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Results for “Alcohol-Induced Disorders”

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At least 127 records · Page 7Linked to original sources
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↗
PubMed1981

Neuroendocrine effects of fetal alcohol exposure.

While the actions of alcohol on endocrine function in adults are well-documented, the effects of fetal exposure to alcohol on neuroendocrine function in neonates and adults are only beginning to be investigated. Recent reports are reviewed which demonstrate effects of fetal alcohol exposure on pituitary-adrenal function, GH secretion, thyroxine levels and sexual differentiation in newborn rodents. Our studies of the long-term effects of fetal and early postnatal exposure to alcohol on pituitary-adrenal and body temperature responses to a challenge dose of ethanol in adult rats are described. Both responses are enhanced in prenatally, but not in postnatally exposed rats, indicating that the effects of fetal alcohol exposure on physiological systems, such as the endocrine and thermoregulatory systems, persist to adulthood. Based on apparent similarities in the somatic and cerebral deficits which occur following fetal alcohol exposure and neonatal corticosteroid treatment, a hypothesis is developed for the role of alcohol-induced activation of the HPA axis during gestation in the adverse effects of fetal alcohol exposure.

Adolescent↗
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↗
PubMed1995

The natural history of nonalcoholic fatty liver: a follow-up study.

Nonalcohol-induced fatty liver is widely believed to be a benign condition with little or no risk of disease progression. There have been occasional reports of progression to cirrhosis but none in the absence of preexisting fibrosis on the index biopsy specimen even when co-existing hepatitis was present (steatohepatitis). From our histological database (1978 to 1985), we identified 161 patients with fatty liver seen at our institution and traced the case notes of 156. One hundred five patients were initially excluded as having an alcohol-induced cause, and the remaining 51 either were seen in the clinic (37) or had died, in which cases copies of their death certificates were obtained (14). A further 7 patients were excluded after clinic attendance gave evidence of alcohol excess and another 4 after review of their initial biopsy showed the presence of fibrosis or steatohepatitis. The apparent cause of the steatosis in the 40 included patients with strictly nonalcohol-induced pure fatty liver was obesity in 12, diabetes in 4 (1 obese patient), and cachexia associated with extrahepatic malignancy in 6. Four of the remaining 19 had serological evidence of an autoimmune disorder, but none of these had any clinical or histological features of autoimmune liver disease. Nine patients had evidence of hyperlipidemia, 3 of whom were also obese. At a median follow-up of 11 years (7 to 16), 12 of 26 living patients had abnormal results of liver blood tests and had repeat liver biopsies performed. None had progressed to steatohepatitis or cirrhosis; 1 obese patient had developed mild fibrosis 9.8 years after her index biopsy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗