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Results for “Alcohol-Induced Disorders”

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At least 109 records · Page 6Linked to original sources
PubMed1986

[The nature, properties and mechanism of formation of alcohol hyalin].

The term "alcohol hyalin" designates several types of acidophilic inclusions in the cytoplasm of hepatocytes in acute alcoholic hepatitis. While similar material occurs in a number of non-alcoholic hepatopathies and extrahepatically, alcohol hyalin serves as an important marker of the alcohol-induced liver disease. Alcohol hyalin is mainly a protein material (fibrillar or granular) containing a number of polypeptides related to cytokeratin system, as well as some unique components. Its formation has multiple pathologic consequences including necrosis of hepatocytes, inflammatory processes in the liver resulting in cirrosis, and systemic autoimmune disorders. Three main hypotheses on mechanism of alcohol hyalin formation are discussed.

Alcoholism↗
PubMed1989

[Alcohol-induced liver cirrhosis as a cause of portal hypertension].

Basic data on pathomorphology and symptomatology of the alcohol-induced liver cirrhosis accompanied by portal hypertension are discussed. Respective data were compared with the group of cirrhotic patients not abusing alcohol. A high percentage of encephalopathic disorders and nearly 50% of the patients suffering from the hemorrhage from esophageal varices were the first sign of the cirrhosis in both groups. Despite hemorrhage from esophageal varices a few patients obtained surgical help preventing recurrence of the hemorrhage. Liver functional reserve, incidence of encephalopathies and the degree of liver involvement are in favour for non-alcohol cirrhosis. Inflammatory process in the liver, splenomegaly and hypersplenism were more frequent in the liver cirrhosis of non-alcohol origin.

Adult↗
PubMed1989

Role of electrolytes in the etiology of alcohol-induced hypertension.

Alcohol use is associated with an increased prevalence of hypertension although the responsible mechanisms and hemodynamic correlates have not been well-defined. Disorders of electrolyte and water metabolism with resultant retention of sodium and water are common in alcoholics. However, although volume relates to cardiac output, and cardiac output to blood pressure, plasma volume expansion does not appear to be important in the development of the hypertension associated with chronic alcoholic use. Most available evidence suggests that the primary underlying mechanism is increased vascular resistance. Chronic alcohol administration may produce an increased accumulation of cytoplasmic calcium in vascular smooth muscle with vascular hyperreactivity, vasoconstriction, and increased peripheral resistance. Although precise mechanisms have not been elucidated, this may result from (1) a direct effect of alcohol on plasma membrane permeability, sodium transport, and Na+/Ca2+ exchange, and/or (2) impaired calcium transport due to a secondary abnormality such as magnesium depletion, which is present in alcoholics.

Cardiac Output↗
PubMed1988

[Loss of vision as a complication of acute pancreatitis].

A report is presented on two patients with severe visual loss and scotoma following an episode of alcohol-induced pancreatitis. A 35-year-old man with pancreatitis developed visual loss in both eyes. Ophthalmoscopic examination revealed extensive ischemic infarcts with bilateral hemorrhage and cotton-wool spots, a clinical picture similar to that of (post-traumatic) Purtscher's retinopathy. Goldmann visual fields demonstrated paracentral scotomas. Fundoscopic lesions had disappeared 3 months after the acute event and visual acuity improved gradually from 0.1 to 1.0. In a 36-year-old man, cerebral infarction was established by CT as a possible cause of visual loss. CSF examination revealed Sudan-III positive material suggesting cerebral fat embolism as the cause of cerebral infarcts. Visual fields showed central scotomas. During the 4-year follow-up period there was a gradual improvement in visual acuity.

Acute Disease↗
PubMed1988

[Effect of alcoholic intoxication of female mice prior to pregnancy on the ultrastructure of neurons in the sensorimotor cortex of the progeny].

Sensorimotor cortex in the offspring of female rats alcoholized in the prepregnancy period revealed signs of delayed neuronal development and dystrophic changes in the neurons especially on the 14th day after birth. In 21-day-old animals the reparative changes increased, but normalization of neuronal ultrastructure was not observed. The dystrophic changes suggest that prenatal brain hypoxia plays an important role in the pathogenesis of alcohol-induced neuronal lesions in the offspring.

Animals↗
PubMedDate not supplied

[Relations between disordered exocrine pancreas function, alcohol consumption and age in alcoholics].

During clinical withdrawal treatment, a disturbed exocrine pancreas function was found in 28 per cent of 72 alcohol addicts, which occurred in connection with an alcohol-induced pancreatitis. The clinical course was mainly quiescent. Altered bicarbonate concentrations and enzyme dissociations were found as a result of the secretin pancreozymin test. In alcohol addicts, the maximum activity of the amylase output was reached as early as 20 minutes and that of bicarbonate, trypsin and chemotrypsin not until 40 minutes post stimulationem. The sums of the logarithmically transformed 40-minute output of bicarbonate, amylase and trypsin displayed significant differences between the alcohol-addict and control groups. The degree of severity of the disturbed exocrine pancreas function was essentially a function of the daily amount of alcohol taken by the addict and of the age of the patient. The dysfunction was most evident in the 30-to-50-year-old patients. Chronic consumption of alcohol is assumed to give rise to a selective effect on the hydro-kinetic and ecbolic pancreas function.

Adolescent↗
PubMed1986

Alcohol-induced pathology.

The classical symptom formation of alcoholism is identified along with the main causes of death in a representative cohort of U.S. alcoholics. New findings in alcoholism studies pertaining to allergenic and hypoglycemic pathways are discussed. The failure of current treatment modes based on a behavioral disease model of alcoholism is noted. The evidence for a new model of alcoholism as an inherited predisposition for metabolic/enzymatic dysfunction is presented, along with the potential for a new treatment protocol based on that model.

Alcoholism↗
PubMedDate not supplied

The molecular mechanism of fetal alcohol syndrome (FAS). I. Ethanol-induced growth suppression.

Of the birth defects associated with alcohol consumption during pregnancy, in situ growth retardation resulting in neonates that are small for gestational age is the most common observation in both humans and animal models. A variety of alcohol-induced alterations in maternal, placental and/or fetal physiology have been proposed as the basis for this retarded fetal growth. The molecular mechanism(s) of this retardation, however, is obscure; and it remains to be determined whether the growth suppression is the result of the action of ethanol or its metabolites on embryonic, maternal or placental tissue. Using the embryonic chick as a model which circumvents changes in maternal and placental function, we have measured ethanol-induced growth suppression as a function of embryonic age and ethanol dosage. The data suggest that ethanol per se suppresses the rate of cell division in embryonic tissue resulting in fewer cells/embryo for a given time of gestation. The suppression of cell division is proportional to the ethanol dose and appears to be related to ethanol-induced changes in the metabolism of the prostaglandin hormones and resulting changes in the cyclic-AMP levels of the developing embryos.

Alcohol Dehydrogenase↗
PubMedDate not supplied

Nutritional issues in perinatal alcohol exposure.

Animal models are important in perinatal alcohol research because they provide an opportunity to study the effects of alcohol while controlling for biological, social and environmental factors which are difficult to control in human studies. One of the variables which has often been overlooked in animal studies, however, is nutrition. Even when there has been an awareness of the need for nutritional controls, such controls have been particularly difficult to implement because alcohol and nutrition interact at so many levels. In this review the interactions of alcohol and nutrition are discussed and some of the methods used to separate effects of alcohol from effects of alcohol-induced malnutrition are considered. In particular, the issues of method of alcohol administration as well as effects of alcohol on nutrient intake, nutrient digestion, absorption and utilization, and nutrient requirements are reviewed. Potentiation of ethanol effects by dietary deficiencies during pregnancy, and possible synergistic effects of alcohol and nutritional deficiencies are described. Finally, the problems inherent in pair-feeding and ad lib feeding control procedures, as well as the issues of diet composition and feeding schedule are discussed.

Alcoholism↗
PubMed1978

Relationship between neuropsychological performance and alcohol consumption in alcoholics.

Cognitive performance in drug-free alcoholic patients (n = 95) within 7 days of their last drink was significantly predicted by chronic and recent drinking practices. Conceptually distinct cognitive functions were differentially influenced by various combinations of drinking variables. Consideration of curvilinear relationships enhanced the amount of variance explained, and it is suggested that certain patterns of consumption may accelerate the alcohol-induced decline of brain function.

Adult↗