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)

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

Four aluminum compounds--nitrate, chloride, sulphate and bromide--were administered orally and intraperitoneally to rats and mice. The LD50-values (14 days) were determined. The majority of deaths occurring during the first four days. The clinical and physical signs appearing after intoxication include among other lethargy, decreased locomotor activity, piloerection, weight loss and perorbital bleeding. After 14 days no alterations in liver and renal functions were detected in the animals which received intraperitoneally the LD50-values of aluminum nitrate as a single dose. Aluminum concentrations were highest in liver and spleen. No histopathological lesions could be observed. To compare the efficacies of nine chelating agents on the toxicity of aluminum in mice, the therapeutic index and the therapeutic effectiveness of each chelating agent have been calculated. Malic, succinic, oxalic and malonic acids showed the best results with malic and succinic acids being the most effective. Deferoxamine mesylate (DFOA), sodium salicylate, L-cysteine and citric acid were not so effective as antidotes for acute aluminum toxicity. Aurin tricarboxylic acid (ATCA) should not be used due to its high toxicity.
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PMID:Acute toxicity studies of aluminium compounds: antidotal efficacy of several chelating agents. 358 26

About 150 waterfowl died and another 250 became weak and lethargic from suspected salt poisoning after using White Lake, a highly saline lake in Mountrail County, North Dakota. Frigid temperatures made fresh water unavailable, forcing the birds to ingest the saline waters with resultant toxic effects. Sick birds recovered when removed from the salt water and released into fresh water marshes. Brain sodium levels were higher in dead geese submitted for necropsy than in controls.
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PMID:Salt toxicosis in waterfowl in North Dakota. 362 5

Although used as a condiment and essential supplement since pre-Biblical times, chlorine as a part of the molecule salt has received little research effort by large animal nutritionists. Its low cost and the continued popularity of salt as a condiment and sodium supplement has precluded the appearance of chloride deficiencies. There is great variation in the chloride and sodium content of feedstuffs fed to lactating cows so that some formulations require no supplemental chloride or sodium. Chloride is highly available from feedstuffs, and when dietary chloride is low, the cow can reduce sharply her losses of chloride in urine, feces, skin secretions, and to some degree in milk. Clinical symptoms of chloride deficiency in the lactating cow include pica, lethargy, anorexia, lowered milk yield, constipation, and cardiovascular depression. Metabolic changes are expressed as a severe primary hypochloremia, secondary hypokalemia, and metabolic alkalosis. Requirement for chloride by the lactating cow is about .20%; a working allowance of .25% seems reasonable for cows in positive energy balance. With gradual resolution of the requirements for chloride and more data on chloride in feedstuffs, use of supplemental salt for either sodium or chloride can be reduced greatly.
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PMID:Mineral utilization by the lactating cow--chlorine. 370 Jul 98

We have presented a case of thiazide-induced hyponatremia that followed an unusual course after the patient, suffering from extreme lethargy, was admitted with a serum sodium concentration of 104 mEq/L. Although the electrolyte imbalance was essentially corrected within 20 hours and there was clinical improvement, three days later the patient suddenly lost consciousness. She was comatose for more than a month, apparently from extrapontine myelinolysis. After a dramatic improvement, the patient was discharged with almost no neurologic deficit.
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PMID:Thiazide-induced hyponatremia: an unusual neurologic course. 370 34

Central nervous system symptoms due to hyponatremia is highly dependent on its acuteness and cause. Severe acute hyponatremia (serum sodium less than 125 mEq/l) often causes confusion, lethargy, seizures or frank coma due to brain oedema. If therapy is delayed, hyponatremia carries a high mortality rate, and risk of irreversible brain damage. Hyponatremia should probably be corrected to 125-130 mEq/l at a rate of 1.5-2.0 mEq/l/h. Malnourished alcoholic patients with hyponatremia may represent a special case with possible dangers of central pontine myelinolysis if a very low serum sodium is corrected acutely to normonatremic or hypernatremic levels. Mortality in this subgroup is high whatever the therapy.
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PMID:Hyponatremia: cerebral symptoms and role in central pontine myelinolysis. 370 29

We studied biliary excretion of sodium and chloride in 17 infants with external bile drainage through a "biliostomy" and describe four additional children who became ill from sodium depletion following external biliary drainage procedures for biliary tract anomalies. In the 17 infants, the mean +/- SD bile sodium concentration was 122 +/- 15 mEq/L. The mean +/- SD serum sodium concentration was low (132 +/- 7 mEq/L) (normal, 138 to 145 mEq/L). The mean +/- SD bile volume was 388 +/- 317 mL/day at one year following surgery (range, 40 to 1,000 mL/day). In the four children, clinical manifestations of sodium depletion (lethargy, anorexia, dehydration, and malnutrition) necessitated hospital admission. At that time, the serum sodium concentration ranged from 109 to 129 mEq/L, and the simultaneous urinary sodium concentration ranged from 0 to 5 mEq/L. Although dietary sodium was normal, biliary losses exceeded dietary intake, resulting in salt and water depletion despite renal conservation. Children with biliary drainage procedures are at risk for sodium depletion and should be monitored closely and supplemented accordingly until biliostomy closure is performed.
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PMID:Sodium homeostasis in infants with biliary drainage procedures. 370 30

A patient who developed chronic salicylism associated with salicylate therapy for treatment of juvenile rheumatoid arthritis is described, and the clinical presentation and treatment of chronic salicylism are reviewed. A 5 1/2-year-old boy was receiving aspirin 150/mg/kg/day for treatment of juvenile rheumatoid arthritis. While on salicylate therapy, the patient developed tachypnea and became increasingly hyperthermic, lethargic, and disoriented. The patient developed a maculopapular rash, weakness, and a decreased level of consciousness during the 11 days before admission to the hospital. Physical examination and laboratory determinations revealed that the patient had hypoprothrombinemia, hypoglycemia, and severe hepatic encephalopathy secondary to long-term salicylate toxicity. The patient was treated for hypoglycemia, electrolyte imbalances, thrombocytopenia, and anemia and was discharged after 24 days. Diagnosing chronic salicylism with hepatic dysfunction was difficult because the symptoms are similar to those of stage I to stage II Reye's syndrome. Liver enzymes, including aspartate aminotransferase (also called SGOT), alanine aminotransferase (also called SGPT), alkaline phosphatase, and lactate dehydrogenase, may be elevated in juvenile arthritis patients with hepatic dysfunction. Liver dysfunction usually improves when salicylate therapy is discontinued. Supportive therapy should always be used in symptomatic patients. Children on long-term, high-dose salicylate therapy should be monitored closely, and baseline liver function tests should be performed. The clinical effectiveness of administering sodium bicarbonate in attempts to alkalinize urine and increase salicylate elimination is controversial. In patients with juvenile rheumatoid arthritis who develop chronic salicylism, careful analysis of the patient's medication history, laboratory values, and clinical presentation are necessary to rule out Reye's syndrome.
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PMID:Chronic salicylism in a patient with juvenile rheumatoid arthritis. 370 82

A case of central pontine myelinolysis (CPM) following rapid correction of hyponatremia is reported and a review of the literature is made. The patient was a 63-year-old non-alcoholic female who had no liver or kidney diseases in her past history. She was found unconscious after a series of convulsions and was admitted to the hospital. Eighteen months prior to admission, she had a surgery for a ruptured anterior communicating artery aneurysm. Her postoperative course was uneventful except for an urinary incontinence and mild disorientation. She was initially lethargic with conjugate deviation toward right. Nine days after admission, she still remained lethargic, and laboratory studies showed a serum sodium value of 93 mEq/l, serum osmolarity 206 mOsm/l and urine osmolarity 270 mOsm/l when she was clinically diagnosed as having SIADH. She was treated by a strict elimination of water, and administration of sodium, dexamethasone and demeclocycline. In three days, serum sodium was corrected and returned to 137 mEq/l. However, she deteriorated in consciousness and became comatose and developed quadriplegia. CT scans and cerebral angiograms were normal. One month later, another CT scans demonstrated a well-defined hypodensity area in the pons. Brain stem auditory response (BSAR) showed a prolongation of III-V interpeak latency, especially IV-V interval. Her neurological state was essentially unchanged thereafter and she died of septic shock after 12 months' hospitalization. No permission for autopsy was obtained. The clinical course, CT scans and BSAR reported here are indicative of the diagnosis of CPM.
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PMID:[A case of central pontine myelinolysis]. 374 96

The effects of phenytoin (PHT) on the modifications of ammonia (NH+4) metabolism caused by sodium valproate (VPA) are here studied in order to identify the drug combinations susceptible of evoking stuporous states in epileptics, a rare condition attributed to a hyperammonemic encephalopathy induced by VPA. During chronic treatment with PHT or VPA-PHT, the acute injection of VPA increases the kidney's output of NH+4. During chronic PHT treatments, the acute injection of VPA modifies the liver's NH+4 metabolism and the arterial hyperammonemia is high (mean = 90 mumol/l). During chronic VPA-PHT treatments, the acute injection of VPA does not affect the hepatic NH+4 metabolism, suggesting that adaptation occurs, and the arterial hyperammonemia is moderate (mean = 60 numol/l). Disturbances of the hepatic adaptive mechanisms may explain certain complications observed during multiple-drug regimens.
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PMID:Adaptation of hepatic ammonia metabolism after chronic valproate administration in epileptics treated with phenytoin. 392 65


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