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)

Nine dogs with intermediate- or high-grade lymphoma were prospectively entered into a protocol to be given a total of 15 weekly doses of doxorubicin (10 mg/m2 of body surface, IV) in an attempt to eliminate all clinical evidence of neoplasia, with minimal risk of drug toxicity. Eight of these dogs did not complete the protocol because of progression of the disease. The median number of doses administered to dogs that developed progressive disease before the regimen was completed was 5 (range, 2 to 9). Seven dogs achieved partial (n = 5) or complete (n = 2) remission, with median duration of 14 days (range, 7 to 231 days). The dog that was given all 15 weekly treatments remained in complete remission for 231 days. Complete remission that lasted for 14 days was observed in another dog. Toxicosis developed in 3 dogs; signs of toxicosis were generally mild and included colitis (n = 1), vomiting (n = 1), neutropenia (n = 1), and lethargy (n = 1). The lowest neutrophil count (1,876 cells/microliter) was seen in one dog after 7 doses of doxorubicin were given. Doxorubicin at dosage of 10 mg/m2/wk appears to be safe, but is generally ineffective for treatment of lymphoma.
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PMID:Weekly administration of low-dose doxorubicin for treatment of malignant lymphoma in dogs. 207 76

Toxicosis attributable to fenvalerate and N,N-diethyl-m-toluamide (Deet) exposure was suspected in 2 cats. Clinical signs of toxicosis developed within 4 to 6 hours of dermal application of the pesticide. Clinical signs of toxicosis seen in both cats included hypersalivation, ataxia, and depression. In addition, seizures were seen in 1 cat. Both cats died. Analysis of skin, kidney/urine, liver, and brain tissues confirmed the presence of fenvalerate and Deet. The pyrethroid fenvalerate and the insect repellent Deet are used for the control of fleas and ticks on cats. Suspected fenvalerate/Deet toxicosis in cats is associated with tremors, hypersalivation, ataxia, vomiting, depression, and seizures.
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PMID:Fenvalerate/N,N-diethyl-m-toluamide (Deet) toxicosis in two cats. 229 39

Toxicosis caused by Anabaena spiroides was diagnosed in 7 of 26 finishing hogs in a farrow-to-finish operation in Kentucky. Several sick pigs in the herd had the following clinical signs: vomiting, dull appearance, lethargy, anorexia, muscle tremors, frothing at the mouth, coughing, sneezing, dyspnea, and bloody diarrhea. Of the 7 dead pigs, 2 were necropsied. Tissue speciments and stomach contents were obtained for microscopic, microbiologic, and toxicologic evaluations. In addition, vomitus from sick pigs and pond water samples were collected for laboratory analysis. Direct microscopic examination of pond water, vomitus, and stomach contents revealed nearly pure A spiroides, a toxic blue-green algae. The possible involvement of bacterial toxins in these pigs was not established; however, the laboratory and field data suggested that the clinical signs and death losses were attributable to the consumption of pond water mixed with the bloom of the alga, A spiroides.
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PMID:Blue-green algae (Anabaena spiroides) toxicosis in pigs. 250 12

Bromethalin is a potent neurotoxin capable of inducing fatal cerebral edema in companion animals. Bromethalin decreases adenosine triphosphate production resulting in cerebral edema. Toxicosis can be seen in cats and dogs with oral exposures as low as 0.3 and 2.5mg/kg, respectively. High doses produce severe muscle tremors, hyperthermia, seizures, and death within a couple hours postingestion. The usual presentation after moderate to low exposure develops over 12-24 hours with progressive ataxia, paresis, and hindlimb paralysis. Central nervous system depression continues to semicoma or coma. Diagnosis is based upon history of exposure, development of progressive appropriate clinical signs and chemical confirmation in tissues. Treatment relies heavily upon early emesis induction and prolonged decontamination with pulse dosing of activated charcoal. There is no specific antidote; attempts to control cerebral edema with diuretics and corticosteroids have met with limited success. Significant supportive care is usually required, often including seizure management, nutritional support, and defense against decubital ulceration. Prognosis is guarded to poor.
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PMID:Bromethalin. 2379 84

Oleander poisoning typically results in cardiac arrhythmias, hyperkalemia, and gastrointestinal irritation, and can be fatal. Oleander extracts have also been studied experimentally as hypoglycemic agents. Here, we describe a dog with confirmed oleander toxicosis presenting with classical symptoms and also hypoglycemia. After excluding other likely causes of hypoglycemia, the finding was attributed to oleander toxicosis, which has not been previously reported in dogs. A 7-year-old female spayed Maltese was presented to the emergency service after ingesting oleander leaves. Toxicosis was confirmed by measurement of digoxin using a competitive binding immunoassay, patient level 0.7 ng/mL (0.9 nmol/L) 24-h post-ingestion. Clinical symptoms included vomiting, cardiac arrhythmia, mild hyperkalemia, and hypoglycemia. Treatment was successful with aggressive supportive care, and the dog was discharged from the hospital after 48 h and made a full recovery. This case reviews the presentation and treatment of oleander toxicity but also highlights possible effects of oleander on blood sugar in dogs. Hypoglycemia in this dog, attributed to oleander poisoning, is interesting as it supports experimental research into hypoglycemic properties of oleander extracts.
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PMID:Hypoglycemia associated with oleander toxicity in a dog. 2525 2