Abnormally fucosylated haptoglobin as a marker for alcoholic liver disease but not excessive alcohol consumption or non-alcoholic liver disease

1993 ◽  
Vol 219 (1-2) ◽  
pp. 177-182 ◽  
Author(s):  
W. Chambers ◽  
S. Thompson ◽  
A.W. Skillen ◽  
C.O. Record ◽  
G.A. Turner
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Alcoholic Liver Disease ◽  
Excessive Alcohol Consumption ◽  
Excessive Alcohol ◽  
Fucosylated Haptoglobin

scholarly journals A study of alanine aminotransferase - aspartate aminotransferase as a marker of advanced alcoholic liver disease

2020 ◽  
Vol 7 (4) ◽  
pp. 551
Author(s):  
Aravind G. N. ◽  
Abhilash K. ◽  
Syed Umar Farooq
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Chronic Liver Disease ◽  
Alcoholic Liver Disease ◽  
Alcohol Withdrawal ◽  
Chronic Liver ◽  
Outpatient Basis ◽  
Excessive Alcohol Consumption ◽  
Excessive Alcohol ◽  
The Mean

Background: Alcohol is one of the most common etiology for chronic liver disease. There are several enzymes which remain elevated in both excessive Alcohol consumption and Alcohol induced liver cirrhosis1.  But none is sensitive or specific.  The ratio of Aspartate transaminase (AST) with Alanine transaminase (ALT) is one of the best marker for alcohol liver disease. Current study mainly compares the ratio of AST/ALT with both Alcoholic liver disease and excessive Alcohol consumption patients.Methods: Observational, cross sectional study conducted on 50 patients diagnosed with alcoholic liver disease and 50 patients of alcohol withdrawal syndrome.  Either admitted or seen on outpatient basis at Bangalore medical college and research institute and data was compared among the groups and appropriate statistical methods are applied.Results: The mean ratio of AST/ALT ratio in 50 patients of alcoholic liver disease group was 3.45, whereas the mean ratio in 50 patient of alcohol withdrawal was about 99. When compared statistically this ratio was significant in chronic liver disease group.Conclusions: Most of the patients with heavy alcohol drinking had high AST and alt levels. But ratio of AST/ALT levels was significant high and suggest chronic liver disease secondary to alcohol.

scholarly journals Genetic and Epigenetic Modifiers of Alcoholic Liver Disease

2018 ◽  
Vol 19 (12) ◽  
pp. 3857 ◽  
Author(s):  
Marica Meroni ◽  
Miriam Longo ◽  
Raffaela Rametta ◽  
Paola Dongiovanni
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Alcoholic Liver Disease ◽  
Complex Disease ◽  
Wide Spectrum ◽  
Association Studies ◽  
Phenotypic Variability ◽  
Genome Wide Association Studies ◽  
Epigenetic Factors ◽  
Excessive Alcohol Consumption

Alcoholic liver disease (ALD), a disorder caused by excessive alcohol consumption is a global health issue. More than two billion people consume alcohol in the world and about 75 million are classified as having alcohol disorders. ALD embraces a wide spectrum of hepatic lesions including steatosis, alcoholic steatohepatitis (ASH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). ALD is a complex disease where environmental, genetic, and epigenetic factors contribute to its pathogenesis and progression. The severity of alcohol-induced liver disease depends on the amount, method of usage and duration of alcohol consumption as well as on age, gender, presence of obesity, and genetic susceptibility. Genome-wide association studies and candidate gene studies have identified genetic modifiers of ALD that can be exploited as non-invasive biomarkers, but which do not completely explain the phenotypic variability. Indeed, ALD development and progression is also modulated by epigenetic factors. The premise of this review is to discuss the role of genetic variants and epigenetic modifications, with particular attention being paid to microRNAs, as pathogenic markers, risk predictors, and therapeutic targets in ALD.

scholarly journals Crosstalk between Oxidative Stress and Inflammatory Liver Injury in the Pathogenesis of Alcoholic Liver Disease

2022 ◽  
Vol 23 (2) ◽  
pp. 774
Author(s):  
Yoon Mee Yang ◽  
Ye Eun Cho ◽  
Seonghwan Hwang
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Inflammatory Responses ◽  
Tissue Injury ◽  
Pathological Features ◽  
Excessive Alcohol Consumption ◽  
Excessive Alcohol ◽  
The Relationship

Alcoholic liver disease (ALD) is characterized by the injury, inflammation, and scarring in the liver owing to excessive alcohol consumption. Currently, ALD is a leading cause for liver transplantation. Therefore, extensive studies (in vitro, in experimental ALD models and in humans) are needed to elucidate pathological features and pathogenic mechanisms underlying ALD. Notably, oxidative changes in the liver have been recognized as a signature trait of ALD. Progression of ALD is linked to the generation of highly reactive free radicals by reactions involving ethanol and its metabolites. Furthermore, hepatic oxidative stress promotes tissue injury and, in turn, stimulates inflammatory responses in the liver, forming a pathological loop that promotes the progression of ALD. Accordingly, accumulating further knowledge on the relationship between oxidative stress and inflammation may help establish a viable therapeutic approach for treating ALD.

scholarly journals The effect of moderate alcohol drinking in nonalcoholic fatty liver disease

2020 ◽  
Vol 26 (4) ◽  
pp. 662-669
Author(s):  
Jong Hwa Choi ◽  
Won Sohn ◽  
Yong Kyun Cho
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Alcohol Consumption ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Moderate Alcohol Consumption ◽  
Excessive Alcohol Consumption ◽  
Nonalcoholic Fatty Liver ◽  
Safe Limits ◽  
Excessive Alcohol

Nonalcoholic fatty liver disease (NAFLD) is defined by fat accumulation in liver that is not caused by excessive alcohol consumption. Safe limits of alcohol consumption in NAFLD are usually defined as alcohol consumption of less than 210 g per week for men and 140 g per week for women (30 g/day in men, 20 g/day in women) and alcohol consumption below safe limits is generally regarded as moderate alcohol consumption. Many studies have investigated the effects of moderate alcohol consumption on NAFLD patients. Some studies showed that moderate alcohol consumption prevented the progression of fibrosis in the liver, whereas other reports showed worsening of fibrosis in the liver based on serologic, radiologic and liver biopsy findings compared with effects on total abstainers. NAFLD is also thought to be a hepatic manifestation of metabolic syndrome, and when combined with excessive alcohol consumption results in the development of components of metabolic syndrome and systemic harmful effects. The effects of moderate alcohol consumption on NAFLD have yet to be established.

scholarly journals Innate immunity in alcoholic liver disease

2011 ◽  
Vol 300 (4) ◽  
pp. G516-G525 ◽  
Author(s):  
Bin Gao ◽  
Ekihiro Seki ◽  
David A. Brenner ◽  
Scott Friedman ◽  
Jessica I. Cohen ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Liver Disease ◽  
Alcohol Consumption ◽  
Liver Fibrosis ◽  
Alcoholic Liver Disease ◽  
Chronic Viral Hepatitis ◽  
Western World ◽  
Excessive Alcohol Consumption ◽  
Alcoholic Steatohepatitis

Excessive alcohol consumption is a leading cause of chronic liver disease in the Western world. Alcohol-induced hepatotoxicity and oxidative stress are important mechanisms contributing to the pathogenesis of alcoholic liver disease. However, emerging evidence suggests that activation of innate immunity involving TLR4 and complement also plays an important role in initiating alcoholic steatohepatitis and fibrosis, but the role of adaptive immunity in the pathogenesis of alcoholic liver disease remains obscure. Activation of a TLR4-mediated MyD88-independent (TRIF/IRF-3) signaling pathway in Kupffer cells contributes to alcoholic steatohepatitis, whereas activation of TLR4 signaling in hepatic stellate cells promotes liver fibrosis. Alcohol consumption activates the complement system in the liver by yet unidentified mechanisms, leading to alcoholic steatohepatitis. In contrast to activation of TLR4 and complement, alcohol consumption can inhibit natural killer cells, another important innate immunity component, contributing to alcohol-mediated acceleration of viral infection and liver fibrosis in patients with chronic viral hepatitis. Understanding of the role of innate immunity in the pathogenesis of alcoholic liver disease may help us identify novel therapeutic targets to treat this disease.

scholarly journals Electrolyzed Hydrogen Water Protects against Ethanol-Induced Cytotoxicity by Regulating Aldehyde Metabolism-Associated Enzymes in the Hepatic Cell Line HepG2

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 801
Author(s):  
Satoshi Yano ◽  
Jinyun Wang ◽  
Shigeru Kabayama ◽  
Taichi Hara
Keyword(s):  
Liver Disease ◽  
Alcoholic Liver Disease ◽  
Molecular Hydrogen ◽  
Toxic Substance ◽  
Excessive Alcohol Consumption ◽  
Hydrogen Water ◽  
Hepatocellular Damage ◽  
Electrolytic Hydrogen ◽  
Excessive Alcohol ◽  
Serious Disease

Excessive alcohol consumption can cause multi-systemic diseases. Among them, alcoholic liver disease is the most frequent and serious disease. Electrolytic hydrogen water (EHW) is produced at the cathode during electrolysis of water and contains a large amount of molecular hydrogen and a low content of platinum nanoparticles with alkaline properties. In this study, we found that EHW inhibits ethanol-induced cytotoxicity by decreasing the intracellular acetaldehyde, a toxic substance produced by ethanol degradation, in hepatocyte cell lines HepG2. Analysis of the mechanism of action revealed that EHW inhibits the metabolism of ethanol to acetaldehyde by suppressing alcohol dehydrogenase. EHW also promotes the metabolism of acetaldehyde to acetic acid by activating aldehyde dehydrogenase, which plays to reduce aldehyde toxicity and intracellular reactive oxygen species in HepG2 cells. These functions were correlated with the concentration of molecular hydrogen in EHW, and were abolished by degassing treatment, suggesting that molecular hydrogen may contribute as a functional factor in the suppression of ethanol-induced hepatocellular damage. Furthermore, hydrogen water with high dissolved hydrogen molecule showed the same hepatocellular protective effect against ethanol as the EHW. These results suggest that EHW may be useful in the prevention of alcoholic liver disease.

Alcohol consumption patterns in heavy drinkers with and without alcoholic liver disease (ALD)

2001 ◽  
Vol 120 (5) ◽  
pp. A117-A117
Author(s):  
K DEAR ◽  
M BRADLEY ◽  
K MCCORMACK ◽  
R PECK ◽  
D GLEESON
Keyword(s):  
Liver Disease ◽  
Alcohol Consumption ◽  
Alcoholic Liver Disease ◽  
Consumption Patterns ◽  
Heavy Drinkers
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