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)

Pseudohypoaldosteronism has been described as a syndrome presenting early in life with profound salt wastage, failure to thrive, and lethargy. The mechanism of sodium loss is renal, not related to aldosterone production. Previous cases have been transient, responding to supplemental salt therapy which was discontinued after one to two years. A child whose pseudohypoaldosteronism was first diagnosed in infancy and whose salt loss persisted to 7 years of age is described.
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PMID:Persistent pseudohypoaldosteronism in a 7-year-old boy. 704 Oct 74

The authors review the evidence for the efficacy of the sodium amytal interview with particular reference to psychiatric emergencies and rapid assessment and treatment. Amytal interviews have a valid role in the assessment and initial management of catatonia, hysterical stupor, and unexplained muteness as well as in distinguishing between depressive, schizophrenic, and organic stuporous states. Valid therapeutic indications include the abreaction of traumatic neurosis, recovery of memory in amnesic and fugue states, and recovery of function in conversion disorders. The authors offer a protocol for application of the amytal interview in emergency settings.
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PMID:Overview: clinical applications of the Amytal interview in psychiatric emergency settings. 707 39

Studies with unanesthetized active (non-lethargic) marmots demonstrated circannual rhythms of renal function (clearances of p-aminohippurate, creatinine, and inulin), plasma osmolality, and plasma sodium and potassium concentrations. Effective renal plasma flow, glomerular filtration rate, the clearance of creatinine, and plasma potassium were highest in spring and lowest in the fall and winter. Plasma osmolality and plasma sodium concentrations tended to be highest during the winter months and lowest in the spring and summer. p-Aminohippurate excretion was shown to be a Tm-limited system.
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PMID:Circannual renal function and plasma electrolytes of the marmot. 724 3

Adult female mink (Mustela vison) were fed a diet that contained Fusarium moniliforme culture material that provided dietary concentrations of 89 ppm fumonisin B1, 21 ppm fumonisin B2, and 8 ppm fumonisin B3 for 87 days. During the trial, there was mild lethargy in the mink fed fumonisins, but no other clinical signs or differences in feed consumption (measured during the first two weeks), body weights, or survivability were observed between the fumonisin-treated and control mink. Several hematologic parameters (mean corpuscular hemoglobin concentration, plasma total solids, and lymphocyte concentration) and serum chemical concentrations (globulin, phosphorus, potassium, blood urea nitrogen, creatinine, bilirubin, and cholesterol) and activities (alkaline phosphatase, alanine aminotransferase, amylase, and aspartate aminotransferase) were greater in the mink fed fumonisins than in the controls. Serum albumin/globulin and sodium/potassium ratios and chloride concentrations were lower in the fumonisin-fed mink than in the controls. The concentrations of free sphinganine and the ratio of free sphinganine to free sphingosine in the liver and kidneys of the fumonisin-treated mink were greater than in the control mink. No histopathologic alterations were associated with fumonisin treatment. These results indicate that long-term dietary exposure to F. moniliforme culture material containing 118 ppm total fumonisins is not lethal to adult mink, but can produce adverse physiological effects in the animals.
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PMID:Chronic toxicity of fumonisins from Fusarium moniliforme culture material (M-1325) to mink. 757 84

Acute arsenic toxicity is rare, and there have been no pediatric cases of acute arsenic poisoning in the recent literature. We report a pediatric case of acute arsenic ingestion treated initially with British antilewisite (BAL) and D-penicillamine (DP), and later with dimercaptosuccinic acid (DMSA). A 22-month-old girl ingested 1 oz 2.27% sodium arsenate and developed immediate vomiting and diarrhea. The patient presented to a community emergency department with the following vital signs: blood pressure 96/72 mm Hg, pulse 160 beats/min, respirations 22 breaths/min. She was pale and lethargic. Gastric lavage was performed, and abdominal X-ray was normal. She continued to have gastrointestinal symptoms and received 3 mg/kg BAL. Sinus tachycardia persisted, with heart rate increasing to 200 beats/min. In 12 hours, she was asymptomatic and was started on oral DP. On day 1, 24-hour urine arsenic was 4,880 micrograms/L. She remained asymptomatic and was discharged on day 6 on oral DP. She did well except for a rash that could have been a side effect of DP. On day 8, when the day 5 24-hour urine arsenic level was returned at 650 micrograms/L, the patient was readmitted and started on DMSA. After 4 days on DMSA, the 24-hour urine arsenic level was 96 micrograms/L. White blood cell count and renal and hepatic function remained normal. The excretion half-life was approximately 2.5 days, which is at least 2 to 3 times faster than the spontaneous excretion half-life expected in adults. Long-term follow-up was unavailable.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pediatric arsenic ingestion. 760 32

The use of psychotropic drugs has been associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in a number of case reports. SIADH is characterised by the sustained release of antidiuretic hormone (ADH) from the posterior pituitary. The patients have a reduced ability to excrete diluted urine, ingested fluid is retained, and the extracellular fluid expands and becomes hypo-osmolar. The cardinal signs are hyponatraemia, serum hypoosmolality and a less than maximally diluted urine. Common symptoms include weakness, lethargy, headache, anorexia and weight gain. These symptoms may be followed by confusion, convulsions, coma and death. The early symptoms are vague and nonspecific, and they may even mimic the symptoms of the psychiatric disorder itself. For antidepressants, the risk of SIADH seems to be highest during the first weeks of treatment. For antipsychotics, the risk seems to be more spread out in time. The causative role of the drug may sometimes be difficult to estimate, as even drug-free psychiatric patients, mostly those with schizophrenia, develop SIADH on the basis of psychogenic polydipsia. Smoking is another factor associated with the development of SIADH, and the risk may also increase with age. The acute treatment of SIADH induced by a psychotropic drug includes discontinuation of the drug as well as restriction of fluid intake. In cases with significant clinical symptoms, infusion of sodium chloride is recommended. After the acute management, it is useful to evaluate the causative role of the drug by performing a water loading test and/or drug rechallenge. If continued treatment with an antidepressant or antipsychotic is indicated, a drug with a different pharmacological profile should be chosen, and the serum sodium levels should be monitored closely. If treatment with the drug that caused SIADH must be continued, concomitant treatment with demeclocycline may reduce the tendency of hyponatraemia.
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PMID:Hyponatraemia and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) induced by psychotropic drugs. 761 32

Thirty-six male mink were fed diets that contained 0, 1, 2 or 4% supplemental salt (sodium chloride) and were given drinking water ad libitum for 7 d. Three mink on each diet were then placed on ad libitum, 50% ad libitum or 25% ad libitum drinking water for the next 14 d. Ad libitum water consumption was directly proportional to the salt content of the diets. Feed consumption was inversely related to the level of dietary salt, although water restriction had a greater effect in reducing feed consumption than did the supplemental salt. The clinical signs of salt toxicity-water restriction observed were increased thirst, mild dehydration, decreased feed consumption, decreased body weight, rough coat, crusty nose and eyes, irritability in the early stage, and lethargy in the later stages. In general, serum and urinary sodium and chloride ion concentrations increased with increasing dietary salt concentrations. Expressed as a percent of brain weight, liver, spleen, kidney and heart weights of mink fed supplemental salt were less than the control weights. Adrenal gland weights increased in response to water restriction. Brain sodium concentrations were not affected by salt supplementation when drinking water was provided ad libitum. However, restricting drinking water generally resulted in increased brain sodium concentrations. Mild to moderate micro- or macrovesicular vacuolar changes were observed in the livers of some mink fed each level of dietary salt, but were especially prominent in the mink restricted in drinking water.
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PMID:Effects of supplemental dietary sodium chloride and restricted drinking water on mink. 770 90

A 5-year-old boy had recurrent vomiting and lethargy with lacticacidemia and ketoacidemia since birth. Lipoamide dehydrogenase deficiency was found in muscle and fibroblasts. Therapy with sodium dichloroacetate, thiamine, and carnitine was associated with reduction of the severity and frequency of the decompensation episodes and near normal plasma lactate levels. At 5 years of age, the patient has normal cognitive function and moderate motor impairment.
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PMID:Congenital lacticacidemia caused by lipoamide dehydrogenase deficiency with favorable outcome. 781 30

Hypopituitarism is uncommon in elderly people. We report 12 cases of hypopituitarism diagnosed after the age of 60 (range 63-89, mean 74.9) years over a 10-year period. Aetiology was evident in eight cases, viz. pituitary tumour in six and previous post-partum haemorrhage and giant aneurysm of carotid artery in one each. The presentation was often non-specific with symptoms such as lethargy, pallor, falls, urinary incontinence, confusion, fever and flexion contractures. Subtle clues to the condition were missed in four cases resulting in delayed diagnosis. Although levels of pituitary trophic hormones are generally low in this condition, the thyrotrophin (TSH) was normal in seven cases in the present series. Normal levels of serum sodium and potassium did not exclude cortisol deficiency. Hormone replacement therapy resulted in improved quality of life. Physicians dealing with elderly patients should bear this easily treated condition in mind.
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PMID:Hypopituitarism: a difficult diagnosis in elderly people but worth a search. 776 67

One hundred fifty lactating mink on one ranch in southern Ontario were monitored over the lactation period in 1989 for evidence of clinical disease, and serial blood samples were collected for biochemical analysis. Antemortem blood samples were collected and necropsies performed on the 17 females that developed nursing disease and on 17 controls matched to the same stage of lactation and on ten nonlactating controls. Twenty-two additional nursing disease cases were selected from seven ranches in the following year and processed similarly. The clinical signs typically observed in affected females were sudden onset lethargy and anorexia followed by dehydration, ataxia, and a reluctance to move. The major clinical-pathologic findings were a marked increase in serum osmolality and total protein, urea nitrogen, creatinine, phosphorus, glucose, and potassium concentrations and a decrease in sodium and chloride concentration. In addition, the animals were acidotic, there was a reduction in the urine specific gravity, and the hemogram was consistent with a stress response. Emaciation and dehydration were the only pathologic changes consistently present in cases of nursing disease and not in controls. In almost all cases, bacteria were not cultured from the liver, spleen, and mammary gland, but Campylobacter jejuni was cultured from the intestinal contents of 15/17 affected mink and 2/5 controls. Aleutian disease virus antibody was not present in any of the affected mink. Lipid vacuoles in hepatocytes and renal tubular epithelium, hypertrophy of cells in the adrenal cortex, and pulmonary congestion and atelectasis were present in both diseased females and controls, as were various sporadic inflammatory lesions. Nursing disease may result from energy depletion due to lactation. All lactating females are affected by this process; clinical disease reflects the terminal physiologic decompensation of the most susceptible individuals.
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PMID:Nursing disease in mink: clinical and postmortem findings. 811 44


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