Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17174 (aspartate aminotransferase)
 14,872 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

24 patients with advanced, histologically proven cancer were treated with difluoromethylornithine 2.25 g/m2 orally every 6 h for the first 7 days of each 4-week treatment cycle. These patients also received daily i.m. doses of recombinant human alpha 2a-interferon (IFN) on Days 3 through 7 of each cycle. IFN doses of 3, 6, 12, 24, 36, and 48 X 10(6) units/m2 have been studied utilizing three patients at each daily dose level. Three additional patients have been observed at each of the two highest doses for better toxicity definition. This combination produced slight transient declines in leukocyte and platelet counts and transient rises in serum aspartate aminotransferase; however, these changes were no more pronounced at the higher IFN doses than at daily doses of 6 X 10(6) units/m2. Mild nausea and vomiting occurred in most patients and mild diarrhea also was common at all IFN dose levels. Chills, fever, myalgia, lethargy and fatigue, and anorexia were also observed at all IFN doses; however, lethargy and fatigue (lassitude) seemed to be the major factor which limited patient tolerance of IFN to 48 X 10(6) units/m2 daily. No ototoxicity was identified clinically or audiometrically and no life-threatening toxicity has occurred. Initial Phase II studies in melanoma are currently in progress.
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PMID:Phase I study of difluoromethylornithine in combination with recombinant alpha 2a-interferon. 314 Oct 46

The medical records of 14 hyperthyroid cats with thyroid carcinoma were analyzed retrospectively regarding historical, physical, laboratory, and thyroid scintiscan findings, treatment, and treatment outcome. Breed predilection was not detected, and older castrated male cats were most commonly affected. The most common clinical signs detected by owners were weight loss, polydipsia, polyuria, polyphagia, hyperactivity, and anorexia. Physical examination findings included tachycardia, palpable cervical mass, hyperactivity, cardiac murmur, and abnormal coat. Common abnormal laboratory findings were high serum thyroxine and triiodo-thyronine concentrations and high serum alanine transaminase, alkaline phosphatase, and aspartate transaminase activities. Azotemia, hyperphosphatemia, and hyperglycemia were noticed less frequently. The most common thyroid scintiscan findings were multiple nodular areas of high radionuclide uptake in the cervical region, thoracic inlet, and cranial mediastinum. The most common morphologic diagnosis was mixed compact and follicular carcinoma, with follicular and papillary carcinomas being less common. Most cats responded well to treatment of the thyroid tumor, with rapid resolution of the historical and physical examination findings. The most common necropsy findings were local tumor invasion, regional lymph node metastases, cardiomyopathy, and interstitial nephritis.
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PMID:Thyroid carcinoma causing hyperthyroidism in cats: 14 cases (1981-1986). 318 90

Chronic hepatic disease was diagnosed in 6 horses with history of anorexia and weight loss. These horses consistently had abnormally high serum gamma-glutamyltransferase activities, total and direct bilirubin and blood ammonia values, and sulfobromophthalein clearance times, whereas serum iditol dehydrogenase, aspartate transaminase, and alkaline phosphatase activities were variable. In the 6 horses, histologic examination of the liver revealed lesions of chronic hepatitis with varying degrees of fibrosis. All 6 horses had ingested kleingrass (Panicum coloratum) for variable periods. Three healthy horses fed kleingrass hay for 90 days developed hepatic lesions and increases in serum gamma-glutamyltransferase activities similar to those in the 6 horses with chronic hepatitis. Characteristic hepatic lesions in both groups of horses included bridging hepatic fibrosis, cholangitis, and hepatocellular regeneration.
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PMID:Kleingrass-associated hepatotoxicosis in horses. 319 74

Oral administration of lantana leaves (6 g/kg body weight) and isolated toxins (125 mg/kg body weight) to rabbits caused ictericity, anorexia and decrease in fecal output. There was increased size of the kidneys, and the livers were ochre-colored and fragile but there was no hepatomegaly. Histopathologically, lantana-intoxicated rabbits had swellings of hepatic cells, portal fibrosis, dilatation of bile canaliculi and biliary hyperplasia. Kidneys had proliferation of mesenchymal cells in glomerular tufts, degeneration of tubules, swelling of tubular epithelial cells and pyknosis of nuclei. The intoxicated animals had elevated levels of conjugated and unconjugated bilirubin in plasma, the major increase being in the conjugated form (suggestive of obstructive jaundice). There were marginal changes in the activities of acid phosphatase and glutamate oxaloacetate transaminase in the plasma.
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PMID:Toxicity of lantana (Lantana camera L) leaves and isolated toxins to rabbits. 338 48

As the results of treatment in Wilson's disease are so dependent on the stage at which penicillamine therapy is started, the antecedent history in 34 patients with Wilson's disease was analysed with particular respect to the earliest manifestations of the disease. Lethargy and anorexia (70%) jaundice (56%) and abdominal pain (48%) were the commonest symptoms and less common were intellectual deterioration (22%) and recurrent epistaxes (22%). The duration of symptoms before diagnosis ranged from five days to three years (mean 10.5 months) and in only five of the patients was the diagnosis established before referral. Analysis of the physical signs at presentation showed hepatomegaly (81%) and splenomegaly (70%) to be common and the only signs which were significantly more common in the 13 fatal cases were jaundice and ascites. In three of these and in one other patient who survived the clinical course was exceptionally severe and was indistinguishable from fulminant hepatic failure. Based on the severity of abnormality of serum aspartate aminotransferase, bilirubin, and prothrombin time on admission a prognostic index was derived which enabled complete separation of fatal and nonfatal cases and when subsequently used in a further nine index cases correctly predicted the outcome. Two further cases found to have indices in the fatal category did well after liver transplantation, which needs to be considered as soon as the diagnosis is established in cases with such severe liver damage.
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PMID:Wilson's disease: clinical presentation and use of prognostic index. 379 21

A 4-year-old cat was examined because of anorexia and lethargy. The cat became icteric within 3 days of admission. Values for aspartate transaminase, alanine transaminase, total bilirubin, alkaline phosphatase, and cholesterol were higher than normal. Radiography revealed hepatomegaly, with loss of detail in the cranioventral portion of the abdomen. Further diagnostic procedures were not permitted, and the cat was euthanatized. At necropsy, cholecystitis, cholangitis, and numerous choleliths were found. Cholelithiasis is a rare cause of obstructive jaundice in the cat.
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PMID:Cholelithiasis in a cat. 397 77

Analysis of 56 patients with obstructive jaundice due to carcinoma of the pancreas or extrahepatic biliary tree showed that unexpected features were present in 25%. Presentation with painless jaundice was uncommon, and the symptoms were more often non-specific, with malaise, anorexia, and vomiting. Abdominal pain was frequent, and the condition was found in young patients. One-fifth presented with serum alkaline phosphatase levels of less than 30 K.A. units. Some had high serum aspartate aminotransferase levels, more characteristic of hepatocellular jaundice. A mathematical model may be helpful in correctly weighting these various criteria.
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PMID:Pitfalls in the diagnosis of jaundice due to carcinoma of the pancreas or biliary tree. 451 75

The clinical and clinicopathologic effects of excess oral pyridoxine hydrochloride (150 mg/kg body weight/day) and clioquinol (200 mg/kg body weight/day) alone and in combination were evaluated in adult Beagle dogs over an experimental period of approximately 100 days. Anorexia and loss of body weight occurred in the first weeks of the trial period in each treatment group, but was most severe in dogs given both compounds. Dogs in each treatment group (10 of 10 pyridoxine-treated dogs, 6 of 13 clioquinol-treated dogs and 12 of 13 pyridoxine plus clioquinol-treated dogs) developed neurologic disease, manifested principally by ataxia. Pyridoxine-treated dogs had proprioceptive loss involving both fore- and hindquarters, characterized by stiff, spastic, dysmetric leg movements. In clioquinol-treated dogs, dysmetric leg movements were accompanied by failure to support body weight in the hindquarters, but similar forelimb involvement occurred in severely affected dogs. The neurologic disease in dogs given both compounds varied; signs in some dogs resembled those of affected dogs of the pyridoxine-treated group, and in others, those in clioquinol-treated group. Erythrocyte counts, hemoglobin concentrations and packed cell volumes were reduced in dogs in each treatment group and were lowest in dogs given both compounds. Plasma protein was mildly reduced in dogs given pyridoxine or pyridoxine plus clioquinol. Few or no differences were present in the leukocyte counts, blood urea nitrogen concentrations, in activities of serum alanine aminotransferase and aspartate aminotransferase, and in concentrations of sodium, chloride or potassium in treated dogs as compared to control dogs.
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PMID:The subacute neurotoxicity of excess pyridoxine HCl and clioquinol (5-chloro-7-iodo-8-hydroxyquinoline) in beagle dogs. I. Clinical disease. 645 37

Naturally occurring cases of poisoning of cattle by Cestrum parqui were characterised by ataxia, depression, recumbency, convulsions and death. Three cattle were dosed experimentally by intrarumenal administration of fresh plant material. One calf died 48 h after receiving 30 g (wet weight) of plant/kg bodyweight. Doses of 11 and 17 g/kg caused only mild intoxication, with dullness and anorexia lasting 2 days. In natural and experimental cases the main lesion was hepatic periacinar necrosis. Elevated levels of plasma aspartate transaminase and prolonged prothrombin times were demonstrated in experimental cases. Haemorrhage beneath the serosa and into the intestinal lumen occurred in field cases, but not in the experimental. It is concluded that C. parqui poisoning in cattle is a primary hepatotoxicity.
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PMID:Cestrum parqui (green cestrum) poisoning in cattle. 651 79

Eleven adult Basenji dogs with immunoproliferative small intestinal disease (IPSID) were studied. Two items of history related to the digestive tract were characteristic: (i) chronic intractable diarrhea in most dogs, and (ii) progressive emaciation. Anorexia was intermittent in only a few dogs. In addition, skin lesions of various degrees of severity were observed, including alopecia of pinnae and ventrum, hyperpigmentation and hyperkeratosis of pinnae, and necrosis and ulcerations of margins of pinnae. The cause of the skin lesions was not determined; however, hypothyroidism did not appear to contribute to the skin changes. Standard hematologic and serum chemical values were not consistently abnormal. However, a poorly regenerative anemia, mild neutrophilia, and increased aspartate aminotransferase and alanine aminotransferase activities were generally observed in severely affected dogs. The Pelger-Huet anomaly was identified in dog 3. Maldigestion and malabsorption as determined by the N-benzoyl-L-tyrosyl-p-aminobenzoic acid and d-xylose test was documented to varying degrees in dogs with IPSID. Maldigestion was correlated with functional pancreatic exocrine insufficiency. Severe malabsorption was documented in only 3 dogs. Serum gastrin values were evaluated in these dogs because of a prior observation of parietal cell hyperplasia and gastric ulceration. Hypergastrinemia was documented in 3 dogs. Additional studies will be necessary to determine whether an acid hypersecretory state contributes to the pathogenesis of IPSID in Basenjis.
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PMID:Clinical and laboratory characterization of Basenjis with immunoproliferative small intestinal disease. 660 87


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