[Alcohol-induced hematologic disorders].
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Alcoholism↗
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Results for “Alcohol-Induced Disorders”
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[Osteonecrosis, alcoholism and liver steatosis].
Ethylism represents at the present time one of the most frequent etiological factors of primitive osteonecrosis of the femoral head. In relation to a case of osteonecrosis of the femoral head associated with multiple bone infarcts in a chronic alcoholic, also presenting recurring jaundice, alcohol-sensitive hyperlipidaemia, and moderate anaemia, the authors review the role of fatty embolisms in the formation of primitive osteonecrosis of the femoral head. These fatty embolisms may be the result of alcohol-induced hyperlipidaemia, possibly an associated pancreatic disorders, or in particular of hepatic steatosis. A systematic histological study of 10 recent unselected cases of primitive osteonecrosis of the femoral head confirmed the extreme frequency of such embolisms (8 cases out of 10).
Adult↗
[The natural history of alcohol-induced pancreatitis (authors transl)].
Alcohol-induced pancreatitis (AIP), although essentially a chronic pathological disorder, covers a wide spectrum of clinical syndromes ranging from fulminating to more chronic and even painless varieties. The clinical features, complications and treatment of AIP are presented with special reference to differences between the clinically acute and chronic forms of the disease.
Abdomen, Acute↗
Psychiatric manifestations of Cushing's syndrome: response to lowering of plasma cortisol.
The incidence of psychiatric abnormalities has been assessed in 38 patients with Cushing's syndrome and two with alcohol-induced pseudo-Cushing's syndrome. Twenty-six patients were examined by one of us using a standardized psychiatric interview, and this group included all those with severe to moderate psychiatric disorders. Depression was the commonest symptom: five patients (13%) were markedly or severely depressed, four (10%) were moderately depressed and 13 (32%) were mildly depressed. Four patients exhibited other, non-depressive psychiatric symptoms and only 14 (35%) were judged free from psychiatric abnormality. The first line of treatment was to reduce the circulating cortisol level either by adrenalectomy or by treatment with oral metyrapone; both patients with alcohol-induced pseudo-Cushing's syndrome were treated by alcohol withdrawal. Once the plasma cortisol level was successfully controlled, depressive symptoms were relieved in all five patients with marked or severe depression and in three of the four who were moderately depressed. Mild depressive symptoms were relieved in six of the 13 affected. It is concluded that metyrapone may be of considerable value in the management of the acute psychiatric states which may occur in Cushing's syndrome and these findings are discussed in the light of their possible pathogenesis.
Adolescent↗
Serum beta2-microglobulin in liver disease.
The concentration of beta 2-microglobulin in serum was determined in seventy-one patients with various liver disorders. Elevated values were found in most patients with chronic active or chronic persistent hepatitis and in over 80% of patients with alcohol-induced liver cirrhosis. In contrast, patients with alcohol-induced fatty liver, the serum beta 2-microglobulin concentrations were mostly within the normal range. Significant correlation (P less than 0.001) was noted between the elimination rate of galactose from blood and the serum beta 2-microglobulin concentration in patients with alcoholic liver damage but not in patients with chronic hepatitis. The reasons for the increased S-beta 2-microglobulin concentrations in liver diseases are unknown. Several explanations including a release of beta 2-microglobulin from necrotic liver cells or an increased synthesis of beta 2-microglobulin consequent to inflammation in the liver are possible. Alternatively, raised beta 2-microglobulin levels may reflect the hepatic synthesis during reparative growth.
Adult↗
Enhancement of ethonol-induced withdrawal convulsions by blockade of 5-hydroxytryptamine receptors.
Male Swiss-Webster mice were made physically dependent on ethanol using the ethanol vapour inhalation technique. Animals pretreated with methysergide, a known 5-hydroxytryptamine receptor blocking agent, had significantly greater alcohol-induced withdrawal convulsions than saline pretreated controls. These findings suggest that the reduction of 5-HT at receptor sites may result in the augmentation of the withdrawal convulsions.
Animals↗
Causal effects of cholelithiasis on hepatopancreatobiliary diseases: a multi-cohort Mendelian randomization study.
BACKGROUND: Cholelithiasis is commonly associated with multiple hepatopancreatobiliary diseases, yet whether these relationships reflect causal mechanisms or shared risk factors remains unclear. METHODS: We performed a phenome-oriented two-sample Mendelian randomization (MR) analysis to evaluate the causal impact of genetic liability to cholelithiasis across hepatopancreatobiliary outcomes. Independent genome-wide significant variants were selected as instrumental variables. Primary analyses used inverse variance weighting, complemented by sensitivity analyses, reverse MR, and multivariable MR adjusting for body mass index (BMI). RESULTS: Genetic predisposition to cholelithiasis was associated with increased risk of acute pancreatitis and extrahepatic cholangiocarcinoma (eCCA), with consistent directionality across datasets.The association with acute pancreatitis was interpreted as a positive control, whereas the null association with alcohol-induced acute pancreatitis served as a negative control. No causal association was observed for portal vein thrombosis. Sensitivity analyses, including MR-PRESSO and MR Steiger filtering, supported the robustness and directionality of the causal estimates. Reverse MR analyses showed no consistent evidence supporting reverse causality. Multivariable MR indicated that observed effects were not fully explained by BMI-related pathways. CONCLUSION: These findings suggest that cholelithiasis susceptibility may contribute to the broader hepatopancreatobiliary disease network, extending its clinical relevance beyond a localized biliary disorder.
Mendelian Randomization Analysis↗
Polygenic Susceptibility in Peripartum, Alcohol-Induced, and Cancer Therapy-Related Cardiomyopathies.
IMPORTANCE: Rare monogenic variants linked to nonischemic dilated cardiomyopathy (DCM) are enriched among individuals with secondary cardiomyopathies, such as peripartum (PPCM), alcohol-induced (ACM), and cancer therapy-related (CCM) cardiomyopathies. However, it remains unclear whether a polygenic predisposition to DCM also contributes to these conditions. OBJECTIVE: To assess the association of a DCM polygenic score with PPCM, ACM, and CCM, and to evaluate the contributions of monogenic and polygenic susceptibilities to these secondary cardiomyopathies. DESIGN, SETTING, AND PARTICIPANTS: This was a retrospective genetic association analysis of data from the Mass General Brigham (MGB) Biobank (n = 42 137, 2008-2025), with replication in the UK Biobank (n = 295 160, 2005-2010), FinnGen (n = 417 950, 2017-2025), and the Veterans Affairs Million Veteran Program (n = 516 066, 2011-2025). In MGB Biobank, medical records were reviewed to ascertain secondary cardiomyopathy cases and antecedent clinical risk factors. EXPOSURES: DCM polygenic risk score and DCM monogenic variants. MAIN OUTCOMES AND MEASURES: The primary outcomes were the association of the DCM polygenic risk score with PPCM, ACM, and CCM and the prevalence of monogenic variants and a high polygenic score among individuals with cardiomyopathy. RESULTS: The mean (SD) age in the MGB Biobank was 55.7 (17.0) years at enrollment, and 24 551 (58.3%) were female. Across the 4 study cohorts, 3414 individuals with secondary cardiomyopathy were identified, including 70 with PPCM, 2281 with ACM, and 1063 with CCM. The DCM polygenic score was associated with PPCM (odds ratio [OR], 1.82 per SD; 95% CI, 1.43-2.30), ACM (OR, 1.56; 95% CI,1.34-1.82), and CCM (OR, 1.64; 95% CI,1.24-2.15) (all with P < .001). Monogenic variants were enriched but present in 7 of 113 individuals with medical record-reviewed cardiomyopathy in MGB, while 66 had a high polygenic score, which conferred an approximately 3-fold increased odds of cardiomyopathy. Most individuals with cardiomyopathy lacked antecedent clinical risk factors. CONCLUSIONS AND RELEVANCE: In this cohort study, individuals with PPCM, ACM, and CCM were enriched for monogenic DCM variants and a high DCM polygenic score, suggesting a shared genetic susceptibility influenced by distinct environmental precipitants. These findings support a shared genetic architecture between secondary cardiomyopathies and DCM, although additional work with larger numbers of individuals with cardiomyopathy is needed to confirm these findings.
Humans↗
Corneal endothelial anomalies in the fetal alcohol syndrome.
The fetal alcohol syndrome involves various neural crest-derived structures thus causing systemic and ocular malformations. This study investigated anomalies of the corneal endothelium, a neural crest-derived tissue, in eight children affected by fetal alcohol syndrome without known anterior segment anomalies. We performed specular biomicroscopy on the central corneal endothelium. The data were then compared with those from 80 age-matched healthy children, applying the same methods. Significant differences were found between patients with fetal alcohol syndrome and healthy subjects for mean cell density (P = .032), polymegethism (P = .000), and percentage of hexagonal cells (P = .000). We also found a close correlation between endothelial anomalies and auditory dysfunction in the patients with fetal alcohol syndrome. These alterations may be a consequence of alcohol-induced toxic effects on neural crest cells destined to form both the corneal endothelium and the organ of Corti in the same embryogenic period.
Adolescent↗
Effects of combined pre- and postnatal ethanol exposure (three trimester equivalency) on glial cell development in rat optic nerve.
This study evaluated the effects of a combined gestational and 10 day postnatal alcohol exposure (human three trimester equivalency) on the development of glial cells in the rat optic nerve. Pregnant rats were exposed to alcohol via a liquid diet, then their pups were artificially reared and further exposed to alcohol for 10 postnatal days via a gastrostomy fed liquid diet. Control animals, born of pair fed dams, were artificially reared on pair fed isocaloric diets. Optic nerve tissues were prepared for light and electron microscopic studies from animals on gestational days (G) 15 and 20 and postnatal days (P) 5, 10, 15, 20 and 90. There were fewer glial cells per cross-section on day 15 and the cross-sectional areas of optic nerves were smaller on days G20, P15 and P90 in the ethanol exposed animals. There was an alcohol-induced delay in the appearance of immature cells within the oligodendroglia lineage and a decrease in the number of oligodendroglia present at 15 and 20 days, indicating a delay in the maturation of oligodendroglial cells. These effects were compensated for by 90 days. Maturation of the astrocytic cell lineage was generally unaffected by the alcohol although there was evidence of increased numbers of cells in the lineage. There was no consistent indication of alcohol-induced degeneration of glial cells or their organelles. Thus, alcohol exposure for all of gestation and 10 postnatal days in the rat causes a delay in oligodendrocyte maturation but appears to have no long-term effects on the glial cell population of the optic nerve. Such a delay, by contributing to delays in myelin development, could help to explain some of the neurological dysfunctions associated with developmental alcohol exposures.
Aging↗
The effect of prenatal alcohol exposure on attention in the rat.
The effect of prenatal exposure to alcohol on the development of basal heart rate and on the elicitation and habituation of the heart rate orienting response was examined in three experiments with rats. In all experiments, Etoh dams consumed large, daily amounts of alcohol and their weight gain during pregnancy was less than that of ad lib or pairfed dams. In addition, Etoh-exposed pups weighed less and grew more slowly than their ad lib or pairfed counterparts. Although prenatal exposure to alcohol had a significant effect on the ontogeny of basal heart rate, there was no effect on the magnitude of the heart-rate response to a novel olfactory stimulus or on habituation of the heart-rate response to that stimulus. Implications of the present findings for models of alcohol-induced attention deficits are discussed.
Animals↗
Drug- and alcohol-induced psychiatric syndromes.
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Drug Prescriptions↗
Alcohol and nutrition.
Alcoholic patients frequently have evidence of nutritional deficiency the consequences of which may be seen in all systems of the body. Alcoholism is theoretically a completely preventable disorder which requires more attention by the general public, practising physicians and research workers. Rehabilitation of the established alcoholic will sometimes be limited by failure to modify behaviour or because of nutritionally induced brain damage but we are beginning to understand some of the mechanisms by which malnutrition evolves (Figure 2). Better methods must be developed to limit alcohol-induced tissue injury in patients whose drinking cannot be controlled. The final mechanisms of liver injury remain to be established. Cirrhosis may be induced in animals ingesting a good diet but this does not ensure adequate delivery and utilization of nutrients at the subcellular level. Cirrhosis takes a long time to evolve and the natural history, including longitudinal nutritional profiles in man, has not been established. Therefore, although normal liver morphology is sometimes seen in alcoholics with gross stigmata of malnutrition suggesting that factors other than malnutrition are important, it may be that critical nutrients have not been deficient for long enough in these individuals or severe depletion has been intermittent. Whether or not malnutrition is of decisive importance in the toxicity of alcoholic liver injury in man, adequate replacement is essential for protection and repair of liver cells. Established daily minimal requirements are not adequate for patients with active liver disease. Hepatocyte injury reduces the capacity of this major storage site and causes release of vitamins (co-enzymes) into the circulation in the form of holoenzymes. Liver damage reduces the conversion of nutrients into their metabolically useful forms required for catabolic processes and to meet increased needs for DNA/RNA synthesis necessary for repair of damaged cells and to replace necrotic cells. The choice and route of therapy must take account of the patient's metabolic needs and their absorptive defects. The effects of alcohol and maternal undernutrition on the fetus/neonate may cause intra-uterine death or varying degrees of brain damage, thus limiting the potential of the next generation.
Alcoholism↗
Storage and retrieval processes of alcohol-induced amnesia.
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Adolescent↗
Isolated corticotrophin-deficiency found through alcohol-induced hypoglycemic coma.
A case of hypoglycemic coma after alcohol ingestion was observed in a chronic alcoholic. Upon close examination isolated corticotrophin-deficiency was found. It is suggested that ethanol-induced hypoglycemia may be consistent with dysfunction of mitochondria in hepatic cells and that there may be disorder of the hypothalamus in the chronic drinker.
Adrenocorticotropic Hormone↗
Major depression or alcohol-induced organic affective syndrome?
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Alcoholism↗
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↗
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↗