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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To add information about sporadic Legionnaires' disease, 87 cases of L. pneumophila pneumonia were reviewed. Twenty cases were nosocomial infections and 67 cases were community-acquired. Most cases (64%) occurred between July and October. The mean age of patients was 51.4 years and males outnumbered females 2.5:1.0. Thirty-one percent of patients were receiving corticosteroid, immunosuppressive, or antineoplastic chemotherapy when illness began. Immunosuppression at onset of illness was more common in nosocomial infections (90%) than in community-acquired infections (14%). Seventy percent of patients had underlying diseases. Malignancies, renal failure, and transplantation were the most common conditions underlying nosocomial infections. Chronic lung disease and malignancies were the most common diseases underlying community-acquired infections. The case-fatality rate in nosocomial infection (70%) was greater than that in community-acquired disease (22%). Clinical, laboratory, and radiologic features of the cases were examined. Illness ranged from mild to severe. Extrapulmonary findings of encephalopathy and renal failure were more common in fatal than in non-fatal cases. Indirect immunofluorescent and microagglutination antibody responses plateaued by the fourth week of illness. Twenty-nine patients died. The case-fatality rate of patients receiving erythromycin (6%) was less than that of patients receiving penicillin (36%), ampicillin (28%), cephalosporin (32%), or aminoglycosides (41%). Despite erythromycin therapy, the case fatality rate for nosocomial L. pneumophilia pneumonia was unacceptably high (25%).
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PMID:Sporadic Legionnaires' disease: clinical observations on 87 nosocomial and community-acquired cases. 646 87

Eleven patients with familial hemophagocytic lymphohistiocytosis (FHLH) are described. They all belonged to four Jewish families of Iranian and Iraqi origin. Parental consanguinity was found in three families. The age of onset of disease ranged from 6 weeks to 36 months. All patients had fever, wasting, and enlargement of the liver and spleen. In addition, lymph-node enlargement and neurologic complications were common. The most consistent laboratory findings were pancytopenia, atypical lymphomonocytoid cells in the peripheral blood, abnormal liver function test results, and increased cerebrospinal fluid protein. The course was fatal in all patients. Nine of the 11 patients died within 2 weeks to 3 months of presentation, and 2 patients achieved temporary remissions but died of disease within 8 and 24 months, respectively. Response to antibiotic therapy or to the administration of corticosteroids and cytotoxic drugs was unimpressive. Pancytopenia complicated by sepsis or bleeding, hepatic failure, or encephalopathy were the terminal events. This report draws attention to the existence of FHLH in Jews of Iranian-Iraqi origin in whom parental consanguinity is very common.
Cancer 1984 Nov 15
PMID:Familial hemophagocytic lymphohistiocytosis (FHLH) in Israel. I. Description of 11 patients of Iranian-Iraqi origin and review of the literature. 648 37

The authors report two cases of neoplastic encephalopathy. In one patient with oviduct carcinoma it had the form of cerebellopathy. In the other case of renal carcinoma it appeared as encephalopathy with a nearly exclusive involvement of cerebral hemispheres. The reaction of microglia, lymphocytes and diffuse demyelination found in these cases are regarded by the authors as a result of autoimmunization in the course of malignant neoplasm. Attention is called to the importance of axial computer tomography in the intravital diagnosis of this encephalopathy.
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PMID:[Neoplastic encephalopathy in the light of 2 observed cases]. 652 28

An acute episode of encephalopathy after the infusion of 16 g methotrexate is reported in a 12-year-old girl with osteogenic sarcoma. The complication occurred during the 11th treatment course, when severe vomiting and diarrhea were followed by a low urine output with consecutive toxic concentrations of methotrexate in serum and cerebrospinal fluid leading to severe systemic and central nervous system toxicity. The onset of the central nervous system toxicity was acute with slurred speech, paresis of the external rectus eye muscles, ataxia, and hemiparesis, and symptoms resolved completely after 30 hours by treatment with calcium leucovorin and forced diuresis. After management of the cerebral and systemic toxicity, high-dose methotrexate treatment could be reinstituted, and was followed by no further complications. In contrast to the transient cerebral dysfunctions, probably caused by embolization of tumor tissue in the early course of high-dose methotrexate treatment, the acute neurologic syndrome observed in the current case after the prolonged use of methotrexate seemed to be related to direct central nervous system toxicity of the drug.
Cancer 1984 May 01
PMID:Transient encephalopathy during the late course of treatment with high-dose methotrexate. 658 97

The authors have studied 119 cases of partial epilepsies, selected from the patients treated in the Centre Saint-Paul between 1966 and 1970 according to the following criteria: seizures beginning before the age of 12; electro-clinical evolution known about for at least 5 years (mean duration: 13 years 3 months). The cases are separated in 4 groups according to the severity of epilepsy: (1) complete recovery and withdrawal of treatment; (2) no seizure with treatment; (3) persisting seizures with treatment; (4) frequent and severe seizures with treatment. The severe epilepsies are characterized by an early commencement of fits (before 3 years), associated symptoms of encephalopathy, lack of familial antecedents, association of several types of seizures, or the existence of a particular critical semiology (either complex partial motor seizures, or succession of simple motor and complex semiology, sudden fall, or reflex triggering). However, it is also necessary to consider the syndromic grouping of signs which is of greater value than a simple analysis of benignity or malignancy factors.
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PMID:[The partial epilepsies in childhood--evolution and prognosis factors (author's transl)]. 680

Seven patients with bone or soft tissue sarcomas but without metastatic CNS disease developed a chronic leukoencephalopathy after high-dose (8000-15,000 mg/m2) iv methotrexate (MTX) chemotherapy with leucovorin (LV) rescue. Approximately 12 MTX-LV treatments were administered over a 3-7 month period. None of the patients had cranial irradiation. The syndrome usually began several months after the initiation of chemotherapy with subtle personality changes followed by a progressive dementia, focal seizures, pseudobulbar palsy, spastic quadriparesis, and stupor. Computerized tomographic scans revealed diffuse white matter hypodensity in five patients and atropic changes in five patients. Serum MTX concentrations were elevated in four of six patients prior to several MTX-LV treatments, suggesting that MTX persisted in tissues for a long time. Abnormally high levels of MTX were detected in the cerebrospinal fluid of all four patients several days after an MTX-LV treatment, at a time when their encephalopathy was most severe. Pathologic brain material was obtained from three patients and revealed a spectrum of abnormalities. The syndrome observed in our patients clinically resembles the one described in children with acute lymphatic leukemia who received cranial irradiation and large cumulative amounts of low-dose (12-20 mg/m2) systemic MTX without LV.
Cancer Treat Rep 1980
PMID:Leukoencephalopathy following high-dose iv methotrexate chemotherapy with leucovorin rescue. 697 Jun 16

In order to assess the prevalence of venocclusive disease in autopsied recipients of bone marrow transplantation, we reviewed coded liver histology from 204 consecutive autopsied recipients transplanted for leukemia (142), other malignancies (5), or aplastic anemia (57). Twenty-seven patients with leukemia, 2 with carcinoma, and 3 with aplasia had venocclusive disease and survived 2-86 days post-transplant. Early lesions showed subintimal edema and hemorrhage within small central venules and centrilobular congestion with hepatocyte degeneration. Later lesions showed subtotal to complete fibrous obliteration of the central venule lumina and centrilobular sinusoidal fibrosis. Thirteen patients had a subclinical course, and 19 were symptomatic. Venocclusive disease was life-threatening or lethal in 13. Typical symptoms developed 1-3 wk post-transplant and consisted of sudden weight gain, hepatic enlargement, ascites, high bilirubin, and encephalopathy. Statistical analyses showed a significantly higher prevalence of venocclusive disease associated with transplantation for leukemia (P = 0.014), pretransplant conditioning with more rigorous chemoradiotherapy regimens (P < 0.001) and three- to fourfold increase of venocclusive disease in patients whose conditioning included dimethyl busulfan (P < 0.005). Abnormal liver tests before transplant were also more prevalent among patients with venocclusive disease. No factors predicted the clinical outcome of established venocclusive disease. Venocclusive disease showed no association with hepatic graft-versus-host disease even among prolonged cases with severe periportal hepatitis and cholestasis. Other centrilobular lesions (hepatocyte degeneration, sinusoidal fibrosis, and phlebosclerosis) were identified in 23 patients. These non-specific changes may occur with viral hepatitis, graft-versus-host disease or chemoradiotherapy effects.
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PMID:An analysis of hepatic venocclusive disease and centrilobular hepatic degeneration following bone marrow transplantation. 700 4

We treated 13 adult patients with acute leukemia or chronic myelocytic leukemia (CML) in blast phase using succinylated Acinetobacter glutaminase-asparaginase (SAGA) administered on a daily dose schedule. SAGA reduced the peripheral blast count in two patients with acute lymphoblastic leukemia and two with blastic CML; however, no patient achieved either complete or partial remission. Marked central nervous system toxic effects (encephalopathy and coma) were observed, limiting treatment in patients whose disease appeared responsive; this effect finally prompted early discontinuance of the trial. Other toxic effects observed included nausea, hyperglycemia, and respiratory alkalosis. Hypersensitivity reactions to the enzyme were not seen. Pharmacologic analyses showed that prolonged blood glutamine depletion was achieved only by daily enzyme administration; however, we noted the importance of performing amino acid analysis on blood which was deproteinized immediately following phlebotomy. Our results demonstrate excessive central nervous system toxicity when glutaminase-asparaginase is administered on a daily schedule. Because of this effect, we propose that future trials of similar enzymes be limited to short courses of enzyme therapy, possibly with the addition of antimetabolites or amino acid analogs, which could enhance the antitumor effect without increasing toxicity.
Cancer Treat Rep 1982 Jul
PMID:Clinical evaluation of succinylated Acinetobacter glutaminase-asparaginase in adult leukemia. 704 29

A case of fatal encephalopathy following administration of misonidazole (MISO) is reported. Anorexia and dehydration preceded signs of encephalopathy after a cumulative dose of 18 g (11 g/m2) of MISO in five weekly doses. Serum MISO levels four hours after weekly administrations were markedly elevated. Postmortem examination revealed focal cortical neuronal necrosis and hemorrhage with focal demyelination. The possible relationship of dehydration or altered drug metabolism to the development of MISO central nervous system toxicity is noted.
Cancer 1982 Feb 01
PMID:Fatal misonidazole-induced encephalopathy: an RTOG case report. 705 5

In an attempt to decrease the activation of 5-FU by normal cells relative to cancer cells, 20 patients with metastatic cancer were given 72 courses of 5-FU and allopurinol (HPP) in a phase I trial. 5-FU was given daily by iv bolus injection for 5 consecutive days every 4 weeks: HPP, 300 mg orally every 8 hours for 6 consecutive days, was started 24 hours before the first injection of 5-FU. HPP appeared to modulate 5-FU toxicity by allowing higher doses (18-21 mg/kg daily for 5 days) to be given. Unexpectedly, neurotoxicity was the dose-limiting toxicity; it was slowly reversible and manifested primarily as encephalopathy, with some patients having cerebellar signs. Gastrointestinal and hematologic toxic effects were mild and infrequent. Because of the high incidence of neurotoxicity and low response rate, this program does not appear to offer any advantages over conventional dose schedules of 5-FU alone.
Cancer Treat Rep 1982 Sep
PMID:High-dose allopurinol modulation of 5-FU toxicity: phase I trial of an outpatient dose schedule. 711 49


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