Diaz LE; Montero A; Gonzalez-Gross M; Vallejo AI; Romeo J; Marcos A. Influence of alcohol consumption on immunological status: A review. European Journal of Clinical Nutrition 56(Supplement) S50-S53, 2002. (16 refs.)
The aim of this review is to present and discuss the effect of different levels of alcohol consumption on the immune system. Not only the amount consumed but also the type of alcoholic beverage have to be taken into account in order to determine the consequences on activity, number, distribution, balance, interaction and response of immunocompetent cells. The association between alcohol exposure and the risk of developing an alcohol-related disease is multifactorial. In fact, age, gender, smoking habits, dietary intake and exercise are involved among other factors. The evaluation of the host cellular and humoral immune responses has shown that alcohol may induce some benefits when consumption is moderate. Moreover, those alcoholic beverages that contain antioxidants, such as red wine, could be protectors against immune cell damage. According to the literature consulted, the daily consumption of 10-12 g and 20-24 g of alcohol for women and men, respectively, is considered to be a moderate intake; the type of beverage has been established not to be important when defining moderation. Particular attention is often focused on the U- or J-shaped curve which also suggests that light to moderate drinking produces a protective effect. Such an inverse relationship indicates a reduction of risk for both light and moderate consumers and a higher risk not only for hard drinkers, but also for non- consumers. Copyright 2002, MacMillan Crest, Ltd.
Editor. Medical consequences of alcohol abuse. Alcohol Research & Health 24(1): 27-31, 2000. (3 refs.)
Griffiths HJ, Parantainen H, Olson P: Alcohol and bone disorders, Alcohol Health and Research World 17(4): 299–304, 1993.
Guidot DM; Hart CM. Alcohol abuse and acute lung injury: Epidemiology and pathophysiology of a recently recognized association. (review). Journal of Investigative Medicine 53(5): 235-245, 2005. (61 refs.)
Alcohol is the most commonly used and abused drug in the United States. The deleterious health effects of alcohol can be attributed both to its acute intoxicating effects, which result in temporary impairment of judgment and motor skills, and to its more chronic and toxic effects on the liver, pancreas, heart, and brain, all of which may result in irreversible organ damage. Although recognized for more than a century as a major risk factor for pneumonia, alcohol abuse was until recently perceived to have no significant effects on lung structure and/or function. However, within the past decade, epidemiologic studies have revealed that alcohol abuse independently increases the risk of acute respiratory distress syndrome (ARDS) two- to fourfold in patients with sepsis or trauma and may play a role in ARDS pathogenesis in as many as half of all patients with the syndrome. Although alcohol abuse alone does not cause acute lung injury, it renders the lung susceptible to dysfunction in response to the inflammatory stresses of sepsis, trauma, and other clinical conditions recognized to cause ARDS. Recent investigations in both animal models of chronic ethanol ingestion and in human subjects with a history of alcohol abuse have explored this previously unrecognized connection between alcohol and acute lung injury and have uncovered multiple derangements, which we now characterize as the "alcoholic lung." This review summarizes the epidemiologic association between alcohol abuse and acute lung injury and the recent experimental findings that are unraveling the underlying pathophysiology. Copyright 2005, Slack, Inc.
Gutjahr E; Gmel G; Rehm J. Relation between average alcohol consumption and disease: An overview. (review). European Addiction Research 7(3): 117-127, 2001. (161 refs.)
Objective: To conduct an overview of alcohol-related health consequences and to estimate relative risk for chronic consequences and attributable fractions for acute consequences. Methods: Identification of alcohol-related consequences was performed by means of reviewing and evaluating large-scale epidemiological studies and reviews on alcohol and health, including epidemiological contributions to major social cost studies. Relative risks and alcohol-attributable fractions were drawn from the international literature and risk estimates were updated, whenever possible, by means of meta-analytical techniques. Results: More than 60 health consequences were identified for which a causal link between alcohol consumption and outcome can be assumed. Conclusions: Future research on alcohol-related health consequences should focus on standardization of exposure measures and take into consideration both average volume of consumption and patterns of drinking. Copyright 2001, S. Karger Publishers
Halsted CH. Nutrition and alcoholic liver disease. (review) Seminars in Liver Disease 24(3): 289-304, 2004. (137 refs.)
Malnutrition is a common finding in chronic alcoholics, and protein calorie malnutrition (PCM) is universal and predictive of survival in patients with established alcoholic liver disease (ALD). These patients also demonstrate frequent deficiencies of folate, thiamine, pyridoxine, and vitamin A, which enhance the likelihood of anemia, altered cognitive states, and night blindness. The etiologies of malnutrition in ALD patients are multiple and interactive and include anorexia with inadequate dietary intake, abnormal digestion of macronutrients and absorption of several micronutrients, increased skeletal and visceral protein catabolism, and abnormal interactions of ethanol and lipid metabolism. Numerous, and mostly inadequately controlled, studies have evaluated the potential efficacies of oral, enteral, and parenteral nutrition approaches to treatment of ALD, with mixed results on liver function, clinical improvements, and short- or long-term survival. Targeted metabolic treatments include supplementation with S-adenosylmethionine (SAM) or phosphatidylcholine derivatives, each with promising experimental bases but inconclusive clinical trials. Copyright 2004, Thieme Medical Publications
Henry JA. Management of drug abuse emergencies. Journal of Accident & Emergency Medicine 13(6): 370-372, 1996. (17 refs)
This provides a succinct overview of the presentation and management of drug abuse emergencies as these occur in emergency services. There are separate sections that address opioids, benzodiazepines, cocaine, LSD, amphetamines, and ecstasy (amphetamine derivatives.) There is also attention directed to initial assessment, signs and symptoms suggestive of drug use, and the likely range of purity different drugs. The issues associated with body stuffing (swallowing drugs to avoid apprehension) and body packing (ingestion of drugs or insertion into body cavities as part of drug trafficking) are also noted. Copyright 1998, Project Cork
Henry JA. Metabolic consequences of drug misuse. British Journal of Anaesthesia 85(1): 136-142, 2000. (49 refs.)
Metabolic consequences of drug misuse are not uncommon, and are increasing as illicit drug use becomes more widespread. Although the range of medical problems produced is very wide, metabolic problems most commonly occur with heroin, cocaine, and the ecstasy group of drugs, which are the main focus of this review. Discussion of heroin begins with a review of the emergency measures to be taken in response to overdose. It is also noted that a substantial number of deaths associated with heroin may be due to anaphylactoid reactions in part due to contaminants. Rhabdomyolosis is a serious consequence of overdose and associated damage can lead to renal failure and require dialysis. Alcohol is a common cofactor in rhabdomyolosis. Hyperkalaemia and hypocalcaemia are commonly part of the picture. Heroin leucoencephalopathy is also noted, that has been associated with smoking heroin, and caused 11 deaths in the Netherlands in the mid 1980s a contaminant, never identified was the suspected cause. Medical emerencies associated with the use of ecstasy are reviewed: hyperthermic collapse, cardiovascular collape, disseminated intravascular coagulation, rhabdomyolosis, and acute renal failure. The management of the hyperthermic patient is reviewed, followed by a discussion of liver damage and also hyponatraemia. The metabolic effects of cocaine use are then reviewed, again including rhabdomyolosis, hyperthermia, and cardiovascular incidents. Copyright 2000, Macmillan Journals
Joshi PC; Guidot DM American Journal of Physiology and Lung Cell Molecular Physiology 292: L813-L823, 2007. (84 refs)
Epidemiological evidence gathered only in the past decade reveals that alcohol abuse independently increases the risk of developing the acute respiratory distress syndrome by as much as three- to fourfold. Experimental models and clinical studies are beginning to elucidate the mechanisms underlying this previously unrecognized association and are revealing for the first time that chronic alcohol abuse causes discrete changes, particularly within the alveolar epithelium, that render the lung susceptible to acute edematous injury in response to sepsis, trauma, and other inflammatory insults. Recent studies in relevant animal models as well as in human subjects are identifying common mechanisms by which alcohol abuse targets both the alveolar epithelium and the alveolar macrophage, such that the risks for acute lung injury and pulmonary infections are inextricably linked. Specifically, chronic alcohol ingestion decreases the levels of the antioxidant glutathione within the alveolar space by as much as 80-90%, and, as a consequence, impairs alveolar epithelial surfactant production and barrier integrity, decreases alveolar macrophage function, and renders the lung susceptible to oxidant-mediated injury. These changes are often subclinical and may not manifest as detectable lung impairment until challenged by an acute insult such as sepsis or trauma. However, even otherwise healthy alcoholics have evidence of severe oxidant stress in the alveolar space that correlates with alveolar epithelial and macrophage dysfunction. This review focuses on the epidemiology and the pathophysiology of alcohol-induced lung dysfunction and discusses potential new treatments suggested by recent experimental findings. Copyright 2007, American Physiological Society
Kosten TR; O'Connor PG. Management of drug and alcohol withdrawal. (review) New England Journal of Medicine 348(18): 1786-1795, 2003. (67 refs)
|This review covers the general presentation and management of withdrawal from sedatives (alcohol and benzodiazepines), opiates, and stimulants, and considers the role of the generalist physician and referral versus direct treatment.
Lingford-Hughes AR; Welch S; Nutt DJ. Evidence-based guidelines for the pharmacological management of substance misuse, addiction and comorbidity: Recommendations from the British Association for Psychopharmacology. (review). Journal of Psychopharmacology. 18(3): 293-335, 2004. (403 refs.)
The British Association for Psychopharmacology guidelines for the treatment of substance misuse, addiction and comorbidity with psychiatric disorders primarily focus on their pharmacological management. They are based explicitly on the available evidence and presented as recommendations to aid clinical decision making for practitioners alongside a detailed review of the evidence. A consensus meeting, involving experts in the treatment of these disorders, reviewed key areas and considered the strength of the evidence and clinical implications. The guidelines were drawn up after feedback from participants. The guidelines primarily cover the pharmacological management of withdrawal, short- and long-term substitution, maintenance of abstinence and prevention of complications, where appropriate, in substance misuse, addiction and comorbidity with psychiatric disorders. Copyright 2004, Sage Publications
Levitsky J; Mailliard ME. Diagnosis and therapy of alcoholic liver disease. (review) Seminars in Liver Disease 24(3): 233-247, 2004. (173 refs.)
Alcoholic liver disease (ALD) presents considerable challenges to clinicians. Screening for alcohol abuse and alcoholism should be routine and repeated annually with close attention to signs and symptoms of liver disease. In patients with evidence of liver dysfunction or injury, consideration should be given to performance of liver biopsy for diagnosis and prognosis and prior to initiation of medication with the potential for significant side effects. Therapy depends on the spectrum of pathological liver injury: alcoholic fatty liver, alcoholic hepatitis, and cirrhosis. Abstention is the foundation of therapy for an alcohol problem. Alcoholic fatty liver should improve with abstention, but the similarity to the pathogenesis of nonalcoholic fatty liver and potential for progressive injury merits consideration of lipotropic agents. The continuing mortality, poor acceptance of corticosteroids, and identification of tumor necrosis factor-alpha (TNF-alpha) as an integral component has led to studies of pentoxifylline and, recently, anti-TNF antibody to neutralize cytokines in the therapy of severe alcoholic hepatitis. Antioxidant therapy of alcoholic cirrhosis has significant promise but will require large clinical trials. Copyright 2004, Thieme Medical Publishing
McLellan AT. Is addiction an illness: Can it be treated? (review) Substance Abuse 23(3 Supplement): 67-94, 2002. (199 refs.)
This chapter consider the questions regarding the effectiveness of treatment from several perspectives, and the evidence available in each area. It begins by exploring if dependence is an illness. In doing so it considers if it can be reliably diagnosed, if it has a a predictable course, and are there physiological changes that occur. It then examines evidence for the efficacy of medications and medically oriented behavioral interventions. The next section reviews the research on specific treatment elements, covering th past 15 years. The final section discusses why addiction medicine is perceived as less effective than care of other medical disorders. Comparisons are made to other medical disorders. Copyright 2002, Project Cork
Meister K; Whelan E; Kava R. The health effects of moderate alcohol intake in humans: An epidemiologic review. Critical Reviews in Clinical Laboratory Sciences 37(3): 261-296, 2000. (193 refs.)
A large body of scientific evidence associates the moderate intake of alcohol with reduced mortality among middle-aged and older people in industrialized societies. This association is due largely to a reduced risk of death from coronary hart disease, which appears to outweigh any possible adverse effects of moderate drinking. The regular consumption of small amounts of alcohol is more healthful than the sporadic consumption of larger amounts. No beneficial effect of moderate drinking on mortality has been demonstrated in young adults (premenopausal women and men who have not reached their forties). It is theoretically possible that moderate drinking in young adulthood might reduce the risk of later heart disease; however, this has not been clearly demonstrated. For some individuals (e.g., those who cannot keep their drinking moderate, pregnant women, and those who are taking medications that may interact adversely with alcoholic beverages), the risks of alcohol consumption, even in moderation, outweigh any potential benefits. Because even small amounts of alcohol can impair judgement and coordination, no one should drink alcoholic beverages, even in moderation, before driving a motor vehicle or performing other activities that involve attention and skill. Copyright 2000, CRC Press, Inc
Meng Q; Gao B; Goldberg ID; Rosen EM; Fan SJ. Stimulation of cell invasion and migration by alcohol in breast cancer cells. Biochemical and Biophysical Research Communications 273(2): 448-453, 2000. (30 refs.)
Increasing epidemiological studies suggest that alcohol consumption confers a high risk for development of breast cancer. In this study, we found that biologically relevant concentrations of alcohol elicited a significant stimulation of cell adhesion, migration, and invasion in MCF-7 human breast cancer cells. Moreover, the promotion of invasion and migration potential by alcohol was associated with the significant decrease of E-cadherin, alpha, beta, and gamma three major catenin, and BRCA1 expression. In addition, an enhanced expression of BRCA1 significantly blocked alcohol-stimulated cell invasion. Thus, our present study suggests that alcohol as a breast cancer risk factor plays an important role not only in carcinogenesis, but also in promotion of cell invasion and migration. Copyright 2000, Academic Press, Inc.
National Institute on Alcohol Abuse and Alcoholism: Tenth special report to the U.S. Congress on alcohol and health, Rockville MD: National Institute on Alcohol Abuse and Alcoholism, 2000.
This in the 10th Special Report to the U.S. Congress on Alcohol and Health, mandated by the legislation that created the National Institute on Alcohol Abuse and Alcoholism. The intent is to summarize the knowledge base. It covers a range of topics from epidemiology, to genetics, neuroscience, toxicology, prevention, and treatment. The overview of current research is divided into eight chapters: Chapter 1 deals with drinking over the life span, and includes Issues of biology, behavior, and risk. Chapter 2 focuses on alcohol and the brain, neurosciences and neurobehavior. Chapter 3 considers genetic and psychosocial influences. Chapter 4 focuses upon medical consequences. Chapter 5 addresses prenatal alcohol exposure. Economical and health service issues are addressed in Chapter 6. Chapter 7 addresses prevention and is followed by treatment research. Copyright 2001, Project Cork
Nordstrom-Klee B; Delaney-Black V; Covington C; Ager J; Sokol R. Growth from birth onwards of children prenatally exposed to drugs: A literature review. Neurotoxicology and Teratology 24(4): 481-488, 2002 (47 refs.)
Reductions in birth weight and length have been independently attributed to prenatal exposure to alcohol, cigarettes and cocaine. While pregnant women often use multiple substances, studies have not consistently controlled for exposure to other agents or other important differences in maternal lifestyle associated with the use of these substances. Despite these difficulties, the preponderance of evidence suggests that prenatal alcohol and cocaine independently reduce birth measurements. This review synthesizes the scientific literature focusing on prenatal exposures and the relationship to child growth. First examined are studies that investigated the link between prenatal exposures and birth weight and length, followed by the effects of these substances on childhood growth. Studies vary in the number of subjects, cohort characteristics, measurement of exposure and control for potential confounders. Differences in sample characteristics and size, as well as degree of statistical control for potential confounders and the examination of moderating characteristics, have led to differing conclusions regarding the long-term effect of prenatal substance exposure on growth. Large-scale, well-designed studies are needed to clearly examine the unique contribution of both varying prenatal exposures and the magnitude and timing of these exposures on childhood growth deficits. Copyright 2002, Pergamon Press
Oscar-Berman M; Marinkovic K. Alcoholism and the brain: An overview. Alcohol Research & Health 27(2): 125-133, 2003. (28 refs)
Alcoholism can affect the brain and behavior in a variety of ways, and multiple factors can influence these effects. A person’s susceptibility to alcoholism–related brain damage may be associated with his or her age, gender, drinking history, and nutrition, as well as with the vulnerability of specific brain regions. Investigators use a variety of methods to study alcoholism–related brain damage, including examining brains of deceased patients as well as neuroimaging, a technique that enables researchers to test and observe the living brain and to evaluate structural damage in the brain. Public Domain