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)

A 23 year old male developed abdominal pain, diarrhoea, and vomiting several hours after poisoning with acute triphenyltin intoxication in a suicide attempt. Severe ataxia, dysmetria, nystagmus, and blurring of vision soon supervened. Disturbance of consciousness and confusion developed 12 days later and lasted for two months. A delayed sensorimotor polyneuropathy was shown by electrophysiological studies to be due to axonal degeneration and demyelination. The neuropathy rapidly recovered after consciousness was regained.
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PMID:Acute triphenyltin intoxication: a case report. 750 Jan 18

A 46-year-old healthy man suffered from sore throat, fever and right otalgia. On the next day, he developed hoarseness and difficulty in swallowing. On the 6th day, he suffered from vertigo, nausea and vomiting associated with unsteady gait. He was admitted to the otorhinolaryngology department in our hospital and pointed out to have vesicles at his right ear. On the 13th day, he was referred to our service. On admission, no vesicles were noted at the right ear or pharynx. Neurological examination revealed mild nuchal rigidity and marked hoarseness, associated with poor elevation of soft palate and loss of pharyngeal reflex on the right side. He also had horizontal-clockwise rotatory nystagmus in primary gaze and ataxic gait. There was no hearing loss nor facial palsy. No other abnormal neurological findings were noted. The cerebrospinal fluid showed pleocytosis associated with increased protein. The viral antibody titre for herpes zoster was significantly elevated on 18th day in serum as well as in cerebrospinal fluid. Vertigo, nausea, vomiting, ataxia and difficulty in swallowing were all disappeared by the 25th day, whereas hoarseness was improved but still noted 6 months later. Among cranial nerves, trigeminal and facial nerves are the most commonly affected in patients with herpes zoster, but there have been a few reported cases of the 9th and 10th cranial nerve involvement in the literature. In these previously reported cases, all were written before the era of serological diagnosis, and herpes zoster was diagnosed by the vesicles at the ear or pharynx.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of unilateral VIIIth, IXth and Xth cranial nerve involvement with herpes zoster]. 216 88

Poisonings resulting from DEET are rarely encountered in companion animals. In human patients, DEET toxicosis has been associated with the development of a toxic encephalopathy characterized by tremors, seizures, behavioral changes, and abnormal movements. Generally, DEET toxicosis in companion animals is of short duration and is characterized by vomiting, tremors, ataxia, and excitation. Treatment for DEET toxicosis includes symptomatic therapy and decontamination.
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PMID:Diethyltoluamide (DEET) insect repellent toxicosis. 218 Jan 85

Review of all reports involving anthelmintics in dogs and cats to the IAPIC between January 1, 1986 and August 10, 1988, revealed that ivermectin (extra-label use) and piperazine accounted for over 50% of the calls assessed as toxicoses and suspected toxicoses. Both ivermectin and piperazine are gamma-aminobutyric acid (GABA) agonists and their major effects appear to be on the central nervous system. Ivermectin toxicoses at estimated doses of greater than or equal to 100-less than 500 micrograms/kg were reported more than once only in the collies (n = 25) and Australian shepherds (n = 10); these two breeds accounted for 46% (69 of 150) of the toxicoses and suspected toxicoses calls in dogs. Ataxia, behavioral disturbances, tremors, mydriasis, weakness/recumbency, apparent blindness, hypersalivation/drooling (dogs only), and coma were the most commonly reported clinical signs in dogs and cats with suspected ivermectin toxicoses. Shock, dyspnea, vomiting, and ataxia were the most common clinical signs attributed to the microfilaricidal activity of ivermectin. Piperazine was the anthelmintic with the greatest number of reports of toxicoses and suspected toxicoses in cats. Piperazine neurotoxicity in cats and dogs usually was manifested by muscle tremors, ataxia, and/or behavioral disturbances within 24 hours after estimated daily dose(s) between 20 and 110 mg/kg.
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PMID:Ivermectin and piperazine toxicoses in dogs and cats. 218 Jan 89

Twenty-six cases of accidental 5-fluorouracil (5-FU) ingestions by dogs were reviewed from phone calls to the Illinois Animal Poison Information Center. Cases were collected from January 1, 1987 to December 31, 1988. Of the 26 calls involving 5-FU exposures, 12 were classified as "toxicosis," 13 as "suspected toxicosis," and one as "exposure." Dogs were the only species involved in 5-FU cases received during this time. Accurate estimates of the amount of 5-FU ingested by dogs could be made in 17 cases. Ingestion of more than 20 mg/kg of 5-FU was associated with the development of toxicosis. None of the 12 dogs that ingested oral doses in excess of 43 mg/kg (estimated) survived. Clinical signs associated with 5-FU poisoning in the dog were death, seizures, vomiting (with and without blood), tremors, diarrhea (with and without blood), ataxia, and depression. Clinical signs generally developed within 45 to 60 minutes after exposure, and deaths occurred 6 to 16 hours after ingestion.
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PMID:5-Fluorouracil toxicosis in the dog. 226 27

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

Dilantin toxicity has been well described and has generally been noted to include signs and symptoms of nystagmus, ataxia, nausea, and vomiting. Dilantin's depressive effects are seldom mentioned. Two patients are presented who, although stable while on the rehabilitation unit, developed vegetative signs of depression soon after discharge. Both were found to have toxic levels of Dilantin. Neither revealed the classic neurologic or gastrointestinal complaints. Although one patient had documented family and social stressors, the other had a stable home life. Both patients recovered remarkably once their Dilantin dosages were adjusted. In such patients who present with change in mood, sleeping, and eating patterns, Dilantin toxicity should be suspected. Serum blood levels should be checked, and dosage adjusted before the addition of antidepressant medication. Possible causes for Dilantin-associated depression are discussed in detail.
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PMID:Dilantin toxicity and vegetative depression: a report of two cases. 224 39

Seventeen adults with cerebellar stroke confirmed by computerized tomography were reviewed, and divided into two groups: the first group consisted of 10 patients with cerebellar softening, and the second one included 7 cases with cerebellar hemorrhage. The diagnostic rests primarily upon the symptoms and clinical signs. They consist of acute onset of vertigo, headache, nausea or vomiting, ataxia-disequilibrium, then progressing signs of brain stem compression with gaze palsy, cranial nerve palsies and a decreasing level of consciousness. The computerized tomography is the diagnostic test of choice. The interpretation of the scan and of the brain stem and its surrounding cisterns gives decisive help in accessing the indications for surgical treatment.
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PMID:[Cerebellar infarcts and hemorrhages: differential diagnosis]. 242 23

Brain stem glioma is the third most common childhood brain tumor, comprising 10-15% of this group of neoplasms. Typical presenting symptoms include ataxia, diplopia and headache, while signs of increased intracranial pressure occur later in the clinical course. Although prolonged failure to thrive, characterized by cachexia and vomiting are rare manifestations of brain stem lesions, in this study we report a 9.5-year-old boy with failure to thrive since infancy which remitted after excision of a brain stem astrocytoma.
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PMID:Chronic dysphagia, vomiting and gastroesophageal reflux as manifestations of a brain stem glioma: a case report. 248 55

Vomiting was suppressed in cats pretreated with 8-OH-DPAT and then challenged with an emetic stimulus; motion, xylazine or cisplatin. The antiemetic effect is likely due to stimulation of postsynaptic serotonin-1A receptors. The most parsimonious explanation is that it acts at a convergent structure, presumably at or near the vomiting center. If so, 8-OH-DPAT may block emesis elicited by virtually any other stimulus. A supplementary experiment revealed that lorazepam suppressed motion sickness at a dose that produced ataxia, but did not suppress xylazine-induced emesis. These results do not support the possibility that the antiemetic effects of 8-OH-DPAT were the result of anxiolytic activity.
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PMID:8-OH-DPAT suppresses vomiting in the cat elicited by motion, cisplatin or xylazine. 253 22


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