Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten of 100 mature ewes were afflicted with acute oxalate toxicosis within 40 hours after being temporarily penned in a lot that contained considerable growing Rumex crispus (curly dock). Clinical signs of toxicosis included excess salivation, tremors, ataxia, and recumbency. Affected ewes were markedly hypocalcemic and azotemic. Oxalate crystals were not observed in urine. Gross postmortem lesions were minimal and nondiagnostic in 2 ewes that died peracutely, but perirenal edema and renal tubular degeneration were clearly observable in ewes euthanatized on the third day of toxicosis. Diagnosis of oxalate toxicosis was confirmed by histopathologic findings. Samples of Rumex spp contained 6.6 to 11.1% oxalic acid on a dry-weight basis, a concentration comparable with that in other oxalate-containing plants that have caused acute oxalate toxicosis.
 ...
PMID:Acute oxalate poisoning attributable to ingestion of curly dock (Rumex crispus) in sheep. 236 22

Eight dogs with ethylene glycol intoxication were treated with 4-methylpyrazole, an alcohol dehydrogenase inhibitor. Dogs had clinical signs referable to ethylene glycol ingestion including ataxia, depression, vomiting, polyuria, and dehydration. Metabolic abnormalities included high anion gap metabolic acidosis, serum hyperosmolality, isosthenuria, and monohydrate and dihydrate calcium oxalate crystalluria. Serum and urine ethylene glycol concentrations were determined to confirm ingestion of ethylene glycol. A 50-mg/ml solution of 4-methylpyrazole in propylene glycol was administered iv as follows: initial treatment, 20 mg/kg of body weight; at 17 hours after admission, 15 mg/kg; at 25 hours after admission, 5 mg/kg. By 24 hours after admission, all dogs had clinical and metabolic improvement. Of the 8 dogs, 7 were released within 3 days of admission. Four of the 8 dogs returned for follow-up evaluation, at which time biochemical or hematologic abnormalities were not observed.
 ...
PMID:4-Methylpyrazole as treatment for naturally acquired ethylene glycol intoxication in dogs. 258 8

Ingestion of ethylene glycol was responsible for severe azotemia, acidosis, and abnormal anionic gap value in a pygmy goat. Clinical signs consisted of ataxia, polydipsia, decreased rumen motility, and constipation. Nervous signs included depression, absence of menace response, vertical nystagmus, and terminal convulsions. Four days after onset of clinical signs, antidotal treatment was ineffective. Lesions and oxalate crystals in the kidney were typical of ethylene glycol or plant oxalate toxicosis in other species. Toxicologic analysis revealed ethylene glycol in the rumen content and glycolic acid in urine and ocular fluid.
 ...
PMID:Ethylene glycol toxicosis in a pygmy goat. 319 47

Fifteen dogs were given 9.5 ml of ethylene glycol/kg of body weight, orally. Physical examination and clinical laboratory findings were evaluated at 1 and 3 hours after ingestion. Three of these dogs were also evaluated at 6, 9, 12, 24, 48, and 72 hours after ingestion. At 1 and 3 hours, the dogs were depressed, ataxic, and polydipsic with increased urine output and serum osmolality. Plasma bicarbonate and urine osmolality were decreased. The osmolal and anion gaps were increased at 1 and 3 hours, respectively. Calcium oxalate crystalluria was first observed at 6 hours. Diminished renal excretory function was not evident until 48 hours. Depression, ataxia, metabolic acidosis, polydipsia, and polyuria in the presence of serum hyperosmolality were early (1 and 3 hour) findings that indicated ethylene glycol intoxication in dogs.
 ...
PMID:Early clinicopathologic findings in dogs ingesting ethylene glycol. 652 24

Clinicopathologic findings were retrospectively evaluated in 26 cats and 24 dogs with ethylene glycol intoxication. Common clinical signs were ataxia, depression, vomiting, and hypothermia. Characteristic alterations in the hemogram and serum chemical profile included neutrophilia, lymphopenia, azotemia, hyperphosphatemia, hypocalcemia, hyperglycemia, and decreased whole blood bicarbonate. Common urinalysis findings included isosthenuria, proteinuria, glucosuria, hematuria, calcium oxalate and hippurate crystalluria, and the presence of renal epithelial cells, white blood cells, and granular and cellular casts in the urine sediment. The high death rate (78%) was attributed to delays in presentation, diagnosis, and therapy.
 ...
PMID:Clinicopathologic findings in dogs and cats with ethylene glycol intoxication. 669 34

Ducks maintained over winter in an area used for automobile storage and repair were poisoned by anti-freeze. Signs were weakness, depression, ataxia, and death. Post-mortem lesions consisted of marked nephrosis; numerous oxalate crystals occluded the renal tubules. Levels of ethylene glycol were markedly elevated compared with levels in normal tissues. To further characterize the disease, six healthy ducks were given ethylene glycol in oral doses ranging from 1.1 to 17.8 ml/kg. As the dosage was increased, blood and tissue concentrations of ethylene glycol increased and time to death decreased. Histologic lesions were similar to those seen in the accidentally poisoned ducks.
 ...
PMID:Ethylene glycol intoxication in ducks. 702 Jun 83

Acute Halogeton glomeratus poisoning occurred in 16 of 680 range cattle during and following a trail drive. Signs of toxicosis included posterior ataxia, recumbency, coma, and death. Histopathologically, abundant, refractile calcium oxalate crystals were seen in renal tubules. Inasmuch as the plant is generally unpalatable for cattle, poisoning in this case was enhanced by a preceding period of food deprivation.
 ...
PMID:Halogeton poisoning in range cattle. 741 Jan 53

A four-year-old wire-haired dachshund developed progressive neurological signs of ataxia, intention tremor and finally dysuria. Two years later, histopathology showed that neurons throughout the brain and spinal cord were distended with lipopigment which was also present in macrophages. Ultrastructurally, the pigment in the neurons occurred predominantly as electron-dense membranous whorls and stacks. There were a few vacuolated macrophages in the meninges. Hepatocytes were highly vacuolated and electron microscopy suggested that they were empty membrane-bound vesicles. The disease was diagnosed as mucopolysaccharidosis IIIA because of its similarity to other biochemically confirmed cases in the same breed and in a New Zealand huntaway dog. Additional lesions included calcium oxalate uroliths, severe secondary calcification of tissues including the brain and storage deposits in some neurons, and lesions which may have been associated with high levels of the substrate, heparan sulphate.
 ...
PMID:Histological diagnosis of mucopolysaccharidosis IIIA in a wire-haired dachshund. 1137 Aug 81

Oxaliplatin is a reference drug in the treatment of digestive-tract tumors, especially colorectal cancer. Its toxicity profile is dominated by a peripheral sensitive neuropathy, with neuromuscular manifestations. This neurotoxicity has 2 components: an acute toxicity characterized by a rapid onset of cold-induced distal dysesthesia and/or paresthesia, muscular contractions, numbness, stiffness, usually transient but able to evolve into a chronic, persistent sensory peripheral neuropathy that eventually causes functional impairment. A persistent sensory peripheral neuropathy may develop with prolonged treatment, eventually causing superficial and deep sensory loss, sensory ataxia and functional impairment. This neurotoxicity is frequent, 80%of the patients and becomes chronic in 15 to 20%of the patients, sometimes irreversible. The mechanism of this neurotoxicity has been elucidated: an increased neuronal excitability is due to the action of oxaliplatin on voltage-gated sodium channels through chelation of calcium by the oxaliplatin metabolite. The prevention of this neurotoxicity is a major goal, taking in account the wide indications of this drug. Different approaches have been or are evaluated, based on pathogenic or practical concepts: 1) modifications of the administration schedule; 2) substances acting upon sodium channels : calcium-magnesium, carbamazepine, gabapentine, venlafaxin; 3) detoxifying agents and antioxydants: glutathion, amifostine, alphalipoic acid, tocopherol ; 4) substances used in other kinds of neuropathy: glutamine, alphalipoic acid; 5) neurotrophic factors: NGF, LIF; 6) oxaliplatin analogs, with a DACH platin, without oxalate. Calcium-magnesium infusion seem to be an efficient and safe approach. Further studies are necessary for a better understanding and prevention of this neurotoxicity, potentially severe.
 ...
PMID:[Oxaliplatin neurotoxicity]. 1649 18

Forty seven of 150, 15-month-old long weaners died of an acute renal disease syndrome following introduction into an old maize field with a heavy stand of Amaranthus spp. The clinical syndrome was characterised by sudden onset neurological disease with ataxia and recumbency. Subcutaneous oedema, ascites and perirenal oedema with urine odour were the major gross necropsy findings. Renal histopathology revealed marked coagulative renal tubular necrosis of the proximal and distal straight tubules with intertubular haemorrhage. Acute renal failure and perirenal oedema has been described in cattle, pigs, horses and sheep associated with the ingestion of A. hybridus L. and A. retroflexus L. This perirenal oedema syndrome has been widely reported in the Americas, while in South Africa intoxication with the amaranths has only previously been associated with nitrate and possibly oxalate poisoning in cattle.
 ...
PMID:An outbreak of perirenal oedema syndrome in cattle associated with ingestion of pigweed (Amaranthus hybridus L.). 1823 43


1 2 Next >>