scholarly journals Alcohol and hepatocarcinogenesis

2020 ◽  
Vol 26 (4) ◽  
pp. 736-741
Author(s):  
Makiko Taniai

An excessive alcohol intake may result in fatty liver, acute/chronic hepatitis, cirrhosis, and lead to hepatocellular carcinoma (HCC). The aim of this review is to clarify the present condition and the mechanisms of alcohol-related hepatocarcinogenesis and clinical risk factors for alcohol-related HCC. There are several possible mechanisms through which alcohol may induce hepatocarcinogenesis, including the mutagenic effects of acetaldehyde toxicity through the formation of protein and DNA adducts and the production of reactive oxygen species due to the excessive hepatic deposition of iron, changes to lipid peroxidation and metabolism, inflammation and an impaired immune response and modifications to DNA methylation. Furthermore, it has been reported that alcohol accelerates liver carcinogenesis through several signaling pathways including gut-liver axis. From a clinical perspective, it is well known that alcohol interacts with other factors, such as age, gender, viral hepatitis, obesity, and diabetes leading to an increased risk of HCC.

2019 ◽  
Vol 6 (1) ◽  
pp. e000260 ◽  
Author(s):  
Hiroshi Matsushita ◽  
Akinobu Takaki

BackgroundAlcohol is classified as a Group 1 carcinogen by the International Agency for Research on Cancer because it induces hepatocellular carcinoma (among other cancers) in humans. An excessive alcohol intake may result in fatty liver, acute/chronic hepatitis, and cirrhosis and eventually lead to hepatocellular carcinoma. It has been reported that alcohol abuse increases the relative risk of hepatocellular carcinoma by 3- to 10-fold.Aim and MethodsTo clarify the known mechanisms of alcohol-related carcinogenesis, we searched Pubmed using the terms alcohol and immune mechanism, alcohol and cancer, and immune mechanism and cancer and summarized the articles as a qualitative review.ResultsFrom a clinical perspective, it is well known that alcohol interacts with other factors, such as smoking, viral hepatitis, and diabetes, leading to an increased risk of hepatocellular carcinoma. There are several possible mechanisms through which alcohol may induce liver carcinogenicity, including the mutagenic effects of acetaldehyde and the production of ROS due to the excessive hepatic deposition of iron. Furthermore, it has been reported that alcohol accelerates hepatitis C virus-induced liver tumorigenesis through TLR4 signaling. Despite intense investigations to elucidate the mechanisms, they remain poorly understood.ConclusionThis review summarizes the recent findings of clinical and pathological studies that have investigated the carcinogenic effects of alcohol in the liver.


2015 ◽  
Vol 42 (5) ◽  
pp. 835-840 ◽  
Author(s):  
Shaowei Wu ◽  
Eunyoung Cho ◽  
Wen-Qing Li ◽  
Jiali Han ◽  
Abrar A. Qureshi

Objective.Alcohol intake has been associated with an increased risk of psoriasis. However, the association between alcohol intake and risk of psoriatic arthritis (PsA) has been unclear. We evaluated the association between alcohol intake and risk of incident PsA in a large cohort of US women.Methods.Our present study included a total of 82,672 US women who provided repeated data on alcohol intake over the followup period (1991–2005). Self-reported PsA was validated using the Psoriatic Arthritis Screening and Evaluation (PASE) questionnaire. Cox proportional hazards models were used to estimate the age-adjusted and multivariate-adjusted HR and 95% CI for the PsA in association with alcohol intake.Results.We documented 141 incident PsA cases during 14 years (1,137,763 person-yrs) of followup. Compared to non-drinkers, the multivariate HR for PsA were 0.70 (95% CI 0.48–1.01) for 0.1–14.9 g/day, 1.43 (95% CI 0.67–3.08) for 15.0–29.9 g/day, and 4.45 (95% CI 2.07–9.59) for ≥ 30.0 g/day of cumulative average alcohol intake. Risk estimates were generally consistent when using updated alcohol intake and baseline alcohol intake in 1991 as the exposures, and when the analysis was restricted to those who developed psoriasis during the followup.Conclusion.Excessive alcohol intake was associated with an increased risk of incident PsA in a cohort of US women.


Author(s):  
Erika N Aagaard ◽  
Brede Kvisvik ◽  
Mohammad O Pervez ◽  
Magnus N Lyngbakken ◽  
Trygve Berge ◽  
...  

Abstract Aims Increased left ventricular mechanical dispersion by 2D speckle tracking echocardiography predicts ventricular arrhythmias in ischaemic heart disease and heart failure. However, little is known about mechanical dispersion in the general population. We aimed to study mechanical dispersion in the general population and in diseases associated with increased risk of cardiovascular disease. Methods and results The present cross-sectional study consists of 2529 subjects born in 1950 included in the Akershus Cardiac Examination (ACE) 1950 study. Global longitudinal strain (GLS) was assessed from 17 strain segments, and mechanical dispersion calculated as the standard deviation of contraction duration of all segments. The cohort was divided according to the median value of mechanical dispersion, and multivariable linear regression models were performed with mechanical dispersion as the dependent variable. The prevalence of coronary artery disease (CAD), hypertension, obesity, and diabetes (P < 0.01 for all) was significantly higher in subjects with supra-median mechanical dispersion. In a multivariable clinical model, CAD (B = 7.05), hypertension (B = 4.15; both P < 0.001), diabetes (B = 3.39), and obesity (B = 1.89; both P < 0.05) were independently associated with increasing mechanical dispersion. When echocardiographic indices were added to the multivariable model, CAD (B = 4.38; P < 0.01) and hypertension (B = 2.86; P < 0.001) remained significant in addition to peak early diastolic tissue velocity e’ (B = −2.00), GLS (B = 1.68), and ejection fraction (B = 0.22; P < 0.001 for all). Conclusion In a general middle-aged population, prevalent CAD and hypertension were associated with increasing mechanical dispersion, possibly indicating elevated risk of fatal arrhythmias and sudden cardiac death. Albeit weaker, systolic and diastolic dysfunction, were also associated with increasing mechanical dispersion.


2021 ◽  
pp. 1-12
Author(s):  
L. Díaz de León-Martínez ◽  
C.M. López-Mendoza ◽  
Y. Terán-Figueroa ◽  
R. Flores-Ramírez ◽  
F. Díaz-Barriga ◽  
...  

Cervical cancer (CC) is one of the most serious threats to the lives of women; co-factors in addition to oncogenic human papillomavirus (HPV) infection may be important in causing CC. Women in Mexico are exposed to dietary aflatoxin B1, a potent carcinogen, which may act as a co-factor, in inducing progression to CC. Scarce studies are addressing environmental risks associated with the development of CC, thus the study aimed to establish a relationship between the presence of AFB1 and the detection of human papillomavirus in the genome of Mexican women. Forty samples from cervical tissue of women infected with HPV were obtained; positive results regarding the HPV type (16 and/or 18) were found in 92.5% women and the presence of AFB1-DNA adducts were detected in 77.5% of the same positive HPV samples. Detection of AFB1-DNA adducts and genomic concentrations were correlated with the detection of two oncogenic types of HPV 16 and 18. AFB1-DNA positivity and higher genomic concentrations of AFB1-DNA adducts were correlated with an increased risk of oncogenic detection of HPV in cervical samples from women in Mexico. As a secondary objective, a hypothetical interaction of the adducts with the NRF2 pathway has been proposed, therefore activation of p62 and in turn E6 and E7 (HPV proteins) would inhibit the formation of autophagosomes, which would result in a presence or recurrence of CC.


2021 ◽  
Author(s):  
Rea Mittal ◽  
Lilly Su ◽  
Devyani Ramgobin ◽  
Ashwani Garg ◽  
Rahul Jain ◽  
...  

Alcohol use disorder (AUD) is highly prevalent and can lead to many cardiovascular complications, including arrhythmias. Chronic alcohol use has a dose-dependent relationship with incidence of atrial fibrillation (AF), where higher alcohol intake (>3 drinks a day) is associated with higher risk of AF. Meanwhile, low levels of chronic alcohol intake (<1 drink a day) is not associated with increased risk of AF. Mechanistically, chronic alcohol intake alters the structural, functional and electrical integrity of the atria, predisposing to AF. Increased screening can help identify AUD patients early on and provide the opportunity to educate on chronic alcohol use related risks, such as AF. The ideal treatment to reduce risk of incident or recurrent AF in AUD populations is abstinence.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Donna M Buchanan ◽  
Surya Mundluru ◽  
James H O’Keefe ◽  
Kimberly J Reid ◽  
Fengmeng Tang ◽  
...  

Background: Prior studies show light to moderate alcohol use is associated with reduced mortality and cardiovascular events, whereas heavy use increases mortality and cardiovascular risks. The association of alcohol use and post-myocardial infarction (MI) symptoms is unknown. We explored the association between alcohol use and risk of having angina 1 year after an MI. Methods: Upon enrollment in the 19-center prospective PREMIER registry, acute MI patients (n=2481) were asked about alcohol use. Angina (any vs. none) was assessed at 1 year with the Seattle Angina Questionnaire. The association of alcohol use and 1-year angina was modeled using a hierarchical multivariable modified Poisson regression model. Results: Overall, 47% reported never drinking and others reported having the following # of drinks/day: 42% < 1; 6% 1 to 2; 3% > 2 to 4; 2% > 4. After adjusting for demographic, clinical, and treatment variables, patients that reported never drinking were 45% more likely to have angina than moderate drinkers (1 to 2 drinks/day). However, > drinks/day was associated with an 81% greater risk of angina than moderate alcohol use. Those drinking < 1 drink/day or > 2 to 4 per day had similar angina risk compared to moderate drinkers. Results did not vary by gender (p > .05 for interaction). Conclusions: This study extends prior evidence of a dose-dependent relationship between alcohol use and other cardiovascular benefits/risks to post-MI angina. Moderate alcohol consumption (1 to 2 drinks/day) was associated with reduced risk of angina 1 year after MI compared to abstinence or heavy alcohol consumption. Excessive alcohol use (>4 drinks/day) was associated with increased risk of angina.


Sign in / Sign up

Export Citation Format

Share Document