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)

Lethargy, hyperpyrexia, tremor, and rigidity associated with leukocytosis and elevation of the creatine kinase level occurred in a patient with a closed head injury who was being treated with haloperidol for control of agitation. This constellation of symptoms, known as the neuroleptic malignant syndrome (NMS), partially improved when the neuroleptic medication was stopped, but complete resolution of the syndrome did not occur until the patient was treated with bromocriptine. Because haloperidol is the most widely used medication for the agitation that develops in patients with significant closed head injuries, neurosurgeons should be aware of the NMS. The NMS is caused by neuroleptic medications and may initially present with unexplained hyperpyrexia, leukocytosis, and elevated creatine kinase levels. Halting the neuroleptic, supportive care, and the use of dantrolene sodium and bromocriptine are the treatment modalities of choice for this syndrome, which has a mortality rate of 20 to 30% and may be linked to malignant hyperthermia.
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PMID:Neuroleptic malignant syndrome complicating closed head injury. 396 Feb 97

Methyl salicylate (oil of wintergreen) in the form of candy flavoring was ingested by a 21-month-old male infant who subsequently developed vomiting, lethargy, and hyperpnea. A "swallow" of the solution resulted in a serum salicylate concentration of 81 mg/dL six hours after ingestion. The infant was treated with parenteral fluids and sodium bicarbonate and he recovered rapidly. Hazards associated with salicylate use in this form include lack of parental awareness of the substance's toxic potential, the attractiveness of the candy-like odor, and the availability of the liquid in non-child-resistant packaging containing potentially lethal quantities.
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PMID:Candy flavoring as a source of salicylate poisoning. 399 Dec 73

A study of the effects of 4 milk preparations on the early growth of low birth-weight newborns in Ceylon is reported. The following parameters were studied: mortality; weight gain; tolerance, as indicated by the incidence of diarrhea and the presence of sugar in the stools; blood glucose levels; and blood urea and serum sodium levels. A powdered and partially skimmed cow's milk, Nestogen, was used as it is available in the government hospitals throughout the island. 2 strengths constituted Formulas 1 and 2, and by addition of sucrose to the latter, a 3rd of higher calorie value was prepared. The 4th formula was breast milk. The study population from 3 nurseries consisted of 112 babies between 1250 and 2057 grams birth-weight, those of lighter weight being excluded as many required intravenous therapy initially. Weights were checked daily, and as soon as babies were able to suck adequately, they were allowed home. Mean blood glucose levels were within the normal range in babies appropriate and small for gestational age on all 4 milks. There was a high incidence of diarrhea among babies on all 3 Nestogen formulas. On Formulas 1 and 2, diarrhea occurred between the 4th and 12th day, and, in all cases, preceded weight loss and dehydration. Babies with diarrhea on Formula 3 showed symptoms between the 3rd and 5th days, and in each case lethargy, weight loss, dehydration, and in some, fever, were followed by diarrhea. Blood urea nitrogen levels increased with the protein content of the diet and may have reflected a diminished extra cellular fluid volume due to extra renal fluid losses. Mortality rates were similar in the Nestogen fed babies; no breast fed babies died. In sum, the comparison showed breast milk to be overall superior for those who could suck. A higher protein feed was associated with more rapid weight gain but addition of sucrose produced intolerance. Higher strengths of Nestogen which obligate greater urinary fluid are probably unsafe in a hot climate which induces considerable insensible losses of water.
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PMID:Feeding studies in Ceylonese babies. 449 4

The efficacy of phenytoin sodium and chlorpromazine hydrochloride in the reduction of spasticity was evaluated in both open and controlled studies. In each study, the majority of patients exhibited both objective and subjective signs of improvement. Reduction of motor tone in spastic muscles, as well as improvement in functiional status, was observed. Most patients experienced greater benefit from the combination of phenytoin and chlorpromazine than from either drug alone. The use of the drugs in combination permitted decreased chlorpromazine doses and reduced unwanted side effects such as lethargy and somnolence. These drugs may exert their action by suppressing fusimotor efferent as well as afferent discharged from muscle spindles. The results suggest that the fusimotor system is an important pharmacologic target in the treatment of spasticity.
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PMID:Phenytoin and chlorpromazine in the treatment of spasticity. 624 2

Congenital adrenocortical unresponsiveness to ACTH is characterized by hyperpigmentation, muscular weakness, and episodes of hypoglycemia, with lethargy or coma and convulsion, and without signs or symptoms of salt wasting. Endocrinological evaluation reveals low levels of serum and urinary glucocorticoids, elevated levels of plasma ACTH and unresponsiveness to exogenous ACTH. On the other hand, aldosterone secretion or excretion is normal and is elevated during a low sodium diet. We reported on two patients with this syndrome. Case A, a 4 year-old-girl, showed skin hyperpigmentation, hypoglycemia, convulsion and coma. She was tall wlth a marked advance of bone age. Case B, a 4 year-old-boy, showed skin hyperpigmentation, fatigability and muscular weakness. Both of them revealed low urinary excretion of THE, THF, cortolone, and beta-cortolone and low levels of plasma cortisol. The levels of urinary glucocorticoids and plasma cortisol did not respond to ACTH administration. During a low sodium diet, urinary aldosterone excretion was elevated, urinary sodium excretion ws decreased, and the patients were able to conserve sodium normally. We also summerized other reported cases and discussed the etiology of this syndrome.
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PMID:[2 cases of congenital adrenocortical unresponsiveness to ACTH (author's transl)]. 625 Sep 21

Three dogs with hypoadrenocorticism did not have characteristically abnormal serum concentrations of sodium, potassium, and chloride and had not been treated with glucocorticoids. Diagnosis was based on lack of adrenocortical response to exogenous adrenocorticotropic hormone. Clinical signs included lethargy, weakness, anorexia, vomiting, and weight loss. The case demonstrated that the diagnosis of canine hypoadrenocorticism should not be excluded on the basis of normal serum electrolyte values.
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PMID:Atypical hypoadrenocorticism in three dogs. 626

Two female infants with nonketotic hyperglycinemia (NKH) were treated with diazepam for the control of seizures. The first infant had seizures, lethargy, and respiratory distress in the first 24 hours of life. The diagnosis of NKH was made at 3 weeks of age and she was then placed on a regimen of strychnine and a low-protein diet. Strychnine therapy was discontinued after three months of treatment because there was no improvement in the seizure control or in the patient's condition. At 5 months of age the patient was referred to our clinic for further work-up. The second infant had seizures, hypotonia, and respiratory distress shortly after birth. She was treated with phenobarbital and diphenylhydantoin, which had no effect on her seizures. The baby was referred to our clinic at 8 months of age and diagnostic studies revealed NKH. All previous medications were stopped and both infants were placed on diazepam, a competitor for glycine receptors in the CNS. Choline and folic acid were added for one-carbon unit transfer and sodium benzoate to bind excessive glycine. Both infants responded to this treatment with cessation of seizures; they became more responsive and alert, and their EEGs showed remarkable improvement despite the persistence of elevated glycine levels in plasma, CSF, and urine. Diazepam as a competitor for the receptors of glycine may prove helpful in controlling the intractable seizures associated with NKH.
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PMID:Nonketotic hyperglycinemia: treatment with diazepam--a competitor for glycine receptors. 630 Jul 46

The purpose of the present study was to develop a controllable experimental model in the dog that would consistently and predictably produce a malignant hypertensive crisis, and to determine the sequential changes in renal function, salt and water balance, and hormones that are involved in the transition from benign to accelerated hypertension. Norepinephrine (NE) was infused continuously into the renal artery of unilaterally nephrectomized dogs that were maintained on 50 mEq sodium/day. The infusion rate of NE was increased each day according to the following schedule: 0.05, 0.1, 0.2, 0.3, 0.4, and 0.5 microgram/kg/min. During the first 4 to 5 days of intrarenal NE infusion, there was a progressive decrease in glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), and increases in plasma renin activity (PRA), mean arterial pressure (MAP), and filtration fraction. At the end of this period of benign hypertension, MAP had risen from a control value of 91 +/- 4 to 132 +/- 8 mm Hg, in association with approximately a 10-fold increase in PRA and a 40% reduction in renal function. Then, suddenly, during the subsequent 24-hour infusion period, the MAP increased abruptly in all animals (MAP = 156 +/- 8 mm Hg), and a hypertensive crisis occurred. This crisis was associated with the following: salt and water depletion, hyponatremia, hypovolemia and hemoconcentration, polydipsia, marked activation of the renin-angiotensin-aldosterone system, increased plasma cortisol concentration, hemolysis, marked impairment in renal function, lethargy, and vomiting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malignant hypertensive crisis induced by chronic intrarenal norepinephrine infusion. 637 96

Ketotifen 1 mg b.d. (oral) and sodium cromoglycate 20 mg q.i.d. (inhalation) were compared in a double-blind crossover trial in 43 asthmatic outpatients. Comparison of diary card scores and pulmonary function tests showed significant improvement over a 12 week period on each drug. Comparison of the diary card scores and pulmonary function tests showed no significant difference between the drugs after 12 weeks of treatment. Twenty-six patients experienced sedation and/or lethargy whilst on ketotifen and 11 patients had similar side effects whilst on cromoglycate. Physician preferences based on diary card and pulmonary function data showed an approximately equal number of preferences for each medication and also a small group of patients in which no preference could be made. The present trial suggests that both ketotifen and cromoglycate are effective in the management of outpatient asthma. When all the patients are considered as a group no distinction can be made between the two drugs; on the basis of physician assessment of each patient, it appears that some patients may do better on ketotifen and others on cromoglycate.
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PMID:Evaluation of ketotifen (HC20-511) in bronchial asthma. 641 21

Stuporous states induced by sodium valproate (VPA) are accompanied by an isolated marked hyperammonemia. In reality, hyperammonemia occurs after administration of VPA even in the absence of neurological complications. The hyperammonemia is of purely renal origin and results from modifications in glutamine metabolism, this compound being the main precursor of amino acid neurotransmitters. Combined administration of VPA and phenobarbitone increases the level of hyperammonemia due to lack of detoxification by the liver of the excess of ammonia produced by the kidneys. The anatomical site of origin of the ammoniogenesis, and its intensity, were studied in two patients with a history of stuporous states during combined VPA-phenobarbitone treatment. A single injection of VPA at a later date when they were being treated by combined phenobarbitone-carbamazepine therapy, induced disturbances in ammonia metabolism which did not differ qualitatively from those observed when intolerance to VPA is lacking. It is therefore not possible to rely on simple biological tests to detect patients at risk. Correlation is also lacking between the degree of hyperammonemia and disorders of vigilance. Ammonia does not therefore appear to be the only factor responsible for neurological complications and the role of other factors must be investigated. These include: disturbances of metabolism of inhibitory and excitatory aminoacid neurotransmitters, the condition of the cerebral parenchyma, and the excitatory effect of sodium valproate which could act to varying degrees in synergy with the hyperammonemia to provoke a stuporous state.
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PMID:[Role of hyperammonemia in stuporous states induced by sodium valproate]. 642 Aug 66


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