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)

Many psychiatric patients have polydipsia and polyuria without identifiable underlying medical causes. Hyponatremia develops in some polydipsic patients and can progress to water intoxication with such symptoms as confusion, lethargy, psychosis, and seizures or death. This syndrome is sometimes called "compulsive water drinking," "psychogenic polydipsia," and "self-induced water intoxication." Although the underlying pathophysiology of the syndrome is unclear, several factors have been implicated in producing polydipsia and symptomatic hyponatremia. These include a possible hypothalamic defect, the syndrome of inappropriate secretion of ADH (SIADH), and neuroleptic medication. Evaluation of psychiatric patients with polydipsia includes a search for other medical causes of polydipsia, polyuria, hyponatremia, and SIADH. Treatment modalities currently available include fluid restriction and medications.
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PMID:Polydipsia and hyponatremia in psychiatric patients. 328 1

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

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

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

Cerebrospinal fluid (CSF) involvement in myeloma is rarely seen. Recently we experienced a case with this lesion. A 70-year-old man developed consciousness level disorder during the course of bronchopneumonia. Neurological examination revealed stuporous consciousness, neck stiffness and Kernig's sign. Immunoelectrophoresis showed monoclonal IgG in serum. CSF which was obtained through lumbar puncture was clear and its pressure was 155 mm H2O. It contained 207 white cells/3 mm3; glucose, 54 mg/dl; and protein, 33 mg/dl. The differential count of the CSF was (in %) monocytes, 48.0; plasma cells, 25.5; neutrocytes, 15.5; and lymphocytes, 11.0. Cytoplasm and nucleus of the plasma cells were in various sizes. Some irregular multiple nuclei, flaming cells and grape cells were also observed in them. The cytoplasm of the plasma cells fluoresced with antisera against lambda chains IgG. The value of immunofluorescent technique in identifying plasma cells in the CSF is emphasized.
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PMID:[Abnormal cerebrospinal fluid plasma cells in a case of myeloma]. 371 84

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

A tetrodotoxin-like substance, denoted ephippiotoxin, was obtained from the tissue of Brachycephalus ephippium, a small pumpkin-coloured frog collected in the Atlantic Forest of the southeast region of Brazil. Ephippiotoxin is a dialyzable substance soluble in water, methanol and ethanol, but insoluble in organic solvents such as chloroform and other apolar solvents. After treatment with active charcoal (Norit-A) and purification with ion-exchange Amberlite IRC-50 resin (NH4 + form), a freeze-dried residue was obtained, with a toxicity of c. 117 micrograms/kg (mice, i.p.). Ephippiotoxin showed the same mobility as crystalline tetrodotoxin (Sankyo) when submitted to thin-layer chromatography (silica gel G) using seven different solvent systems. White mice (20 +/- 1 g) injected i.p. with either B. ephippium tissue extracts or semi-purified toxin showed partial paralysis of the hind limbs, lethargy, altered breathing rhythm and clonic convulsions. Death occurred within 1.5-30 min after injection, depending on the dose. Ephippiotoxin induced atrioventricular diastolic blockade in the toad heart. It also inhibited the response of toad striated muscle to direct and indirect electric stimulation and blocked the compound action potential of isolated frog sciatic nerve.
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PMID:A tetrodotoxin-like substance found in the Brazilian frog Brachycephalus ephippium. 377 95

Presented is the case of a normal two-month-old girl who developed seizures secondary to water intoxication. The infant had been fed 20 to 30 oz of water daily for three days, while her usual formula was withheld because of vomiting and diarrhea. On the day of admission, the infant exhibited signs of water intoxication in the form of lethargy, vomiting, and seizures. Hyponatremia, hypothermia, and hyperglycemia were noted on admission, and are common features of the syndrome. The patient responded well to fluid restriction and salt replacement. Previous reports have attributed water intoxication to feeding mismanagement, vigorous hydration, dilute formulas, and swimming lessons.
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PMID:Water intoxication with seizures. 396 5

Previous studies have shown that manganese (Mn) deficiency in rats results in reduced activity of manganese superoxide dismutase (MnSOD) and increased levels of mitochondrial lipid peroxidation. These findings suggested to us that the Mn-deficient rat may be especially susceptible to the toxic effects of ethanol, as the metabolism of this compound results in production of superoxide anion. Offspring from Mn-sufficient and Mn-deficient adult rats were given either 20% (wt/vol) ethanol or distilled-deionized water as their drinking fluid for 14 d. Response to ethanol feeding was different between Mn-sufficient and deficient rats as evidenced by severe reductions in caloric intake and body weight observed in the Mn-deficient rats. Furthermore, after 14 d of ethanol feeding, these rats were extremely lethargic and in poor physical condition. Although Mn-sufficient rats responded similarly to the deficient rats during the first 6 d of ethanol feeding, they increased their caloric intake and body weight during the remainder of the experimental period. MnSOD activity in the ethanol-fed Mn-sufficient and Mn-deficient rats was similar, thus the alcohol-induced toxicity observed in the deficient rats was not due to reduced MnSOD activity. Iron-induced lipid peroxidation may be one of the mechanisms leading to the toxicity observed, as ethanol feeding resulted in liver Fe levels that were 30% higher than those in Mn-deficient rats that were not fed ethanol.
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PMID:Manganese deficiency: effects on susceptibility to ethanol toxicity in rats. 398 Dec 64

A 9-year-old male Boxer with signs of lethargy, weight gain, polyuria, polydipsia, eosinopaenia and lymphopaenia was diagnosed as having hyperadrenocorticism. Concurrent central diabetes insipidus was diagnosed using a water deprivation test and antidiuretic hormone response test. A contrast radiographic technique was used to outline a pituitary mass. A chromophobe adenoma and secondary hypothyroidism were found on post-mortem examination.
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PMID:Pituitary tumour causing multiple endocrinopathies in a dog. 402 18


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