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Chronic Alcohol Use (chronic + alcohol_use)
Selected AbstractsAlcohol and injuries: a review of international emergency room studies since 1995DRUG AND ALCOHOL REVIEW, Issue 2 2007CHERYL J. CHERPITEL Abstract This paper provides a review of emergency room (ER) studies on alcohol and injury, using representative probability samples of adult injury patients, and focuses on the scope and burden of the problem as measured by estimated blood alcohol concentration (BAC) at the time of the ER visit, self-report drinking prior to injury, violence-related injury and alcohol use disorders. A computerized search of the English-language literature on MEDLINE, PsychINFO and the National Institute on Alcohol Abuse and Alcoholism (NIAAA) Alcohol and Alcohol Problems Science Database (ETOH) was conducted for articles published between 1995 and 2005, using the following key descriptors: (1) emergency room/emergency department/accident and emergency, (2) alcohol/drinking and (3) injuries (intentional and unintentional). Findings support prior reviews, with injured patients more likely to be positive for BAC and report drinking prior to injury than non-injured, and with the magnitude of the association substantially increased for violence-related injuries compared to non-violence-related injuries. Indicators of alcohol use disorders did not show a strong association with injury. Findings were not homogeneous across studies, however, and contextual variables, including study-level detrimental drinking pattern, explained some of the variation. This review represents a broader range of ER studies than that reported previously, across both developed and developing countries, and has added to our knowledge base in relation to the influence of contextual variables on the alcohol-injury relationship. Future research on alcohol and injury should focus on obtaining representative samples of ER patients, with special attention to both acute and chronic alcohol use, and to organisational and socio-cultural variables that may influence findings across studies. In-depth patient interviews may also be useful for a better understanding of drinking in the injury event and associated circumstances. [source] Alcohol exposure and paracetamol-induced hepatotoxicityADDICTION BIOLOGY, Issue 2 2002STEPHEN M. RIORDAN In contrast, serious hepatotoxicity at recommended or near-recommended doses for therapeutic purposes has been reported, mainly from the United States and in association with chronic alcohol use, leading to the widely held belief that chronic alcoholics are predisposed to paracetamol-related toxicity at relatively low doses. Yet the effects of alcohol on paracetamol metabolism are complex. Studies performed in both experimental animals and humans indicate that chronic alcohol use leads to a short-term, two- to threefold increase in hepatic content of cytochrome P4502E1, the major isoform responsible for the generation of the toxic metabolite from paracetamol, although increased oxidative metabolism of paracetamol at recommended doses has not been demonstrated clinically. A reduced hepatic content of glutathione, required to detoxify the reactive metabolite, has been documented in chronic alcoholics, due probably to associated fasting and malnutrition, providing a metabolic basis for any possible predisposition of this group to hepatotoxicity at relatively low paracetamol doses. Simultaneous alcohol and paracetamol ingestion reduces oxidative metabolism of paracetamol in both rodents and humans, predominantly as a consequence of depletion in cytosol of free NADPH. The possibilities that chronic alcohol use may predispose to paracetamol-related hepatotoxicity and that alcohol taken with paracetamol may protect against it, based on these metabolic observations, are examined in this review. [source] Alcohol and Hepatitis C Virus,Interactions in Immune Dysfunctions and Liver DamageALCOHOLISM, Issue 10 2010Gyongyi Szabo Hepatitis C virus infection affects 170 million people worldwide, and the majority of individuals exposed to HCV develop chronic hepatitis leading to progressive liver damage, cirrhosis, and hepatocellular cancer. The natural history of HCV infection is influenced by genetic and environmental factors of which chronic alcohol use is an independent risk factor for cirrhosis in HCV-infected individuals. Both the hepatitis C virus and alcohol damage the liver and result in immune alterations contributing to both decreased viral clearance and liver injury. This review will capture the major components of the interactions between alcohol and HCV infection to provide better understanding for the molecular basis of the dangerous combination of alcohol use and HCV infection. Common targets of HCV and alcohol involve innate immune recognition and dendritic cells, the critical cell type in antigen presentation and antiviral immunity. In addition, both alcohol and HCV affect intracellular processes critical for hepatocyte and immune cell functions including mitochondrial and proteasomal activation. Finally, both chronic alcohol use and hepatitis C virus infection increase the risk of hepatocellular cancer. The common molecular mechanisms underlying the pathological interactions between alcohol and HCV include the modulation of cytokine production, lipopolysaccharide (LPS)-TLR4 signaling, and reactive oxygen species (ROS) production. LPS-induced chronic inflammation is not only a major cause of progressive liver injury and fibrosis, but it can also contribute to modification of the tissue environment and stem cells to promote hepatocellular cancer development. Alteration of these processes by alcohol and HCV produces an environment of impaired antiviral immune response, greater hepatocellular injury, and activation of cell proliferation and dedifferentiation. [source] Effect of Alcohol Consumption on CpG Methylation in the Differentially Methylated Regions of H19 and IG-DMR in Male Gametes,Implications for Fetal Alcohol Spectrum DisordersALCOHOLISM, Issue 9 2009Lillian A. Ouko Background:, Exposure to alcohol in utero is the main attributable cause of fetal alcohol spectrum disorders (FASD) which in its most severe form is characterized by irreversible behavioral and cognitive disability. Paternal preconception drinking is not considered to be a significant risk factor, even though animal studies have demonstrated that chronic paternal alcohol consumption has a detrimental effect on the physical and mental development of offspring even in the absence of in utero alcohol exposure. It has been documented that alcohol can reduce the levels and activity of DNA methyltransferases resulting in DNA hypomethylation and that reduced methyltransferase activity can cause activation of normally silenced genes. The aim of this study was to establish a link between alcohol use in men and hypomethylation of paternally imprinted loci in sperm DNA in genomic regions critical for embryonic development, thus providing a mechanism for paternal effects in the aetiology of FASD. Methods:, Sperm DNA from male volunteers was bisulfite treated and the methylation patterns of 2 differentially methylated regions (DMRs), H19 and IG-DMR, analyzed following sequencing of individual clones. The methylation patterns were correlated with the alcohol consumption levels of the volunteer males. Results:, There was a pattern of increased demethylation with alcohol consumption at the 2 imprinted loci with a significant difference observed at the IG-DMR between the nondrinking and heavy alcohol consuming groups. Greater inter-individual variation in average methylation was observed at the H19 DMR and individual clones were more extensively demethylated than those of the IG-DMR. CpG site #4 in the IG-DMR was preferentially demethylated among all individuals and along with the H19 DMR CpG site #7 located within the CTCF binding site 6 showed significant demethylation in the alcohol consuming groups compared with the control group. Conclusion:, This study demonstrates a correlation between chronic alcohol use and demethylation of normally hypermethylated imprinted regions in sperm DNA. We hypothesize that, should these epigenetic changes in imprinted genes be transmitted through fertilization, they would alter the critical gene expression dosages required for normal prenatal development resulting in offspring with features of FASD. [source] Influence of chronic alcohol abuse and ensuing forced abstinence on static subjective accommodation function in humansOPHTHALMIC AND PHYSIOLOGICAL OPTICS, Issue 3 2001Hugh Campbell Summary Purpose. Acute alcohol ingestion can change accommodation, but the long term effects of sustained alcohol consumption on accommodative function have not been studied in detail. This study was thus undertaken on individuals with a history of alcohol abuse. Methods. Thirty-seven male individuals aged 25,56 years (average 40 years) from an alcohol rehabilitation centre in Inverness, Scotland, were assessed on admission and after a week of forced abstinence. The results were compared to a paired age-matched set of control male subjects. The static amplitude of accommodation was measured by an RAF rule, and the pupil size measured with a pupil gauge. Results. On admission, the group mean measured amplitude of accommodation was 4.7±2.2 D (mean±SD). These values for the alcoholics were lower than age-matched controls (of5.9±2.9 D). The slope of the age-dependent decline in RAF rule accommodation measures was significantly smaller for the alcoholics compared to controls (at 0.215±0.027 D/year versus0.332±0.015 D/year, respectively; p <0.001), with the younger alcoholics showing a greater impairment. Following abstinence, there was no measurable change in accommodation measured, indicating the lower amplitude in the alcoholics was not attributable to circulatory alcohol levels. The resting pupil diameter in the alcoholics was4.37±0.63 mm compared to the controls of3.97±0.75 mm, with a higher incidence of small pupils (,3 mm) in the controls. Conclusions. The results indicate that chronic alcohol use can adversely affect subjective static accommodation, especially in younger alcoholics, as well as cause slight mydriasis. [source] Analysis of Prior Health System Contacts as a Harbinger of Subsequent Fatal Injury in American IndiansTHE JOURNAL OF RURAL HEALTH, Issue 1 2005Teri L. Sanddal BS ABSTRACT: Context: Many American Indian nations, tribes, and bands are at an elevated risk for premature death from unintentional injury. Previous research has documented a relationship between alcohol-related injury and subsequent injury death among predominately urban samples. The presence or nature of such a relationship has not been documented among American Indians living in the northern plains. Purpose: The purpose of this study was to identify and characterize any association between prior injury and/or alcohol use contacts with the Indian Health Service (IHS) and subsequent alcohol-related injury death that may suggest opportunities for mitigation. Methods: Death certificates of American Indians who died from injury (ICD-9-E 800-999) in a rural IHS area over 6 consecutive years were linked to IHS acute-care facility records and toxicology reports. Deaths and prior IHS contacts were stratified by alcohol use as a contributing factor. Of the 526 injury deaths involving American Indians in the IHS area studied, 411 (78%) were successfully linked to IHS records. One hundred fifty-two of these cases met the inclusion criteria, with an additional 98 cases identified as a comparison group. Findings: No differences in alcohol use at time of death between groups with and without prior health care contact (for injury or alcohol) could be determined (81% vs 73%). A significant relationship was found between previous visits for acute or chronic alcohol use and subsequent alcohol-related fatalities (P =.01). Conclusions: Based on these findings, injury-prevention activities in the population studied should be initiated at the time of any health-system contact in which alcohol use is identified. Intervention strategies should be developed that convey the immediate risk of death from injury in these patients. [source] | ||||||||||