Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
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Toxic irreversible encephalopathic syndromes developed in 2 patients treated with lithium carbonate and haloperidol. Symptoms consisted of lethargy, fever, tremulousness, confusion, and extrapyramidal and cerebellar dysfunction, accompanied by leucocytosis and elevated serum enzyme, blood urea nitrogen, creatinine and fasting blood glucose levels. One patient suffered widespread irreversible brain damage; the other was left with persistent dyskinesias. Although causal factors have not been identified, this report and others in the literature suggest that diffuse irreversible encephalopathy may occasionally develop in individuals with abnormal brain sensitivity to the lithium carbonate/haloperidol combination. Evidence for this is based on the fact that in our patients and others mentioned in the literature the dosage and blood levels of lithium were not high.
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PMID:Toxic irreversible encephalopathy induced by lithium carbonate and haloperidol. A report of 2 cases. 641 23

The main purpose of this work was to study changes in the balance of fluids, electrolytes and blood metabolites in neonatal piglets with severe transmissible gastroenteritis. Six two day old conventional piglets were infected with transmissible gastroenteritis virus while six others were used as normal controls. Blood samples were collected in heparin when the infected piglets were moribund. The following variables were measured: packed red cell volume, total plasma protein and bicarbonate, blood pH, blood urea nitrogen and plasma glucose, creatinine, chloride, inorganic phosphorus, sodium, potassium, magnesium and calcium. Vomiting and diarrhea appeared 12 to 24 hours postinoculation in the infected piglets and they were moribund one or two days later. Before becoming moribund, most of the piglets fell rapidly into a lethargic and comatose state. The most evident changes in their blood variables were an increase in packed cell volume, total protein, blood urea nitrogen, phosphorus and magnesium levels and a decrease in pH and bicarbonate concentration as well as a severe hypoglycemia. The results suggest that severe hypoglycemia coupled with metabolic acidosis and dehydration might be an important factor contributing to the high mortality rates caused by transmissible gastroenteritis in neonatal piglets. The hypoglycemia results from a combination of the inadequate glucose metabolism inherent to neonatal piglets and the acute maldigestion and malabsorption resulting from the diffuse and severe villous atrophy induced by the virus.
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PMID:Hypoglycemia: a factor associated with low survival rate of neonatal piglets infected with transmissible gastroenteritis virus. 647 97

A symptomatic elevation in plasma ammonium concentration, termed hyperammonemia, is associated with numerous congenital and acquired conditions (Table 11). In some cases, such as urea cycle disorders, ammonia is the principal toxin. In other instances, such as portal systemic encephalopathy, it is but one of a number of metabolic disturbances, However, in either case hyperammonemic episodes should be treated aggressively to prevent coma, subsequent brain damage, or death. This involves restricting protein intake, providing adequate calories, and giving agents that remove accumulated nitrogen. Long-term therapy relies on diagnosing the specific disease rate. This rarely requires invasive procedures such as liver biopsy. In most cases measurement of plasma amino acids and urinary organic acids will identify the defect. Treatment involving restriction of nitrogen intake, vitamin supplementation, or stimulation of alternative pathways of waste nitrogen excretion can then be instituted. Early therapy, especially in patients with neonatal-onset hyperammonemia, is imperative to avoid severe brain damage. On this basis, the plasma ammonium level should be determined in virtually every newborn with lethargy, hypotonia, poor feeding, seizures, and/or respiratory distress of unclear origin (Table 12).
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PMID:Hyperammonemia. 651 17

11 adult female dogs were given periodic intravenous injections of uranyl nitrate [UO2(NO3)2 . 6H2O] to create a syndrome of chronic uremia. Initially, dogs usually received 2.0 mg/kg of uranyl nitrate; subsequent doses were generally less. After the initial injection, there was an abrupt fall in creatinine clearance and rise in plasma urea nitrogen. Low and relatively constant creatinine clearances (10.2 +/- SD 2.7 ml/min) were easily maintained with further injections. Dogs developed proteinuria, aminoaciduria, weight loss, and plasma amino acid levels similar to those of chronically uremic humans and rats. With creatinine clearances of 4 ml/min or less, dogs became listless and lethargic, and daily activity and food intake decreased. Repeated injections of uranyl nitrate appear to be an easy and reliable method for creating a model of chronic uremia in dogs.
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PMID:Chronic uremia syndrome in dogs induced with uranyl nitrate. 736 Feb 99

Ornithine transcarbamylase deficiency is an X-linked recessive disorder of urea biosynthesis characterized by recurrent, often fatal, hyperammonemic encephalopathy in affected males; carrier females are usually asymptomatic. We report here the clinical and laboratory findings in five symptomatic heterozygous females with ornithine transcarbamylase deficiency. In each case, the onset of symptoms occurred in the 1st year of life, but diagnosis was delayed by up to 15 years. Symptoms included recurrent vomiting with lethargy (five patients), dietary protein intolerance (five), irritability (four), severe acute encephalopathy (three), ataxia (three), and acute hemiparesis (two). All eventually showed evidence of developmental delay or learning difficulties. Two of the three who experienced severe, acute, hyperammonemic encephalopathy suffered serious, permanent neurologic sequelae. Three of the patients showed decreased ornithine transcarbamylase activity in liver obtained by needle biopsy, and the other two had marked orotic aciduria associated with hyperammonemia. Neuroimaging studies demonstrated persistent abnormal lobar attenuation and abnormal signal on computed tomographic scan and magnetic resonance imaging. All patients showed marked symptomatic improvement on treatment with dietary protein restriction supplemented by pharmacologic measures to increase nonprotein nitrogen excretion. Ornithine transcarbamylase deficiency should be considered in the differential diagnosis of acute or chronic encephalopathy in females at any age.
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PMID:Ornithine transcarbamylase deficiency in females: an often overlooked cause of treatable encephalopathy. 749 56

The purpose of this study was to determine the effects of recombinant human GH (rhGH; 0.025 mg/kg.day) and one of two doses of recombinant human insulin-like growth factor-I (rhIGF-I; 0.015 and 0.060 mg/kg, twice daily) on body composition in elderly women. Sixteen healthy elderly women (mean age +/- SEM, 71.9 +/- 1.3 yr) were randomly assigned to receive either rhGH (GH; n = 5), low dose rhIGF-I (n = 6), or high dose rhIGF-I (n = 5). A 2-week predrug baseline period was followed by 4 weeks of hormone treatment, with a standardized diet fed throughout. All groups experienced a significant increase in serum IGF-I and IGFBP-3 levels over the treatment period, accompanied by significant decreases in IGF-II (P < 0.05). Fat mass decreased in all groups, with significant increases in lean body mass and nitrogen retention occurring in the high dose IGF and GH groups. Total body water did not change, whereas increases observed in intracellular fluid approached significance (P = 0.06). These anabolic changes were accompanied by numerous negative side-effects in the GH and high dose IGF groups, including headaches, lethargy, joint swelling/pain, and bloatedness. The low IGF dose was well tolerated. These results demonstrate that the administration of rhGH and rhIGF-I for 4 weeks results in anabolic changes in body composition in elderly women.
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PMID:The effects of recombinant human insulin-like growth factor-I and growth hormone on body composition in elderly women. 753 17

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

Whole-carcass residues of the rodenticide zinc phosphide (Zn3P2) and hydrolyzed phosphine (PH3) were determined for voles (Microtus spp.) that died following ingestion of a 2% Zn3P2 steam rolled oat (SRO) groats bait. Procedures involved: a three-day acceptance test to assess vole consumption (n = 27) of control SRO groats and several one-day Zn3P2- (n = 13) or control-bait (n = 4) tests to characterize onset of pharmacotoxic signs and to obtain fatally-dosed carcasses for residue analyses. Carcasses were stored in liquid nitrogen (LN2) to maximize retention of Zn3P2/PH3 residues prior to chemical determinations. Linear regressions were computed between pairs of consumption and residue variables. Main results were the following: (1) mean (+/- SD) consumption of control bait was 2.5 (+/- 0.9), 3.0 (+/- 0.9), and 2.8 (+/- 0.8) g on days 1, 2, and 3, respectively (> or = 10.6 +/- 4.6% of body weight); (2) all test-bait voles (n = 13) died approximately 4-12 h after bait presentation, with lethargy and respiratory distress key signs of toxicosis; (3) whole-carcass Zn3P2 residues averaged 1.73 mg (min-max: 0.31-4.95), and PH3 residues averaged 10.6 micrograms (min-max: 0.5-21.0); and (4) significant linear regressions were found between bait consumption/Zn3P2 intake and body weight (r2 = 0.64, p < or = 0.001), carcass Zn3P2 and bait consumption/Zn3P2 intake (r2 = 0.32, p < or = 0.043), and carcass Zn3P2 and body weight (r2 = 0.60, p < or = 0.002). Certain analytical and hazards issues are discussed.
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PMID:Regressors of whole-carcass zinc phosphide/phosphine residues in voles: indirect evidence of low hazards to predators/scavengers. 775 4

Effects of restricted tube-feeding (25% of energy requirements) of protein, lipid, or carbohydrates on body weight loss; hematologic and clinical chemical variables; plasma lipid and amino acid concentrations; nitrogen balance; and hepatic histologic features and lipid concentrations were compared with values in voluntary-fasting cats (control, CON). Twelve obese cats (6.1 +/- 0.1 kg, > 40% above optimal body weight) were randomly assigned to 4 matched treatment groups (n = 3)--protein (PRO), lipid (LIP), carbohydrate (CHO), and CON--and were offered a low-palatability diet for 4 weeks. Cats of the PRO, LIP, and CHO groups were also tube-fed isocaloric amounts (88 kcal of metabolizable energy) of a casein-soybean protein mixture, corn oil, or a dextrin-dextrose mixture, respectively, during the 4 weeks. All cats fasted, rather than eat the low-palatability purified diet. Cats of the PRO group lost weight at a lower rate (P < 0.05) than did cats of other groups. After 4 weeks of fasting, serum alkaline phosphatase activities were higher than reference values in all cats of the CON and LIP groups and in 2 cats of the CHO group. At that time, 1 cat of the LIP group had lethargy, hepatomegaly, and hyperbilirubinemia. Total hepatic lipid and triglyceride concentrations increased in all groups during the study, but the increase was significantly (P < 0.05) less in cats of the PRO group, compared with those of the CON and LIP groups, and those of the CHO group, compared with those of the LIP group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of protein, lipid, or carbohydrate supplementation on hepatic lipid accumulation during rapid weight loss in obese cats. 799 98

Nutritional support of patients with HIV or acquired immune deficiency syndrome (AIDS) has many similarities to other disease states in that the same nutritional products and techniques are used. Some patients with HIV, and many with AIDS without secondary infection, experience a metabolic milieu similar to patients with cancer cachexia. In providing dietary counselling to the HIV patient, we encounter many of the obstacles that must be overcome to improve nutrition in cancer: anorexia, gastrointestinal discomfort, lethargy, and poor nutrient utilization, which limit the ability for nutritional repletion. When a secondary infection is superimposed on HIV, patients resemble more highly catabolic trauma patients or patients in the intensive care unit (ICU), where, despite aggressive efforts to feed, there is usually a net nitrogen wasting leading to the more rapid development of cachexia. However, even in this setting, feeding will limit substantially net catabolism when compared to total starvation. Because the nutritional needs of HIV patients vary greatly, individual strategies have to be designed as the patient moves through the stages of disease. Patients are generally able to consume adequate nutrition either as regular food or dietary supplements during the latency period of viral replication. Once secondary infections become prevalent, artificial diets administered by tube or by vein may be required during the period of active secondary infections, with dietary supplements often helpful during more quiescent periods. Patients with HIV are among the most challenging for clinicians providing nutritional support. Knowledge from treatment of patients with other diseases may be useful, but more data must be gathered on the unique aspects of aetiology and treatment of the anorexia, malabsorption, and ultimate wasting associated with AIDS.
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PMID:Nutrition support and the human immunodeficiency virus (HIV). 811 86


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