[Massive hyperlipemia in alcoholic intoxication].
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Several thousand blood samples were taken from alcoholized drivers at the Blood Alcohol Examination Centre of the Institute of legal Medicine at Cologne University. These samples showed blood alcohol contents (BAC) as well as GGT, CDT, methanol, acetone and isopropanol levels which indicated alcohol addiction. The blood samples were selected by the drivers' ages and their BAC, but in some cases the GGT also played a role. In the majority of cases 1 or 2 parameters were measured. In 200 cases all four indicators were determined. The four parameters characterize a different problematic drinking behaviour. GGT characterizes chronic, long-term misuse, CDT characterizes occasional misuse, methanol characterizes current addicted drinking and acetone and isopropanol characterize metabolic disorders caused by alcohol. The importance of parameters is thoroughly discussed, also in relation to incorrectly measured positive values and the relation between alcohol consumption and -problems. Methanol values above 10 mg/kg, GGT activities above 100 U/l and CDT levels above 60 U/l provide sufficient proof of there being an alcohol problem which requires treatment. The levels of other indicators need not be above normal to determine this. The proportion of drivers under the influence of alcohol with problematic alcohol levels increases significantly when the BAC is above 2.0 per mille. However, there have been drivers with alcohol problems with lower BAC levels. DUI offenders addicted to alcohol are quite frequently over 40 years old. A correlation between the single indicators and the BAC is rarely found. If a correlation is to be found, it would be most likely with drivers whose BAC lies above 2.0 per mille. The mentioned indicators would detect an alcohol problem from the blood sample taken for the blood alcohol test. Alcohol problems may be detected and treated shortly after the DUI offence. This method is comparatively cheaper than medical-psychological-examinations as well as being based on objective and verifiable parameters.
Paroxystic alcohol intoxications are classically defined by the alternation of acute and massive intoxications and abstinence periods but occur mostly in chronically drinking patients. Loss of control, sensation seeking and impulsivity are common features of these disorders that are often associated with multiple drug use. They also seem to be characterized by underlying biological and genetic risk factors and antisocial personality disorder.
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Acute alcohol intoxication causes diuresis presumably resulting from inhibition of vasopressin (also called antidiuretic hormone) release from the posterior pituitary gland. In contrast, in alcoholics during withdrawal from alcohol, vasopressin release is stimulated, resulting in water retention (antidiuresis) and dilutional hyponatremia. The purpose of this study was to evaluate the role of this biphasic response of vasopressin secretion to alcohol in normal persons. We studied eight healthy men who took part in two study sessions: one involving the ingestion of ethanol (1.2 g/kg of body weight) and the other the ingestion of the same volume of fruit juice during 3 hr from 6 to 9 PM. Starting at 6 AM the following morning, subjects were loaded with water (20 ml/kg of body weight within 15 min). During the first 3 hr of the study, ethanol intake increased diuresis, whereas from midnight to 6 AM, a phase of antidiuresis was obtained. Antidiuresis continued during water loading when the retention of water was 44 +/- 6% during the alcohol experiment and 12 +/- 4% during the control session (p < 0.05). During the alcohol-induced diuresis, the plasma arginine vasopressin levels did not differ from the control experiment, but were higher during the phase of antidiuresis from 10 PM to 6 AM (p < 0.05- < 0.01). Also, after water loading at 8 and 9 AM, they were higher in the alcohol study than in the control experiment (p < 0.05). After alcohol ingestion, serum osmolality was higher than the corresponding control values from 8 PM to 2 AM (p < 0.01- < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Acute alcohol ingestion can lead to psychiatric emergencies. The main syndromes observed are states of agitation, acute anxiety episodes and suicide or attempted suicide. States of agitation are mainly due to simple or pathological inebriety. Any case of acute alcoholic intoxication requires a full clinical examination and a simple laboratory work-up. Behavioral disorders linked to pathological inebriety can be improved by moderate doses of sedatives such as benzodiazepine, carbamate, tetrabamate or neuroleptic drugs for the most agitated states. States of anxiety generally regress with non-neuroleptic tranquilizers, and attempted suicide mainly requires close surveillance or intensive care.
Chronically alcoholized intoxication (1.5--2 months) induces adaptation of cerebral neurones to changing equilibrium states of biochemical processes by altering the activity of enzymes of GABA metabolism, reduction of alanine and aspartate transaminase activity and increase of LDH and succinate dehydrogenase activity. In the cerebellum and cerebral hemispheres during alcohol abstinacy the activity of GABA-T, succinate dehydrogenase and aspartate transaminase was reduced while that of LDH and alanine transaminase was increased. The administration of fusarinic acid (100 mg/kg i. p.) to control animals induced a sharp increase of GAD activity in both structures of the brain. The stimulatory effects of fusarinic acid were not observed when it was administered to animals receiving alcohol chronically. Motor activity or rats was markedly reduced during chronical alcoholism and the first days of alcohol abstinacy (24--48 h), as well as following injection fusarinic acid and homopantothenic acid. The increase of locomotion and the vertical component of motor activity was observed only following one week or one month after alcohol abstinacy.
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Coma and vomiting are the commonest symptoms in young teenagers intoxicated by alcohol. Severe toxicity, manifested as coma, occurs at lower blood alcohol concentrations in young teenagers than in adults. The effect of ethanol on the state of consciousness is directly proportional to blood alcohol concentration. Among children under 5 years of age the risk of hypoglycaemia is increased. A significant risk in acute alcohol intoxication is the rapid development of coma, which in cold environments could lead to fatal hypothermia. Preschool-age children are reported to eliminate ethanol twice as fast as adults, whereas young teenagers eliminate it at the adult rate. The biochemical disturbances in children 11 to 16 years of age with alcohol intoxication resemble those of adults. Mild acidosis of a respiratory or metabolic origin and mild hypokalaemia are common findings in young teenagers. Fluid replacement with glucose-containing fluids and follow-up are generally the only treatments needed for complete recovery. Motives leading to alcohol intoxication are a wish to get drunk, experimenting, problems in human relations, and attempted suicide. The underlying problems are often family-related, such as divorce, an alcoholic parent and a lower socioeconomic group.
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Although both alcohol intoxication and withdrawal have been demonstrated to produce significant endocrine alterations, no data exist on the effects of acute withdrawal on immune functions. Therefore, the current study investigated the effect of alcohol intoxication and acute withdrawal on plasma cortisol, prolactin and catecholamines, and blood leukocyte subset distribution in alcohol-dependent subjects. Nine male alcoholics admitted to the university clinic for alcohol dependence and 9 age-matched controls participated in the study. Blood was drawn from the alcohol-dependent subjects at 10:30 a.m. on day 0 (chronic alcohol intoxication), at the same time during acute alcohol withdrawal (day 1) and following the resolution of acute withdrawal (day 7). Blood was drawn from age- and gender-matched healthy control subjects at the corresponding time points. Plasma was then analyzed for hormone concentrations and blood examined for leukocyte subsets by flow cytometry. Alcohol-dependent patients displayed significantly elevated plasma cortisol during intoxication and withdrawal, which decreased to control levels following resolution of acute withdrawal. Small elevations of plasma prolactin and catecholamines were also observed during intoxication. Furthermore, alcohol-dependent subjects showed reduced absolute numbers of CD4(+) and CD8(+) T cells and natural killer cells compared with healthy controls across all time points. In contrast, although monocyte numbers were lower in alcohol-dependent patients during intoxication, acute alcohol withdrawal increased the number of monocytes in patients. Thus, alcohol dependence produces a general suppression of leukocyte subset populations in blood. However, resolution of acute alcohol withdrawal is associated with a return of plasma cortisol to control levels, and a concomitant increase in peripheral blood monocyte numbers.
Alcohol intoxication is being recognized increasingly as the major factor in pathogenesis after burn injury. Findings from multiple studies support the suggestion that, in comparison with burn-injured patients who sustained injury in the absence of alcohol intoxication, burn-injured patients who sustained injury under the influence of alcohol exhibit higher rates of infection and are more likely to die. Thus, infection becomes the primary cause of death in burn-injured patients. Because the intestine is considered to be a major source of bacteria, studies in experimental animals have been designed to examine whether alcohol intoxication before burn injury enhances bacterial translocation from the intestine. Results of these studies have shown a several-fold increase in bacterial translocation from the intestine in the group of animals receiving combined insult of alcohol intoxication and burn injury compared with findings for the groups receiving either insult alone. Alcohol intoxication and burn injury independent of each other have also been shown to cause an increase in bacterial translocation. The gastrointestinal tract normally maintains a physical mucosal and immunologic barrier that provides an effective defense in keeping bacteria within the intestinal lumen. However, in injury conditions these defense mechanisms are impaired. Intestinal bacteria consequently gain access to extraintestinal sites. Intestine-derived bacteria are implicated in causing systemic infection and in subsequent multiple organ dysfunction in both immunocompromised patients and patients with injury, such as burn and trauma. In this article, we discuss three potential mechanisms that are likely to contribute to the increase in bacterial translocation in alcohol intoxication and burn injury: (1) increase in bacterial growth in the intestine, (2) physical disruption of mucosal barrier of the intestine, and (3) suppression of the immune defense in the intestine.
OBJECTIVE: To highlight the clinical criteria of persons who are accused of being under the intoxicating effect of alcohol brought to medicolegal officer by the police. METHODS: Included cases of alcohol intoxication reported to the medicolegal sections of three major government hospitals of Karachi i.e., Jinnah Post Graduate Medical Centre, Civil Hospital and Abbasi Shaheed Hospital, Karachi, during the period January to December 1996. RESULTS: During one year of study, 338 persons were brought from police stations all over Karachi to the medicolegal sections of the above three hospitals. Out of these, 260 persons were disposed off by the medicolegal officers by use of their clinical judgement, 78 persons were suspected to be under the effect of alcohol intoxication and were referred to the chemical examiner where urine and blood analysis for alcohol was positive in 40 and negative in 38 cases. Only one fatal case of alcohol intoxication was reported to the chemical examiner and the viscera sent for examination were positive for alcohol. CONCLUSION: The incidence of the positive cases of alcohol intoxication on laboratory analysis was 11.8% while negative results were obtained in 11.2% cases, out of 23% cases referred to the chemical examiner, indicating that the bulk of cases i.e. 76.9% were disposed off on clinical criteria only which is a crude method of assessment of cases of acute alcohol intoxication.
Effect of chronic alcoholic poisoning on the activity of alcohol dehydrogenase (ADH) in the liver of rats was studied during ontogenesis. The activity of the enzyme was detectable for the first time in the fetal liver days 17-18 of the ontogenesis and reached the level seen in adult rats day 25 after the birth. ADH activity was dramatically increased in the liver of fetuses and progeny of females alcoholized before and during the entire pregnancy period as well as of females alcoholized before and during mating. Alcoholization of females before and over the first 15-16 days of pregnancy did not modulate the activity of liver ADH in the fetuses and progeny despite the fact that this activity in the mothers liver was 2.5 times as high as that in control.