Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ingestion of a moderate dose of ethanol (0.8 g/kg) by volunteers prior to 4-h inhalation exposure to m-xylene (6.0 or 11.5 mmol/m3) caused marked alterations in xylene kinetics. After ethanol intake the blood xylene level rose about 1.5-2.0-fold and urinary methylhippuric acid excretion declined by about 50% suggesting that ethanol decreased the metabolic clearance of xylene by about one half during xylene inhalation. This effect was noticeable up until a few hours after completed xylene exposure. Urinary excretion of 2,4-xylenol, the minor m-xylene metabolite, was generally not decreased by ethanol and sometimes the reverse seemed to be the case. The disturbance of xylene kinetics can be hypothesized to be caused mainly by ethanol-mediated inhibition of microsomal metabolism. When four volunteers who ingested ethanol prior to m-xylene inhalation at the higher concentration were monitored for blood acetaldehyde, transiently raised levels were found without notable effects on ethanol elimination. This observation may explain why some individuals experienced dizziness and nausea during the combined ethanol-xylene exposure.
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PMID:Metabolic interaction between m-xylene and ethanol. 709 64

A serious, relatively unrecognized, occupational health problem involves the interaction of ethyl alcohol and chemical agents used in industry. Workers who drink alcohol and are exposed to certain chemical agents may experience adverse health effects such as nausea, dizziness, headache, and liver damage. This report reviews the synergistic interactions of ethanol with compounds such as the thiurams, amides, oximes, halogenated hydrocarbons, and metals. Also discussed is the effect of ethanol as a cofactor with vinyl chloride in the etiology of cancer.
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PMID:The interaction of ethyl alcohol and industrial chemicals. 717 Oct 89

Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are the major enzymes responsible for ethanol metabolism in humans. Both enzymes exhibit genetic polymorphisms among racial populations. About half of the Chinese population lack mitochondrial ALDH2 activity and such a deficiency has been believed to be a negative risk factor for the development of alcoholism. To assess ethanol and acetaldehyde metabolism in Chinese with different ALDH2 genotypes, we genotyped 273 male adults at the ADH2, ADH3, and ALDH2 loci by using polymerase chain reaction-directed mutagenesis and restriction fragment length polymorphisms. Of the 143 individuals homozygous for both the ADH2*2 and the ADH3*1 alleles, 80, 55, and 8 were identified as ALDH2*1/*1, ALDH2*1/*2, and ALDH2*/*2, respectively. Five each from the above three ALDH2 genotypic subjects underwent alcohol elimination testing. Blood ethanol and acetaldehyde levels were determined at various times up to 130 min after intaking a low dose of ethanol (0.2 g/kg body weight) by using head-space gas chromatography and high-performance liquid chromatography with fluorescence detection, respectively. The mutant homozygotes of ALDH2*2/*2 and the heterozygotes exhibited significantly higher peak acetaldehyde concentrations and also greater areas under the blood concentrations-time curve (AUC) than did the normal homozygotes of ALDH2*1/*1, with the mutant homozygotes both being the largest. The mutant homozygotes displayed significantly higher peak ethanol levels and AUC compared to the normal homozygotes. Of the 17 subjective feeling items tested, palpitation, facial warming, effects of alcohol, and dizziness were found to be most pronounced among the mutant homozygotes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ethanol and acetaldehyde metabolism in chinese with different aldehyde dehydrogenase-2 genotypes. 748 Mar 58

A 29-year-old man suffered from dystonic writer's cramp for over three years. When he wrote, typed and did other tasks using right hand, dystonic involuntary movement triggered medial rotation of the arm, wrist extension and shoulder elevation. Medication, biofeedback, and botulinum injection were performed without much success. We tried to block the sensory input from muscles by using lidocaine and ethanol. We made injections of 0.5% lidocaine 50ml and 99% ethanol 5ml into muscles with abnormal activity at the frequency of twice a week for about six months. After the treatment, dystonic movement was remarkably improved and he was then able to write, type and perform other tasks with the right hand. Side effects included pain of the injection site, nausea and dizziness, which lasted for a few hours. This "muscle afferent block" did not cause muscle weakness. We speculate that muscle afferent plays a pivotal role in dystonia so that its blocking may be of clinical use.
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PMID:[Muscle afferent block for the treatment of writer's cramp]. 872 Mar 30

This study compared the effect of subcutaneous nicotine injections (2 x 0.3 mg and 2 x 0.6 mg) with saline on subjective and physiological measures in 18 never-smokers and 18 smokers (24-h nicotine deprived), under conditions of rest and cognitive testing. Prior to the injections the mood of the smokers had deteriorated to a level significantly below that of the never-smokers as a result of tobacco withdrawal. Cognitive tests caused reductions in calmness and increased alertness but there was no evidence of nicotine improving mood in either group under either condition. The 0.6 mg dose worsened mood in never-smokers and caused unpleasant symptoms (e.g. dizziness and arm pain) in both groups. Compared with smokers, never-smokers experienced stronger symptoms of nicotine toxicity and a greater reduction in alertness in response to the 0.6 mg dose, suggesting chronic tolerance to some nicotine effects in smokers. Nicotine produced similar increases in heart rate and decreases in finger pulse volume in both groups. Our results imply that if nicotine has a mood enhancing effect it occurs only after tolerance has been acquired to its primary adverse effects, and that its ability to reverse the mood deterioration caused by tobacco withdrawal is susceptible to situational factors such as our experimental conditions.
Drug Alcohol Depend 1997 Mar 14
PMID:Mood and physiological effects of subcutaneous nicotine in smokers and never-smokers. 908 82

We studied the frequency of use of flumazenil by emergency departments in our region and compared it to recommendations made by specialists in poison information at our poison control center. For a 5-mo period, we prospectively collected cases involving benzodiazepines or zolpidem. Data was documented only from calls from emergency departments. Emergency department personnel were asked the following: If given, the dose and frequency, contraindications, and adverse reactions. Each case was followed to completion. Flumazenil was not given in 55 cases. Of the remaining 14 cases in which it was given, 10 of the cases received flumazenil prior to poison control center consultation. We noted 1 case of dizziness. Ten cases given flumazenil had contraindications (eg ethanol abuse or possible seizurogenic coingestants). Despite possible contraindications, flumazenil was given 10/14 times (71%) prior to calling the poison control center. These results point to potential overuse of this antidote where contraindications or cautions are suspected in the overdosed patients. Our study suggests that when flumazenil use is contemplated by an emergency department physician, a poison control center consult may have a contrary recommendation.
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PMID:Emergency department use of flumazenil prior to poison center consultation. 925 Nov 78

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

An oral solution available as ethanol-free droplets of the fixed drug combination tilidine-HCl 50 mg/naloxone-HCl 4 mg (CAS 27107-79-5 and CAS 465-65-6, respectively; Tilidin-ratiopharm plus Tropfen) was investigated in 12 healthy volunteers together with an ethanol-containing reference preparation for comparable bioavailability. The study was conducted in an open, randomized, two-way cross-over design applying single doses of 20 droplets (equivalent to 50 mg tilidine-HCl/4 mg naloxone-HCl) of either formulation in the fasting state. The drug plasma profiles were monitored for a period of 48 h by means of LC-MS/MS for tilidine and its active metabolite nortilidine, whereas GC-MS was employed in order to determine naloxone and its phase I metabolite, 6-beta-naloxole. Maximum concentrations (Cmax) achieved were 22.28 ng/ml (tilidine) and 92.78 ng/ml (nortilidine) for the test preparation. Corresponding values for the reference preparation were 24.95 ng/ml (tilidine) and 100.73 ng/ml (nortilidine). The extent of drug absorption (AUC0-infinity) amounted to 38.83 ng h/ml and 467.63 ng h/ml for the prodrug tilidine and the metabolite nortilidine of the test preparation and corresponded well to 43.81 ng h/ml and 493.85 ng h/ml of the reference. Regarding the rate of drug absorption, essentially identical tmax and Rabs values for both tilidine and nortilidine of either preparation in addition pointed to well comparable liquid formulations and equipotent analgesia may be inferred from opioid pharmakokinetic profiles. Pharmacokinetics of the opioid antagonist naloxone and 6-beta-naloxole were also determined and resulted in well coinciding profiles for both preparations. Thus despite the fact that only minimum oral naloxone bioavailabilities were observed, plasma level monitoring of naloxone and 6-beta-naloxole allowed for demonstration of systemic exposure of opioid antagonistic compounds throughout a period of 2-3 h after oral drug administration. Due to the limited number of subjects involved, the primary aim of the study did not consist in demonstration of drug bioequivalence. Rather a comparable bioavailability between preparations was assumed if AUC and Cmax point estimators of 90% confidence intervals would be contained within a 0.80-1.20 range. The study outcome revealed that all four investigated analytes met this requirement, whilst nortilidine pharmacokinetic parameters even fulfilled commonly accepted bioequivalence criteria, i.e. inclusion of 90% confidence intervals of AUC- and Cmax-ratios within acceptance limits of 80% and 125%. Increased data variation observed with bioavailability parameters of tilidine, naloxone and 6-beta-naloxole prevented their bioequivalence demonstration based on only 12 study participants. In conclusion, single doses of two different tilidine/naloxone 50 mg/4 mg liquid formulations revealed well comparable bioavailability for all 4 analytes investigated. Both treatments were fairly well tolerated. Most frequently reported adverse events were dizziness, headache and nausea, which all recovered without sequelae and necessity of concomitant treatment.
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PMID:Bioavailability investigation of a new tilidine/naloxone liquid formulation compared to a reference formulation. 1044 8

Although there is general agreement that chronic ingestion of alcohol poses great risks for normal cardiovascular functions and peripheral-vascular homeostasis, a direct cause and effect between the real phenomena of alcohol-induced headache and risk of brain injury and stroke is not appreciated. "Binge drinking" of alcohol is associated with an ever-growing number of strokes and sudden death. It is becoming clear that alcohol ingestion can result in profoundly different actions on the cerebral circulation (e.g., vasodilation, vasoconstriction-spasm, vessel rupture), depending upon dose and physiologic state of host. Using rats, it has been demonstrated that acute, high doses of ethanol can result in stroke-like events concomitant with alterations in brain bioenergetics. We review recent in vivo findings obtained with 31P-NMR spectroscopy, optical reflectance spectroscopy, and direct in vivo microcirculatory studies on the intact brain. Alcohol-induced hemorrhagic stroke is preceded by a rapid fall in brain intracellular free magnesium ions ([Mg2+]i) followed by cerebrovasospasm and reductions in phosphocreatine (PCr)/ATP ratio, intracellular pH, and the cytosolic phosphorylation potential (CPP) with concomitant rises in deoxyhemoglobin (DH), mitochondrial reduced cytochrome oxidase aa3 (rCOaa3), blood volume, and intracellular inorganic phosphate (Pi). Using osmotic mini-pumps implanted in the third cerebral ventricle, containing 30% ethanol, it was found that brain [Mg2+]i is reduced 30% after 14 days; brain PCr fell 15%, whereas the CPP fell 40%. Such animals became susceptible to stroke from nonlethal doses of ethanol. Human subjects with mild head injury have been found to exhibit early deficits in serum ionized Mg (IMg2+); the greater the degree of early head injury (30 min-8 h), the greater and more profound the deficit in serum IMg2+ and the greater the ionized Ca (ICa2+) to IMg2+ ratio. Patients with histories of alcohol abuse or ingestion of alcohol prior to head injury exhibited greater deficits in IMg2+ (and higher ICa2+/IMg2+ ratios) and, unlike the subjects without alcohol, did not leave the hospital for at least several days. Women, for some unknown reason, exhibit a much higher incidence of morbidity and mortality from subarachnoid hemorrhage (SAH) than men. Data on 105 men and women with different types of stroke indicate that, on the average, a 20% deficit in serum IMg2+ is seen; total Mg (TMg) or blood pH is usually near normal. Women with SAH, however, exhibit much lower IMg2+ and higher ICa2+/IMg2+ ratios; the presence of ethanol in the blood is associated with even more depression in IMg2+ in SAH in women. It is possible that prior alcohol ingestion is, in large measure, responsible for a great deal of this unexplained higher incidence of SAH in women. It has recently been reported that the cyclical changes in estrogenic hormones appear to control the serum IMg2+ level in young women. A surge in estrogenic levels prior to SAH could thus precipitate, in part, the SAH. In other human studies, it has been shown that migraines and headache, dizziness, and hangover, which accompany ethanol ingestion, are associated with rapid deficits in serum IMg2+ but not in TMg. The former, and the alcohol-associated headache, can be ameliorated with IV administration of MgSO4. Premenstrual tension-headache (PTH) and its exacerbation by alcohol in women is also accompanied by deficits in IMg2+, and elevation in serum ICa2+/IMg2+; IV MgSO4 corrects the PTH and the serum deficit in IMg2+. Animal experiments show that IV Mg2+ can prevent alcohol-induced hemorrhagic stroke and the subsequent fall in brain [Mg2+]i, [PCr], pHi, and CPP. Other recent data indicate that alcohol-induced cellular loss of [Mg2+]i is associated with cellular Ca2+ overload and generation of oxygen-derived free radicals; chronic pretreatment with vitamin E prevents alcohol-induced vascular injury and pathology in the brain. (ABSTRACT TRUNCATED)
Alcohol 1999 Oct
PMID:Association of alcohol in brain injury, headaches, and stroke with brain-tissue and serum levels of ionized magnesium: a review of recent findings and mechanisms of action. 1054 55

The livers of some larger fish such as shark, tuna and seabass have been reported to be responsible for a peculiar poisoning causing headaches and desquamation. This type of poisoning can also be induced by ingestion of the livers of the sea whale, the polar bear and the seal. Since these animals contain an extremely large quantity of vitamin A in their livers and the symptoms of poisoning in the patients resembled those of patients with acute hypervitaminosis A, the poisoning was believed to have been caused by excessive vitamin A intake. We observed an episode of acute fish liver intoxication in which 3 man experienced dizziness, headache, blurred vision, nausea, vomiting, fever, and desquamation after ingesting the liver of the grouper fish Cephalopholis boenak (C. boenak). One of the patients had full-blown symptoms and presented with a high fever, headache, dizziness, generalized aching pain, and superficial vesicles and bullae of the skin. The treatment was mainly supportive. In the follow-up period, he subsequently developed hair loss and diffuse peeling of the skin on his palms and soles. Acute fish liver intoxication is rare, especially in subtropical regions. Symptomatologically, the clinical pictures of these patients were comparable to acute hypervitaminosis A or retinoid intoxication. The average vitamin A content in the grouper (C. boenak) is high enough to cause acute vitamin A intoxication. Moreover, ethanol may play a potentiating role in this type of event.
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PMID:Acute fish liver intoxication: report of three cases. 1058 20


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