Alcohol intoxication in hospitalized young teenagers.

The scientific literature concerning alcohol intoxication is enormous. However, less is known of alcohol-induced disturbances in children and adolescents and most of those reports concern cases of hypoglycemia in children under five years of age. We studied the clinical status and chemistry, especially acid-base balance, in 36 young teenagers treated at hospital for alcohol intoxication. On physical examination 6 patients were somnolent, 18 were comatose and 12 were in deep coma. The impairment of consciousness was directly proportional to the blood ethanol concentration. Acidosis was a central finding, and it was caused by a combination of respiratory and metabolic factors (a high blood PCO2 and a low base excess; r = 0.97, p < 0.001); the finding of respiratory acidosis dominated. Base excess correlated negatively with beta-hydroxybutyrate and lactate, as expected. All the metabolic products measured--acetate, beta-hydroxybutyrate and lactate--were significantly elevated compared with the control patients. No hypoglycemia was found. Prior treatment with intravenous glucose decreased vomiting and normalized the serum lactate concentration and PO2. Hypokalemia was the most common abnormality in serum electrolytes. In four patients the rate of fall of blood ethanol concentration was 2.8-3.3 mmol/h (0.13-0.15 g/l-1 h-1) and the mean acetate concentration was 0.8 mmol/l (SE 0.3). Biochemical disturbances in young teenage alcohol intoxicants resemble those previously found in adults. The severe toxicity by ethanol, manifesting in coma, occurs in lower blood alcohol concentrations in children than in adults.

Cumulative 10-year risk of symptomatic duodenal and gastric ulcer in patients with or without chronic gastritis. A clinical follow-up study of 454 outpatients.

The cumulative rate of symptomatic peptic ulcer (PU) was examined in a 10-year clinical follow-up study of 454 consecutive outpatients who had undergone diagnostic gastroscopy, from whom routine biopsy specimens were taken from the antral and corpus mucosa, and who were found to be ulcer-free before and at the time of this initial gastroscopy. During the follow-up period 34 (11%) of 321 patients who showed gastritis in the biopsy specimens at the initial gastroscopy had contracted symptomatic PU (18, 5, 7, and 4 cases of duodenal, pyloric, antral, and angular or corpus ulcer, respectively), which was verified by endoscopy. Only 1 (0.8%) of 133 patients with normal antral and corpus mucosa had contracted PU. It was calculated that the 10-year cumulative probability of PU was 10.6% (95% confidence interval (CI95), 7.2-14.0%) in the patients with gastritis, whereas this probability was only 0.8% (0-2.2%) in the patients who had normal antral and corpus mucosa in the initial specimens. The cumulative probability of PU was found to be highest, 27.3% (1.0-53.6%), in middle-aged men (41-60 years of age) who had chronic antral gastritis or chronic pangastritis (gastritis in both antrum and corpus). It is concluded that chronic gastritis precedes the appearance of PU and that the cumulative 10-year risk of PU is very low when both antral and corpus mucosa are normal but may be high if chronic gastritis is present.

The effect of glucocorticoids, beta-2-adrenoceptor agonists, theophylline and propranolol on the rate of ethanol elimination and blood acetate concentration in humans.

The effects of a single dose and of prolonged administration of glucocorticoids and of a single dose of salbutamol, theophylline or propranolol on the rate of ethanol elimination and blood acetate concentration were examined in healthy male students. Mean ethanol elimination rate and mean blood acetate concentration were increased significantly after acute intake of glucocorticoids. After chronic administration of glucocorticoids, the rate of ethanol elimination was significantly increased, whereas blood acetate concentration showed a tendency to increase, but did not reach statistical significance. Changes were found neither in ethanol elimination rates nor in blood acetate levels after single doses of salbutamol, theophylline and propranolol.

Increased rate of ethanol elimination and elevated blood acetate in asthmatics on corticosteroid, beta-2-sympathicomimetic and theophylline treatment.

The rate of ethanol elimination and blood acetate concentrations after a peroral dose of alcohol were measured in eight asthmatic patients receiving high-dose corticosteroid, sustained release theophylline and beta-2-sympathicomimetic treatment and in eight nonalcoholic, healthy controls. Mean ethanol elimination rate (ER) and mean blood acetate concentration (AC) were significantly (P less than 0.01) higher in asthmatics (ER = 134.8 +/- 12.9 mg/kg/hr, AC = 1.13 +/- 0.25 mM) than in controls (ER = 100.2 +/- 12.3 mg/kg/hr, AC = 0.64 +/- 0.10 mM). In the asthmatics there was a significant negative correlation between the age and the rate of ethanol elimination (r = -0.890, P less than 0.01); in the control group, however, this correlation was of lower degree (r = -0.423) and did not achieve statistical significance. Enhanced ethanol metabolism in asthmatics is possibly due to the effect of drugs. Our results suggest that ethanol elimination rate is increased in asthmatics receiving medication and that the effect is most significant in younger age groups.

Increased serum acetate as a marker of problem drinking among drunken drivers.

727 consecutive drunken drivers were studied for laboratory markers of excessive alcohol consumption. Serum gamma-glutamyltransferase and alanine aminotransferase showed no differences and aspartate aminotransferase and blood alcohol concentration only small differences between groups of first and repeating drunk driving offenders. The best laboratory test to differentiate the repeating offenders with probably more serious alcohol problems from the first offenders was in our material serum acetate, the mean serum acetate level of the repeating offenders being highly significantly (P less than 0.001) higher than that of the first offenders or nonalcoholic controls. Serum acetate also differentiated first offenders from nonalcoholic controls (P less than 0.001). Our results suggest that serum acetate could be used for the screening of problem drinking among drunken drivers.

Increased blood acetate: a new laboratory marker of alcoholism and heavy drinking.

Blood acetate concentration of 51 intoxicated patients was measured and compared to conventional laboratory markers of chronic alcoholism. Mean blood acetate concentration of 23 chronic alcoholics and 17 heavy drinkers was significantly (p less than 0.0005) higher than that of 53 nonalcoholic volunteers or 11 occasional drinkers. Blood acetate level was completely independent of blood ethanol concentration ranging from 0.20 to 2.90 promille. Blood acetate was elevated in 65% of both chronic alcoholics and heavy drinkers. Gammaglutamyltransferase was abnormal only in 35%, aspartate aminotransferase in 21% and mean corpuscular volume in 12% of heavy drinkers. Combination (acetate + gammaglutamyltransferase) correctly detected 87% of alcoholics and 71% of heavy drinkers. During ethanol oxidation the upper normal limit of blood acetate is 0.75 mM. The specificity of increased blood acetate is as high as 92%. Increased blood acetate is indicative for metabolic tolerance to alcohol and it may be so far the most sensitive and specific laboratory marker of chronic alcoholism and heavy drinking.