[Hypacusia after acute alcoholic intoxication. Description of a case].
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The function of the hypothalamo-pituitary-gonadal system has been studied in 118 males with different stages of alcoholism. Comparison with the control group has shown decreased levels of interstitial cell stimulating hormone (ICSH), follicle-stimulating hormone (FSH), and testosterone, and elevated concentrations of prolactin (Prl). Differences in the parameters of hormonal activity expressed in a varying degree of a decrease in FSH, ICSH, and testosterone, and a Prl elevation are related to change in mutual regulatory influences between the gonads and hypothalamo-pituitary complex. The most informative parameters were concentrations of Prl and testosterone (considering elevation in the former and reduction in the latter hormone) and the ratio of their concentrations. Difference of these parameters in each group (corresponding to the stages of alcoholism) may be used as an additional diagnostic criterion of chronic alcohol intoxication.
This study tested the hypothesis that prolonged consumption of alcohol directly or indirectly, through endotoxin influx in the circulation, stimulates the Kupffer cells to produce macrophage inflammatory protein-2 (MIP2) and up-regulates the expression of adhesion molecules, i.e., CD18 on PMNs and its counter-receptor, intercellular adhesion molecule-1 (ICAM-1), on hepatic cells. As a result, enhanced sequestration and cell-cell interaction among these cell types may occur in the liver, which in turn could result in altered hepatic function and hepatotoxicity. This hypothesis was tested in alcohol-fed, specific pathogen-free, male Sprague-Dawley rats. After 16 weeks of feeding, endotoxin (0.2 +/- 0.043 EU/mL) and MIP2 (625 +/- 100 pg/mL) were detected in the sera of alcoholic rats but not in the pair-fed rats. Concomitantly, serum aspartate transaminase (AST) activity was significantly increased. Small lipid deposition and inflammatory-like changes in the liver were also observed. Isolated Kupffer cells from alcohol-fed rats released large amount of MIP2 (> 600 pg/10(6) Kupffer cells/24 hr) in vitro compared with Kupffer cells from pair-fed rats (< 150 pg/10(6) Kupffer cells/24 hr). At the same time, the expression of CD18 and ICAM-1 on polymorphonuclear neutrophils (PMNs) and hepatic cells was increased more than twofold. Monoclonal antibody 1F12, an anti-CD18 antibody, attenuated hepatic injury in vivo, and in PMN-hepatocyte coculture in vitro in the alcohol-fed group. Another factor that could contribute to hepatic injury was MIP2, which was cytotoxic to alcoholic hepatocytes in vitro. This was reversed by cycloheximide, thus suggesting the indirect hepatotoxic effect of MIP2. In addition, isolated PMNs and Kupffer cells from alcohol-fed rats released large amounts of superoxide, which may also play a role in hepatic injury. These results demonstrate that MIP2 and adhesion molecules may contribute, at least in part, in the initiation of hepatic injury during alcohol intoxication.
During a drinking experiment 20 young male volunteers were asked to estimate the amount of their BAC and commented on their driving ability and their readiness to participate in road traffic. During the resorption phase the majority of the volunteers estimated their BAC too low, whereas in the early elimination phase most of their estimates were to high. The majority of the volunteers felt able to drive throughout the whole experiment which demonstrates an impairment of essential control functions as early as low to medium alcohol intoxication.
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Significant ethanol intoxication can be detected by measuring a large osmolar gap, i.e. a large difference between the measured and calculated plasma osmolality. In our laboratory, measurement of the osmolar gap with the application of a correction factor has been used as a screening test for alcohol intoxication and has been shown to be rapid and effective and to compare favourably with an accepted method for assaying ethanol (alcohol dehydrogenase). In only a few clinical situations is a more specific and accurate assay for ethanol required. In interpreting the result, it must be stressed that substances other than ethanol may occasionally cause a raised osmolar gap.
BACKGROUND: At present there are only intriguing and preliminary clinical results regarding the efficacy of metadoxine (pyridoxol L-2-pyrrolidone-5-carboxylate) in acute alcohol intoxication. The present study was planned with the aim of investigating the effectiveness of metadoxine in the management of patients affected by acute ethanol intoxication. METHODS: A double-blind, randomized, multicenter, placebo-controlled trial was carried out on 58 patients of both sexes with acute ethanol intoxication. Patients were treated with a single dose of 900-mg intravenous metadoxine (n = 29) or with placebo (n = 29). Patients were clinically and biochemically evaluated at 0.5, 1, 2, 3, 6, 9, and 12 hr after treatment. RESULTS: Treatment with metadoxine significantly decreased the half-life of ethanol in blood (from 6.70 +/- 1.84 to 5.41 +/- 1.99 hr; p < 0.013) and showed a faster rate of ethanol elimination. The effects on ethanol half-life in blood were accompanied by a faster onset of recovery from intoxication, defined as the time of the transition of blood ethanol levels to the immediately lower range defined by intoxication categories (in g/liter: 0 to 0.5, absent; 0.51 to 1.0, mild; 1.1 to 2.5, moderate; >2.5, severe). Thus the median time to onset of recovery was 0.95 hr with metadoxine and 2.34 hr with placebo (p = 0.013). The effects of treatment on blood alcohol levels were paralleled by a significant decrease in the rating of the toxic clinical symptomatology. At 2 hr the improvement of toxic symptoms (in percent of maximum possible) was 68 +/- 28 vs. 44 +/- 27% in controls (p < 0.002). CONCLUSIONS: In patients with acute ethanol intoxication metadoxine accelerated the elimination of ethanol from blood, which led to faster recovery from intoxication, and improved the behavioral toxic symptomatology. Metadoxine could be helpful in the management of acute ethanol intoxication.
This study evaluated the accuracy of the post-rotational nystagmus test (PRN) on the basis of the results of 1006 PRN tests performed at the Institute for Forensic Medicine in Ljubljana between 1998 and 2002 during standardized medical examinations in cases of suspected drunk driving. The evaluation of PRN test results with blood alcohol concentration (BAC) as a reference was based on classification into the following categories and characteristics: true positives (TP), true negatives (TN), false positives (FP), false negatives (FN), sensitivity, specificity, positive predictive values (PPV), negative predictive values (NPV), and accuracy. An optimal cut-off value of 10 s for post-rotational nystagmus time was chosen with the help of a receiver operating characteristic (ROC) curve for the BAC limit of 0.5 g/kg. The results of the decision analyses were: TP = 584, FP = 43, FN = 229, TN = 150, sensitivity = 0.718, specificity = 0.777, PPV= 0.931, NPV= 0.396, and accuracy = 0.730. The area under the ROC curve (AUC) was 0.813. Based on the AUC, the post-rotational nystagmus test is a good test for predicting alcohol intoxication over 0.5 g/kg. As a part of the physician's examination, it contributes significantly to the description of the clinical state.
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