Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A healthy 19-year-old recruit in a French artillery regiment drank 250 mL of a mixture of beer and wine that had rinsed in a hot 155-mm gun-barrel. Fifteen minutes later, he complained of nausea followed by seizures. He was comatose for 24 h, presenting signs of encephalopathy. A moderate renal failure was noted initially and worsened to an extensive tubular necrosis with anuria on the day after the incident. The first toxicological investigations only showed a 0.31 g/L blood ethanol. Then inductively-coupled plasma (ICP) emission-spectrometry revealed very high concentrations of tungsten in the "beverage" as well as in gastric content, blood and urine (1540 mg/L, 8 mg/L, 5 mg/L, and 101 mg/L, respectively). The nature of the metal was confirmed by ICP coupled to mass spectrometry. A simple and reliable ICP quantitative assay of tungsten in biological fluids, hair and nails was then developed. It showed high blood levels (> 0.005 mg/L) until day 13 in spite of six hemodialyses, and in urine until D33. Tungsten was also incorporated in hair and nails. To the best of our knowledge, such an intoxication has never been reported before though this drinking seems to be traditional in the French Artillery. It has probably been favored by the unusually high volume of beverage absorbed and by the new alloy of the gun, containing tungsten. The clinical evolution was satisfactory over weeks and the patient was declared totally cured after five months.
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PMID:Tungsten determination in biological fluids, hair and nails by plasma emission spectrometry in a case of severe acute intoxication in man. 914 46

When administered orally, naltrexone undergoes extensive biotransformation and is metabolized to 6 beta-naltrexol and other minor metabolites. Naltrexone has been recently approved by the Food and Drug Administration for the treatment of alcohol dependence. An important clinical issue with naltrexone treatment is predicting patient compliance, which may be influenced by adverse side effects experienced during the medication. We investigated whether subjective side effects were related to urinary concentrations of naltrexone and its metabolite 6 beta-naltrexol 3 hr after administration of 50 mg po naltrexone in 24 male moderate-to-heavy social drinkers. The results showed significantly higher levels of urinary 6 beta-naltrexol (p < 0.05) in those subjects who experienced one or more side effect (i.e., headache, nausea, anxiety, or erection). Urinary naltrexone levels did not differ between the groups. Results also showed an approximate 10:1 ratio of 6 beta-naltrexol to naltrexone levels and a significant positive correlation between the parent compound and metabolite, suggesting parallel renal clearance. The results of this study suggest a possible mechanism for the side effects observed after acute administration of naltrexone.
Alcohol Clin Exp Res 1997 Aug
PMID:Naltrexone biotransformation and incidence of subjective side effects: a preliminary study. 926 42

Acute effects of ethanol (0.55 g/kg) and the opioid antagonist naltrexone (50 mg) on auditory event-related brain potentials (ERP) (i.e., electrical brain activity time-locked to sensory stimuli) were investigated in 13 healthy social drinkers, using a double-blind, placebo-controlled, design. The subjects' task was to attend to tones presented to a designated ear while ignoring tones to the other, and to detect deviant tones among the attended tones. When administered alone, naltrexone significantly reduced the amplitude of the later part of negative difference (Nd[l]), suggesting impaired selective attention. However, this effect might have been caused by naltrexone-induced nausea. Ethanol, when ingested alone, attenuated the amplitude of the N1, and increased the peak latencies of the mismatch negativity (MMN) and N2b that have been suggested to reflect automatic change detection in audition and allocation of attentional resources to processing of stimulus deviance, respectively. In contrast, the P1 amplitude was augmented by alcohol, but only when the tones were attended. When ethanol and naltrexone were simultaneously ingested, however, the alcohol-induced P1 amplitude augmentation was canceled, thus tentatively suggesting opioidergic mediation of this alcohol effect. In contrast, the MMN peak latency was increased significantly more in the interaction condition than in the ethanol condition, thus suggesting that the detrimental effects of alcohol on involuntary attention switching were augmented by naltrexone. Furthermore, the N2b amplitude was significantly suppressed in the interaction condition, suggesting attentional impairment.
Alcohol 1998 Feb
PMID:Effects of naltrexone and ethanol on auditory event-related brain potentials. 947 56

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

Twenty healthy social drinkers (9 women and 11 men) drank either 50 g of ethanol (mean intake 0.75 g/kg) or 80 g (mean 1.07 g/kg) according to choice as white wine or export beer in the evening over 2 h with a meal. After the end of drinking, at bedtime, in the following morning after waking-up, and on two further occasions during the morning and early afternoon, breath-alcohol tests were performed and samples of urine were collected for analysis of ethanol and methanol and the 5-hydroxytryptophol (5-HTOL) to 5-hydroxyindol-3-ylacetic acid (5-HIAA) ratio. The participants were also asked to quantify the intensity of hangover symptoms (headache, nausea, anxiety, drowsiness, fatigue, muscle aches, vertigo) on a scale from 0 (no symptoms) to 5 (severe symptoms). The first morning urine void collected 6-11 h after bedtime as a rule contained measurable amounts of ethanol, being 0.09 +/- 0.03 g/l (mean +/- SD) after 50 g and 0.38 +/- 0.1 g/l after 80 g ethanol. The corresponding breath-alcohol concentrations were zero, except for three individuals who registered 0.01-0.09g/l. Ethanol was not measurable in urine samples collected later in the morning and early afternoon. The peak urinary methanol occurred in the first morning void, when the mean concentration after 80 g ethanol was approximately 6-fold higher than pre-drinking values. This compares with a approximately 50-fold increase for the 5-HTOL/5-HIAA ratio in the first morning void. Both methanol and the 5-HTOL/5-HIAA ratio remained elevated above pre-drinking baseline values in the second and sometimes even the third morning voids. Most subjects experienced only mild hangover symptoms after drinking 50 g ethanol (mean score 2.4 +/- 2.6), but the scores were significantly higher after drinking 80 g (7.8 +/- 7.1). The most common symptoms were headache, drowsiness, and fatigue. A highly significant correlation (r = 0.62-0.75, P <0.01) was found between the presence of headache, nausea, and vertigo and the urinary methanol concentration in the first and second morning voids, whereas 5-HTOL/5-HIAA correlated with headache and nausea. These results show that analysing urinary methanol and 5-HTOL furnishes a way to disclose recent drinking after alcohol has no longer been measurable by conventional breath-alcohol tests for at least 5-10h. The results also support the notion that methanol may be an important factor in the aetiology of hangover.
Alcohol Alcohol
PMID:Urinary excretion of methanol and 5-hydroxytryptophol as biochemical markers of recent drinking in the hangover state. 971 4

The aims of this study are to investigate whether self-reported facial flushing postalcohol consumption (PAC) among subjects with ALDH2*1/*1 can be attributed to ADH2 or ADH3 and whether the prediction of ALDH2 genotype can be improved by examining the combination of flushing and other accompanying reactions of PAC sensitivity. Fifty-eight subjects of Han ancestry in Taiwan were interviewed for alcohol-sensitivity reactions and their blood samples were genotyped for ALDH2, ADH2, and ADH3. For subjects with ALDH2*1/*1 (n = 46), 70% reported to have no flushing PAC and 30% reported flushing PAC. When subjects with ALDH2*1/*1 had ADH2*1/*1 (n = 11), all reported to have no flushing; otherwise, 35% (for ADH2*1/*2, n = 17) and 44% (for ADH2*2/*2, n = 18) reported flushing. For subjects with ALDH2*1/*1 and at least one ADH2*2 allele, the genotype of ADH3 was not associated with self-reported flushing. PAC flushers with ALDH2*1/*1 (50%) were more likely to report nausea than those with ALDH2*1/*2 (8%). The probability of ALDH2*1/*1 given flushing reported was 0.29, while the probability of ALDH2*1/*1 given both flushing and nausea reported was 0.71. The results indicate that self-reported flushing is determined by both ALDH2 and ADH2 and that prediction of ALDH2 genotype on the basis of self-reported flushing and nausea can help identify subjects at increased risk for alcoholism.
Alcohol Clin Exp Res 1998 Aug
PMID:Self-reported flushing and genotypes of ALDH2, ADH2, and ADH3 among Taiwanese Han. 972 71

Steroid hormone action involves binding to cognate intracellular receptors that, in turn, bind to respective response elements and thus modulate gene expression. The present study shows that the gonadal steroids, 17beta-estradiol and progesterone, may also act as functional antagonists at the 5-hydroxytryptamine type 3 (5-HT3) receptor in whole-cell voltage-clamp recordings of HEK 293 cells stably expressing the 5-HT3 receptor. Functional antagonistic properties at this ligand-gated ion channel could also be shown for 17alpha-estradiol, 17alpha-ethinyl-17beta-estradiol, mestranol, R 5020, testosterone, and allopregnanolone but not for pregnenolone sulfate and cholesterol. An antagonism at the 5-HT3 receptor could further be observed with the aromatic alcohol 4-dodecylphenol but not with phenol or ethanol. Thus, the modulation of 5-HT3 receptor function by steroids or alcohols is dependent on their respective molecule structure. The antagonistic action of steroids at the 5-HT3 receptor is not mediated via the serotonin binding site because the steroids did not alter the binding affinity of [3H]GR65630 to the 5-HT3 receptor, and kinetic experiments revealed a quite different response pattern to 17beta-estradiol when compared with the competitive antagonist metoclopramide. BSA-conjugated gonadal steroids labeled with fluorescein isothiocyanate bound to membranes of HEK 293 cells expressing the 5-HT3 receptor in contrast to native HEK 293 cells. However, there was no dose-dependent displacement of the binding of gonadal steroids to membranes of cells expressing the 5-HT3 receptor in binding experiments or fluorescence studies. Thus, gonadal steroids probably interact allosterically with the 5-HT3 receptor at the receptor-membrane interface. The functional antagonism of gonadal steroids at the 5-HT3 receptor may play a role for the development and course of nausea during pregnancy and of psychiatric disorders.
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PMID:Functional antagonism of gonadal steroids at the 5-hydroxytryptamine type 3 receptor. 973 11

Opioid compounds are commonly used analgesics. After opioid administration, troublesome subjective effects, such as dysphoria, dizziness, nausea, and pruritus, have been reported. While some if not all of these are believed to occur due to central nervous system effects of opioids, the anecdotal reports heard from volunteers in our other studies suggest that a peripheral opioid antagonist reduced some of these effects. In this double-blind randomized placebo-controlled study, we evaluated the efficacy of oral methylnaltrexone, a selective peripheral opioid receptor antagonist, to decrease subjective effects after administering morphine to normal human volunteers. After intravenous morphine injection (0.05 mg/kg), significant increases in subjective ratings were obtained on 'nauseous', 'skin itch', 'stimulated', and 'flushing'. Oral methylnaltrexone 19.2 mg/kg significantly decreased these four ratings. Plasma methylnaltrexone concentrations at two different oral doses were also measured to correlate between pharmacological effects of the compound and its plasma levels. Our results suggested that methylnaltrexone has a potential therapeutic value in decreasing some undesirable subjective effects associated with opioid medications.
Drug Alcohol Depend 1998 Oct 01
PMID:Efficacy of orally administered methylnaltrexone in decreasing subjective effects after intravenous morphine. 980 Jan 45

A 36-year-old man with a history of depression presented to the emergency department after ingesting approximately 3,000 mL of ethylene glycol antifreeze in a suicide attempt. The patient's ethylene glycol concentration, 1,889 mg/dL, was higher than any level previously documented in the medical literature. Although his course was complicated by nausea, emesis, lethargy, metabolic acidosis, and kidney failure, the patient survived without persistent kidney failure or other chronic problems. Sustained hemodialysis and ethanol infusion were instituted in the ED, on the basis of the patient's history, before laboratory confirmation of the ingestion was obtained.
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PMID:Emergency department hemodialysis in a case of severe ethylene glycol poisoning. 986 97

The mechanisms underlying the suppressant effects of naltrexone (NTX) on ad libitum alcohol drinking in a bar/restaurant setting were investigated in heavy beer drinkers. Fifty-one male and female heavy drinkers (mean age = 22) received 50 mg of NTX or placebo (PBO), p.o., on two separate occasions in a randomized, double-blind crossover protocol. After 7 days of taking medication, subjects were provided with the opportunity to consume beer ad libitum during two, 90-min test sessions that were held 1 to 2 weeks apart. Blood samples were collected on test days to ensure medication compliance and to measure blood levels of NTX and the active beta-naltrexol. Less beer was consumed during NTX treatment. NTX decreased urges to consume alcohol. NTX-treated subjects also took significantly longer to finish each glass of beer and were more likely to terminate beer drinking early. Self-report stimulation and ratings of positive mood states were lower during NTX treatment. Negative side effects of NTX, such as nausea and headache, were reported more frequently with NTX. Not all of the subjects decreased their beer intake on NTX, and some subjects drank more beer. Nonresponders to NTX were not related to blood levels of the active metabolite beta-naltrexol or to a family history of alcoholism. Overall, the results of this study suggest that NTX affects a number of the components of alcohol drinking sequence, including lowering cravings, decreasing the positive reinforcing effects of alcohol, and increasing headache and nausea, each of which may contribute to reducing alcohol intake.
Alcohol Clin Exp Res 1999 Feb
PMID:Effects of naltrexone on alcohol self-administration in heavy drinkers. 1006 45


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