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

A young man, in good health until the age of 22, developed progressive personality changes, lethargy, motor diffuculities, urinary bladder dysfunction, and convulsions. Spinal fluid abnormalities included monocytic pleocytosis and selective increase of gamma globulins. The clinical features and the structural lesions in the central nervous system are reminiscent of disseminated-diffuse sclerosis. Oligodendrocytes appeared normal in number and showed nonspecific abnormalities. Comparison of the structural lesions found in this case with those described in seven reports of demyelination indicates that the separation of this syndrome, as a distinct entity, may not be justified. We suggest that such cases be classified as myelinoclastic disorders, in the same category with multiple sclerosis and its variants.
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PMID:Unusual demyelinating disease. A form of diffuse-disseminated sclerosis. 4 12

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

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

The clinical aspects of Mycoplasma pneumoniae infection in 103 children under 12 years admitted to hospital over an eight-year period were reviewed retrospectively. Respiratory illnesses occurred in 87 (85%) cases. The prevalence of lower respiratory tract involvement was similar in both pre-school and school children. Cough was the commonest symptom at all ages. Coryzal symptoms and wheeze were common in pre-school children. Most infants had signs of pharyngitis or otitis media. Non-specific symptoms--fever, lethargy, malaise, anorexia and vomiting--were common accompaniments in children older than one year of age. Non-respiratory illnesses in 16 (15%) patients included gastroenteritis, convulsions, non-specific skin rashes and limb pains. The duration of stay in hospital ranged from two to 30 days (median five days) with apparent clinical recovery and resolution of chest X-ray abnormalities within three months in 78 (76%) patients seen for review.
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PMID:Mycoplasma pneumoniae infection. A retrospective review of 103 hospitalised children. 53 6

The toxicity of aminophylline and caffeine was studied in adult and 2-day-old rats following a single subcutaneous injection of the respective drug. Following the injection of high doses of either methylxanthine, adult rats developed convulsions, tremors, lethargy and licking of lips. In adult rats, the LD50 of caffeine and aminophylline was the same after 24 h and after 1 week of observation: caffeine 265 mg/kg, and aminophylline 202 mg/kg (theophylline base 172 mg/kg). In young rats, the LD50 was greater when the observation was carried out for 1 week than at 24 h after the injection; at 24 h: caffeine 220 mg/kg, and aminophylline 169 mg/kg (theophylline base 144 mg/kg); at 1 week: caffeine 155 mg/kg, and aminophylline 140 mg/kg (theophylline base 119 mg/kg). Young rats failed to gain weight at a normal rate after administration of either methylxanthine. The greater toxicity of both methylxanthines in newborn animals may be at least partly due to the extremely slow elimination of theophylline and caffeine in the neonate.
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PMID:Comparative toxicity of caffeine and aminophylline (theophylline ethylenediamine) in young and adult rats. 69 26

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

Tyzzer's disease, distemper, and mycotic pneumonia were diagnosed at necropsy of a 6-week-old mixed breed pup. The illness was characterized by lethargy, poor appetite, dysentery, and convulsions, the latter developing just prior to death. The necropsy findings included pale, dilated large intestine and swollen, dark liver. Histologically, multifocal hepatic necrosis, similar to that of Tyzzer's disease in other species of animals, was observed. Bacillus piliformis was found in hepatocytes and necrotic areas of the liver.
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PMID:Naturally occurring Tyzzer's disease as a complication of distemper and mycotic pneumonia in a dog. 95 24

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


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