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)

16 patients of studies AML-BFM-83 and -87 with allogeneic bone marrow transplantation (BMT) in first complete remission (CR) were compared with matched controls with postremission chemotherapy (CT-MC). CT-MC were selected from 250 non-grafted patients with a minimum of remission duration corresponding to the median interval between remission and allogeneic BMT (7.3 and 3.6 months in studies BFM-83 and BFM-87). Matched pair criteria according to prognostic significance were: blast cell reduction day 15 in bone marrow, FAB subtypes, white blood cell count, age, and time to CR. Therapy results in BMT and CT-MC groups were comparable: 2 relapses and 2 treatment-related deaths after BMT vs. 5 relapses. The probability for event-free interval of 9 years was: .73 (SD .12) in the BMT group vs. .67 (SD .12) in the CT-MC group. Early and late toxicity was higher in the BMT group. 3 children of the BMT group had tolerable or severe sequelae (convulsive seizures, hemiparesis). Currently, there is no advantage for allogeneic BMT in first CR according to our results. Only high risk patients should be grafted as soon as possible after achieving CR.
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PMID:[Comparison of chemotherapy alone with allogeneic bone marrow transplantation in first full remission in children with acute myeloid leukemia in the AML-BFM-83 and AML-BFM-87 studies--matched pair analysis]. 151 60

The combination of high-dose busulfan (16 mg/kg) and 200 mg/kg cyclophosphamide is gaining increasing significance as a preparative regimen prior to autologous, syngeneic, or allogeneic marrow transplantation. A new regimen of high-dose busulfan in conjunction with a reduced dose of 120 mg/kg cyclophosphamide has recently been described as a preparative regimen prior to allogeneic transplantation. To determine the drug-related nonhematologic toxic effects of this new regimen without confounding factors associated with allogeneic transplantation, we conducted a pilot study using this new regimen in 20 patients with acute myeloid leukemia (AML) in first remission prior to autologous unpurged marrow transplantation. All patients experienced transient non-life-threatening acute drug-related toxicity with skin reactions in 20 (100%), nausea and vomiting in 20 (100%), oral mucositis in 18 (90%), hepatic functional impairment in 17 (85%), hemorrhagic cystitis in three (15%), and generalized seizures in two (10%) of these patients, respectively. Two procedural, fatal complications resulted from infectious causes that were not directly related to the speed of hematopoietic reconstitution or the toxicity of the preparative regimen. The 3-year event-free survival estimate (55% +/- 11%) and probability of leukemic recurrence (38% +/- 11%) attained with this new regimen in recipients of autografts in first remission of AML are promising and challenge comparisons with preparative regimens employing combinations of cytotoxic agents or total body irradiation (TBI).
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PMID:Acute toxicity and first clinical results of intensive postinduction therapy using a modified busulfan and cyclophosphamide regimen with autologous bone marrow rescue in first remission of acute myeloid leukemia. 215 49

Cerebral aspergillosis is one of the most common mycotic infections in the central nervous system causing different clinical features such as brain abscess, granuloma, meningitis, and encephalitis. Cerebral aspergillosis, however, may lead to a cerebral vascular accident such as intracranial hemorrhage or cerebral infarction. In this report, we present two patients with cerebral aspergillosis accompanied by intracranial hemorrhage. A total of 124 reported cases of cerebral aspergillosis are reviewed to ascertain the pathogenesis of the associated vascular lesion. The first patient was a 9-year-old girl, who developed drowsiness with a headache during the medical treatment for acute myelocytic leukemia. CT disclosed subarachnoid and intraventricular hemorrhage. The autopsy revealed that the aspergillus arteritis was the cause of repeated hemorrhage. The second patient was a 15-year-old boy with allergic purpura and renal failure, who suddenly developed a stupor with convulsive seizure. CT disclosed an intracerebral hemorrhage in the right parieto-occipital area. The patient gradually deteriorated and died in spite of the surgical removal of the hematoma. The autopsy revealed that the hemorrhage was caused by the aspergillus arteritis. Cerebral aspergillosis has two routes of infection to the central nervous system: hematogenous dissemination from the distant site (usually the lung) and direct extension from the contiguous site (usually the paranasal sinuses or orbit). The primary mechanism of neuropathology is different between these two types. Primary cerebral arteritis is most often seen in patients with the former type, whereas primary basal meningitis occurs in the latter. The incidence of clinico-pathological features is different between hematogenous dissemination type and direct extension type.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral aspergillosis as a cerebral vascular accident]. 339 19

Amsacrine (AMSA) has been shown to be an effective therapeutic agent in the treatment of adult acute nonlymphocytic leukemia (ANLL). The Eastern Cooperative Oncology Group studied the efficacy and toxicity of high-dose amsacrine (200 mg/m2/day for 5 days) in 38 adult patients with refractory and relapsed ANLL. The complete remission rate was low (8%). This dose level of amsacrine caused severe mucositis in 24% of patients and marked liver function abnormalities in 11%. Seizures did not occur, and two reversible cardiac events were not clearly attributable to amsacrine administration. Escalation of amsacrine beyond currently recommended total doses of 600-750 mg/m2 is unlikely to be of benefit.
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PMID:High-dose amsacrine (AMSA) therapy of relapsed and refractory adult acute nonlymphocytic leukemia. A phase II study. 654 66

Thirty-seven patients with acute leukemia in relapse were treated with a three-drug combination that included a 3- or 4-day course of AMSA with total doses ranging from 600 mg/m2 to 740 mg/m2 I.V., cytosine arabinoside 25 mg/m2 I.V. followed by 200 mg/m2 by continuous infusion daily for 5 days, and thioguanine 100 mg/m2 p.o. q 12h for 5 days. Eight of the 25 patients with acute nonlymphoblastic leukemia achieved a complete remission and 3 a partial remission. None of the five patients with acute lymphoblastic leukemia achieved a response and there was one partial remission in the seven patients with myelodysplastic syndrome or blastic CML. Reversible toxicity included nausea and vomiting (78%), alopecia (100%), pancytopenia (100%), mild stomatitis (63%), and hepatic dysfunction (24%). One patient developed seizures and cardiac arrhythmias. The activity of this combination in heavily treated patients with ANLL is comparable to that of the anthracycline-containing regimens, and its use in previously untreated patients with ANLL should now be explored.
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PMID:Treatment of acute leukemia in relapse with 4'(9-acridinylamino) methanesulfon-m-anisidide (AMSA) in combination with cytosine arabinoside and thioguanine. 689 90

Between October 1988 and December 1992, 167 patients with leukemia receiving marrow transplants from HLA-identical donors and conditioned with cyclophosphamide (120 mg/kg) were randomized to additional treatment with either busulfan (16 mg/kg, n = 88) or total body irradiation (TBI; n = 79). The busulfan-treated patients had an increased cumulative incidence of veno-occlusive disease of the liver, ie, 12% compared with 1% in the TBI group (P = .009). Furthermore, hemorrhagic cystitis occurred in 24% of the busulfan patients versus 8% in the TBI patients (P = .003). In patients with advanced disease beyond first remission or first chronic phase, transplantation-related mortality was 62% among the busulfan-treated patients compared with 12% among the TBI recipients (P = .002). These differences between the two groups were statistically significant in multivariate analysis. Seizures were seen in 6% of the busulfan-treated patients and were absent in the TBI group (P = .03). Grade II-IV of acute graft-versus-host disease (GVHD) was similar in the two groups, but grade III-IV and chronic disease was more common in the busulfan-treated group (P = .04). Death associated with GVHD occurred in 17% of the busulfan-treated group and 2% of the TBI group (P = .003). Patients treated with busulfan had a 3-year actuarial survival of 62%, which was worse than the 76% among those treated with TBI (P < .03). In multivariate analysis, poor survival was associated with advanced disease (P < .0001), no posttransplant septicemia (P = .0006), grade II-IV GVHD (P = .006), and busulfan treatment (P < .02). The incidence of relapse did not differ between the two groups. Relapse-free survival was also similar in the two treatment groups on analysis of data from all patients, children, patients with early disease, and those with acute myeloid leukemia, acute lymphoblastic leukemia, and chronic myeloid leukemia. However, in adults (P = .05) and patients with advanced disease (P = .005), leukemia-free survival was significantly better in those treated with TBI. We conclude that patients treated with busulfan have more early toxicity and an increased transplant-related mortality in patients with advanced disease. TBI is therefore the treatment of choice, especially in adults and patients with advanced disease. However, busulfan is an acceptable alternative for patients with early disease and for those in whom TBI is not feasible.
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PMID:A randomized trial comparing busulfan with total body irradiation as conditioning in allogeneic marrow transplant recipients with leukemia: a report from the Nordic Bone Marrow Transplantation Group. 816 51

Idiopathic hyperammonemia (IHA) has been described as a rare complication of intensive chemotherapy, but there is little data regarding its occurrence after bone marrow transplantation (BMT). IHA is defined as elevated plasma ammonia concentrations (> 200 mumol/l) in the absence of significant liver function abnormality. From a 21 year BMT database of 2358 patients, we have identified 12 patients (0.5%) with IHA, ages 19 to 46 years. Diagnoses included ALL (n = 2), AML (n = 4), CLL (n = 1), CML (n = 3) and aplastic anemia (n = 2). Eight received marrow from a matched sibling donor, three from an unrelated donor and one autologous marrow. IHA occurred between 14 and 106 days after transplant (median, 25 days). Most frequently patients presented with symptoms of a metabolic encephalopathy, with lethargy and confusion evolving into unresponsiveness, metabolic coma and in eight cases, seizures. At diagnosis of IHA, liver functions were normal or only modestly abnormal. Ten of the 12 patients died 1 to 9 days (median 3.5 days) after diagnosis of IHA despite treatment with combinations of dialysis and ammonia-trapping therapy. While IHA is a rare complication of BMT, it is associated with a high mortality. Early recognition of the syndrome by measurement of plasma ammonia concentrations in patients with neurological symptoms may improve outcome.
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PMID:Idiopathic hyperammonemia: a frequently lethal complication of bone marrow transplantation. 880 24

Subacute encephalopathy developed in four patients within one to two months after undergoing high-dose chemotherapy and bone marrow transplantation or peripheral blood progenitor (stem) cell transplantation for breast cancer, acute myeloid leukemia, and non-Hodgkin's lymphoma. None of the patients had previously known neurologic disorders, central nervous tumor or infection. Two patients presented with generalized tonic, clonic seizures, and two with confusion and lethargy. In all patients lumbar puncture and CT scans of the brain were normal, while magnetic resonance imaging (MRI) demonstrated multifocal predominantly white matter lesions. Phenytoin therapy was given to the two patients with seizures and all four patients improved without specific therapeutic intervention. Repeat MRIs became normal within three months. We report a delayed and transient encephalopathy which appears to be a unique complication of high-dose cytotoxic chemotherapy. The corresponding brain lesions may not be appreciated on CT scans, suggesting an expanded role for MRI studies in patients who develop neurologic findings while undergoing high-dose cytotoxic therapy.
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PMID:Delayed, transient encephalopathy after marrow transplantation: case reports and MRI findings in four patients. 884 58

Involvement of CNS with leukemic cells is well recognized complication of acute lymphatic leukemia (ALL) in childhood, but with recent improvements in systemic treatment and longer survival the incidence of this complication has increased in adults. Neurological symptomatology in patients with CNS leukemia is due to meningeal infiltration, but sometimes also to diffuse and nodular cerebral infiltration. Between January 1991 and December 1994, 36 patients suffering of acute leukemia, 28 with ALL, and 8 with acute myeloid leukemia (AML) were demonstrated to have neuroleukemia by the following criteria: (1) the presence at lumbar puncture (LP) pleocytosis and blast cells on CSF sediment (without positive bacteriologic and fungal cultures), and (2) the presence of neurological symptoms and signs. All 36 patients had 46 episodes of CNS involvement. All patients had neurological examinations during every episode, and according to the neurological abnormalities were classified into four categories. LP was performed in all, and CSF sediments obtained by sedimentation in Sayk's chambers, were routinely stained by MGG and cytochemical stains to detection of leukemic cells (Fig. 1). EEG was done during 21 episodes, CT scan during 15. We divided patients into four groups according to the most prominent neurological symptoms and signs. First was the group included 23 episodes (50%), (18 ALL, 5 AML), where symptoms and signs of meningeal irritation predominated, mimicking the clinical picture of meningitis. This meningeal syndrome can sometimes produce differential diagnostic problems with CNS infections, when CSF examination is of primary importance. Second was the group of 9 patients (6 ALL and 3 AML) with 10 episodes (21.74%) where cranial nerve symptoms and signs-predominated, or were exclusively present. Most frequently affected were bulbomotors, facials and opticus. Third group consisted of 8 ALL patients (8 episodes, 17.39%) with dominant spinal root symptomatology, caused by pathological infiltration of either spinal roots or meninges surrounding them. This group includes also one patient with mononeuritis multiplex and the other with painful polyneuropathy. All patients in this group had pain on straight leg raising, but we stress here that all patients from other groups had positive Lazarevitsh's sign, too. So, it can be a good differential diagnostic parameter for distinguishing toxic medicamentous polyneuropathy from leukemic poliradiculoneuropathy. Fourth group included 5 patients (5 episodes, 10.87%). 4 ALL and 1 AML, where cerebral symptoms, such as seizures, hemiparesis and psychoorganic syndromes were prominent. CSF was obtained during all episodes by lumbar puncture. The protein concentration ranged from 21-3180 mg/dl, and was above normal (45 mg/dl) during 28 episodes. Mild hypoglycoracchia was present during 16 episodes. Cell count ranged from 11-4816 cells/cm3, malignant cells were identified during all episodes with same morphological and cytochemical characteristics of identified type of leukaemia. It has been established that the most valuable diagnostic procedure in CNS leukemia is CSF examination, and detection of blasts is sufficient for diagnosis. All other procedures like EEG, myelography and CT have only supplemental diagnostic significance. Finally, in this study we showed that neurological symptomatology in patients with acute leukemia is not dependent of the type of leukemia, moreover different types of AL can have same neurological manifestations. As others, we sometimes used the term CNS leukemia in this paper, although it is clear that meninges and peripheral nervous system are most often involved. This is the reason why we suggest that neuroleukemia, or NS leukemia should be used as more appropriate expressions.
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PMID:[Neuroleukemia in adults]. 910 25

Refractory anemia with excess blasts in transformation (RAEB-T) is a pre-leukemic syndrome that can progress to acute myelogenous leukemia (AML). Although leptomeningeal disease in AML is rare and it is commonly associated with specific cytogenetic abnormalities, it has not been documented in RAEB-T. We report a woman who experienced seizures and had subarachnoid enhancement on MRI suggestive of leukemic infiltrates in the leptomeninges. Her bone marrow aspirate revealed 6.6% blasts and the presence of Auer rods, findings consistent with a diagnosis of RAEB-T. Subsequent cytogenetic analysis detected an uncommon deletion of chromosome 11q23, and the breakpoint on chromosome 11 is identical to that seen in AML patients having leptomeningeal disease and translocation between chromosome 9 and 11. Although RAEB-T is not considered as leukemia and is thought unlikely to involve the central nervous system, the presence of leptomeningeal disease and 11q23 deletion in our patient suggests that cytogenetic abnormality may be an important determinant of neurological complications, regardless of a diagnosis of RAEB-T or AML which is based on cellular morphology.
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PMID:Leptomeningeal disease in pre-leukemic syndrome: cytogenetic abnormality versus cellular morphology. 946 87


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