Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cyclophosphamide has been considered one of the reference drugs of chemotherapy in randomized trials in hormone-refractory prostate cancer by the National Prostatic Cancer Project (NPCP). Ifosfamide, another oxazaphosphorine agent, and an analog of cyclophosphamide, appears to be more active and less toxic in a broad spectrum of tumors. Fifteen patients with metastatic hormone-refractory prostate cancer were treated with continuous infusion of ifosfamide 2 g/m2 per day for 2 days, together with the uroepithelial protective agent Mesna 2.4 g/m2 per day for 2 days, both to be repeated every 3 weeks. All patients have failed on previous hormonal therapy and 7 patients had received previous chemotherapy. The median age was 66 years. Fourteen patients were evaluable; none of whom achieved an objective response. Four patients were stabilized and 10 had disease progression while on chemotherapy. Major toxicity included 2 reversible encephalopathy, 3 grade I reversible renal toxicity, and 1 hemorrhagic cystitis. We concluded that ifosfamide given in this schedule in this group of patients is not an active agent in prostate cancer.
Cancer Invest 1990
PMID:Phase II trial of ifosfamide in the treatment of metastatic hormone-refractory patients with prostatic cancer. 212 44

Primary care physicians have a crucial role in recognition of potentially emergent conditions in patients with known or suspected cancer. This task presents a significant challenge because the initial manifestations of these conditions are usually nonspecific. In most cases, therapy is far more effective when diagnosis is made at the earliest possible point. Thus, physicians should become familiar with conditions commonly seen in cancer patients, such as superior vena cava syndrome, malignant pericardial effusion, spinal-epidural metastasis, and altered mentation from brain metastases, metabolic encephalopathy, or hypoglycemia.
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PMID:Emergent signs of cancer. Recognizing them early in the office or ER. 214 60

Although polymicrobial bacteremia has been described in several previous series, there has been no recent study of patients using rigorous statistical analysis. Our objective was to characterize a present-day patient population with polymicrobial bacteremia and to define factors prognostic of survival. Polymicrobial bacteremia accounted for 6% of all positive blood cultures at a university hospital and a Veterans Administration hospital over a 2 1/2 year period in the late 1980s. The majority of these patients were elderly with significant underlying diseases, notably malignancies, and 56% of all episodes were nosocomially acquired. Enterobacteriaceae have remained the most common organisms, though the frequency of gram-positive cocci isolated has increased compared to older studies. Gastrointestinal, genitourinary, and skin and soft-tissue sources were the most common, although the incidence of infections due to central venous catheters appeared to be increasing. The source of 25% of bacteremia was not identified despite newer diagnostic techniques. By univariate analysis, mortality, which was 36% overall, correlated with thrombocytopenia, respiratory failure, disseminated intravascular coagulation, encephalopathy, severity of underlying disease, hemolysis, adult respiratory distress syndrome, use of steroids, renal insufficiency, institution, presence of central lines, and nosocomial acquisition. Using stepwise logistic regression analysis, mortality was predicted by respiratory failure, severity of underlying disease, and hemolysis. We conclude that polymicrobial bacteremia remains an important entity in the present-day hospitalized population, with an increasing frequency of gram-positive organisms and catheter sources, and a large proportion of undiagnosed etiologies.
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PMID:Polymicrobial bacteremia in the late 1980s: predictors of outcome and review of the literature. 218 Dec 31

Following its early entry into the central nervous system (CNS), HIV-1 alters cerebral cell architecture and may subsequently affect higher cognitive functions, leading eventually in some patients to HIV-1 encephalopathy. The CNS may also be the target of opportunistic infections and malignancy secondary to HIV-1 immunosuppression. Studies at the cellular, anatomical, and behavioral levels present evidence for significant involvement of the CNS in HIV-1 disease, while initial reports of treatment strategies hold promise for providing some amelioration in affected individuals.
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PMID:Central nervous system effects of human immunodeficiency virus type 1. 218 20

Acute changes in mental status (AMS) develop in children with cancer from a multitude of cancer- and treatment-related complications. To determine the incidence, etiology, and outcome of children with cancer who had AMS, the medical records of all children under 18 years of age with systemic cancer (excluding primary central nervous system tumors) who had AMS in our institution during the years 1981 through 1987 were reviewed. AMS developed in 89 of 815 children at risk (11%). The AMS was caused by seizures in 53 (60%), an encephalopathy in 24 (27%), and a stroke syndrome in 12 (13%). AMS occurred in 42 of 305 (14%) with leukemia, 16 of 139 (12%) with lymphoma, 14 of 136 (10%) with sarcoma, 10 of 104 (9%) with neuroblastoma, and 7 of 104 (5%) with other malignancies. Children with acute lymphocytic leukemia were more prone to having seizures (61%), while children with nonacute lymphocytic leukemia were almost equally likely to have encephalopathies, strokes, or seizures. Children with lymphoma were admitted for treatment most often with an encephalopathy (44%). Etiologies for AMS were evaluated vigorously, and one or more etiologies were identified in 80 of 89 (89%) patients. Dependent on the type of tumor, the anticancer treatment used and, timing during the course of illness AMS occurred, specific diagnoses were more likely. Neurologic morbidity and mortality were dependent on the cause of AMS. Children with seizures that were initially difficult to control were more likely to require long-term anticonvulsant therapy.
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PMID:Acute mental status changes in children with systemic cancer. 230 89

Children presenting with advanced leukaemia and non-Hodgkin's lymphoma may develop life-threatening complications in the early stages of management. Major metabolic disturbances with encephalopathy, septicaemic shock, pneumonitis, massive haemorrhage, or the physical effects of tumour masses may on occasion warrant intensive therapy. Close liaison between paediatric oncologists, oncological surgeons, and anesthesiologists is essential in establishing admission criteria for such cases and in defining therapeutic end points in the event of multisystem failure. This paper discusses the principles of intensive care management of patients with haematological malignancies by considering two cases who developed the tumour lysis syndrome with respiratory and renal failure. A case associated with metabolic encephalopathy is also described.
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PMID:Tumour lysis syndrome and the anaesthesiologist: intensive care aspects of paediatric oncology. 234 46

A panel of nine monoclonal antibodies raised against human hemopoietic cells was used for immunohistological labeling of frozen sections of human nervous tissues and tumors. Three antibodies showed a remarkably consistent labeling pattern when tested on 18 samples of normal or reactive tissue, on 31 neurogenic and 17 non-neurogenic tumors in an indirect immunofluorescence technique. VIM C6, an antibody recognizing cells of the granulocyte series, showed surface labeling of normal and reactive glial cells and of all types of glioma regardless of the grade of malignancy. VIT 13, an antibody recognizing activated T-cells, labeled the processes of normal, reactive, and neoplastic glia in a manner very similar to but not identical with glial fibrillary acidic protein (GFAP). VIB C5, an antibody recognizing B cells and granulocytes, showed surface labeling restricted to malignant cells (malignant gliomas and primitive neuroectodermal tumors) and fetal brain, thus recognizing, within the nervous system, an oncofetal antigen. Due to this operational specificity within the nervous system, some of the antibodies described here might have a role as diagnostic markers for CNS tumors. This study confirms and expands previous data that sharing of antigenic determinants by hemopoietic cells and nervous tissue or neurogenic tumors is common. However, the significance of such cross-recognition is still obscure. It is tempting to speculate that cross-reacting auto-antibodies might contribute to tissue damage in some immune-mediated neurologic diseases (myasthenia gravis, multiple sclerosis, CNS involvement in systemic lupus erythematosus) or to impairment of immunoregulation in multiple sclerosis or glioma patients. Furthermore, sharing of surface determinants might be responsible for the dual tissue tropism of some viruses, including the lymphotrophic virus (HTLV) in the encephalopathy of the acquired immune deficiency syndrome (AIDS).
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PMID:Shared antigenic determinants between human hemopoietic cells and nervous tissues and tumors. 241 Oct 97

Fludarabine phosphate (NSC 312878), an adenosine deaminase resistant analogue of 9-beta-D-arabinofuranosyladenine, has entered clinical trials. Eleven patients with acute leukemia in relapse received 14 courses of fludarabine phosphate as a 5-day continuous infusion administered at doses of 40 to 100 mg/m2/day. Toxicity was characterized by uniform myelosuppression, as well as occasional nausea, vomiting, and hepatotoxicity. Three episodes of metabolic acidosis and lactic acidemia were noted. In addition, three patients suffered neurotoxicity. Two of these three patients had a severe neurotoxicity syndrome characterized by blindness, encephalopathy, and coma. Neither patient recovered neurological function. Neuropathological findings at autopsy were characterized by a diffuse, necrotizing leukoencephalopathy which was most severe in the occipital lobes. The medullary pyramids and posterior columns were also severely affected. This sporadic fatal neurotoxicity was observed only at doses greater than 40 mg/m2/day. The maximum tolerated dose for a 5-day infusion of fludarabine phosphate is thus 40 mg/m2/day.
Cancer Res 1986 Nov
PMID:Fludarabine phosphate (NSC 312878) infusions for the treatment of acute leukemia: phase I and neuropathological study. 242 88

Previous work suggested that methotrexate (MTX) may cause encephalopathy by inhibiting biosynthetic pathways for dopamine and serotonin in the brain. We examined this issue by measuring the neurotransmitter metabolites homovanillic acid and 5-hydroxyindoleacetic acid in the lumbar CSF of rhesus monkeys receiving continuous intracerebroventricular infusions of MTX or dichloromethotrexate. Infusion of the lowest dose (0.05 mg/day) produced a large (300%) rise in homovanillic acid levels and a modest elevation in 5-hydroxy-indoleacetic acid. During higher dose infusion, which was associated with clinical encephalopathy, the biogenic amine metabolites fell from their previous elevated levels. In one encephalopathic monkey, an injection of 1 mg of leucovorin produced a marked elevation in CSF monoamine metabolites within 1 hour and rapid clinical recovery. In contrast, leucovorin produced no change in monoamine metabolites in control animals. The data suggest that MTX may block egress of monoamine metabolites from CSF at the lower doses and suppress neurotransmitter turnover at toxic doses which cause encephalopathy. Serial measurements of CSF monoamine metabolites deserve further investigation as biochemical markers for toxic effects of MTX on neuronal metabolism in the CNS.
Cancer Treat Rep 1986 Oct
PMID:Effects of intraventricular methotrexate on cerebrospinal fluid monoamine metabolites in rhesus monkeys. 242 91

Fourteen patients developed severe central nervous system (CNS) toxicity after receiving an investigational antitumor agent, fludarabine phosphate (FAMP). The CNS toxicity has the distinctive features of delayed onset and progressive clinical course. Visual deficits were the most common presenting symptom and developed eventually in most cases. Deterioration of mental status and progressive encephalopathy were also observed. The development of clinical CNS toxicity appears dose-related; thirteen of 36 patients (36.1%) who received FAMP at high doses (greater than or equal to 96 mg/m2/day for 5-7 days per course) developed neurotoxicity, while only one of 443 patients (0.2%) who received the drug at low doses (less than or equal to 125 mg/m2 per course) developed similar toxicity. Although the precise mechanism responsible for this toxicity is yet unknown, progressive demyelination appears to be the responsible process. Extensive review of the clinical data failed to identify factors which might contribute to the development of CNS toxicity. Patients on trials of FAMP should be meticulously monitored for the possible development of neurotoxicity.
Cancer Treat Rep 1986 Oct
PMID:Central nervous system toxicity of fludarabine phosphate. 242 92


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