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)

Glomerular disease was diagnosed by histopathologic examination in 11 related Bullmastiff dogs, and clinical and laboratory data were collected retrospectively. Four female and seven male dogs between the ages of 2.5 and 11 years were affected. Clinical signs, including lethargy and anorexia, were nonspecific and occurred shortly before death or euthanasia. In five affected dogs serial blood samples were obtained, and dramatically elevated blood urea nitrogen and creatinine levels were demonstrated up to 2.75 years before death. Protein-creatinine ratios were elevated in six of six dogs and were above normal 3.5 years before death in one dog. The kidneys appeared grossly normal to slightly smaller than normal at necropsy. Histologic abnormalities of the kidneys were consistent with chronic glomerulonephropathy with sclerosis. Examination of the pedigrees of related affected dogs yielded evidence supporting an autosomal recessive mode of inheritance.
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PMID:Familial glomerulonephropathy in the Bullmastiff. 1523 31

Ammonia, normally produced from catabolism of amino acids, is a deadly neurotoxin. As such, the concentration of free ammonia in the blood is very tightly regulated and is exceeded by two orders of magnitude by its physiologic derivative, urea. The normal capacity for urea production far exceeds the rate of free ammonia production by protein catabolism under normal circumstances, such that any increase in free blood ammonia concentration is a reflection of either biochemical or pharmacologic impairment of urea cycle function or fairly extensive hepatic damage. Clinical signs of hyperammonemia occur at concentrations > 60 micromol/L and include anorexia, irritability, lethargy, vomiting, somnolence, disorientation, asterixis, cerebral edema, coma, and death; appearance of these findings is generally proportional to free ammonia concentration, is progressive, and is independent of the primary etiology. Causes of hyperammonemia include genetic defects in the urea cycle ("primary") or organic acidemias ("secondary"), as well as genetic or acquired disorders resulting in significant hepatic dysfunction. Thus, because of the neurotoxic implications of hyperammonemia and the typical absence of other specific laboratory abnormalities, appearance of the clinical signs should trigger an emergent search for elevated blood ammonia concentration.
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PMID:Hyperammonemia, bane of the brain. 1549 74

Four groups comprising 16 broiler birds each were given benzalkonium chloride (BC) at 100, 300, 500 and 700 ppm in drinking water for 40 days and one group of 16 birds (control) was kept on plain water. Clinical signs in higher dose groups were respiratory distress, drooling of saliva, difficulty in deglutition, inappetence, apathy, lethargy and loss of body weight. Better body weight gain was recorded in 100 ppm dose rate. At 300 ppm, no significant body weight variation was recorded, whereas, at 500 and 700 ppm dose rates, significantly poor body weight gain was recorded. Major pathological changes were seen in 500 and 700 ppm groups, which exhibited formation of yellow diphtheritic plaques in the buccal cavity, swollen and pale commissures of beak and shortening of tongue. Minute necrotic and ulcerative foci were seen in oesophagus and crop. Hyperplastic and hypertrophic alterations were seen in mucosa of the upper digestive tract. Crop of 300 ppm group revealed formation of well developed epithelial nest with pseudoepitheliomatous hyperplasia at the margin of the lesion. Serum alanine transaminase, urea and uric acid in 500 and 700 ppm groups were elevated whereas no significant variations were observed in the 100 and 300 ppm groups. BC could enhance performance of broiler birds at 100 ppm dose rate. It should not be used beyond 300 ppm.
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PMID:Pathology of benzalkonium chloride toxicity and its effect on body weight gain in broiler birds. 1558 18

A review of records from the AnTox database of the American Society for the Prevention of Cruelty to Animals Animal Poison Control Center identified 43 dogs that developed increased blood urea nitrogen concentration, serum creatinine concentration, or both as well as clinical signs after ingesting grapes, raisins, or both. Clinical findings, laboratory findings, histopathological findings, treatments performed, and outcome were evaluated. All dogs vomited, and lethargy, anorexia, and diarrhea were other common clinical signs. Decreased urine output, ataxia, or weakness were associated with a negative outcome. High calcium x phosphorus product (Ca x P), hyperphosphatemia, and hypercalcemia were present in 95%, 90%, and 62% of the dogs in which these variables were evaluated. Extremely high initial total calcium concentration, peak total calcium concentration, initial Ca x P, and peak Ca x P were negative prognostic indicators. Proximal renal tubular necrosis was the most consistent finding in dogs for which histopathology was evaluated. Fifty-three percent of the 43 dogs survived, with 15 of these 23 having a complete resolution of clinical signs and azotemia. Although the mechanism of renal injury from grapes and raisins remains unclear, the findings of this study contribute to an understanding of the clinical course of acute renal failure that can occur after ingestion of grapes or raisins in dogs.
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PMID:Acute renal failure in dogs after the ingestion of grapes or raisins: a retrospective evaluation of 43 dogs (1992-2002). 1623 10

The purpose of this investigation was to determine the effects of an activated charcoal (AC) suspension containing propylene glycol and glycerol on serum osmolality, osmolal gap, and lactate concentration in dogs. Six healthy adult dogs were administered 4 g/kg AC in a commercially available suspension that contained propylene glycol and glycerol as vehicles. Blood samples were taken before and 1, 4, 6, 8, 12, and 24 hours after the administration of the test suspension. Samples were analyzed for osmolality, blood gases, and concentrations of lactate, sodium, potassium, serum urea nitrogen, and glucose. Osmolal gaps were calculated for each time point. Mean serum osmolality, osmolal gap, and lactate concentration were significantly increased after suspension administration compared to baseline. Serum osmolality increased from 311 mOsm/kg at baseline to 353 mOsm/kg, osmolal gap increased from 5 to 52 mOsm/kg, and lactate concentration increased from 1.9 to 4.5 mmol/L after suspension administration (all P < .01). Three of the 6 dogs vomited between 1 and 3 hours after the administration of the test suspension, and 4 of 6 dogs were lethargic. All dogs drank frequently after AC administration. Commercial AC suspension administered at a clinically relevant dose increases serum osmolality, osmolal gap, and lactate concentration in dogs. These laboratory measures and the clinical signs of vomiting, lethargy, and increased frequency of drinking might complicate the diagnosis or monitoring of some intoxications (such as ethylene glycol) in dogs that have previously received AC suspension containing propylene glycol, glycerol, or both as vehicles.
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PMID:Effects of oral administration of a commercial activated charcoal suspension on serum osmolality and lactate concentration in the dog. 1623 12

Piroplasmosis, a disease endemic to most tropical and subtropical areas, appears to be spreading to more temperate zones. This article gives a review of equine piroplasmosis and describes an acute case of infection with Babesia caballi in a Dutch Standard bred foal after a short stay at a stud in Normandy (France). A 3-month-old stallion foal was presented with lethargy, fever of 41 degrees C, and pale mucosal membranes. Haematology revealed a low packed cell volume (14 l/l) leucytosis (25 G/l) and a high blood urea nitrogen concentration (20.1mmol/l). Infection with B. caballi was diagnosed on the basis of Giemsa staining blood smears and was confirmed by polymerase chain reaction in combination with RLB. Treatment with imidocarb dipropionate and a blood transfusion resolved the haemolytic crisis.
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PMID:[A literature review of equine piroplasmosis after an episode of acute babesiosis in a Dutch Standardbred foal after a stay in Normandy]. 1645 88

A 5-year old Tinker gelding was referred to the Department of Equine Sciences with a left eye uveitis and fever. At presentation the horse showed a mild lethargy, fever and decreased vision of the left eye. Rectal examination revealed an enlarged left kidney, with a hard and an irregular surface. The cranial mesentery artery had an enlarged and irregular aspect. Blood analysis showed anaemia, leucocytosis, increased blood urea nitrogen and creatinine and a hyperproteinemia. Urine analysis repeatedly showed a marked proteinuria and an increased gammaGT/creatinine ratio. The amount of abdominal fluid was slightly increased. However, the aspect, amount of cells and protein were normal. In the following two days the fever persisted and the horse showed anorexia and severe neurological signs. The horse was euthanized with permission of the owner. Post mortem examination showed a generalized parasitic infestation of Halicephalobus gingivalis in the uvea of the left eye, the kidneys and the central nerve system.
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PMID:[Halicephalobus gingivalis infection in a 5-year-old Tinker gelding]. 1650 77

Valproate-induced hyperammonemic encephalopathy (VHE) is an unusual complication characterized by a decreasing level of consciousness, focal neurological deficits, cognitive slowing, vomiting, drowsiness, and lethargy. We have thoroughly reviewed the predisposing factors and their screening, the biochemical and physiopathological mechanisms involved, the different treatments described, and those that are being investigated. Etiopathogenesis is not completely understood, although hyperammonemia has been postulated as the main cause of the clinical syndrome. The increase in serum ammonium level is due to several mechanisms, the most important one appearing to be the inhibition of carbamoylphosphate synthetase-I, the enzyme that begins the urea cycle. Polytherapy with several drugs, such as phenobarbital and topiramate, seems to contribute to hyperammonemia. Hyperammonemia leads to an increase in the glutamine level in the brain, which produces astrocyte swelling and cerebral edema. There are several studies that suggest that treatment with supplements of carnitine can lead to an early favorable clinical response due to the probable carnitine deficiency induced by a valproate (VPA) treatment. Development of the progressive confusional syndrome, associated with an increase in seizure frequency after VPA treatment onset, obliges us to rule out VHE by screening for blood ammonium levels and the existence of urea cycle enzyme deficiency, such as ornithine carbamoyltransferase deficiency. Electroencephalography (EEG) is characterized by signs of severe encephalopathy with continuous generalized slowing, a predominance of theta and delta activity, occasional bursts of frontal intermittent rhythmic delta activity, and triphasic waves. These EEG findings, as well as clinical manifestations and hyperammonemia, tend to normalize after VPA withdrawal.
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PMID:Valproate-induced hyperammonemic encephalopathy. 1677 19

Ornithine transcarbamoylase (OTC) deficiency is the most common hereditary urea cycle disorder. It is an X-linked recessive disorder that usually presents with encephalopathy and hyperammonaemia. We report a 14-month-old female carrier of OTC deficiency, who presented with a history of intermittent vomiting for 5 weeks and irritability and lethargy for 1 week. She was found to be in acute liver failure, with elevated transaminases, coagulopathy and a consistently low urea. Identifying an OTC mutation and ruling out other possible causes of acute hepatic failure confirmed the diagnosis. She was placed on low-protein diet supplemented with essential amino acids, and her liver enzymes, hyperammonaemia and coagulopathy corrected. Three other female patients have been reported with OTC deficiency presenting with severe cryptogenic hepatitis; our patient is unique in that the presentation of her disease was dominated by acute liver failure on a back ground of normal growth and development, no liver enlargement, and mild hyperammonaemia. OTC deficiency should be considered in the differential diagnosis of infants presenting with acute hepatocellular dysfunction, especially in females.
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PMID:Ornithine transcarbamoylase deficiency presenting with acute liver failure. 1680 8

A 1-year-old guinea pig presented with anorexia, lethargy, and weight loss, 1 week after ingesting a peace lily leaf. Laboratory findings were suggestive of renal failure and included elevated blood urea nitrogen and creatinine with concurrent isosthenuria. The guinea pig was euthanized 1 month later due to worsening clinical signs.
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PMID:Renal failure in a guinea pig (Cavia porcellus) following ingestion of oxalate containing plants. 1693 58


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