapy should be restricted to such patients.
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PMID:Prognosis and treatment of seizures in children with acute lymphoblastic leukemia. 763 3


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