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)

Overnight metabolic studies in 39 poorly controlled insulin-treated diabetic patients aged 9 to 66 years showed hypoglycaemia (blood-glucose less than 2 mmol/1) in 22 patients; it lasted 3 h or more in 17. Hypoglycaemic symptoms were very mild or absent, but 19 patients had other features of overtreatment with insulin. These included lethargy, depression, night sweats, morning headaches, fits (3 patients), glycogen-laden hepatomegaly (3), and acquired tolerance to high doses of insulin (mean 1 u/kg/24 h). The best clinical clue to recurrent nocturnal hypoglycaemia was the intermittent occurrence of symptoms, however "mild" and infrequent these appeared to be. Reduction of insulin by a mean of 25% in these patients (without change of species) did not result in loss of overall control; 1 patient with recurrent ketoacidosis was stablished on 40% of his initial dose. It is difficult, sometimes impossible, to achieve good overnight control with conventional once or twice daily insulin therapy. Since patients readily become tolerant of low blood-glucose levels, reliance on urine tests and symptoms of hypoglycaemia as a guide to dosage easily produces a spiral of overtreatment.
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PMID:Unrecognised nocturnal hypoglycaemia in insulin-treated diabetics. 8 75

The potential toxicity of FE-S15 (B. Braun-Melsungen), a soybean-oil fat emulsion used in parenteral nutrition, was studied in dogs. Forty pure-bred beagles, in two experimental groups (FE-S15 at 9 and 4 g/kg/day) and two corresponding control groups (receiving Dextrose-Ringer's solution), were given daily infusions for 28 days via a central venous catheter. Vital signs and hematologic, biochemical, and bacteriologic changes were monitored closely. When compared with control groups, no significant weight loss was observed in either group; the food intake decreased only in animals receiving fat in high doses. Hemoglobin and hematocrit decreased in all groups during infusion, the greatest fall observed in the group receiving high-dose fat infusion where the hematocrit declined from 45.5% to 31.7%. This decrease was significantly different from the controls only during one observation period. Clinical signs, such as lethargy, vomiting, diarrhea, loss of appetite and fever were observed infrequently in both experimental and control animals, more often in those treated with high-dose fat infusion. It appears that the fat emulsion FE-S15 causes only minor side effects but otherwise is well tolerated in dogs at a potentially toxic level.
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PMID:Studies of the toxicity of an intravenous fat emulsion. i. Hematologic changes and survival after administration of a soybean oil (FE-S15) in beagles. 11 23

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

The potential toxicity of FE-S15, a soybean oil fat emulsion used in parenteral nutrition, was studied in dogs. Forty pure bred beagles, divided into two experimental groups (FE-S15 at 9 and 4 gm/kg BW/day) and two corresponding control groups (receiving Dextrose Ringer's Solution) were given daily infusions for 28 days via a central venous catheter. When compared with control groups no significant weight loss was observed in either experimental group; the food intake decreased only in animals receiving fat in high doses. Hemoglobin and hematocrit decreased in all groups, the greatest fall observed in the group receiving high dose fat infusion was the hematocrit decline from 43.9% to 31%. This decrease was significantly different from the control only during one observation period. The total serum lipids, triglyceride and phospholipid concentrations of the animals receiving fat in high doses increased 3-4 times in comparison to that of the control group; cholesterol increased 5 times. The serum protein level fell from 6.5 to 5.1 gm/dl in animals receiving 9 gm/kg BW/day while animals receiving 4 gm/kg BW/day had a significant increase to 8.4 gm/dl. Except for an overall decreased activity clinical sign such as lethargy, loss of appetite, vomiting, and diarrhea were infrequent and equally observed in experimental and control animals. The post mortem examination did not reveal changes that must be attributed to the administered fat. It is concluded that the fat emulsion FE-S15 is fairly well tolerated in dogs at a potentially toxic level.
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PMID:[Tolerance studies of an intravenous fat emulsion (FE-S15) with beagle dogs]. 57 61

Plasma glucose and insulin have been studied during lethargy and spontaneous arousal of hibernating hedgehogs. During lethargy, plasma glucose and insulin were low and showed no variation. Glucose and insulin injections given during lethargy showed no effects on plasma insulin and glucose respectively but confirmed a very low plasma clearance of glucose and insulin. During spontaneous arousal, the increase in plasma insulin occured before the increase in blood glucose and at about the time that utilization of blood glucose was restored.
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PMID:Plasma glucose and insulin in the hibernating hedgehog. 66 77

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

Clinical and autopsy data indicate that ventriculitis persists despite parenteral and intralumbar antibiotic therapy. In the present study, ventriculitis was documented as postmortem examination in nine newborns. These studies indicate that ventriculitis occurs commonly in neonates with meningitis, particularly when there is delayed sterilization of CSF culture, A clinician has to bear in mind the diagnosis of ventriculitis when: 1) There is poor clinical and/or laboratory response to the usual therapy. 2) He has a critically ill patient with lethargy, convulsions and bulging fontanels. 3) He culture an unusual organism. 4) He faces a suspected complication of meningitis: subdural effusion, ventriculitis or abscess. 5) A CSF from ventricular puncture with more than 150 WBC, glucose less than 50 mg. and protein more than 200 mg.
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PMID:[Neonatal meningoventriculitis]. 83 10

An experimental model of clinical liver failure, using total devascularization of the liver is described in the pit. The survival time was 1495 +/- 75 (SEM) minutes. Clinically the pigs showed a uniform course. They became lethargic after eight to ten hours and following a period of increasing drowsiness they became comatose. The immediate cause of death was cardio-vasculary collaps. The ammonium ion concentration in the blood increased to 696 +/- 57 umol/l and in cerebrospinal fluid to 664 +/- 57 umol/l. Cerebrospinal fluid glucose concentration was significantly decreased.
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PMID:Total devascularization of the Liver: an experimental model of acute liver failure. 106 34

One infant with congenital hypertrophic pyloric stenosis developed severe hypoglycemia with lethargy, irritability, cyanosis, and convulsions in the immediate postoperative period after Fredet-Ramstedt pyloromytomy. A likely hypothesis for this mechanism has been reported as hepatic glycogen depletion secondary to malnutrition. Any infant with malnutrition, from whatever cause, should be assumed to have glycogen depletion, and repletion should be started and continued with all intravenous fluids given during the preoperative period. Hypoglycemia should be suspected when an infant develops any unusual or unexplained symptoms or findings in the immediate postoperative period. Prompt and intensive treatment with intravenous hypertonic glucose infusion must be begun and continued until blood glucose determinations remain at a safe level with oral feedings alone.
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PMID:Postoperative hypoglycemia in congenital hypertrophic pyloric stenosis. 111 56

A 43-year-old man who presented parkinsonism due to pontine and extrapontine myelinolysis was reported. Late in February, 1990, the patient presented suffered from a flu-like illness and was seen at a community hospital. Physical finding showed the pigmentation on the whole body and hypotension, and laboratory examination revealed severe electrolyte imbalance (serum sodium 100 mEq/l, serum potassium 6.9 mEq/l, serum chloride 68 mEq/l) and hypoglycemia (postprandial serum glucose 78 mg/dl). Given these results, adrenal failure was strongly suspected. Prompt correction of electrocyte imbalance was performed by the infusion of sodium chloride, and four days later the serum sodium level reached 131 mEq/l. On the other hand, the patient was noticed lethargic and showed parkinsonism i.e., rest tremor, cog-wheel rigidity, and hypokinesia. Fourteen days after the onset of neurological abnormalities, the patient was referred to our hospital for further evaluation of parkinsonism. Additionally, neurological examination revealed dysphagia, mutism and positive pyramidal tract sign. On admission brain computed tomography was unremarkable, but on the 14th hospital day it showed low density area in the pons. Brain magnetic resonance imaging also showed a striking increase in T2-weighted signal from the pons, the midbrain, and the bilateral thalamus. Based on these findings, a diagnosis of parkinsonism due to pontine and extrapontine myelinolysis was made, and levodopa therapy was started. After the initiation of levodopa therapy, improvement of tremor, rigidity, and hypokinesia ensued with marked functional benefit, and the patient was discharged on the 49th hospital day. Levodopa was stopped three weeks after discharge but, all neurological abnormalities were not recurrent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of parkinsonism due to pontine and extrapontine myelinolysis]. 130 Feb 56


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