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)

We report Reye syndrome in an 11-year-old boy whose first symptoms were generalized convulsions and coma without clinical or laboratory evidence of liver disease. Serum glutamic oxaloacetic transaminase and lactate dehydrogenase (LDH) values increased strikingly on the third day after the onset of coma. These enzymatic changes were associated with prolongation of prothrombin time. A rise in blood ammonia concentrations began on the fourth day of coma. The diagnosis of Reye syndrome was confirmed by a liver biopsy and at autopsy. This case demonstrates that encephalopathy in Reye syndrome can develop prior to detectable hepatic involvement, and suggests that factors unrelated to generalized liver damage may occasionally play a role in the pathogenesis of this obscure disorder.
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PMID:Reye syndrome without initial hepatic involvement. 84 16

The alpha-keto acid dehydrogenase complex and its component enzymes, lactate dehydrogenase, pyruvate carboxylase, cytochrome c oxidase, succinate-cytochrome c reductase, NADH-cytochrome c reductase, and the concentration of cytochromes and enzymes of beta-oxidation in muscle from a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes were studied and no specific defect was found. These results raise the possibility that the mitochondrial changes in the patient may be secondary.
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PMID:Biochemical studies in mitochondrial encephalomyopathy. 368 14

Lactate dehydrogenase isoenzymes in cerebrospinal fluid were measured during the first 24 h of life in 25 asphyctic neonates. The infants were subjected to clinical and developmental examinations for a mean follow-up period of 15.2 months. The mean values for cerebrospinal LDH2(MH3) and LDH3(M2H2) isoenzymes were significantly higher in asphyctic infants who died from hypoxic-ischemic encephalopathy or who survived but suffered neurologic sequelae, than they were in those asphyctic infants who survived and were normal in the follow-up studies. Therefore, the authors conclude that the lactate dehydrogenase isoenzyme pattern in cerebrospinal fluid may be of value when assessing anoxic brain damage.
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PMID:LDH isoenzymes in CSF in the diagnosis of neonatal brain damage. 376 14

The D(-) isomer of lactic acid appears to cause a form of metabolic encephalopathy experienced by patients who have had jejunoileal bypass for morbid obesity. However, analysis for D(-)-lactate is not routinely available in clinical or reference laboratories. We describe an enzymic centrifugal-analyzer assay for D(-)-lactate in plasma or serum, with use of D(-)-lactate dehydrogenase. The method involves two-point kinetic calibration and preincubation of specimen and NAD+, thus eliminating the need for specimen-blanking or protein-precipitating pretreatment. This rapid, accurate, and precise assay should be helpful in evaluating patients with "short-bowel syndrome" who display confusion, lethargy, ataxia, or other central nervous-system disturbances that may be ascribable to D(-)-lactic acidosis.
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PMID:Kinetic enzymic assay for D(-)-lactate, with use of a centrifugal analyzer. 661 31

Two brothers had intermittent episodes of muscle weakness, lethargy, hyperammonemia, rhabdomyolysis, and elevated activities of creatine phosphokinase (CPK), lactic dehydrogenase, and SGOT in serum associated with low muscle carnitine but normal serum carnitine concentrations. These siblings represent a "mixed" form of carnitine deficiency with the elements of both systemic and myopathic carnitine deficiency. The older sibling died suddenly after a 24-hour fast. The younger boy has received carnitine for three years. During this period, serum CPK activity has remained elevated and increased further during illnesses, but no clinical symptoms of encephalopathy or myopathy have appeared.
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PMID:Encephalopathy and fatal myopathy in two siblings. Their association with partial deficiency of muscle carnitine. 709 Oct 87

Fulminant hepatic failure has been reported in patients with chronic congestive heart failure. Two patients in whom jaundice and coma followed cardiac surgery were studied to find the possible etiology. Clinical, biochemical, and histologic evaluations revealed low cardiac output; elevated levels of bilirubin, lactic dehydrogenase, serum glutamic oxaloacetic transaminase, and alkaline phosphatase; prolonged prothrombin time; and centrizonal necrosis of hepatocytes with sinusoidal dilatation. No other possible causes of hapatic dysfunction and coma were identified. We conclude that acute postoperative congestive heart failure may cause fulminant hepatic failure and metabolic encephalopathy.
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PMID:Hepatic coma after open heart surgery. 738 54

Cerebrospinal fluid (CSF) lactate dehydrogenase was determined in 19 control infants without asphyxia (Group I), 24 infants with perinatal asphyxia (Group II), and 26 asphyxiated infants with seizures (Group III). Mean birthweights, gestational ages, CSF glucose, protein and red blood cells, and the ages at which the lumbar punctures were performed were not significantly different among the three groups. Mean CSF lactate dehydrogenase was significantly higher in Group III than in Groups I and II. Isoenzyme patterns indicated that the origin of the CSF lactate dehydrogenase was neuronal tissue, or a plasma transudate from increased permeability of the blood-brain barrier. There were 10 deaths due to anoxic encephalopathy in Group III, but none in Groups I or II. Follow-up of survivors at 10 to 30 months of age revealed neurological sequelae in three infants in Group I, two in Group II and five in Group III. Mean CSF lactate dehydrogenase in those with sequelae had not been significantly different from that of normal survivors; however, the mean was significantly higher in infants who died with anoxic encephalopathy compared with normal infants. These data indicate that CSF lactate dehydrogenase is significantly elevated in infants with fatal anoxic brain damage, and suggest that determinations may be of prognostic value in non-fatal cerebral hypoxia.
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PMID:Cerebrospinal fluid lactate dehydrogenase in infants with perinatal asphyxia. 739 27

Intravascular lymphomatosis is a rare fatal neoplasm characterized by malignant cells of lymphocytic lineage producing vascular occlusions. The cerebral vasculature is particularly affected. Two patients seen at our institution presented with progressive neurologic deficits including dementia, hemiparesis and myelopathy. Review of an additional 64 reported cases with neurologic involvement indicates that patients developed intermittent fevers, an encephalopathy ranging from acute disorientation to rapidly progressive dementia, and focal signs such as hemiparesis and myelopathy. Common laboratory abnormalities include elevated cerebrospinal fluid protein and a lymphocytic pleocytosis, elevated blood erythrocyte sedimentation rate and serum lactate dehydrogenase. Malignant cells are rarely seen in cerebrospinal fluid, blood or bone marrow. Neuroimaging is usually abnormal with parenchymal lesions seen on cerebral tomography and magnetic resonance imaging along with an occasional meningeal pattern of contrast enhancement. Treatment with corticosteroids, chemotherapy, radiation therapy, or plasmapheresis provided limited benefit. Intravascular lymphomatosis should be considered in the differential diagnosis of unexplained progressive encephalopathy with superimposed focal deficits.
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PMID:Neurologic manifestations of intravascular lymphomatosis. 757 46

During August 1989-August 1994 at the referral-based obstetric practice of MacKay Memorial Hospital in Taipei, Taiwan, obstetricians saw 8 pregnant women with acute pancreatitis. All but 1 patient had gallstones and/or hyperlipidemia. None had ever been diagnosed with pancreatitis or gallstones in the past. None suffered from alcoholism. One woman was lost to follow-up at 33 weeks gestation. No pregnant woman died. Magnesium sulfate and nifedipine controlled preterm labor in 2 patients. Two women underwent cesarean section (fetal distress and elective). Pancreatitis struck all but 1 during the 3rd trimester of pregnancy. One woman presented at 23 weeks gestation with loss of consciousness, abnormally low volume of circulating plasma in the body, upper gastrointestinal bleeding, and a dead fetus. She also had diabetes mellitus which had gone untreated for 2 years. After spontaneous delivery of the dead fetus, she developed metabolic encephalopathy, sepsis, respiratory distress, and acute renal failure. She completely recovered and left the hospital 62 days after arriving. Physicians instituted conservative treatment for pancreatitis and a fat-restricted diet for hyperlipidemia. Labor was induced in 3 women after determining fetal lung maturity. Pancreatitis symptoms diminished after delivery. At 2 weeks postpartum, they underwent cholecystectomy. In fact, all but 3 women underwent cholecystectomy. Five patients had a fever greater than 38 degrees Celsius upon admission. Three patients were jaundiced. All 8 patients experienced nausea and/or vomiting and abdominal pain. Six women had low serum calcium levels. Only 1 had a serum lactic dehydrogenase level above 350 IU/L. Primiparous women were just as likely to develop pancreatitis during pregnancy as multiparous women. These findings suggest that early diagnosis and prompt treatment of acute pancreatitis are essential to a favorable outcome.
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PMID:Acute pancreatitis in pregnancy. 766 Jul 65

Serum lactate dehydrogenase (LDH), aspartate aminotransferase (ASAT), and hydroxybutyrate dehydrogenase (HBDH) activities are significantly elevated in asphyxiated newborns within the first days of life. The approach of the present study was to evaluate firstly if serum levels of these enzymes correlate with the development of hypoxic-ischemic encephalopathy (HIE) and periventricular-intraventricular hemorrhage (PIVH) in full-term and premature asphyxiated newborns, and secondly if postnatally elevated enzyme activities could be predictive for these disorders. ASAT, LDH and HBDH activities were measured in 98 asphyxiated newborns. Blood samples were taken serially at five fixed times: 0 (cord), 12, 24, 72, and 144 hours post partum. All newborns were examined for the development of HIE and PIVH using standardized scoring systems. Fifty percent of the newborns were full-term and 50% were premature. Ten of the full-term (20.4%) and 21 (42.8%) of the premature newborns developed HIE. Nineteen newborns (19.4%) suffered PIVH (full-term/premature, 7/12). The full-term asphyxiated newborns with HIE or PIVH showed significantly elevated ASAT, LDH, and HBDH activities within the first 72 hours of life. In case of the premature asphyxiated newborns, the enzyme activities did not differ significantly between the study groups. The overall predictive values showed a high sensitivity (HIE/PIVH, 90.0%/71.4%), a high specificity (71.0%/88.1%), an acceptable negative predictive value (44.9%/50.0%), and a high positive predictive value (96.5%/94.9%) for the development of HIE and PIVH in full-term asphyxiated newborns. It is concluded that measurements of ASAT, LDH, and HBDH activities are reliable predictors for the development of HIE and PIVH in full-term asphyxiated newborns.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The predictive value of elevation in specific serum enzymes for subsequent development of hypoxic-ischemic encephalopathy or intraventricular hemorrhage in full-term and premature asphyxiated newborns. 854 57


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