Alcohol and Liver Disease (original) (raw)
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Drug and Alcohol Review, 2021
IssuesAlcohol use has been shown to impact on various forms of liver disease, not restricted to alcoholic liver disease.ApproachWe developed a conceptual framework based on a narrative review of the literature to identify causal associations between alcohol use and various forms of liver disease including the complex interactions of alcohol with other major risk factors. Based on this framework, we estimate the identified relations for 2017 for the USA.Key FindingsThe following pathways were identified and modelled for the USA for the year 2017. Alcohol use caused 35 200 (95% uncertainty interval 32 800–37 800) incident cases of alcoholic liver cirrhosis. There were 1700 (uncertainty interval 1100–2500) acute hepatitis B and C virus (HBV and HCV) infections attributable to heavy‐drinking occasions, and 14 000 (uncertainty interval 5900–19 500) chronic HBV and 1700 (uncertainty interval 700–2400) chronic HCV infections due to heavy alcohol use interfering with spontaneous clearance. ...
Narrative review on alcoholic liver disease: from fibrosis to cancer
Digestive Medicine Research, 2021
Background and Objective: Chronic alcohol consumption results in fatty liver, steatohepatitis, fibrosis, cirrhosis and cancer. Ethanol stimulates hepatocarcinogenesis through hepatic fibrosis and through specific fibrosis independent mechanisms. This review tries to explain how fibrosis is initiated by ethanol and how it represents the basis for the development of hepatocellular cancer (HCC). In addition, it is illustrated how other ethanol specific mechanisms add their carcinogenic potential to this process. Ethanol-specific mechanisms such as oxidative stress, acetaldehyde and metabolic alterations damage hepatocytes with the activation of hepatic stellate cells (HSCs) and the initiation of the fibrotic process. In addition, ethanolmediated gut dysbiosis results in the uptake of endotoxins from the gut to the liver with the activation of Kupffer cells (KCs) and HSCs to secrete extracellular matrix (ECM). Ethanol also induces cytochrome P4502E1 (CYP2E1) to enhance its own oxidation. This induction has enormous negative consequences involved in hepatocarcinogenesis. Methods: According to the literature available on PubMed in English language from 1970 to 2021, this review summarizes mechanisms by which ethanol stimulates hepatic fibrogenesis linked to carcinogenesis and hepatic cancer development independent of fibrosis. Key Content and Findings: Chronic alcohol consumption with a daily quantity of more than 40 grams is associated with an increased risk for cirrhosis of the liver and finally hepatocellular cancer (HCC). In addition to cirrhosis various other ethanol-mediated mechanisms contribute to hepatic cancer development. Modifying risk factors include the amount of alcohol consumed, genetics, female gender, and other underlying liver diseases. Conclusions: The two major drivers of fibrogenesis and thus carcinogenesis are gut dysbiosis and oxidative stress due to the induction of cytochrome P4502E1 with its negative consequences, the generation of reactive oxygen species (ROS), which contribute to both fibrogenesis and carcinogenesis. In addition, the induction of CYP2E1 results in the activation of various pro-carcinogens and in the loss of retinoic acid. Ethanol also alters DNA-and histone methylation and acetylation with its impact on carcinogenesis and suppresses the immune response by various mechanisms. Most recent data implicate that the inhibition of CYP2E1 improves non-cirrhotic alcoholic liver disease (ALD). Clinically individuals with a daily intake of more than 40 grams ethanol should reduce their alcohol intake. If they are not able to do so, they should seek medical help for the treatment of their alcohol use disorder (AUD). For early detection of ALD they should undergo hepatic screening examinations.
Alcohol use disorder and the liver
Addiction, 2020
Alcohol use disorders (AUD) cause a range of physical harms, but the major cause of alcohol-related mortality is alcohol-related liver disease (ALD), in some countries accounting for almost 90% of alcohol-related deaths. The risk of ALD has an exponential relationship with increasing alcohol consumption, but is also associated with genetic factors, other lifestyle factors and social deprivation. ALD includes a spectrum of progressive pathology, from liver steatosis to fibrosis and liver cirrhosis. There are no specific treatments for liver cirrhosis, but abstinence from alcohol is key to limit progression of the disease. Over time, cirrhosis can progress (often silently) to decompensated cirrhosis and hepatocellular carcinoma (HCC). Liver transplantation may be suitable for patients with decompensated liver cirrhosis and may also be used as a curative intervention for HCC, but only for a few selected patients, and complete abstinence is a prerequisite. Patients with AUD are also at risk of developing alcoholic hepatitis, which has a high mortality and limited evidence for effective therapies. There is a strong evidence base for the effectiveness of psychosocial and pharmacological interventions for AUD, but very few of these have been trialled in patients with comorbid ALD. Integrated specialist alcohol and hepatology collaborations are required to develop interventions and pathways for patients with ALD and ongoing AUD.
Alcohol consumption is well entrenched in the fabric of many cultures especially in the western world. It is legal, readily available and relatively cheap. There is a rising incidence in consumption in the developing countries. This incidence has contributed to the dependence and behavioural anomalies associated with its excessive consumption. Sustained excessive alcohol consumption is a brain-centred behavioural disorder; it might lead to liver disease but also predisposes to development of cardiovascular, renal, neurological and endocrine disorders. Alcohol liver disease [ALD] remains an important complication and cause of morbidity and mortality from alcohol abuse. It is surprising then that less than 20% of heavy drinkers progress to advanced disease. The reason for this remains largely speculative. This article is a review of alcoholic liver disease.
Journal of Mind and Medical Sciences, 2019
Liver cirrhosis is a significant public health problem, being an important cause of mortality and morbidity, responsible for approximately 1.8% of the total number of deaths in Europe. Chronic alcohol consumption is the most common cause of liver cirrhosis in developed countries. Europe has the highest level of alcohol consumption among all the global World Health Organisation (WHO) regions. In this paper, we briefly review major factors leading to excessive alcohol consumption in order to draw attention to the fact that alcoholic liver cirrhosis is more than a simple liver disease, and if those risk/causal factors can be prevented, the incidence of this disease could be reduced greatly. Although excessive alcohol consumption is regarded as the cause of alcoholic liver cirrhosis, the etiology is complex, involving multiple factors that act in synchrony, and which, if prevented, could greatly reduce the incidence of this disease. Children of addicts are likely to develop an alcohol-related mental disorder; however, there is no "gene for alcoholism".
Alcohol-Related Liver Disease: Basic Mechanisms and Clinical Perspectives
International Journal of Molecular Sciences
Alcohol-related liver disease (ALD) refers to the liver damage occurring due to excessive alcohol consumption and involves a broad spectrum of diseases that includes liver steatosis, steatohepatitis, hepatitis, cirrhosis, and hepatocellular carcinoma (HCC). The progression of ALD is mainly associated with the amount and duration of alcohol usage; however, it is also influenced by genetic, epigenetic, and environmental factors. The definite diagnosis of ALD is based on a liver biopsy, although several non-invasive diagnostic tools and serum biomarkers have emerging roles in the early detection of ALD. While alcohol abstinence and nutritional support remain the cornerstone of ALD treatment, growing evidence has revealed that the therapeutic agents that target oxidative stress or gut-liver axis, inflammatory response inhibition, and liver regeneration enhancement also play a role in ALD management. Furthermore, microRNAs modulation and mesenchymal stem cell-based therapy have emerging ...
Alcohol Induced Fatty Liver: A Tragic Inception of Wrong Turn
2019
Alcohol is a noteworthy reason for liver cirrhosis in the Western world and records for most of instances of liver cirrhosis found in region general emergency clinics in the UK. Alcoholic liver disease is a term that incorporates the liver appearances of alcohol overconsumption, including fatty liver, alcoholic hepatitis, and constant hepatitis with liver fibrosis or cirrho-sis. As per the American Liver Foundation (ALF), somewhere in the range of 10 and 20 percent of substantial consumers will develop cirrhosis. The disease is a piece of a progression. It might begin with fatty liver disease, at that point advancement to alcoholic hepatitis, and after that to alcoholic cirrhosis. Be that as it may, it's conceivable an individual can develop alcoholic liver cirrhosis while never having alcoholic hepatitis. Symptoms of alcoholic liver cirrhosis regularly develop when an individual is between the ages of 30 and 40. All things considered, it takes around one hour for the body to utilize (separate) one standard beverage as characterized by U.S. rules (for example 12 ounces of 4.5% brew, 5 ounces of 11% wine, or 1.5 ounces of 35% alcohol). Utilization of 60-80 g every day (14 g is viewed as one standard beverage in the US, i.e., 1.5 fl oz hard alcohol, 5 fl oz wine, 12 fl oz lager; drinking a six-pack of brew day by day would be amidst the range) for a long time or more in men, or 20 g/day for ladies fundamentally builds the danger of hepatitis and fibrosis by 7% to 47%. Of all endless substantial consumers, just 15-20% develop hepatitis or cirrhosis, which can happen correspondingly or in progression. The purpose for is accepted to be the liver has gigantic ability to recover and notwithstanding when 75% of hepatocytes are dead, it keeps on working as should be expected. As indicated by NIAAA (1993), somewhere in the range of 10% and 35% of substantial consumers develop alcoholic hepatitis. While development of hepatitis isn't specifically identified with the portion of alcohol, a few people appear to be more prone to this response than others. This is called alcoholic steato-necrosis (Steatosis) and the inflammation seems to incline to liver fibrosis.