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)

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

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

Rickets is a common and paradoxical feature of infantile malignant osteopetrosis and results from the inability of osteoclasts to maintain a normal calcium-phosphorus balance in the extracellular fluid. Despite a markedly positive total body calcium balance, rickets arises when the serum calcium x phosphorus product is insufficient to mineralize newly formed chondroid and osteoid. In five children with malignant infantile osteopetrosis, there were clinical, radiographic, biochemical, and histologic findings of rickets. Characteristic biochemical abnormalities included hypocalcemia, hypophosphatemia, and elevated levels of serum acid phosphatase, alkaline phosphatase, c-terminal parathyroid hormone, and 1,25-dihydroxyvitamin D. The urinary calcium/creatinine ratio was markedly depressed. The serum calcium x phosphorus product was below 30 in all children at the time the rickets was diagnosed, and above 40 by the time the rickets had resolved. Baseline bone density measurements were markedly elevated in all children (> 5 standard deviation above normal) and showed even significant increases (> 7 SD) when the rickets was treated with vitamin D and calcium. The children showed marked clinical improvement, decreased lethargy, increase in mobility and activity, and stimulation of appetite, without any additional adverse hematologic or neurologic effects. The rickets was reversible in all children: in one by HLA-identical sibling bone marrow transplantation and in four by physiologic doses of vitamin D and calcium. The parathyroid and renal responses to hypocalcemia were appropriate, but glucocorticoids, used in treating the hematologic complications of the disease, may have blunted the intestinal response to maximal vitamin D stimulation. This latter blockade can be overcome by increasing dietary calcium. By liberalizing rather than by restricting calcium and phosphorus intake, hypocalcemia can be minimized, phosphorus metabolism can be improved, and rickets can be cured.
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PMID:Osteopetrorickets. The paradox of plenty. Pathophysiology and treatment. 839 71

Clinical signs that included lethargy, inappetence, diarrhea, and vomiting and that progressed to seizures were observed in 40 feeder pigs that were approximately 70 days old. The pigs were fed ground red wheat and whole milk and were housed in a barn that did not allow exposure to direct sunlight. Analysis of samples of feed obtained from the farm indicated inadequate quantities of calcium and phosphorus as well as a low ratio of these 2 nutrients. Serum and tissue concentrations of vitamin A were less than normal. Low serum calcium concentrations, high serum phosphorus concentrations, and high alkaline phosphatase and creatine kinase activities were compatible with low vitamin D concentrations.
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PMID:Seizures and acute death attributable to hypovitaminosis A and suspected hypovitaminosis D in feeder pigs. 849 85

Patients with chronic renal failure (CRF) can develop problems such as lethargy, tetany, and muscle spasms, which can increase their morbidity and mortality. Because of their non-functioning kidneys, patients with CRF require in-depth and comprehensive monitoring of calcium (Ca) and phosphorus (P) levels. This article presents advanced nursing actions and critical thinking strategies for use by the critical care nurse when caring for patients with CRF.
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PMID:Balancing calcium and phosphorus levels in chronic renal failure patients. 939 11

Gadobenate dimeglumine formulation (E7155), at doses of 0 (physiological saline), 0.25, 0.5, 1 and 2 mmol/kg/day of body weight, was administered intravenously to male and female beagle dogs once daily for 4 consecutive weeks in order to evaluate the subacute toxicity of the test article. Reversibility of toxicity was evaluated during a 4-week recovery period at 1 and 2 mmol/kg/day. No toxicologically significant changes were observed at 0.25 and 0.5 mmol/kg/day. In animals receiving 1 or 2 mmol/kg/day, transient swelling and redness of the facial and eye areas, lethargy, decreased activity, emesis, retching, watery or unformed stool, decreased body weight or body weight gain, decreased food consumption, decreased hematocrit and hemoglobin concentration, increased APTT, increases in plasma ALP, GPT or gamma-GT, decreased plasma inorganic phosphorus, total protein or albumin, increased liver or kidney weight, subacute inflammatory infiltrates, loss of centrilobular hepatocytes or hepatocellular cytoplamic vacuolation in the liver, vacuoles in the epithelial cells of the renal tubles and/or hypocellularity in the bone marrow were seen. The results of toxicokinetic analysis showed that systemic exposure was similar in males and females, and there was no accumulation of the test material over the treatment period, although AUC tended to be enhanced by slightly more than the proportionate dose increase. These effects were recovered or tended to be reversed after a post-dosing period for 4 weeks. In conclusion, the No Observed Adverse Effect Level (NOAEL) was 0.5 mmol/kg/day.
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PMID:[General toxicity study of gadobenate dimeglumine formulation (E7155) (4)--4-week repeated dose intravenous toxicity study followed by 4-week recovery period in dogs]. 1063 79

Mature female natural dark mink (Mustela vison) were fed 0.0006 (control), 0.016, 0.053, 0.180, or 1.40 ppb 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for 131-132 d to ascertain the chronic toxic effects of TCDD in mink, including reproduction. Consumption of the 1.4 ppb TCDD diet resulted in lethargy, bloody stools, and 16.7% mortality. Final mink body weights were inversely proportional to the dietary TCDD concentrations. Due to subnormal mink breeding, definitive effects of TCDD on mink reproductive performance were not ascertained; however, there were significant dose-dependent decreases in kit (young mink) birth weight and survival from birth to 3 w of age in the groups that had reproduction. There were also significant differences in adult minkwhite blood cell counts, plasma total solids, serum iron, phosphorus, albumin, total protein, total CO2, cholesterol, osmolality, and anion gap concentrations, and alanine aminotransaminase activity between the various dietary groups. During the latter stages alopecia and thickened, deformed, and elongated toenails were observed in the adult mink fed 1.4 ppb TCDD. At termination the mink fed 1.4 ppb TCDD had ascites, gastric ulcers, intestinal hemorrhages, depletion of adipose tissue, and mottled and/or discolored livers, spleens, and kidneys. Focal lymphocytic meningitis in region of the olfactory bulb was present in 42% of the mink fed 1.4 ppb TCDD. These results confirmed the high sensitivity of mink to TCDD and revealed a toenail abnormality not previously reported for mink fed TCDD.
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PMID:Chronic toxicity of dietary 2,3,7,8-tetrachlorodibenzo-p-dioxin to mink. 1138 52

Two adult guinea pigs were examined because they were lethargic and reluctant to walk. Additionally, I guinea pig had otitis media, and the other had dental malocclusion. Both guinea pigs had been fed a commercially available diet of cereals and pellets enriched with vitamin C and formulated for this species. Radiographically, the guinea pigs had coarse trabecular bone patterns, skeletal deformations, pathologic fractures, and polyarthritic degenerative joint disease. A double cortical line was also evident on several long bones, the pelvis, and the vertebrae. A diagnosis of osteopenia was confirmed by use of dual-energy x-ray absorptiometry. Analysis of a food sample fed to 1 guinea pig revealed calcium and phosphorus contents of 0.524 and 0.425%, respectively (Ca:P ratio, 1.23:1). Microscopic examination of bone tissue from both guinea pigs revealed severe fibrous osteodystrophy. Nutritional secondary hyperparathyroidism caused by calcium-phosphorus imbalance was considered to be the underlying cause of osteodystrophia fibrosa in both guinea pigs.
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PMID:Osteodystrophia fibrosa in two guinea pigs. 1143 72

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

A commercially available, renal failure diet was used to manage suspected renal failure in a 10-week-old Shetland sheepdog puppy. Rickets subsequently developed, possibly from low phosphorous intake and an increased calcium to phosphorus ratio. Decreased dietary calcium in addition to decreased phosphorus may have played a role in decreasing bone mineral density. Lethargy, decreased long bone growth, angular limb deformity, and osteopenia occurred, but these signs resolved within 3 months with nutritional management.
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PMID:Dietary-related skeletal changes in a Shetland sheepdog puppy. 1639 96


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