Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two infants with lethargy, vomiting, convulsions, coma and marked metabolic acidosis were found to have very high concentrations of methylmalonic acid in their serum and urine. In vitro studies of fibroblasts demonstrated that the infants had different variants of methylmalonic acidemia.Vitamin B(12) was given in two different forms at 1 month of age and at 12 months of age. Each trial continued for 4 months but neither infant showed a clinical or biochemical response.In both infants hyperglycinemia, neutropenia and thrombocytopenia developed during acute metabolic crises only. Hypoglycemia was found in patient 2. Hyperammonemia was severe in patient 2 during acute crises but never appeared in patient 1. When clinically well, both infants continued to excrete abnormal amounts of methylmalonic acid in the urine and both had persistent compensated metabolic acidosis.Marked hyperuricemia developed in patient 1 at 18 months of age and led to progressive renal failure. Allopurinol therapy was necessary to keep the uric acid concentration within the normal range. Renal function returned to normal, as indicated by a marked increase in the renal clearance of creatinine and uric acid.Patient 1 is physically and mentally retarded, and has moderate hypotonia, hepatomegaly and persistent vomiting. Patient 2 has developed normally.The urine concentrations of methylmalonic acid in the four parents were normal.
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PMID:Methylmalonic acidemia: 6 years' clinical experience with two variants unresponsive to vitamin B12 therapy. 3 17

Body fluid gas pressure and electrolytes of patients with ruptured aneurysm were continuously analyzed. Intracranial pressure (ICP) was regulated at the level of 120-100 mm H2O by cerebral ventricular drainage. There was no significant change in the pH, PCO2, HCO3-, Na+, K+, Ca++ in the cerebrospinal fluid (CSF) of patients with slight or moderate disturbance of consciousness (lethargic-drowsy state). The PcsfO2 of the patients with marked disturbances of consciousness (semicoma-coma) was significantly low. PcsfO2 of the patients with cerebral vasospasm was significantly lower than for those without vasospasms. PcsfO2/PaO2 was 0.27 +/- 0.01 in the patients with vasospasm and 0.50 +/- 0.01 in those with vasospasm. PcsfO2 tended to decrease in patients with markedly bloody CSF. When the bloody CSF was cleared by ventricular drainage, PcsfO2 increased. PcsfO2 did not return to a normal value in the patients with marked disturbances of consciousness despite sufficient arterial oxygen tension. This suggests that PcsfO2 and PcsfO2/PaO2 should provide a convenient index for the prognosis of patients with ruptured aneurysm.
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PMID:Body fluid oxygen tension and prognosis in patients with ruptured aneurysm. 4 45

A 52-year-old man had a prolonged history of nondeforming migratory polyarthritis and a short episode of pericarditis preceding the onset of bilateral vitreitis and retinitis. The clinical course was characterized by progressive deterioration of vision, increasing lethargy, and dementia, leading to coma and death from pneumonia (21 months later). No intestinal manifestations were recorded. Both eyes, which were removed postmortem, disclosed numerous PAS-positive macrophages throughout the inner retina and vitreous. Electron microscopic studies of the macrophages displayed intracytoplasmic, degenerating, rod-shaped bacteria and membranous structures identical to those seen in the intestine, brain, heart, and other tissues of patients with Whipple's disease. Clinicians should include Whipple's disease, and reticulum cell sarcoma, in the differential diagnosis of patients with bilateral retinitis and vitreitis, especially if these disorders are associated with CNS manifestations.
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PMID:Ocular involvement in Whipple's disease: light and electron microscopic observations. 7 12

Four patients who were rendered comatose or stuporous by drug intoxication, but who were not hypoxic, are described. Three patients received high doses of chlormethiazole for alcohol withdrawal symptoms, and one took a suicidal overdose of nitrazepam. The patient with nitrazepam overdose and two of those with chlormethiazole intoxication conformed to the criteria of 'alpha coma', showing non-reactive generalized or frontally predominant alpha activity in the EEG. The fourth patient who was unconscious after chlormethiazole administration exhibite generalized non-reactive activity in the slow beta range. All four recovered completely without neurological sequelae following the withdrawal of the offending agents. The similarities between the effects of structural lesions and pharmacological depression of the brain stem reticular formation are discussed. It is suggested that in both situations disturbed reticulo-thalamic interactions are important in the pathogenesis of alpha coma. It is concluded that when this electroencephalographic and behavioural picture is seen in drug intoxication, in the absence of significant hypoxaemia, a favourable outcome may be anticipated.
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PMID:Alpha and beta coma in drug intoxication uncomplicated by cerebral hypoxia. 8 36

Two newborn infants, male (A) and female (B), with lethal hyperammonaemia are described in the same family. In both, symptoms started on the second day of life. Lethargy and hypotonia were the most prominent initial findings and were followed by convulsions and coma. In both, blood ammonia levels rose to 570 mumol/u (795 microgram/100 ml) a few hours before death, which occurred on the third and fourth day of life respectively. Assay of liver urea cycle enzymes in baby B showed a complete absence of mitochondrial carbamyl phosphate synthetase activity.
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PMID:Neonatal hyperammonaemia with complete absence of liver carbamyl phosphate synthetase activity. 20 10

The continuous infusion of a concentrated, high-caloric glucose solution intravenously into underfed or 3-day-starved rats at a rate of 390 kcal/kg/day results in hypophosphatemia, muscular weakness, neuropathy, lethargy, occasional convulsions, and eventual coma and death. This sequence of events is not observed in similarly infused normal rats. It is a model of a fatal parenteral nutrition syndrome which occurs in undernourished patients. Rats in coma had an eightfold increase in the blood glucose level, a 1.6-fold increase in serum osmolarity, a 16% to 20( decrease in brain water content, and normal blood ketones. A lag phase of at least 8 hr and often 12 to 24 hr occurred following the start of the hyperosmotic glucose infusion before the blood glucose began to accumulate progressively and the syndrome developed. The onset of the syndrome could be prevented by the administration of large amounts of insulin required to keep the blood sugar from exceeding 250 mg/dl. Thus the rat model of the fatal hyperalimentation syndrome is a form of hyperglycemic, hyperosmolar, nonketotic coma caused by brain dehydration.
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PMID:Weakness, neuropathy, and coma following total parenteral nutrition in underfed or starved rats: relationship to blood hyperosmolarity and brain water loss. 21 10

Water hemlock is a ubiquitous plant that can be mistaken for a turnip as in the case reported. Oral ingestion causes an explosive illness consisting of nausea, vomiting, abdominal cramps, and grand mal seizures that can progress to cyanosis and death. In the reported case a 30-year old man was found semi-comatose some 75 minutes after ingesting a "turnip". The history revealed profuse emesis shortly after eating lunch that changed from bile to frank blood. There was a mean orthostatic blood pressure change of 30 torr, with an increase in the heart rate of 10%. Neurologic examination revealed a lethargic patient. Following administration of 4 liters of Ringer's lactate the patient's blood pressure stabilized and with continued isotonic fluid maintenance he improved rapidly. This case indicates that appropriate management should be directed toward protecting the patient's airway from gastric aspiration, restoring the intravascular and extracellular volume deficit, and controlling cerebral edema.
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PMID:A case of water hemlock poisoning. 49 28

Reye's syndrome in infancy is not a well-defined entity and is infrequently diagnosed. Eight infants 6 months of age or younger had a prodromal viral illness followed by the rapid onset of lethargy, seizures, and coma, resulting in the diagnosis of Reye's syndrome. All had abnormal results of liver function tests including elevations of blood ammonia level. Three patients had pathological studies that confirmed fatty visceral infiltration. The data on these patients, as well as a review of the literature, indicate that the most prominent clinical findings in Reye's syndrome in infancy include marked respiratory abnormalities with tachypnea and apneic episodes; frequent occurrence of seizures in the early stages of the illness; and hypoglycemia in most cases. A strong socioeconomic bias was noted in these patients, with the infants coming primarily from lower socioeconomic, urban environments, while older children with Reye's syndrome have been observed to be predominantly middle-class and from suburban or rural areas.
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PMID:Reye's syndrome in infancy. 68 88

Hypercalcemia causes lethargy and coma in patients with head and neck cancer. It is important to realize that coma may be due to hypercalcemia and need not be a terminal event in the progress of the tumor. Also, the development of hypercalcemia in a previously normocalcemic patient requires investigation as to the cause of the hypercalcemia. I report two cases of comatose patients, hypercalcemic from bony metastases from tongue cancer, in whom treatment by furosemide and intravenous fluid diuresis, prednisone, sodium phosphate, and mithramycin produced worthwhile remissions. Hypercalcemia may be due to (1) bony metastases, (2) pseudohyperparathyroidism, (3) unrelated associated parathyroid tumors, or (4) a second primary tumor. Even with treatment, hypercalcemia is a bad prognostic sign in patients with head and neck cancer.
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PMID:Hypercalcemia and head and neck cancer. Bony metastases from tongue cancer. 69 40

Underfed rats infused intravenously with a glucose-amino acid solution at the rate of 390 kcal/kg/day developed a syndrome of muscular weakness, neuropathy, lethargy and precoma or coma associated with severe hypophosphatemia. The movement of phosphate into the cells was studied to determine where it went and into which organic compounds it was incorporated. All but 8% of the labeled phosphate was found in liver, muscle, bone, and carcass residue. Liver cells took up as much phosphate as bone and twice as much as muscle, on weight basis. About 90% of the labeled phosphate entering liver was found in the acid-soluble fraction. The specific activity of liver phosphate increased in the infused underfed rats compared to uninfused underfed rats. Infusion of the underfed rat until signs of the syndrome appeared was associated with a 2.7- to 5-fold increase over the correspondingly infused normal rat in the labeling of glucose-6-phosphate, glucose-1-phosphate, and 6-phosphogluconate. No increase over the infused normal rat was observed in most of the other sugar phosphate compounds nor in the non-sugar phosphate compounds such as phospholipids, nucleic acids or proteins. he changes in sugar phosphates observed in the underfed rats probably reflect the enzymatic atrophy associated with underfeeding and the consequent inability to respond to the huge glucose load.
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PMID:Intracellular distribution of phosphate in the underfed rat developing weakness and coma following total parenteral nutrition. 82 10


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