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At least 235 records · Page 13Linked to original sources
PubMed1993

Nutrition in the pathogenesis of alcoholic liver disease.

The data and experimental results reviewed here allow the construction of the following hypothesis: alcohol-induced liver disease results from a combination of two phenomena. The first is the induction of the maximum activity of CYP 2E1 by several dietary factors, i.e. (1) low carbohydrate-high fat diet; and (2) the dietary fats composed of PUFA (Yang et al., 1992). The second is the production of lipid peroxidation induced by CYP 2E1 oxidation of ethanol maintained at high blood alcohol levels (> 200 mg %) with the availability of PUFA as substrate (Ekstrom and Ingelman-Sundberg, 1988; Koop, 1992). Thus, lipid peroxidation may be the final common pathway which supports the induction of ALD. Further, it may provide the common denominator which links ALD pathogenesis to non-alcoholic steato-hepatitis (NASH) (French et al., 1989b), where CYP 2E1 is induced by high fat diet and/or diabetes (Dong et al., 1988).

Alcohol Drinking↗
PubMed1996

Visual pathway hemorrhage associated with alcohol-induced coagulopathy.

Hemorrhage confined to the optic pathways is rare. We describe a patient with diffuse hemorrhage of the intracranial optic nerves, optic chiasm, and optic tracts, attributed to alcohol-induced coagulopathy. The hemorrhage resolved completely as the patient's vision improved, and subsequent neuroimaging studies showed atrophy of the affected structures.

Adult↗
PubMed1996

Alcoholic cardiomyopathy: clinical and experimental pathological changes.

In this review we survey the features of alcohol-induced lesions in the heart, in both the clinical and laboratory-animal setting. The data indicates a diverse range of lesions that contribute to the genesis of the entity alcoholic cardiomyopathy (also referred to as alcoholic heart muscle disease). Biopsies of affected patients reveal lesions similar to dilated cardiomyopathy though quantitative morphometry can distinguish between the two disorders. Biochemical analysis reveals an increase in the activities of some enzymes, though the pathogenetic nature of these alterations are unknown, but may well be adaptive. The induction of ischaemia in acute ethanol exposure may contribute to the heart muscle damage, though long term experimental studies indicate that heat shock proteins are reduced, making the heart more vulnerable to cardiac dysfunction. Changes in the rate of protein turnover induced by alcohol appear to be a central feature in animal studies and it is very likely that similar changes occur in man.

Acetaldehyde↗
PubMed1994

Thiamine utilization in the pathogenesis of alcohol-induced brain damage.

There is increasing evidence for the role of thiamine deficiency in ethanol neurotoxicity and in development of alcoholic organic brain disorders other than Wernicke-Korsakoff syndrome [WKS] and cerebellar degeneration. Investigations in humans and in animal models have implicated a reduction in the activities of thiamine-utilizing enzymes as the metabolic basis of tissue injury due to thiamine deficiency. We have investigated the interactions of the thiamine-utilizing enzyme transketolase [Tk], derived from human fibroblasts, lymphoblasts, and various brain regions, with its cofactor, thiamine pyrophosphate [TPP], in an attempt to elucidate the molecular basis of selective brain damage in alcoholism-associated thiamine deficiency. There were no significant differences in the isoelectric pattern of Tk among the nine brain regions (white matter and grey matter) examined. However, Tk activity/mg protein, increase in Tk activity with addition of excess TPP (TPP effect), and TPP-dependent rate of formation of active Tk holoenzyme (tau) varied 2.5-, 6-, and 4-fold, respectively, among these brain regions. These differences in tissue requirements for TPP may contribute to the selective vulnerability of certain brain regions to alcoholism-associated thiamine deficiency, and may influence the pattern of clinical impairment in the individual patient.

Alcohol Amnestic Disorder↗
PubMed1994

Recent findings on the mechanisms by which alcohol damages the developing nervous system.

General etiologic categories related to possible mechanisms of fetal alcohol-induced brain damage are explored. Possible general mechanisms include alterations in protein synthesis, prostaglandins, gangliosides, hypoxia and free radical damage. A multiple systems cascade is presented to illustrate how multiple mechanisms could act together to produce a variety of effects.

Animals↗
PubMed1996

[Alcohol and drug abuse: a retrospective analysis of incidence in a regional hospital 1993-1994].

This retrospective study analyzes and compares the incidence of admissions for alcohol and drug (i.e.: heroin and cocaine) induced diseases to the internal medicine service of Locarno Regional Hospital (61 beds plus intensive care unit) between January 1, 1993 and December 31, 1994. Of 4038 admissions, 298 (7.4%) were related to alcoholism and drug addiction. 4.2% of all hospital days were due to alcohol abuse, whereas 3.2% were related to drug abuse (of these 1.8% were for HIV-associated diseases and 0.9% for withdrawal treatment). The male/female ratio was 3:1 in both groups, the average age of women being significantly lower in the alcoholic group (50.5 +/- 14.4 years vs. 58.1 +/- 12.9; p = 0.003). Over 90% of the patients with alcohol-induced conditions continued to consume alcohol. On the contrary, only 16% of the HIV-positive patients were still drug-addicted. The in-hospital mortality was 6% (5% in the alcoholic group; 1.6% and 12%, respectively, in the HIV-negative and HIV-positive groups of drug addicts). This study confirms the high prevalence of diseases related to alcohol and drug abuse. Women are less affected, but show complications of alcohol abuse earlier. Despite the HIV epidemic in our area, the admissions of alcoholics to the hospital are more frequent than those of drug addicts. Most of the drug addicts with an HIV-associated condition are in remission, whereas alcoholics with alcohol-induced diseases continue, for the most part, to be alcohol-dependent.

Adolescent↗
PubMed1997

Alcohol-induced Purkinje cell loss with a single binge exposure in neonatal rats: a stereological study of temporal windows of vulnerability.

Previous research has shown that the early neonatal period of rats is one of enhanced vulnerability to cerebellar Purkinje cell loss associated with binge-like alcohol exposure, with a prominent sensitive period during the first neonatal week. In this study, an unbiased count of the total number of Purkinje cells was obtained using the stereological optical fractionator, in groups of rats given a single binge-like alcohol exposure either during the most vulnerable neonatal period [postnatal day (PD) 4] or during a later, less vulnerable period (PD 9). Using artificial rearing methods, rats were given 6.6 g/kg of alcohol either on PD 4 or on PD 9, delivered as a 15% (v/v) solution in milk formula on two consecutive feedings of the designated day. Control groups included an artificially reared gastrostomy control and a normally reared suckle control. The mean peak blood alcohol concentrations were not different between the PD 4 and PD 9 alcohol groups, averaging 374 and 347 mg/dl, respectively. The rats were perfused on PD 27. A uniform random sample of sections was obtained from serial frozen sections through the cerebellum, stained with thionin, and Purkinje cells were counted from a uniform random sample of locations on each section with the three-dimensional optical fractionator. The number of Purkinje cells in the suckle control and gastrostomy control groups did not differ from each other, averaging 3.94 (+/- 0.19) and 3.58 (+/- 0.22) x 10(5) cells, respectively. Binge exposure on PD 4 induced significant cell loss (mean of 2.05 +/- 0.20 x (10(5) Purkinje cells), whereas binge exposure on PD 9 did not induce significant Purkinje cell loss (3.70 +/- 0.39 x 10(5) Purkinje cells). These findings confirm that a single neonatal binge alcohol exposure produces pathological Purkinje cell loss, provided that it occurs during the period of enhanced vulnerability coinciding with the early stages of dendritic outgrowth.

Animals↗
PubMed1997

Binge-like alcohol exposure of neonatal rats via intragastric intubation induces both Purkinje cell loss and cortical astrogliosis.

Binge-like alcohol exposure in neonatal rats on postnatal days 4 to 9 via artificial rearing results in a well-documented transient astrogliosis in the cerebral cortex. A recent study, which replicated the astrogliosis using artificial rearing, found that alcohol administered via daily exposure cycles in a vapor inhalation chamber on postnatal days 4 to 9 failed to elicit the effect, thus suggesting that the gliosis was an interactive effect of the artificial rearing administration and not specific to alcohol. The present study evaluated the effects in an intragastric intubation model that replicated the dosing parameters of the artificial rearing while avoiding the stress of surgery and extended maternal separation. In coronal frozen sections through parietal cortex labeled immunohistochemically for glial fibrillary acidic protein, the pups exposed to alcohol by intubation had a significantly greater density of glial fibrillary acidic protein-positive astrocytes per unit volume, compared with littermate controls intubated with a maltose-dextrin formula; alcohol also induced fibrillary hypertrophy of the labeled astrocytes. In the cerebellum, alcohol induced a significant reduction in Purkinje cell number as determined using the optical disector method. These outcomes extend previous findings that neonatal binge alcohol exposure induces acute cortical astrogliosis and Purkinje cell loss, and confirm that the alcohol-induced astrogliosis is not an artifact of artificial rearing.

Alcoholic Intoxication↗
PubMedDate not supplied

Alcohol's impact upon glycobiology.

This report reviews and illustrates ways in which some of the problems linked to excessive alcohol intake may develop from alcohol-induced alterations of eukaryotic cell surface molecules. Alcohol is the number one drug of abuse in the US, affecting at least 15 million Americans and causing annual losses of more than $80 billion and 100,000 lives. An estimated 20-40% of all persons admitted to general hospitals have alcohol-related problems and are often undiagnosed alcoholics being treated for the consequences of their drinking. Chronic alcohol-related cirrhosis of the liver is the ninth leading cause of death in the US, with over 28,000 deaths annually. Alcohol has harmful effects on almost every organ system in the body, producing cardiovascular disorders, liver disease, neuropathological illness and fetal injury. The etiologic mechanisms for these effects of alcohol is a research area of considerable importance to the National Institute for Alcohol Abuse and Alcoholism.

Alcoholism↗
PubMed1976

[Alcohol-induced lesions of the nerve and muscle].

A review is given on the most important neurologic sequelae after long lasting abuse of alcohol. The paper especially deals with the clinical features of neuropathic and myopathic disorders in alcoholics. Electromyography (including electroneurography) is considered to be a major diagnostic aid in these conditions.

Adult↗
PubMed1998

Neonatal ethanol exposure impairs eyeblink conditioning in weanling rats.

Eyeblink conditioning depends on an identified brainstem-cerebellar circuit and may be useful in functional studies of early cerebellar damage produced by neurotoxicants. The present study asked whether binge-like neonatal ethanol exposure that damages the cerebellum would also result in eyeblink conditioning deficits. On postnatal day (PND) 23 to PND24, three groups of Long-Evans rat pups were tested for eyeblink conditioning: (1) ETOH, a group that received intragastric administration of 5.25 g/kg/day of ethanol on PND4 through PND9 via artificial rearing; (2) GC, a gastrostomy control group that received calorically matched milk formula on those days; and (3) SC, suckle controls that were reared normally with their dams. Eyeblink conditioning was severely impaired in the ethanol-treated group relative to the GC and SC groups, which did not differ. This impairment did not reflect sensory, motor, or motivational effects of ethanol treatment, because startle responses to the auditory conditioned stimulus and reflexive eyeblink responses to the unconditioned stimulus did not differ across the three treatment groups. These results suggest that neonatal binge ethanol exposure disrupted brain development in a manner that selectively impaired associative processes involved in eyeblink conditioning, consistent with alcohol-induced damage to the brainstem-cerebellar circuit necessary for this form of learning.

Animals↗
PubMed1998

Chronic pancreatitis: a historical and clinical sketch of the pancreas and pancreatitis.

Chronic pancreatitis (CP), a disease described only in 1946 by Comfort and colleagues is currently a global disease. Chronic alcoholism, albeit is the most frequent etiologic factor for the disease in most of the affluent nations, a form of CP of undetermined etiology, tropical calculous pancreatitis (nutritional pancreatitis, Afro-Asian pancreatitis, or tropical calculous pancreatopathy) has been recognized to be prevalent in many developing nations. Hereditary pancreatitis inherited as an autosomal dominant disease is reported from all parts of the world. A landmark is the recent discovery of a gene that transmits the disease. Nearly 10% of cases of CP are truly "idiopathic" with no identifiable cause. Recent studies indicate that the idiopathic variety of CP has two subsets--a juvenile form and a senile or late onset form, with distinct clinical features. It is extremely rare to see CP secondary to hyperlipidemia or hypercalcemia. These etiologic associations appear to be overemphasized. Epidemiological studies indicate that alcoholism is growing in incidence all over the world along with an increase in all alcohol-associated disorders such as cirrhosis of the liver or pancreatitis. A genetic predisposition to alcoholic pancreatitis is suspected based on population studies, but not proven. The influence of cigarette smoking in enhancing alcohol-induced injury to the pancreas underscores the health hazard associated with alcoholism and cigarette smoking--two habits that often coexist in many individuals. The recent finding that all forms of CP are premalignant further emphasizes the need to enforce preventive measures. The hope is that CP is a preventable disease. The despair is that alcoholism is increasing and spreads across geographic and religious boundaries.

Alcoholism↗
PubMed1998

Alcohol abuse: potential role in electrolyte disturbances and kidney diseases.

The present review summarizes the current knowledge on the multiple effects of alcohol overconsumption on the kidney function as well as on water, electrolyte and acid-base homeostasis. In contrast to the well known transitory diuretic effects, the overall long-term effect of chronic alcohol overconsumption is water and salt retention with expansion of extracellular volume. Furthermore, depletion of magnesium, phosphate and calcium is also frequently found in alcohol-dependent patients. These electrolyte disturbances may be associated with the alcohol-induced hypoparathyroidism and parathyroid hormone resistance of the skeletal muscle as well as with the decrease of serum osteocalcin. Metabolic acidosis with lower arterial blood pH and plasma bicarbonate concentrations was revealed in alcoholic patients upon admission and a significant correlation between chronic alcohol overconsumption and increased incidence of hyperuricemia and gout attacks was also reported. Alcohol seems to have dual effects on the blood pressure. Increased blood pressure was demonstrated in men above 80 g and in women above 40 g ethanol consumption daily. In contrast, young adults consuming only 10 to 20 g per day had lower blood pressure than the abstinent group indicating a J-curve relationship. This is in line with the lowered risk for coronary heart disease associated with regular consumption of small alcohol amounts. The mechanisms responsible for the association between alcohol overconsumption and postinfectious glomerulonephritis have not been elucidated yet. Finally severe alcohol abuse predisposes to acute renal failure and seems to be associated with the general catabolic effects.

Acute Kidney Injury↗
PubMed1998

Acute vision loss resulting from complications of ethanol abuse.

BACKGROUND: Alcoholism affects about 10% of men and 3% to 5% of women in their lifetime. It is a primary chronic disease with genetic, psychosocial, and environmental factors that influence its development and manifestations. METHODS: A 47-year-old alcoholic male manifested mild nutritional optic atrophy, chronic anemia, pancreatitis, and previous gastrojejunostomy and pancreaticojejunostomy. After an acute episode of hypovolemic blood loss from peptic ulceration, there was increased bi-temporal optic nerve head pallor with permanent vision loss, central scotoma, and an acquired red-green color vision defect. RESULTS: The genetic, psychosocial, and systemic effects of ethanol abuse--including anemia, cardiomyopathy, gastric/duodenal ulceration, pancreatitis, and neurologic deficits--are reviewed. Appropriate treatment and management of ocular manifestations and complications from alcoholism are discussed. Prophylactic topical therapy may be indicated to restore the balance between intraocular tension and optic nerve head perfusion in an attempt to prevent further axonal loss. CONCLUSION: Alcohol-induced nutritional optic neuropathy should not be viewed as an isolated ocular entity, but rather as a potentially treatable neurologic problem. An interdisciplinary approach is essential optimal in the management of the alcoholic patient.

Acute Disease↗
PubMed1998

[Functional involvement of diazepam binding inhibitor (DBI) in the establishment of drug dependence].

In this paper, we have reviewed the possibility of the functional involvement of an endogeneous neuropeptide for benzodiazepine receptors, diazepam binding inhibitor (DBI), in the development of drug dependence and the establishment of its withdrawal symptoms. The cerebral levels of DBI protein and its mRNA significantly increased in alcohol-dependent mice, and alcohol-withdrawal caused further increases of both DBI protein and its mRNA. These increases in the mouse cerebral cortex diminished over 14 days after alcohol-withdrawal. In the cerebrocortical neurons, similar patterns of DBI protein and its mRNA were observed during long-term exposure to alcohol and after its withdrawal. Simultaneous exposures of benzodiazepine receptor agonist, antagonist and inverse agonist with alcohol abolished the alcohol-induced increase in DBI mRNA expression in the neurons. Furthermore, the DBI contents and its mRNA expressions were also increased in the cerebral cortex obtained from nicotine-dependent mice and the neurons after long-term treatment with nicotine. The nicotine-induced increases in DBI content and its mRNA expression in the mouse cerebral cortex and the neurons were completely abolished in the presence of an antagonist for nicotinic acetylcholine receptor. These results suggest that the changes in the levels of cerebral DBI induced by continuous treatments with alcohol and nicotine may be involved in the establishment of dependence by alcohol and nicotine, and such changes may be regulated by the benzodiazepine and nicotinic acetylcholine receptors, respectively.

Alcoholism↗
PubMed1998

[Alcohol-induced cognitive impairment is reversible. Neuropsychological tests but not MRT show improvement after abstinence].

Of alcoholic patients who underwent MRI (magnetic resonance imaging) of the brain and neuropsychological tests shortly after discontinuation of heavy drinking, a subgroup underwent repeat MRI scans and neuropsychological assessment one year later. The reduction in drinking habits was associated with cognitive improvement but no significant difference in MRI variables including T1-relaxation time.

Adult↗