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Results for “Alcohol-Induced Disorders”

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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↗
PubMed1995

[Nutritional status of patients with alcoholic liver diseases: comparison of the situation in the seventies and at present].

AIMS. 1) To evaluate the nutritional status of a group of alcohol abusers, relatively to their liver function and morphology, and 2) to compare these data with those of a previous study carried out by out team ten years ago. According to their body weight, 135 alcohol abusers were divided into three groups: normal-weight, over-weight and under-weight. The severity of their hepatopathy was defined as: 1. slight hepatopathy; 2. alcohol-induced hepatitis; 3. alcohol-induced hepatitis plus cirrhosis; 4 child A cirrhosis; 5. child B cirrhosis. RESULTS. 1. The overweight group was homogeneously distributed among the several degrees of compensated hepatopathy. 2. There was a marked reactivity to skin tests (Multitest) in patients with alcohol hepatitis without cirrhosis, independently of nutritional disorders. 3. Only decompensated cirrhosis may cause caloric-protein malnutrition; consequently, nutritional disorders due to alcohol abuse appear late and they are unlikely to play a leading role in the pathogenesis of liver disease due to alcohol abuse. Obesity, on the other hand, may facilitate the onset of liver steatosis.

Adult↗
PubMed1993

Derangement of astrogliogenesis as a possible mechanism involved in alcohol-induced alterations of central nervous system development.

We have postulated that the brain alterations observed after "in utero" alcohol exposure could be due, in part, to a direct effect of ethanol on astrogliogenesis. In the present work we summarize the main findings concerning the effect of prenatal exposure to alcohol on astrocytes in primary culture. We have found that this treatment alters astrocyte growth and the content and synthesis of DNA and proteins. However, "in utero" exposure to ethanol also causes important alterations in the astrocyte cytoskeleton which could be related to an alteration in the amount and activity of several plasma membrane glycoproteins. These results agree with ones obtained "in vivo" and suggest that ethanol-induced alterations in astrogliogenesis could be an important mechanism underlying the CNS disfunctions observed after prenatal exposure to ethanol.

Animals↗
PubMed1995

Treating anxiety in patients with alcoholism.

The clinical management of patients who present with anxiety syndromes combined with alcohol abuse or dependence is reviewed. A critical step is to make the differential diagnosis between alcohol-induced anxiety (principally alcohol withdrawal) and anxiety disorders per se. Interview and examination techniques useful in making this differential are presented. Clinical management of and pharmacotherapy for alcohol withdrawal are outlined. Anxiety disorders that can be comorbid with alcoholism include panic disorder, social phobia, obsessive compulsive disorder, generalized anxiety disorder, and posttraumatic stress disorder. Psychotherapeutic and pharmacotherapeutic measures for each of these in the setting of alcoholism are suggested, and various possible interrelationships between anxiety disorders and alcoholism are considered. Although anxiety disorders may contribute to the underlying etiology of alcoholism in some cases, alcohol abuse tends to take on a life of its own. Treatment of an anxiety disorder can rarely, if ever, be expected to cure alcoholism. Therefore, the need to institute simultaneous treatment aimed at establishing and maintaining sobriety is emphasized. Research on anxiety disorders and alcoholism is as yet inadequate to fully answer many clinical questions about their relationship and their appropriate diagnosis and management. More research is needed in this area.

Adolescent↗
PubMed1994

[Alcohol and its effect on porphyrin metabolism].

Urinary and fecal levels of porphyrins were measured spectrophotometrically for 388 patients. 66 of them suffered from melanodermic skin lesions without hepatic affection, 95 had chronic hepatic diseases and 227 exhibited porphyria cutanea tarda. The results were considered in relation to the lesion and alcohol habits. Alcohol proved to provoke manifestations of porphyrin disbolism. High protoporphyrin fecal concentrations serve early indications of alcohol-induced damage to the liver. Alcohol abuse results in persistent disorders of porphyrin metabolism in subjects with chronic active hepatitis and hepatic cirrhosis. In established clinical and biochemical syndrome of porphyria cutanea tarda alcohol contributes to further progression of fermentopathy specific for relevant porphyria.

Adolescent↗
PubMedDate not supplied

[Comparison of the effects of tianeptine and paroxetine on amnesic deficits induced by prolonged alcohol drinking in mice].

Previous experiments have shown that chronic ethanol consumption in mice for 12 months produced memory deficits associated with both alterations in diencephalic structures (ie, cellular loss, hypometabolism, particularly in mamillary bodies) and with hippocampal and cortical cholinergic hypofunction (Béracochéa et al., Pharmacol Biochem Behav 1992; 42: 749-53). The present study was aimed at comparing the effects of tianeptine and paroxetine (10 mg.kg-1, i.p.), that have opposite properties on serotoninergic transmission, on this alcohol-induced memory deficits. For this purpose, animals were submitted to a T-maze sequential alternation task in which they were given daily series of 6 successive trials separated by a 30-second interval. Behavioural testing began following a 4-week complete withdrawal period. The experiment was conducted in two steps. In the first part, animals received no treatment. Results showed that, as compared to the control group (pair-fed, n = 7), alcohol-treated mice (n = 20) displayed a trial-specific impairment of alternation rates. Specifically, they were impaired on the last three trials (4-6) of the series (52.2 vs 81.0%, p < 0.001), but performed normally on the first ones (2-3), suggesting thereby an increased sensitivity to proactive interference (Béracochéa et al., Behav Brain Res 1987; 25: 63-74). In the second part of the experiment the alcohol group was divided into three homogeneous groups according to the treatment they received 30 minutes before each daily session (ie, placebo, tianeptine, paroxetine).(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Amnestic Disorder↗