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PubMed1987

Use of enzymes for the diagnosis of alcohol-related organ damage.

Elevated levels of serum enzymes are frequently associated not only with alcohol-related organ damage but also with excessive alcohol consumption and alcoholism without significant tissue injury. However, both in the early detection of alcoholism as well as also in the diagnosis of alcohol-related diseases the sensitivities and specificities of these enzyme markers vary considerably. They may be influenced by nonalcohol-related diseases, enzyme-inducing drugs, nutritional factors, metabolic disorders, age, smoking, etc. Consequently, we have neither a single laboratory test--enzyme marker--nor a test combination that is reliable enough for the exact diagnosis between alcohol- and nonalcohol-related organ damage. In most cases it is possible to determine the tissue from which the elevated enzyme is derived, but only occasionally enzyme changes reflect the quantity of the tissue injury. Gamma-glutamyltransferase (GGT) is the most widely used laboratory marker of alcoholism and heavy drinking, detecting 34-85% of problem drinkers and alcoholics. However, the unspecificity of increased serum GGT limits its use for general screening purposes. Its value in the follow-up of various treatment programs, however, is well established. An elevated level of serum aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) in an alcoholic or a heavy consumer indicates alcohol-induced organ damage. The use of test combinations significantly improves the information received with single serum enzyme determinations. An ASAT/ALAT ratio greater than 1.5 can be considered as highly suggestive for the alcoholic etiology of the liver injury. Still better discrimination between alcoholic and nonalcoholic origin of the liver disease may be achieved by the determination of the ratio of GGT to alkaline phosphatase. If this ratio exceeds 1.4 the specificity of the finding in favor for alcoholic liver injury is 78%. The determination of the mitochondrial isoenzyme of ASAT also improves the diagnostic value of ASAT determination. The ratio of mitochondrial isoenzyme to total over 4 is highly suggestive for alcohol-related liver injury. In general, however, the determination of serum activities of other enzymes such as ornithine carbamyl transferase, lactate dehydrogenase, isocitrate dehydrogenase, sorbitol dehydrogenase, alcohol dehydrogenase, guanase, aldolase, alkaline phosphatase or glutathione S-transferase do not significantly improve the diagnostic information obtained with more conventional laboratory markers of liver injury.(ABSTRACT TRUNCATED AT 400 WORDS)

Alanine Transaminase↗
PubMed1988

Experience-dependent cognitive recovery in alcoholics: a task component strategy.

Visuospatial problem-solving deficits following chronic alcohol abuse may not readily recover spontaneously after drinking cessation but may reverse with appropriate environmental stimulation. To determine if such recovery in alcoholics under age 40 may be accelerated by training with components of an initially impaired task (Trails B), this study employed four groups of alcoholics (N = 53) and a group of matched controls (N = 13). Two alcoholic groups received two consecutive cognitive remediation sessions during the latter 2 weeks of a 1-month treatment program, and two groups of alcoholics received no remediation. Results confirmed that recovery of visuospatial problem-solving skills is facilitated by training with task components (experience-dependent recovery) while spontaneous recovery during the first month of abstinence is minimal for this task. These findings demonstrate the efficacy of cognitive remediation in reversing some alcohol-induced cognitive impairment and have important implications for improving alcohol treatment outcome and adaptive functioning.

Adult↗
PubMed1991

Effect of drugs of abuse on psychiatric symptoms among hospitalized schizophrenics.

In a group of 71 inpatient schizophrenics with no other concurrent psychiatric diagnosis except for dependence on one drug, we ascertained the subjective effect their drug of abuse had on their psychiatric symptoms 2 weeks prior to hospitalization. Psychiatric symptoms were assessed by means of the Hopkins Symptom Checklist (Revised) (SCL-90R). Cocaine addicts, but not alcoholics, reported aggravation more often than improvement of symptoms. Alcoholics reported alcohol-induced symptom improvement with a similar frequency as alcohol-induced symptom aggravation.

Adult↗
PubMed1990

Teratogenic effects of alcohol on brain development.

There is convincing evidence that alcohol is teratogenic both in humans and animals and that its most devastating effects are on the developing brain. However, much information is still needed to determine the circumstances that increase the risk and severity of fetal alcohol-induced brain damage and to identify the mechanisms underlying such damage. Animal research has been used to address these issues because, for the most part, they are unapproachable experimentally in humans. In the past, the rather restricted focus of research into the teratology of alcohol has led to several theoretical biases. Recent findings conflict with these biases. Alcohol-induced damage to the developing brain encompasses a longer developmental time-frame, affects more cell populations, occurs at lower levels of exposure, produces greater numbers of permanent effects, and is modulated by more factors than was initially suggested by earlier teratological studies.

Abnormalities, Drug-Induced↗
PubMed2025

Differential Expression of Erythrocyte Proteins in Patients with Alcohol Use Disorder.

Alcohol Use Disorder (AUD) poses global health challenges, and causes hematological alterations such as macrocytosis and oxidative stress. Disruption of protein structures by alcohol and/or its metabolites may exacerbate AUDs; proteomics can elucidate the underlying biological mechanisms. This study examined the proteins differentially expressed in the cytosol and membrane fractions of erythrocytes obtained from 30 male patients with AUD, comparing them to samples from 15 age- and BMI-matched social drinkers (SDs) and 15 non-drinkers (control). The analysis aimed to identify the molecular differences related to alcohol consumption. The AUD patient subgrouping was based on mean corpuscular volume (MCV), with 16 individuals classified as having a normal MCV and 14 having a high MCV. Proteins were separated via two-dimensional(2D)-gel electrophoresis, digested with trypsin, and identified via Matrix-Assisted Laser Desorption/Ionization Time-of-Flight (TOF) mass spectrometry (MALDI-TOF/TOF). Additionally, levels of malondialdehyde and 4-hydroxyalkenals (MDA + HAE), reduced glutathione (GSH), oxidized glutathione (GSSG), serum carbohydrate-deficient transferrin (%CDT), disialotransferrin (%DST), and sialic acid (SA) were analyzed. The results showed increased MDA + HAE and decreased total thiols in AUD patients, with GSSG elevated and the GSH/GSSG ratio reduced in the AUD MCV-high subgroup. Serum %CDT, %DST, and SA were significantly higher in AUD. Compared to the control profiles, the AUD group exhibited differential protein expression. Few proteins, such as bisphosphoglycerate mutase, were downregulated in AUD versus control and SD, as well as in the MCV-high AUD subgroup. Conversely, endoplasmin and gelsolin were upregulated in AUD relative to control. Cytoskeletal proteins, including spectrin-alpha chain, actin cytoplasmic 2, were overexpressed in the AUD group and MCV-high AUD subgroup. Several proteins, such as 14-3-3 isoforms, alpha-synuclein, translation initiation factors, heat shock proteins, and others, were upregulated in the MCV-high AUD subgroup. Under-expressed proteins in this subgroup include band 3 anion transport protein, bisphosphoglycerate mutase, tropomyosin alpha-3 chain, uroporphyrinogen decarboxylase, and WD repeat-containing protein 1. Our findings highlight the specific changes in protein expression associated with oxidative stress, cytoskeletal alterations, and metabolic dysregulation, specifically in AUD patients with an elevated MCV. Understanding these mechanisms is crucial for developing targeted interventions and identifying biomarkers of alcohol-induced cellular damage. The complex interplay between oxidative stress, membrane composition, and cellular function illustrates how chronic alcohol exposure affects cellular physiology.

Humans↗
PubMedDate not supplied

Alcohol intoxication results in rapid loss in free magnesium in brain and disturbances in brain bioenergetics: relation to cerebrovasospasm, alcohol-induced strokes, and barbiturate anesthesia-induced deaths.

In vivo 31P-nuclear magnetic resonance (31P-NMR) spectroscopy and ion-selective electrode measurements were undertaken to determine if administration of acute doses of alcohol (ALC, 0.2-6.6 g/kg), and lethal doses of barbiturate anesthesia, exert any influence on: (1) brain cellular bioenergetics, intracellular free Mg ([Mg2+]i) and intracellular pH (pHi), and (2) serum levels of ionized Mg (IMg2+), ionized calcium (ICa2+) and K+. Approximately 20-30 min after intraperitoneal administration of ALC to anesthetized rats, brain phosphocreatine (PCr)/ATP and PCr/inorganic phosphate (P(i)) ratios dropped from 2.5 to 1.7 and from 6.6 to 2.2, respectively, P(i) rose 20-200% (depending upon ALC dose), and free ADP and creatine rose significantly. ALC induced rapid decreases in the cytosolic phosphorylation potential (CPP) and free energy of ATP hydrolysis (-delta G/delta E). Following ALC administration, brain [Mg2+]i dropped rapidly (within 4-30 min) and significantly; the greater the dose of ALC, the greater the loss in brain [Mg2+]. Correlations were found between [Mg2+]i, PCr/ATP, CPP and delta G/delta E after ALC but not in control brains. Rats that exhibited ALC-induced strokes and death (unlike barbiturate death) exhibited huge elevations in [Mg2+]i. Although ALC administration does not alter brain pHi at least (up to 70 min), ALC- and barbiturate-induced death produces rapid brain intracellular acidosis. Concomitant with ALC-induced alterations in [Mg2+]i and brain cellular bioenergetics, we noted that ALC administration results in rapid elevations in serum IMg2+ and K+ but not ICa2+. These results suggest that ALC administration and heavy or binge-drinking of ALC (1) can result in rapid alterations in brain bioenergetics, [Mg2+]i and pHi, and (2) result in rapid elevations in serum IMg2+ and K+ in rats. In addition, ALC- and barbiturate-induced deaths do not appear to produce identical alterations in brain bioenergetics and [Mg2+]i, and lastly binge or heavy drinking of ALC may result in stroke-like events and sudden death via rapid alterations in brain cellular bioenergetics.

Alcoholic Intoxication↗
PubMed1979

Alcohol-related diseases and carcinogenesis.

Possible mechanisms whereby alcohol abuse and alcohol-related diseases may promote the development of cancer are analyzed. The mechanisms discussed include: (a) contact-related local effects on the upper gastrointestinal tract; (b) the presence of low levels of carcinogens in alcoholic beverages; (c) induction of microsomal enzymes involved in carcinogen metabolism; (d) various types of cellular injury produced by ethanol and its metabolites and their relationship to cancer, particularly in the liver; (e) the nutritional disturbances frequently associated with alcohol abuse. The relationship between alcohol-induced cirrhosis and hepatocellular carcinoma is also discussed, and case histories of patients seen at the Bronx Veterans Administration Medical Center with hepatocellular carcinoma in the absence of cirrhosis are reviewed. Data are presented demonstrating the induction, by chronic ethanol consumption, of microsomal enzymes which convert procarcinogens to carcinogens. These data were derived from experiments in which the ability of microsomes isolated from liver, intestine, and lung tissues of ethanol-fed and control rats to activate several test carcinogens was examined in the Ames Salmonella-mutagenicity test. The hypothesis is presented that ethanol-mediated induction of enzyme systems which activate procarcinogens to carcinogens in various tissues contributes to the enhanced incidence of cancer in the alcoholic.

Alcoholism↗
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↗
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↗