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PubMed1995

Anticardiolipin antibodies and acute alcoholic intoxication.

Many clinical features have been associated with the antiphospholipid antibodies. In a preliminary prospective study, among 1014 consecutive patients admitted to a Medicine Department, 72 (7.1%) patients were found to be anticardiolipin antibodies (aCL) positive. Eight (11%) of these aCL positive patients had alcoholic intoxication. Chronic alcoholism is known to be associated with a high prevalence of autoimmune disorders. The objective of this study was to determine the prevalence of aCL in patients with acute alcoholic intoxication. Sixty two patients (13 women; 49 men), mean age 35 years (range 17-63 years) referred to the emergency care unit were studied. A control population of 62 apparently healthy subjects, age and sex matched, were also tested. Alcoholaemia, aCL, antinuclear antibodies (ANA), Venereal Disease Research Laboratory (VDRL) and Treponema pallidum immobilisation (TPHA) were determined. The mean alcoholaemia among all patients tested was 2.35 gl-1 (range 0.1-4). aCL were found positive in 10 patients (16%); eight men and two women. Seven patients had aCL IgG level of > or = 15 UG PL/ml while two had IgM level of > or = 12.5 UMPL/ml. One had both elevated aCL IgG and IgM. Statistical analysis confirmed that aCL positivity is more frequently encountered in alcoholic patients compared with an age and sex matched population (P = 0.0298). Among alcoholic patients, 12 (19%) had ANA. Four of them were VDRL positive while all were TPHA negative. Two of the 62 control subjects were found aCL positive. From these data, it can be concluded that increased aCL levels are frequently associated with acute alcoholic abuse.

Adolescent↗
PubMed1991

[Morphogenesis of pneumonia in alcoholic intoxication].

A single moderate dose of ethanol given to 120 Wistar male rats inhibits general immune defence and may facilitate the development of pneumonia. No morphological changes are found in the surfactant system in acute alcoholic intoxication. In chronic alcoholic intoxication with a pronounced withdrawal syndrome, apart from the decrease of general immune defence, lung surfactant system is damaged due to the direct ethanol effect on type II pneumocytes. These are the leading factors in the pneumonia pathogenesis characterized by a grave course and tendency to the abscess formation.

Alcoholic Intoxication↗
PubMedDate not supplied

[Characteristics of the central nervous system metabolism reaction to stress in acute alcoholic intoxication].

In a state of acute alcohol intoxication metabolic response on the stress of the central nervous system was distinctly altered in rats (formation and binding of ammonia in brain and medulla spinalis). The following effects were observed: deamidation of brain proteins was impaired, the intensity of ammonia formation was decreased, content of urea decreased and dynamics of gamma aminobutyric acid, dicarbonic amino acids and their amides was altered.

Alcoholic Intoxication↗
PubMed1989

[Excitatory and inhibitory processes in the spinal cord in alcoholic intoxication].

The reflex reactions of the cat spinal cord were studied in chronic alcohol intoxication The extension of the monosynaptic response latency with simultaneous decrease of its amplitude and the suppression of posttetanic potentiation as well as the breaking of inhibitory processes in spinal cord were found after i. v. injection of alcohol. The disordered functional stat of the spinal cord's segmental apparatus seems to be due to depolarizing effect of alcohol and may be one of the causes of the motor breakdown in alcohol intoxication.

Alcoholic Intoxication↗
PubMed2001

Cigarette smoking, alcohol intoxication and major depressive episode in a representative population sample.

OBJECTIVE: This study investigated the associations of cigarette smoking and alcohol intoxication with major depressive episode. DESIGN: Major depressive episode during the past 12 months was assessed in a national representative cross sectional study using the Short Form of the University of Michigan version of the Composite International Diagnostic Interview (the UM-CIDI Short Form). SUBJECTS: A random sample of 5993 non-institutionalised Finnish people aged 15-75 years was interviewed as a part of the 1996 Finnish Health Care Survey. RESULTS: In logistic regression models the factors associated with major depressive episode in the past 12 months were smoking 10 or more cigarettes daily (odds ratio (OR) 2.26; 95% confidence intervals (95% CI) 1.68, 3.04) and alcohol intoxication at least once a week (OR 2.99; 95%CI 1.70, 5.25). Their effects were independent of each other, and remained significant even after adjusting for other major risk factors (marital status, education, unemployment and chronic diseases). The attributable proportion (a measure of the impact of the risk factors of the disease on the population) for daily smoking of 10 or more cigarettes was 0.15, and for alcohol intoxication at least once a week 0.04. CONCLUSION: Cigarette smoking and alcohol intoxication seem to be important risk factors for major depressive episode. In this population the impact of smoking was greater.

Adolescent↗
PubMed1982

"Pseudo" renal failure after isopropyl alcohol intoxication.

We have described a case of isopropyl alcohol intoxication with the confusing picture of normoglycemia and ketonuria, without evidence of metabolic acidosis. The patient also had a spurious elevation of serum creatinine caused by the high acetone level. The positive ketone test was secondary to high levels of acetone, the main metabolic product of isopropyl alcohol. This is the first case of isopropyl alcohol ingestion in which "pseudo" renal failure has been described.

1-Propanol↗
PubMed2006

Waiting for the patient to "sober up": Effect of alcohol intoxication on glasgow coma scale score of brain injured patients.

BACKGROUND: Between 35% to 50% of traumatic brain injury (TBI) patients are under the influence of alcohol. Alcohol intoxication may limit the ability of the Glasgow Coma Scale (GCS) to accurately assess severity of TBI. We hypothesized that alcohol intoxication significantly depresses GCS scores of TBI patients. METHODS: A 10-year, retrospective analysis of a Level I trauma center registry was undertaken. The study population consisted of all blunt injured TBI patients tested for blood alcohol concentration (BAC, n = 1,075). Patients were divided into two groups; intoxicated (mean BAC 202 +/- 77 mg/dL, n = 504) and nonintoxicated (BAC = 0, n = 571). TBI was classified using ICD-9 codes as concussion alone (ICD-9 850, n = 90) and intracranial injury (ICI, ICD-9 851-854, n = 985). Severity was further classified using the Abbreviated Injury Score (AIS). Mean GCS score was compared between the two groups. Patients who were either intubated or hypotensive upon arrival were analyzed separately to rule out confounding effects on GCS score. Severely intoxicated patients (BAC >250 mg/dL, [mean +/- SD] 309 +/- 54 SD, n = 118) were similarly compared. Finally, multivariate linear regression analysis was undertaken to determine whether BAC level was an independent predictor of GCS score while controlling for confounding factors. RESULTS: Intoxicated and nonintoxicated TBI patients were clinically similar. Alcohol intoxication had little effect on GCS score, with less than a single point difference in all types of TBI, except the most severely injured (AIS 5 injuries, GCS score difference 1.4 points). These results were not altered by endotracheal intubation, systemic hypotension, or severe intoxication. Similarly, BAC was not a significant independent predictor of GCS score in a multivariate model. CONCLUSION: Alcohol intoxication does not result in clinically significant changes in GCS score for patients with blunt TBI. Hence, alterations in GCS score after TBI should not be attributed to alcohol intoxication, as doing so might result in inappropriate delays in monitoring and therapeutic interventions.

Adult↗
PubMed1996

Cross-tolerance between acute alcohol intoxication and endotoxemia.

This study tests two hypotheses: (1) prior exposure to LPS induces cross-tolerance for the hepatic effects of subsequent short-term alcohol intoxication; and (2) short-term alcohol intoxication renders the liver resistant to the effects of acute endotoxemia, resulting in reduced production of superoxide and tumor necrosis factor. In the first group of experiments, male Sprague-Dawley rats were treated intravenously with E. coli lipopolysaccharide (LPS) (0.5 mg/kg) 48 hr before they were given an intravenous bolus of ethanol (1.75 g/kg), followed by 250-300 mg/kg/hr) for 3-5 hr. Superoxide release in the perfused liver was measured after 3-hr ethanol infusion. Pretreatment with LPS attenuated ethanol-mediated superoxide anion release by the perfused liver. The stimulatory effect of phorbol myristate acetate on hepatic release of superoxide was also decreased. In the second group of experiments, rats previously treated with ethanol for 5 hr, received an intravenous injection of LPS (1 mg/kg). At 90 min after LPS, sera were collected for tumor necrosis factor alpha assay. Hepatic release of superoxide anion was determined 3 hr after LPS. Acute ethanol intoxication for 5 hr significantly reduced LPS-induced serum tumor necrosis factor activity and free radical release by the perfused liver. LPS-induced mortality was also decreased. In both groups of experiments serum corticosteroid levels were reduced during cross-tolerance. These results demonstrate that cross-tolerance develops between acute alcohol intoxication and endotoxemia manifesting in reduced hepatic production of cytotoxic cytokines and superoxide anions.

Alcoholic Intoxication↗
PubMed2000

Impaired protein synthesis induced by acute alcohol intoxication is associated with changes in eIF4E in muscle and eIF2B in liver.

BACKGROUND: Acute alcohol intoxication in rats decreases protein synthesis in skeletal muscle and, to a lesser extent, in liver. The purpose of the present study was to examine potential mechanisms for the inhibitory effect of acute ethanol exposure. METHODS: Rats were injected intraperitoneally with either ethanol (75 mmol/kg) or saline, and tissues were examined 2.5 hr later. Rates of protein synthesis in vivo were determined by [3H]phenylalanine incorporation into protein, and various eukaryotic initiation factors (eIFs) were quantitated by Western blot analysis to identify possible mechanisms for regulating translation. RESULTS: Protein synthesis in gastrocnemius and liver was decreased (39% and 21%, respectively) after alcohol administration, compared with saline-injected control animals. Alcohol administration did not alter tissue RNA content but diminished translational efficiency in muscle (43%) and liver (24%). Hepatic eIF2B activity was decreased 24% in alcohol-treated rats, and this was associated with a 95% increase in eIF2alpha phosphorylation. However, alcohol did not alter the amount of 4E-binding protein 1 (4E-BP1) bound to eIF4E, cIF4E bound to eIF4G, or the phosphorylation state of either 4E-BP1 or eIF4E. In contrast to liver, neither eIF2B activity nor the phosphorylation of eIF2alpha was affected in muscle of alcohol-treated rats. However, acute alcohol intoxication increased binding of 4E-BP1 to eIF4E (113%), decreased the amount of cIF4E bound to cIF4G (81%), and decreased the amount of 4E-BP1 in the phosphorylated gamma-form (77%). The plasma concentrations of insulin and insulin-like growth factor-I were unchanged by alcohol, but muscle insulin-like growth factor-I messenger ribonucleic acid abundance was decreased 35%. CONCLUSIONS: These data suggest that acute alcohol intoxication decreases translation initiation and protein synthesis in liver and muscle via different mechanisms. Changes in eIF2B appear to predominate in liver, whereas alterations in eIF4E availability appear more critical in skeletal muscle for controlling translation initiation.

Alcoholic Intoxication↗
PubMed1993

[Proof of alcoholic intoxication in automobile driving by breath alcohol content in Austria from the legal viewpoint].

In Austria, automobile drivers are obligated to undergo a breathalizer test if they are suspected of driving under the influence of alcohol. Drivers cannot be forced to take the test, but if they refuse, their conduct is then dealt with as a violation of civil law and is therefore punishable by law. If the Alcomat test yields an alcohol content of 0.4 ml/l, i.e. relevant amount, the suspect then has the right to demand that a blood test be carried out. If the authorities refuse to give him this test, then the suspect will not be held to have been in excess of the legal alcohol level by the civil authorities in the following proceedings. On the other hand, in a legal criminal proceeding, the suspect will then be found guilty of exceeding the legal alcohol level, if additional evidence--which must be examined by the judge within the framework of the free consideration of evidence (a principle recognized by Austrian law but not, for example, by American law)--suffices to show with relative certainty that the suspect exceeded the alcohol limit as defined in section 81 Z2StGB). If a blood test is completed and the results differ from those of the breathalizer, then the blood test results are used.

Accidents, Traffic↗
PubMed2004

Alcohol intoxication effects on simulated driving: exploring alcohol-dose effects on brain activation using functional MRI.

Driving while intoxicated is a major public health problem. We investigated impaired driving using a simulated driving skill game that presents an 'in-car' view of a road and a readout of speed. We explored brain activation and behavioral alterations from baseline at two blood alcohol concentrations (BACs). Participants received single-blind individualized doses of beverage alcohol designed to produce blood alcohol content (BAC) of 0.04 and 0.08 or placebo. Scanning occurred on a 1.5 Tesla Philips MRI scanner after training to asymptote performance. Analysis was performed using independent component analysis (ICA) to isolate systematically nonoverlapping 'networks' and their time courses. Imaging results revealed seven separate driving-related brain networks with different time courses. Several significant findings were observed for the imaging data. First, dose-dependent functional magnetic resonance imaging (fMRI) changes were revealed in orbitofrontal (OF) and motor (but not cerebellar) regions; visual and medial frontal regions were unaffected. Second, cerebellar regions were significantly associated with driving behavior in a dose-dependent manner. Finally, a global disruptive effect of alcohol on the ICA time courses was observed with highly significant differences in OF and motor regions. Alcohol thus demonstrated some behavioral effects and unique, disruptive, dose-dependent effects on fMRI signal within several brain circuits. The fMRI data also suggest that the deficits observed in alcohol intoxication may be modulated primarily through OF/anterior cingulate, motor and cerebellar regions as opposed to attentional areas in frontoparietal cortex.

Adult↗
PubMed1986

Effects of alcohol intoxication on metamemory and on retrieval from long-term memory.

In a balanced-placebo design, people expected either an alcohol drink or placebo drink and consumed either alcohol (1 ml/kg) or placebo. Shortly thereafter, each person attempted to recall the answers to general-information questions (e.g., "What is the capital of Chile?"), made confidence judgments about the accuracy of recall, made feeling-of-knowing judgments on all nonrecalled items, and received a recognition test. Unanticipated outcomes included: Alcohol intoxication significantly hindered recall from long-term memory, contrary to previous conclusions that alcohol does not affect retrieval; people's expectancy of alcohol had no significant effect on memory or metamemory performance, contrary to its established effects on other kinds of performance; and alcohol intoxication produced no significant overconfidence in judgments about recall or in feeling-of-knowing judgments, contrary to the overconfidence produced in other kinds of judgments such as an intoxicated person's assessment of his driving ability. This last outcome implies that alcohol intoxication does not produce a general lowering of the threshold for confidence but rather has effects that are situation specific.

Adult↗
PubMed1984

Effect of alcohol intoxication on the diagnosis and apparent severity of brain injury.

Because alcohol intoxication is common among brain-injured patients, we performed this study to determine the extent to which alcohol alters the initial assessment of brain injury severity in these patients by depressing the level of consciousness. The Glasgow coma scale was used to measure the level of consciousness of 257 brain-injured adults admitted to the University of Virginia Hospital, both on arrival in the emergency room and 6 to 10 hours later. Improvement in the level of consciousness between the first and second measurements was significantly related to the blood alcohol concentration on admission. Patients with the highest blood alcohol concentrations showed the greatest improvement. Most of this effect occurred in patients with a blood alcohol concentration of 0.20% or higher. Alcohol intoxication is a potential source of bias in the clinical classification of brain injuries according to severity.

Adolescent↗
PubMed1976

Effects of fructose and glucose on ethanol-induced metabolic changes and on the intensity of alcohol intoxication and hangover.

The effects of fructose and glucose on the metabolic changes induced by ethanol and on the intensity of alcohol intoxication and hangover were studied in 109 healthy male volunteers. After 10 hours of fasting, the subjects were given 1.75 g of ethanol per kg body wt during 3 hours under controlled laboratory conditions. Fructose or glucose were adminstered either simultaneously with ethanol or 12 hours later during the hangover period. The intensity of alcohol intoxication and hangover were estimated 10 times during the experimental period of 20 hours using subjective and objective rating scales. Sequential determinations of blood ethanol, acetaldehyde, glucose, lactate, free fatty acids, triglycerides, ketone bodies and capillary blood acid-base balance were also made during the experiment. Under these experimental conditions neither fructose nor glucose had any significant effect on the intensity of alcohol intoxication and hangover. The sugars also had no significant effect on the rate of ethanol elimination or on the blood acetaldehyde concentration during the course of the experiment. Blood glucose concentration was decreased and blood lactate, free fatty acid and ketone body concentrations were increased during the hangover period in the subjects who had been given only ethanol. These subjects also had a marked metabolic acidosis during hangover. Glucose and fructose significantly inhibited the metabolic alterations induced by ethanol. In this respect fructose was more effective than glucose. The results indicate that both fructose and glucose effectively inhibit the metabolic disturbances induced by ethanol but they do not affect the symptoms or signs of alcohol intoxication and hangover. The results support the view that hangover is not directly related to the metabolic effects of ethanol or to its metabolic products.

Acetaldehyde↗