Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical, pathomorphological and serological features of acute canine leptospirosis are evaluated and the IgM- and IgG-specific ELISA for leptospirosis serology in dogs is assessed. The clinical syndrome of acute canine leptospirosis was characterized by depression, anorexia, vomiting and often haemorrhagic diarrhoea. In addition, jaundice, uraemia, elevated creatinine and alkaline phosphatase were observed in the majority of the dogs. In pups invagination of the intestines was a noteworthy finding. The clinical signs and the post-mortem findings were rather non-specific so that the clinical and post-mortem diagnosis had to be confirmed serologically. In acute clinical cases of canine leptospirosis a high anti-leptospiral IgM titre, ranging from 160 in pups to 10240 in adults, was always present, whereas the anti-leptospiral IgG titre and the agglutination titre usually were negative or low. Dogs died from leptospirosis in spite of a high anti-leptospiral IgM titre. Only two dogs having, at the first examination, a high IgM titre in conjunction with a high IgG titre survived an acute infection. The possible role of IgM and IgG in the pathogenesis of an acute leptospiral infection is discussed. Different serological patterns in reference dogs, which were not suffering from acute leptospirosis, are presented.
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PMID:Clinical, pathological and serological features of spontaneous canine leptospirosis. An evaluation of the IgM- and IgG-specific ELISA. 379 34

Six small to medium-sized, middle-aged, female dogs with histories of acute pancreatitis developed clinical signs of extrahepatic biliary obstruction. Clinical findings were similar in the 6 dogs and included icterus. Serum biochemical analyses indicated high concentrations of total bilirubin and cholesterol and high alkaline phosphatase and alanine transaminase activities. Exploratory abdominal surgery was performed in each dog. Each dog had a firm mass involving the body of the pancreas, with obstruction of the distal portion of the common bile duct, marked peripancreatic inflammation, and omental adhesions. Cholecystoduodenostomy, using an open mucosal appositional technique for biliary redirection, was performed in each dog. Clinically, results of surgery were good to excellent (ie, lack of postoperative icterus, anorexia, lethargy, or weight loss and absence or infrequency of vomiting). The mean postoperative evaluation period for the 6 dogs was 35 months (range, 20 to 48 months); 5 dogs were alive and healthy at the end of the study. Histologic examination of tissue specimens of the pancreatic mass indicated chronic active fibrosing pancreatitis in the 6 dogs.
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PMID:Common bile duct obstruction secondary to chronic fibrosing pancreatitis: treatment by use of cholecystoduodenostomy in the dog. 380 35

The acute intravenous, intragastric, subcutaneous, intraperitoneal and intratracheal toxicity of T2 toxin has been studied in rats, mice, guinea-pigs, and pigeons. The acute LD50 values obtained varied between 1.0 and 14 mg X kg-1, there being little difference between the various routes in any given species. T2 caused vomiting in pigeons at doses of one fifth or less the LD50. In rats doses of 3.0 and 5.0 mg X kg-1 T2 produced lymphopenia, reticulocytosis, and in the highest dose groups normoblastaemia. Additionally, changes in plasma alkaline phosphatase and aspartate aminotransferase activities were seen. Histological changes were observed in lymphoid organs and were most severe in the thymus, lymph nodes, and Peyer's patches. The spleen was less severely affected. Gastrointestinal changes consisting of dead and dying lymphoid cells throughout the lamina propria were seen together with, in some cases, mucosal ulceration. The time course of the development and of the reversal of the changes was followed.
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PMID:Acute toxicity of T2 toxin in rats, mice, guinea pigs, and pigeons. 381 Jun 51

In the intestinal epithelium the rapidly proliferating crypt cells, the precursors of the mature enterocytes are extremely sensitive to the effects of cytostatic agents. The symptoms of intestinal impairment: nausea, vomiting, diarrhea, ulceration, are well known both in clinical practice and in experimental chemotherapy. To obtain information about the biochemical nature of these side effects, a study was performed by investigating the influence of clinically used alkylating hexitol derivatives, dianhydrogalactitol and diacetyl-dianhydrogalactitol, on rat intestinal mucosa cells. The biochemical parameters were investigated in isolated intestinal mucosa cells. Cell proliferation was characterized by measuring the activity of thymidine kinase, while digestion was evaluated by assaying the alkaline phosphatase, sucrase and maltase activities localized in the brush border membrane of the villus cells. The dose response studies of the different enzyme activities indicated that inhibition in all cases was dose dependent. The nadir of the intestinal damage and the time of regeneration were influenced both by the dose and the dosage schedule of the drugs.
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PMID:Biochemical changes of intestinal epithelial cells induced by cytostatic agents in rats. 386 86

The subacute toxic effects of cyclopiazonic acid (CPA; given orally) were characterized in the dog (CPA was purified from cultures of Aspergillus flavus). Four groups of dogs were given CPA in gelatin capsules for 90 days at the following dosage levels: 0.05, 0.25, 0.5, and 1.0 mg/kg of body weight; a 5th group was used as controls. All dogs administered the 0.5 and 1.0 mg of CPA/kg dosages and 1 dog given the 0.25 mg of CPA/kg dosage died or were humanely killed before the scheduled termination of the study. Clinical signs of intoxication appeared 2 to 44 days after dosing was started and consisted of anorexia and, in 1 to 2 days, vomiting, diarrhea, pyrexia, dehydration, weight loss, and CNS depression. Grossly, the entire alimentary tract had diffuse hyperemia with focal areas of hemorrhage and ulceration. Other lesions were renal infarcts, necrotizing epididymitis, and ulcerative dermatitis. Microscopic lesions included ulceration, necrosis, vasculitis, lymphoid necrosis, karyomegaly in several organs, and decreased mitotic activity in intestinal crypt epithelium. Ulcerative and necrotic lesions were usually associated with vascular lesions. Clinical pathologic changes were leukocytosis, neutrophilia, lymphopenia, monocytosis, and increased serum alkaline phosphatase activity.
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PMID:Cyclopiazonic acid mycotoxicosis in the dog. 392 55

A case report of cholestatic jaundice in a 25 year old woman, who had had jaundice at age 4 years, and had taken Stediril (a combined oral contraceptive) for 1 month, implicates either the pill or a possibly hereditary hyperlipidemia. The jaundice developed in 2 weeks with vomiting, epigastric pain, anorexia, then discolored urine and feces, and intense pruritus. On hospitalization the patient had moderate bilirubinemia (56 mg/1), low alkaline phosphatase (13 U.K.) and slightly high serum glutamate pyruvate transaminase (270 U.W.). There were elevated serum cholesterol (3 gm/1), triglycerides (2.05 gm/1), total lipids (10.6 gm/1), and a definitely increased pre-beta lipoprotein, suggesting hyperlipidemia type IV (Frederickson classification). Liver biopsy showed fibrosis of the portal spaces lymphocytic infiltration, canalicular and intrahepatocytic thrombi. On laparoscopy the liver had a regular lower border, normal volume color and surface. Albumin, prothrombin and flocculation tests were normal. The patient's jaundice lasted about 1 month, then liver function slowly improved, although pruritus remained intense. Probably this jaundice was due to oral contraceptives, in a patient predisposed either by jaundice in childhood or endogenous hyperlipidemia.
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PMID:[Cholestatic icterus due to oral contraceptives]. 426 76

An intramuscular dose schedule of 15(S)-15-methyl-prostaglandin E2-methyl ester (15-(S)-ME PGE2) was evaluated for its application as a midtrimester abortifacient route. 20 healthy gravidas aged 18-42 years and 8-22 menstrual weeks of gestation were aborted in the Clinical Research Unit of the University of North Carolina Memorial Hospital. The subjects were given 5 mcg of the PGE2 methyl ester every 4 hours. 85% (17/20) aborted within 48 hours, 65% (13/20) of these within 24 hours. Mean induction-abortion interval was 21 hours. Trials were defined as complete in 55%, incomplete in 30%, and failure in 15%. Shivering, fever, pain, vomiting, and diarrhea were the most common side effects. The transient shivering occurred in 13 (65%) of the subjects within 20 minutes of the first dose. Fever usually started after shivering, and both resolved spontaneously. 2 patients had estimated blood loss exceeding 500 ml, but they were not given transfusions. No clinically significant changes occurred in mean hemotocrit, platelet count, serum creatinine, bilirubin, alkaline phosphatase, electrolytes, serum glutamic oxalacetic transaminase, and serum glutamic pyruvic transaminase. Mean blood cell and neutrophil counts increased, but neither increase was statistically significant.
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PMID:Intramuscular administration of 15(S)-15-methylprostaglandin E2-methyl ester for induction of abortion. 442 93

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

In a model developed to study acute pancreatitis in the dog, the disease process was comparable with the spontaneously occurring disease. Infusion of oleic acid into the accessory pancreatic duct induced, grossly and microscopically, acute hemorrhagic pancreatitis with pancreatic atrophy, fibrosis, fat necrosis, and edema. Clinical changes included persistent fever and tachycardia in all dogs and abdominal pain, vomiting, and diarrhea in most. Serum amylase and lipase activities increased markedly as did activities of alkaline phosphatase, aspartate aminotransferase, and alanine aminotransferase. Hematologic alterations included hemoconcentration (despite intensive fluid therapy) and leukocytosis due primarily to neutrophilia and monocytosis. Neither corticosteroid nor anticholinergic therapy begun 24 to 32 hours after oleic acid infusion altered the course of the disease. Dogs survived 8 days and appeared clinically normal when the study was terminated.
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PMID:Effects of an anticholinergic and a corticosteroid on acute pancreatitis in experimental dogs. 617 2

Ketoconazole has only recently been recognized as a cause of hepatic injury, with most reports coming from outside the United States. In order to characterize more fully the U.S. experience, we undertook an analysis of 54 reports of alleged ketoconazole-induced liver injury submitted to the Food and Drug Administration from the time of initial marketing in 1980. Thirty-three reports were considered likely instances of ketoconazole-induced hepatitis. The majority of these cases occurred in women more than 40 yr of age. Jaundice was recorded in 27 individuals after therapy of 11-168 days with an average daily dose of 200 mg. Anorexia, malaise, nausea, and vomiting accompanied liver injury in one-third of cases. No instances of rash or eosinophilia were recorded. Serum transaminase and alkaline phosphatase values were consistent with acute hepatocellular injury in 18 patients, with primarily cholestatic injury in 5 patients, and with a mixed pattern in 9 individuals. Only one death seemed attributable to ketoconazole. In that patient, the drug was continued after the appearance of clinical and biochemical evidence of hepatic injury and massive hepatocellular necrosis was present at autopsy. The incidence of symptomatic, potentially serious hepatic injury appears to be very low, perhaps 1 in 15,000 exposed individuals. The presumed mechanism of injury is metabolic idiosyncrasy, although hypersensitivity has not been completely dismissed in some cases reported in the literature. The incidence of mild, asymptomatic, reversible elevations in serum transaminases occurring in ketoconazole recipients has been estimated to be 5%-10%. Periodic biochemical testing and monitoring for symptoms of hepatitis during ketoconazole therapy is recommended to help prevent the development of serious or fatal hepatic injury.
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PMID:Hepatic injury associated with ketoconazole therapy. Analysis of 33 cases. 631 20


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