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)

Venalot, a mixture of coumarin and troxerutin, in the proportion 1 to 6 respectively, was given orally to baboons at dosages of 0, 100, 300 and 1000 mg/kg/day for 26 weeks. Vomiting, usually within 3 h of administration and considered to be of central origin, in addition to vomiting immediately after dosing, was noted in animals receiving 1000 mg/kg/day. At this level, collapse on several occasions in two animals, one of which died, was also observed. Another animal receiving 1000 mg/kg/day was killed for humane reasons following a period of weight loss, reduced appetite and deterioration in body condition. However, no adverse effect on body weight gain, food or water consumption, ophthalmoscopic or electrocardiographic examinations were noted in any other animals during this study. Increased levels of liver function (serum leucine amino-peptidase (LAP), and serum ornithine carbamyl transferase (OCT) were noted during the dosing period, together with slightly increased liver weights terminally for animals receiving 1000 mg/kg/day; however, as no morphological or ultrastructural changes were noted, these findings were considered to be attributable to hypertrophy.
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PMID:Toxicity of venalot (a mixture of coumarin and troxerutin) in the baboon. 682 41

Reported is the case of a 23-year-old man who ingested 300 mL of Reglone. He developed vomiting five to 10 minutes after ingestion. Shortly thereafter, he developed renal and central nervous system manifestations of toxicity, followed by cardiovascular collapse and death 14 hours after admission. Autopsy findings revealed esophagitis, tracheitis, gastritis, and ileitis. Prompt, aggressive therapy that included fluid replacement and removal of the toxin was unsuccessful.
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PMID:Diquat intoxication. 685 38

1 A 21-year-old student ingested thirty ricin seeds in a suicidal attempt, some of which were masticated. Three hours later he developed severe diarrhoea with vomiting and abdominal cramps, followed by extracellular dehydration and circulatory collapse. 2 Biological changes included haemoconcentration. He recovered following symptomatic treatment by infusion of saline and glucose solutions. 3 Ricin was quantified by a radioimmunologic method using Iodine 125, and showed that only a small part of the ricin contained in the seeds was absorbed.
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PMID:Acute voluntary intoxication by ricin. 686 67

Clinical signs and lesions of levamisole toxicosis include: nausea, vomiting, increased salivation, frequent urination and defecation, colic, dizziness, headache, muscle tremors, ataxia, anxiety, hyperesthesia with irritability, clonic convulsions, depression, rapid respiration, dyspnea, prostration, collapse, hemorrhages in the subepicardium and thalamus, enteritis, hepatic degeneration and necrosis, and splenic congestion. Most of these signs and lesions are similar to those observed in nicotine poisoning. Levamisole causes vasopressor and panting effects which are blocked by ganglionic blocking agents hexamethonium and mecamylamine but are not blocked by atropine. The vasopressor effect of levamisole is blocked by alpha-adrenergic antagonists phentolamine and dibenamine; however, the respiratory effect of levamisole is not affected by these alpha-adrenergic antagonists. Repeated IV injections of levamisole cause a tachyphylactic response. With levamisole-induced tachyphylaxis, the effects of other ganglionic stimulants dimethylpiperazinium and nicotine are also abolished. Levamisole causes an electroencephalographic arousal which is antagonized by atropine sulfate and mecamylamine. There is also a structural similarity of levamisole to nicotine. These studies suggest that levamisole is a nicotine-like compound. Possible treatment of levamisole poisoning is discussed. Drug interactions of levamisole with organophosphates and anthelmintics, eg, pyrantel, methyridine, and diethylcarbamazine, are also discussed.
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PMID:Toxicity and drug interactions of levamisole. 721 95

Congenital Adrenal Hyperplasia (C.A.H.) is an autosomal recessive disorder which is often life threatening during the neonatal period prior to establishment of the diagnosis and instigation of appropriate treatment. In females the condition is usually detected at birth due to genital ambiguity. Unfortunately males or extremely virilized females often remain undetected until they suffer a potentially fatal adrenal crisis. Typically, a crisis occurs within the first couple of weeks of life and is preceded by a history of failure to thrive, lethargy and vomiting which may be misdiagnosed as resulting from pyloric stenosis. Vascular collapse and diminished consciousness ensue if adrenal insufficiency remains undetected. Initial biochemical investigation of the shocked neonate with C.A.H. reveals severe hyperkalaemia and hyponatraemia, which initially may be thought to be due to renal failure. Hypoglycaemia may also be a feature. Initial resuscitation requires intravenous saline and hydrocortisone. Once physiologically stable, oral steroids are used to replace absent glucocorticoids and mineralocorticoids. The psychosocial impact of having a critically ill baby, with a relatively uncommon genetic disorder, who requires lifelong treatment can be overwhelming for parents. There is an ongoing risk of adrenal crisis throughout the child's life during periods of physiological stress. Parents require education on the management of medication during normal childhood illnesses; the early indicators of crisis and instruction in injection technique. In addition to skilled technical nursing interventions for their baby, parents can benefit from accurate information and contact with the C.A.H. support group.
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PMID:Congenital adrenal hyperplasia: a potential diagnosis for the neonate in shock. 762 Feb 64

Tripterygium wilfordii Hook F (TWHF) is a kind of Chinese herbal medicine used for 2000 years. It was applied externally for treatment of arthritis and inflammatory tissue swelling in early years. Recently, this drug has been found to have immunosuppressive effects which could successfully induce remission of some autoimmune disorders without obvious adverse effects. Although there are side effects of gastrointestinal upset, infertility and suppression of lymphocyte proliferation, little information about lethal toxicities has been reported. A case is presented here of a previously healthy young man who developed profuse vomiting and diarrhea, leukopenia, renal failure, profound hypotension and shock after ingestion of an extract of TWHF. In addition to his hypovolemic shock, serial electrocardiograms (ECG), cardiac enzyme studies, and echocardiography also showed some evidence of coexisting cardiac damage. He died of intractable shock 3 days after the abuse of TWHF. Further studies of the pathogenesis of peripheral collapse and possible cardiac toxicity, and determination of the therapeutic range of this drug are necessary before it is used extensively.
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PMID:Hypovolemic shock and mortality after ingestion of Tripterygium wilfordii hook F.: a case report. 762 89

Factors to consider in the care of a newborn infant Family history Extremes of body temperature Poor feeding Vomiting Failure to pass urine or meconium Rapid breathing with or without cyanosis Jaundice Rashes and birthmarks 'Jitteriness' Unusual features Collapse
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PMID:Common problems of newborn infants. 769 2

KW-5092 ([1-[2-[[[5-(piperidinomethyl)-2- furanyl]methyl]amino]ethyl]-2-imidazolidinylidene) propanedinitrile fumarate) is a novel gastroprokinetic agent with acetylcholinesterase (AChE) inhibitory activity and acetylcholine (ACh) release facilitatory activity. The present study examined the effects of KW-5092 on gastrointestinal (GI) motor activity in dogs. In anesthetized dogs, KW-5092 at 0.03 to 1 mg/kg, i.v. dose-dependently enhanced the gastric antral and the colonic motor activity. Neostigmine, an AChE inhibitor, enhanced the motor activity at 0.03 and 0.1 mg/kg, i.v. Ranitidine, a histamine H2-receptor antagonist with AChE inhibitory activity and ACh release facilitatory activity, enhanced the motor activity but decreased blood pressure at 1 to 10 mg/kg, i.v. In conscious dogs, KW-5092 at 0.03 to 1 mg/kg, i.v. or 1 to 10 mg/kg, p.o. dose-dependently enhanced the gastric antral, duodenal, ileal and the colonic motor activities. Neostigmine at 0.1 mg/kg, i.v. or 3 mg/kg, p.o. enhanced the duodenal, ileal and colonic motor activities, but induced excitement, slavering, vomiting and diarrhea. Ranitidine at 3 mg/kg, i.v. enhanced the gastric antral and colonic motor activities, but induced collapse or akinesia. The present results suggest that KW-5092 enhances the GI motor activity in a wide range from the gastric antrum to the colon and does not induce behavioral and cardiovascular side effects. KW-5092 may be a useful drug for the treatment of GI motility dysfunctions.
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PMID:Enhancement by KW-5092, a novel gastroprokinetic agent, of the gastrointestinal motor activity in dogs. 796 26

A case of fulminant hepatitis with microvesicular steatosis resembling Labrea's fever, diagnosed in Vitoria (ES) is reported. The 16 year old boy presented with severe epistaxis, agitation, jaundice and hemorrhagic vomiting and died two days after admission to the emergency unit of the University Hospital. The disease started five days before with fever, myalgias, dark urine and jaundice and progressed with psychic agitation, torpor and coma. The liver and spleen were not palpable. HBsAg was negative in the serum. The autopsy showed acute hepatitis with lytic necrosis confluent in the midzonal and periportal areas with massive microvesicular steatosis in the remaining hepatocytes. Mononuclear cells predominated in the exudate. The reticulum showed condensation in the necrotic areas without typical bands of collapse. The portal tracts were edematous with mononuclear infiltration and mild bile duct proliferation. Absence of cholestasis. Except for the confluent midzonal and periportal necrosis this case showed several clinical and morphological aspects of the Labrea fever described from the East Amazon, demonstrating that the anatomical picture of this disease probably is not in related to a factor peculiar to the Amazon region.
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PMID:Labrea-like hepatitis in Vitoria, Espirito Santo State, Brazil: report of a case. 815 25

Quinine poisoning typically results in a constellation of non-life threatening symptoms which include tinnitus, deafness, nausea, vomiting, vision changes, headache, and hypotension. Cardiac conduction defects, dysrhythmias, and cardiovascular collapse have all been reported after overdose and generally occur within 8 hours of ingestion. We report a unique case of delayed cardiotoxicity following quinine ingestion. Toxicity included marked ventricular conduction abnormalities for which serum alkalinization appeared to be therapeutically beneficial, and torsades de pointes requiring overdrive pacing for termination.
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PMID:Delayed cardiotoxicity following quinine overdose: a case report. 834 May 83


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