25 January 2023 In Liver Disease

Alcohol use and metabolic syndrome are highly prevalent in the population and frequently co-exist. Both are implicated in a large range of health problems, including chronic liver disease, hepatocellular carcinoma, and liver-related outcomes (i.e. decompensation or liver transplantation). Studies have yielded mixed results regarding the effects of mild-moderate alcohol consumption on the risk of metabolic syndrome and fatty liver disease, possibly due to methodological differences. The few available prospective studies have indicated that mild-moderate alcohol use is associated with an increase in liver-related outcomes. This conclusion was substantiated by systems biology analyses suggesting that alcohol and metabolic syndrome may play a similar role in fatty liver disease, potentiating an already existing dysregulation of common vital homeostatic pathways. Alcohol and metabolic factors are independently and jointly associated with liver-related outcomes. Indeed, metabolic syndrome increases the risk of liver-related outcomes, regardless of alcohol intake. Moreover, the components of metabolic syndrome appear to have additive effects when it comes to the risk of liver-related outcomes. A number of population studies have implied that measures of central/abdominal obesity, such as the waist-to-hip ratio, can predict liver-related outcomes more accurately than BMI, including in individuals who consume harmful quantities of alcohol. Many studies even point to synergistic interactions between harmful alcohol use and many metabolic components. This accumulating evidence showing independent, combined, and modifying effects of alcohol and metabolic factors on the onset and progression of chronic liver disease highlights the multifactorial background of liver disease in the population. The available evidence suggests that more holistic approaches could be useful for risk prediction, diagnostics and treatment planning.

23 November 2022 In Liver Disease

Heavy alcohol consumption is a major cause of morbidity and mortality. Globally, alcohol per-capita consumption rose from 5.5 litres in 2005 to 6.4 litres in 2016 and is projected to increase further to 7.6 litres in 2030. In 2019, an estimated 25% of global cirrhosis deaths were associated with alcohol. The global estimated age-standardized death rate (ASDR) of alcohol-associated cirrhosis was 4.5 per 100,000 population, with the highest and lowest ASDR in Africa and the Western Pacific, respectively. The annual incidence of hepatocellular carcinoma (HCC) among patients with alcohol-associated cirrhosis ranged from 0.9% to 5.6%. Alcohol was associated with approximately one-fifth of global HCC-related deaths in 2019. Between 2012 and 2017, the global estimated ASDR for alcohol-associated cirrhosis declined, but the ASDR for alcohol-associated liver cancer increased. Measures are required to curb heavy alcohol consumption to reduce the burden of alcohol-associated cirrhosis and HCC. Degree of alcohol intake, sex, older age, obesity, type 2 diabetes mellitus, gut microbial dysbiosis and genetic variants are key factors in the development of alcohol-associated cirrhosis and HCC. In this Review, we discuss the global epidemiology, projections and risk factors for alcohol-associated cirrhosis and HCC.

27 October 2022 In Liver Disease

BACKGROUND: Although alcohol-related liver disease (ALD) is a global health threat, there are no specific effective treatments for it. Thus, efforts at preventing ALD are important and could be enhanced by using strategies based on validated risk and protective factors for the disease.

METHODS: The literature on factors influencing the risk for ALD was systematically searched from PubMed, Embase, and the Cochrane library databases from inception to June 2022. Factors suitable for quantitative analysis were submitted to meta-analysis using fixed-effects and random-effects models to calculate each factor's risk ratio (RR) and 95% confidence interval (CI).

RESULTS: Ten cohort studies (covering 1,005,339 subjects) that reported a clear causal relationship were included in the analysis, involving 11 potential risk factors (sex, race, education level, body mass index, alcohol consumption, types of alcoholic beverage, duration of drinking, drinking frequency, smoking, coffee consumption, and tea consumption). Three of these factors (sex, alcohol consumption, and smoking) were subjected to meta-analysis, and the results showed that male sex (RR = 2.84, 95% CI = 1.86-4.36), alcohol consumption >/=280 g/week (RR = 4.96, 95% CI = 2.71-9.07), and smoking (RR = 2.39, 95% CI = 1.97-2.89) were risk factors for ALD.

CONCLUSIONS: Many factors are likely to influence the incidence of ALD, and male sex, heavy alcohol consumption, and smoking increase the risk of ALD. The relationship between other factors and ALD risk needs further evaluation.

26 August 2022 In Liver Disease

BACKGROUND: The prevalence of fatty liver disease is potentially increasing in adolescents and young adults (AYAs) due to the obesity and alcohol pandemics. The aim of this study was to assess the prevalence of alcohol-associated fatty liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD) in a representative U.S. cohort utilizing transient elastography to directly measure hepatic steatosis and suspected fibrosis.

METHODS: AYAs (age 15-39 years) with valid FibroScan((R)) measurements in the National Health and Nutrition Examination Survey (NHANES) database (2017-2018) were included in the analyses. Those with viral hepatitis, pregnancy, or ALT/AST > 500 U/L were excluded. The population was divided into those with excessive alcohol consumption (ALQ130) and those without. Controlled attenuation parameter (CAP) score >/= 248 dB/m was used to identify suspected ALD and NAFLD. In those with evidence of ALD, the following cutoffs of liver stiffness measurement (LSM) were used for suspected fibrosis: F >/= F2 at LSM >/= 7.5 kPa and F >/= F3 at >/= 9.5 kPa, respectively. In those with suspected NAFLD, the following LSM cutoffs were used: F >/= F2 at 6.1 and F >/= F3 at >/= 7.1, respectively. Cutoffs were chosen based on published literature to maximize sensitivity.

RESULTS: Comparing to those without, subjects with excessive alcohol consumption tended to be older (29.8 vs 28.5 years), have a higher BMI (29.3 vs 28.9 kg/m2), and be from a White ethnicity (65.3% vs. 55.4%). In subjects with excessive alcohol consumption, suspected ALD was present in 56.59% (95% CI 41.57-70.49). In those with suspected ALD, suspected significant fibrosis (F >/= F2) was present in 12.3% (95% CI 4.74-28.34) and advanced fibrosis (F >/= F3) was present in 6.31% (95% CI 0.69-39.55). Similarly, in subjects without excessive alcohol consumption, suspected NAFLD was present in 40.04% (36.64-43.54). In those with suspected NAFLD, suspected significant fibrosis (F >/= F2) was present in 31.07% (27.25-35.16) and suspected advanced fibrosis (F >/= F3) was present in 20.15% (16.05-24.99).

CONCLUSION: A significant percentage of AYAs are at risk for ALD and NAFLD and a subset of these subjects is at risk for significant fibrosis. Efforts should focus on increasing awareness of the prevalence of ALD and NAFLD in this population and to mitigate modifiable risk factors.

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