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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gyromitra esculenta (Pers.: Fr.) Fr. and a few other mushrooms have caused severe poisonings and even deaths in humans. Clinical data are characterized primarily by vomiting and diarrhoea, followed by jaundice, convulsions and coma. Gastrointestinal disorders distinguish this poisoning. Frequent consumption can cause hepatitis and neurological diseases. The species of concern are mainly G. esculenta and G. gigas (Kromb.) Cooke (non Phill.). Nevertheless, recent advances in chromatography, biochemistry and toxicology have established that other Ascomycetes species also may prove toxic. Gyromitrin (acetaldehyde methylformylhydrazone, G) and its homologues are toxic compounds that convert in vivo into N-methyl-N-formylhydrazine (MFH), and then into N-methylhydrazine (MH). The toxicity of these chemicals, which are chiefly hepatotoxic and even carcinogenic, has been established through in vivo and in vitro experiments using animals, cell cultures and biochemical systems. When we consider the chemical nature and the reactivity of these natural compounds, we suggest that chemical and biochemical mechanisms may explain their intrinsic biological activity.
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PMID:Poisoning by Gyromitra esculenta--a review. 193 97

Acetaldehyde has been reported, but has not been proven, to be the toxic entity resulting from metaldehyde ingestion. To investigate this, male dogs were given a single dose of 600 mg metaldehyde or acetaldehyde/kg of body wt via stomach tube. Clinical signs were monitored, and plasma and urine were assayed for metaldehyde and acetaldehyde. Vomiting occurred less often and in a significantly lower number of metaldehyde-dosed dogs than in acetaldehyde-dosed dogs. Ataxia and tremors occurred significantly more often in metaldehyde-dosed dogs than in acetaldehyde-dosed dogs. Acetaldehyde was not detected in the plasma or urine of metaldehyde-dosed dogs, however, it was found in a sample of vomitus from one of the metaldehyde-dosed dogs. Metaldehyde was found in plasma and urine of metaldehyde-dosed dogs. Urinary excretion of metaldehyde from the metaldehyde-dosed dogs was less than 1%. Urinary excretion of acetaldehyde from acetaldehyde-dosed dogs was essentially nonexistent. Metaldehyde has a larger role in the mechanism of metaldehyde toxicity than previously thought. While acetaldehyde appeared to be of significantly lesser importance, we could not eliminate it as a factor in metaldehyde toxicity in dogs.
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PMID:An investigation of metaldehyde and acetaldehyde toxicities in dogs. 308 27

A double-blind, placebo-controlled study in eight healthy male volunteers was conducted to study possible disulfiram-type reactions and hypoprothrombinemia associated with cefotetan administration. Three doses of cefotetan (2 g) or of placebo were administered at 12-h intervals. Ethanol (0.5 g/kg of total body weight) was ingested 1 h after the third dose. Blood ethanol, serum acetaldehyde, and prothrombin times were measured throughout the study. Heart rate, blood pressure, and clinical signs as well as symptoms suggestive of a disulfiram-type reaction were also noted. Five of eight volunteers that received cefotetan showed significant flushing. A significant increase in heart rate also was noted. No change in mean arterial pressure was observed during the cefotetan phase, and no one experienced nausea or vomiting. No statistical differences were observed between phases with respect to ethanol area under the time-concentration curve, elimination rate, or serum acetaldehyde concentrations. A slight but statistically significant increase in prothrombin time also was observed with cefotetan. This study suggests that patients receiving cefotetan might be at risk to develop disulfiram-type reactions and hypoprothrombinemia.
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PMID:Cefotetan-induced disulfiram-type reactions and hypoprothrombinemia. 347 45

The effects of repeated oral administration of cefuroxime axetil were assessed in Beagles. The test material, an ester, is hydrolysed following absorption from the intestine to yield the therapeutically active moiety, cefuroxime, together with acetic acid and acetaldehyde; in this study cefuroxime and unhydrolyzed cefuroxime axetil were detected in the blood. Cefuroxime axetil was administered twice daily during 27 weeks by gavage of aqueous, suspensions, total daily doses were equivalent to 100, 400 or 1600 mg cefuroxime/kg/day. Apart from three cases of intercurrent illness, unrelated to treatment, the dogs remained in good health. Effects observed in the 1600 mg/kg group included vomiting and slight suppression of body weight gain. Minor variations in haematological measurements included rather low haemoglobin levels, packed cell volumes and erythrocyte counts. Slightly smaller numbers of neutrophils were thought to reflect reduced demand on normal defensive mechanisms due to continued antibiotic treatment. Prolongation of prothrombin time and activated partial thromboplastin time is attributed to disturbance of the intestinal microbial flora and reduced synthesis of vitamin K, on which the dog is highly dependent. Cefuroxime does not have the N-methylthiotetrazole side chain thought to be responsible for inhibition by other cephalosporins of the vitamin K-dependent step in the synthesis of clotting factors. Variations in plasma chemistry included rather low levels of plasma protein. Electrophoresis showed this to be a generalised reduction; only gamma globulins were proportionally decreased and this finding, like the low neutrophil counts, is attributed to the protective action of the antibiotic. Minor metabolic adjustments to the compound are reflected in plasma levels of cholesterol and triglycerides. This spectrum of findings was seen only to a very limited extent in the 400 mg/kg group; the 100 mg/kg group was, with very few exceptions, unaffected by the treatment. Macroscopic post mortem examination and microscopic examination of tissues revealed no treatment-related features indicative of toxicity. Cefuroxime axetil was thus shown to possess very little toxicity when administered repeatedly in large doses to Beagles. The lowest dose level in this study was ten times the proposed daily clinical dose in man.
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PMID:An evaluation of the safety of cefuroxime axetil during six months oral administration to beagle dogs. 382 Mar 42

Potentially serious cardiovascular changes occur in alcoholics as a results of carbimide-ethanol reactions (CERs). Hypotension and tachycardia often occur when blood acetaldehyde levels increase. Hypotension with bradycardia can also occur secondary to vagal stimulation, the results of retching or vomiting. Conservative procedures (e.g., modified Trendelenburg's position) are usually effective in reversing the hypotension but in severe reactions active treatment (intravenous fluids, O2, and drugs) may be indicated. Three case reports are presented to illustrate cardiovascular responses during CERs; for comparison, changes for one subject during a disulfiram reaction are also presented. Caution is recommended in screening alcoholics before treatment with carbimide or disulfiram so as to rule out cardiovascular, hepatic, or renal diseases.
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PMID:Cardiovascular changes during the calcium carbimide-ethanol interaction. 746 Apr 72

Sulfiram, a drug applied topically to treat scabies, produces effects similar to those of disulfiram after subsequent ingestion of ethanol. Disulfiram, used in aversion therapy in the treatment of alcoholism, inhibits hepatic aldehyde dehydrogenase (ALDH) causing an accumulation of acetaldehyde after ethanol ingestion. The increased tissue levels of acetaldehyde cause a spectrum of undesirable side-effects including flushing, nausea, vomiting, and tachycardia, which are referred to as the disulfiram reaction. Previous studies have shown that in vitro sulfiram is a very weak inhibitor of ALDH, but solutions of sulfiram markedly increase in potency with time. In the present study, fresh solutions of sulfiram were exposed to fluorescent room light under ambient conditions and analyzed at timed intervals by HPLC. At least eight products, including disulfiram, were formed in the light-exposed sulfiram solutions, but not in solutions kept in the dark. Structural characterization of two of the photolysis products was obtained by on-line microbore HPLC-mass spectrometry (mu LC-MS) and on-line microbore HPLC-tandem mass spectrometry (mu LC-MS/MS) using continuous flow-liquid secondary ion mass spectrometry (CF-LSIMS) as the primary ionization method. Sulfiram was converted to disulfiram at an initial rate of 0.7%/hr, and the formation of disulfiram correlated with the increase in ALDH inhibition in vitro. The results of this investigation show that while sulfiram is a weak inhibitor of ALDH in vitro, it is readily photoconverted to disulfiram, a very potent inhibitor of ALDH, which may explain the adverse reaction to ethanol after sulfiram therapy.
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PMID:Photolysis of sulfiram: a mechanism for its disulfiram-like reaction. 798 3

Ethanol-induced emesis were investigated using Suncus murinus and the emetogenic mechanisms of ethanol were compared with those of cisplatin. Intraperitoneal injection of ethanol caused dose-dependent emesis with ED50 value of 22.3% (v/v) when injection volume was adjusted to 4 ml/kg. Intraperitoneal and subcutaneous injection of acetaldehyde also caused dose-dependent emesis (ED50 = 3.5% (v/v) with an extremely shorter latency (6% i.p.: 1.0 +/- 0.3 min cf. 40% ethanol: 13.0 +/- 1.9 min). Neither ethanol nor acetaldehyde caused emetic responses when injected intracerebroventricularly. Pretreatment with disulfiram, an inhibitor of liver aldehyde dehydrogenase, potentiated the emetogenic effects of ethanol. Surgical abdominal vagotomy, which blocks cisplatin-induced emesis completely, did not prevent ethanol-induced emesis. 5-HT3 receptor antagonists, which also cause complete inhibition of cisplatin-induced emesis, did not affect the responses. However, ethanol-induced emesis was prevented by the pretreatment with 8-hydroxy-2-(di-n-propylamino)tetrarin hydrobromide (8-OH-DPAT) and N-(2-mercaptopropionyl)-glycine (MPG) dose-dependently. The tackykinin NK1 receptor antagonist (+)-(2S, 3S)-3-(2-methoxybenzylamino)-2-phenyl-piperidine (CP-99,994) also attenuated ethanol-induced emesis. Taken together, these results suggest that 1) acetaldehyde is probably responsible for ethanol-induced emesis, 2) active site for ethanol maybe peripheral, 3) ethanol-induced emesis is mediated by free radicals, and 4) mechanism of ethanol-induced emesis and that caused by cisplatin are different in many respects, although in some they are similar and that the precise pathways remain to be identified. Therefore, the tolerance to emetogenic effects of cisplatin in alcoholic patients cannot be explained as a simple cross desensitization of the pathway.
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PMID:Ethanol-induced emesis in the house musk shrew, Suncus murinus. 901 Apr 80

Sudden death caused by the acute onset of diabetic coma is reported. A 15-year-old female had been suffering from insulin-dependent diabetes mellitus for the prior 8 years and had a fever and vomiting for the past few days. On the 4th day, after the onset of fever and vomiting, she died suddenly, and was autopsied to clarify the cause of death. Macroscopic examination revealed that the pancreas was atrophic (40 g) whereas the liver was markedly enlarged (2,740 g). Histological findings were: 1) The islets of Langerhans were decreased in size and number. They were not positive for aldehyde-fuchsin staining, 2) There were severe fatty changes in the liver cells. The retained blood in the left ventricle was analyzed: glucose, 1,016 mg/dl; acetone, 345 mg/l; acetoacetate, 5.91 mmol/l: D-3-hydroxybutyrate, 4.17 mmol/l; hemoglobin A1c, 10.2%; fructosamine, 416 mumol/l; total serum cholesterol, 220 mg/dl; triglycerides, 205 mg/dl; free fatty acid, 8.0 mEq/l; urea nitrogen, 40 mg/dl. Although the biochemical estimation of the glucose and ketone levels in post-mortem body fluids was recognized as being unreliable, many of these values were far elevated in comparison with those of normal individuals. Thus, we concluded that the cause of death was diabetic ketoacidosis. We also discuss the diagnostic problems of postmortem blood chemistry.
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PMID:Sudden death due to diabetic coma in insulin-department diabetes mellitus: an autopsy report. 918 21

The disulfiram-ethanol reaction is a well-known clinical phenomenon occurring as a result of acetaldehyde accumulation in the blood. Symptoms usually begin within 5-15 minutes after ingestion of ethanol in patients who have taken disulfiram 3-123 hours earlier, and generally occur in the following order: flushing, sweating, palpitations, dyspnea, hyperventilation, increased pulse rate, fall in blood pressure, nausea, vomiting, and drowsiness. Patients need not experience all these symptoms, and recovery is generally complete. Trimethoprim-sulfamethoxazole (cotrimoxazole) is a commonly prescribed antimicrobial agent that may produce a reaction similar to that of disulfiram when taken by patients who drink ethanol. This drug-chemical interaction may result in accumulation of acetaldehyde in the blood.
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PMID:Disulfiram-cotrimoxazole reaction. 969 65

Hydrogen cyanamide is used in agriculture as a plant growth regulator and is applied to many deciduous plants to stimulate uniform budbreak after dormancy, resulting in uniform flowering and maturity. Hydrogen cyanamide is highly toxic, and adverse health effects from contact include severe irritation and ulceration of the eyes, skin, and respiratory tract. The substance also inhibits aldehyde dehydrogenase and can produce acetaldehyde syndrome (e.g., vomiting, parasympathetic hyperactivity, dyspnea, hypotension, and confusion) when exposure coincides with alcohol use. After Dormex (Degussa AG, Trostberg, Germany), a pesticide product containing hydrogen cyanamide (49% by weight), was introduced in Italy in 2000, a total of 23 cases of acute illness associated with exposure to this chemical were identified in early 2001. This led to a temporary suspension of sales and usage of Dormex on February 23, 2002, and strengthening of protective measures, as specified on the pesticide label when sales were resumed on June 20, 2003. This report describes 28 additional cases of hydrogen cyanamide-related illness that occurred during 2002-2004, 14 of which occurred after sales resumed. These illnesses suggest that the preventive measures adopted in Italy in 2003 to protect workers using hydrogen cyanamide are inadequate. Workers exposed to hydrogen cyanamide should be provided adequate information, training, personal protective equipment (PPE), and engineering controls.
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PMID:Update: hydrogen cyanamide-related illnesses--Italy, 2002-2004. 1585 60


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