Search PubMed⌕ Search

Biomedical subjects

E Mezey

Publications and source records attributed to E Mezey.

At least 235 records · Page 13Linked to original sources
PubMed1977

Aging and ethanol metabolism.

The effect of aging on the distribution and elimination of ethanol was studied in a group of 50 healthy subjects ranging in age from 21 to 81 yr (mean, 53.3). Ethanol was administered in a continuous 1-hr infusion at a mean rate of 375 mg/m2 body surface area/min (equivalent to a mean dose of 0.57 gm/kg body weight). Serial blood samples for the determination of ethanol concentration was obtained at 15- to 30-min intervals for up to 4 hr post infusion. Ethanol elimination and distribution were evaluated with the aid of a two-compartment model. Rates of ethanol elimination were not affected by age. Peak ethanol concentration in blood water at the end of the infusion period was correlated with age (r= 0.55, p less than 0.001). Lean body mass and total volume of distirbution fo the ethanol were negatively correlated with age. The smaller volume of distirbution, in association with the decreased lean body mass, most likely explains the higher peak ethanol concentration found in the blood after administration of an ethanol does on the basis of surface area in the old as compared with the young subjects. This study demonstrates that age-related changes in body composition are important factors in the study of ethanol metabolism and its pharmacologic effects.

Adult↗
PubMed1977

Changes in hepatic collagen metabolism in rats produced by chronic ethanol feeding.

The effect of ethanol feeding for a period of 6 months on parameters of hepatic collagen metabolism was studied in the rat. Ethanol feeding resulted in small increases in the fibrous and ground substance components of hepatic collagen as measured by increases in collagen-bound hydroxyproline and hexosamine, respectively. Liver histology revealagen proline hydroxylase and the incorporation of labeled proline into collagen by liver slices, both of which are associated with collagen synthesis, were not changed. Ethanol feeding resulted in increases in the concentration of protein and deoxyribonucleic acid in the Kupffer cells, but in no changes in collagenase activity. An increase in collagen degradation was suggested, however, by the increase in the urinary excretion of hydroxyproline and glycosaminoglycans found after 2 and 6 months of ethanol feeding, respectively. This study demonstrates that fatty infiltration of the liver in the rat, after prolonged ethanol feeding, is associated with increased deposition of chemically detectable collagen and evidence of increased collagen degradation, although no significant changes in parameters associated with hepatic collagen synthesis were found.

Alcoholism↗
PubMed1977

Familial hemochromatosis: characteristics of the precirrhotic stage in a large kindred.

Ffty asymptomatic members of a kindred with familial hemochromatosis were studied in an effort to clarify some of the physiologic abnormalities present in the pre-cirrhotic or latent stage of the disease. Using excess hepatic iron as a marker for inheritance of hemochromatosis, results of liver biopsies on 31 family members suggest an auto-somal dominant mode of inheritance with incomplete expressivity. In addition to a relationship between alcohol intake and excess liver iron, there was a strong association between the level of alcohol intake and the presence of hepatic fibrosis in those subjects with excess iron stores. Both serum iron and transferrin saturation were significantly higher in family members with iron overload than in those who were not affected. Only transferrin saturation was significantly correlated with the severity of hepatic iron deposition. Studies of glucose tolerance (OGTT, IVITT, glucose clamp studies) demonstrated a defect in carbohydrate metabolism associated with deficient insulin secretion and insulin resistance, both of which were related to the degree of hepatic iron depostion. In this kindred we have found no evidence for a contribution of inheritance to the carbohydrate intolerance of hemochromatosis. Iron overload was not related to activity of hepatic collagen proline hydroxylase or urinary excretion of peptide-bound hydroxyproline. Serum ferritin, previously thought to be a reliable marker of reticuloendothelial iron stores, was normal in 19 of 20 family members with iron overload.

Adolescent↗
PubMed1977

Measurement of alcohol-related effects in man: chronic effects in relation to levels of alcohol consumption. Part A.

The effects of chronic alcohol ingestion are quantitatively related to intake, but little information is available on the topic. In part A of this review, intake-effect relationships are examined for chronic dysfunctions of the liver, pancreas, cardiovascular system, testis and fetus. Part B considers central nervous system effects such as the withdrawal syndrome, psychosis, brain damage, memory loss, alterations of attention, sleep disturbances and EEG changes. Alcohol and the elderly, evidence of favorable effects of alcohol and the question of alcoholism are also discussed. In the vast majority of studies the documented daily intake levels have been over 150 g of ethanol (the equivalent of one pint of 80-proof spirits), often in the range of 250-300 g. Other potential risk factors such as malnutrition are rarely considered, and little information is available on the effects of more moderate daily intake. The liver emerges as the most vulnerable organ to regular alcohol use with the hazardous range beginning at a daily intake of 80-100 g of ethanol. There is some evidence beneficial effects, especially in the elderly, of daily intakes of 15-30 g and epidemiological evidence of a lower incidence of myocardial infarction in those with a daily intake approximating 56 g. More information is needed on chronic intake-effect relationship, particulary at levels below 150 g.

Alcoholism↗
PubMed1976

Hepatic collagen proline hydroxylase activity in alcoholic liver disease.

The activity of hepatic collagen proline hydroxylase was examined in biopsy samples as a factor in collagen synthesis in 77 patients with alcoholic liver disease. The urinary excretion of peptide bound hydroxyproline was also measured in most of the patients, as an index of collagen degradation. The highest activities of collagen proline hydroxylase were found in the patients with alcoholic hepatitis. Enzyme activity was markedly increased in patients with non-specific changes on liver biopsy, whereas, patients with fatty infiltration had only mild elevations, and those with inactive cirrhosis had normal enzyme activity. Urinary hydroxyproline was elevated only in patients with alcoholic hepatitis and inactive cirrhosis. Follow-up determinations in 16 patients with alcoholic hepatitis, after 4 to 5 weeks, revealed a decrease in enzyme activity, but no change in urinary hydroxyproline. We conclude that among the types of alcohol-related liver diseases, alcoholic hepatitis is associated with the greatest turnover of hepatic collagen.

Adult↗
PubMed1976

Increased urinary excretion of D-glucaric acid in alcoholism.

Alcoholic patients were found to have increased urinary excretion of D-glucaric acid while drinking. The excretion of D-glucaric acid returned to normal after discontinuation of ethanol intake, and the increase in the excretion could be reproduced by the administration of ethanol. Determination of the urinary excretion of D-glucaric acid may be useful in detecting the ingestion of ethanol or drugs when this information is not available by other means.

Adult↗
PubMed1976

Changes in endocrine pancreatic function produced by altered dietary protein intake in drinking alcoholics.

The effect of dietary protein intake on abnormal endocrine pancreatic function was studied in five male chronic alcoholic patients with a recent history of heavy alcohol and poor dietary intake. Pancreatic function was assessed by means of the pancreozymin-secretin stimulation test. Immediately on admission and throughout the study, the patients were given ethanol, 250 g/day in divided doses. Initial administration of a low protein (25 g) 1800 calorie diet resulted in no improvement in pancreatic function. Institution of a normal protein (100 g) 2600 calorie diet for 10 days led to a return to normal in the output of bicarbonate, amylase, lipase, and chymotrypsin. Readministration of the low protein diet for 10 days resulted in decreased output of amylase and chymotrypsin. The volumes of secretion and outputs of trypsin and protein remained unchanged throughout the study. This study shows that the transient dysfunction of the exocrine pancreas frequently observed in actively drinking chronic alcoholic patients is caused by deficient dietary protein intake.

Adult↗
PubMed1975

Endogenous ethanol production and hepatic disease following jejunoileal bypass for morbid obesity.

In this study, we sought to determine whether or not elevated levels of ethanol were present in the systemic circulation, resulting from endogenous ethanol production, which might contribute to the hepatic damage following jejunoileal bypass for morbid obesity. Venous serum samples for assay of ethanol by gas-liquid chromatography were obtained in 8 normal subjects, 9 obese patients prior to surgery, 20 obese patients 2 weeks to 40 months after jejunoileal bypass, and in 2 dogs before and after jejunoileal bypass. Ethanol was detected after jejunoileal bypass in only 7 of the 20 patients and in the 2 dogs. Serum ethanol concentrations ranged from 0.15 to 4.12 mg/100 ml with a mean of 1.18 +/- 1.59 (SD)( mg/100 ml in the 7 patients and ranged from 0.20 to 2.23 mg/100 ml in the dogs. Incubation of the contents of the bypassed intestine of a dog with dextrose resulted in the production of significant amounts of ethanol. However, there was no correlation between the presence of ethanol in the serum and liver histology, when liver biopsy was obtained, postoperatively. Since ethanol was detected in the serum in only small concentrations and in only one-third of the patients, it is unlikely that ethanol production by bacteria in the intestine is of significance in the pathogenesis of liver disease following jejunoileal bypass.

Acetone↗
PubMed1975

Effect of uremia on rates of ethanol disappearance from the blood and on the activities of the ethanol-oxidizing enzymes.

The effect of uremia on ethanol metabolism was investigated. Uremia was induced in male Spraque-Dawley rats by removal of approximately 85 per cent of the renal mass. Control animals had a sham operation. The mean activity of alcohol dehydrogenase was markedly increased in the uremic rats to 2.12 +/- 0.13 (S.E.M.) mumoles per milligram of protein per hours as compared with a control value of 1.39 +/- 0.13 mumoles per milligram of protein per hour (p less than 0.001). There were no changes in the activity of the microsomal ethanol oxidizing system, in catalase activity present in the microsomes, or in the rates of ethanol disappearance from the blood. Uremia resulted in decreases in microsomal cytochrome -450, but no changes in cytochrome b5, NADPH-cytochrome c reductase, or in the activities of aniline hydroxylase and aminopyrine demethylase. The increase in alcohol dehydrogenase activity could not be reproduced by incubation of liver from a normal rat with uremic rat plasma, uremic human serum, or urea. Also, the increase in the enzyme activity was not associated with changes in leucocyte ascorbic acid levels. The cause and physiologic significance of the increase in alcohol dehydrogenase activity in uremia remain to be elucidated.

Alcohol Oxidoreductases↗