Nonheavy Drinking and Worsening of Noninvasive Fibrosis Markers in Nonalcoholic Fatty Liver Disease: A Cohort Study

Chang, Yoosoo; Cho, Yong Kyun; Kim, Yejin; Sung, Eunju; Ahn, Joong Kyong; Jung, Hyun Suk; Yun, Kyung Eun; Shin, Hocheol; Ryu, Seungho

doi:10.1002/hep.30170

Cited by 121 publications

(108 citation statements)

References 41 publications

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“…To complicate matters, alcohol intake within the limits of the current definition has been demonstrated in various studies to pose a significant risk for progression of liver disease. For instance, in a study of 58,927 Korean subjects with NAFLD and low baseline fibrosis scores assessed by non‐invasive markers (AST to Platelet Ratio Index (APRI) and Fibrosis‐4 (FIB‐4)), light (1.0‐9.9 g/d) or moderate (10.0‐29.9 g/d (10.0‐19.9 g/d for women) alcohol consumption was independently associated with worsening of fibrosis over a median of 4.9 years of follow‐up, compared to those with no alcohol consumption (0 g/d) 28 . Similar findings were reported from multiple other studies that included patients from various ethnic backgrounds, 29,30 though as would be expected.…”

Section: Historical Perspective On Fatty Liver Nomenclaturementioning

confidence: 99%

What's in a name? Renaming ‘NAFLD’ to ‘MAFLD’

Fouad

Waked

Bollipo

et al. 2020

Liver International

228

162

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In medicine, language matters and the words used to name and describe a disease can have a profound impact on patients and their families. Over the last two decades, many criticisms have been voiced about the nomenclature and definition of non-alcoholic fatty liver disease (NAFLD) in regards not only to the prominent role that alcohol plays in the definition but also on the negative impacts of the nomenclature including trivialization, stigmatization and less consideration of the disease in health policy. Recently, a consensus of international experts proposed that the disease acronym be changed from NAFLD to metabolic (dysfunction) associated fatty liver disease or 'MAFLD'. This change goes far beyond a mere semantic revision and may be the first step that catalyses the process to better conceptualize the disease for health promotion, patient orientation, case identification, ongoing clinical trials and for health services delivery. Here we review the history of, and definitions of MAFLD in the context of advancing our understanding of the pathogenesis of the disease. We also address the reasons, signals, promises, challenges and the way going forward from the name change from various stakeholder perspectives. K E Y W O R D S MAFLD, metabolic, nomenclature | 1255 FOUAD et Al.

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Section: Historical Perspective On Fatty Liver Nomenclaturementioning

confidence: 99%

What's in a name? Renaming ‘NAFLD’ to ‘MAFLD’

Fouad

Waked

Bollipo

et al. 2020

Liver International

228

162

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“…In a large longitudinal Korean population cohort of 58,927 individuals with ultrasound‐based steatosis, Chang and colleagues () found light‐to‐moderate alcohol intake associated with a worsening of liver fibrosis over time based on noninvasive fibrosis markers. However, although suitable for ruling out advanced fibrosis, these noninvasive fibrosis markers have a low positive predictive value for fibrosis and have not been validated for assessing change in fibrosis over time.…”

Section: Low Alcohol Intake In the Presence Of Nafld And/or Metabolicmentioning

confidence: 99%

Interaction Between Alcohol Use and Metabolic Risk Factors for Liver Disease: A Critical Review of Epidemiological Studies

Åberg

Färkkilä

Männistö

2020

Alcoholism Clin & Exp Res

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Coexistence of alcohol use and metabolic risk-the 2 commonest population risk factors for nonviral chronic liver disease-is a growing concern. Clinical evidence and mechanistic evidence point to considerable supraadditive interaction effects for the development and progression of chronic liver disease between hazardous alcohol use and metabolic abnormalities including obesity, diabetes, and the metabolic syndrome (MetS). Intermittent binge drinking once monthly or more often seems to be associated with progression of liver disease even when average alcohol intake is within the currently allowed limits for a diagnosis of nonalcoholic fatty liver disease (NAFLD), and supraadditive interaction between binge drinking and the MetS has been reported. There are contradictory findings regarding the association between low alcohol use and liver steatosis, but, clearly, the mechanisms of alcoholic hepatotoxicity extend beyond simple fat accumulation. The presence of liver steatosis seems to amplify alcoholic hepatotoxicity. Recent longitudinal studies of NAFLD subjects report low alcohol use associated with both increased fibrosis progression and an elevated risk for liver cancer and severe liver disease. There is no clear safe limit of alcohol intake in the presence of NAFLD or metabolic risk. The interaction effects between alcohol and metabolic dysfunction merit increased attention in public health policy, individual counseling, and risk stratification. Based on current evidence, a strict dichotomization of liver disease into either pure alcoholic or nonalcoholic may be inappropriate.

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“…Male gender and alcohol consumption might be characteristic features of non‐cirrhotic HCC group. Male sex is a well‐known HCC risk factor, and it has become clear that alcohol consumption is harmful to liver disease and HCC development, even if intake is low. Flemming et al developed a scoring system to estimate the 1‐year risk of developing HCC by evaluating a cohort of 34 932 patients with cirrhosis identified from a national liver transplantation waiting list database in the US.…”

Section: Discussionmentioning

confidence: 99%

The characteristics and risk factors of hepatocellular carcinoma in nonalcoholic fatty liver disease without cirrhosis

Tobari

Hashimoto

Taniai

et al. 2019

J of Gastro and Hepatol

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Background and Aim: We evaluated the characteristics of hepatocellular carcinoma (HCC) in patients who had non-alcoholic fatty liver disease (NAFLD) without cirrhosis. Methods: We prospectively followed NAFLD patients at our University hospital. NAFLD was diagnosed from detection of steatosis by histology or imaging, no alcohol intake, and exclusion of other liver diseases. Cirrhosis was defined by histological features, imaging data, and symptoms. We compared NAFLD-related HCC with or without cirrhosis and non-cirrhotic NAFLD with or without HCC. Results: There were 48 non-cirrhotic HCC patients and 71 cirrhotic HCC patients. Multiple logistic regression analysis revealed that other than liver function factors, male gender (OR: 5.603, 95%CI: 1.577-19.900), light drinker (OR: 2.797, 95%CI: 1.031-7.589), and tumor size (OR: 1.031, 95%CI 1.009-1.055) differ significantly between these two groups. The recurrence rate was significantly lower in the non-cirrhotic HCC group than the cirrhotic HCC group, with risk factors being des-γ-carboxy prothrombin and the number of HCCs. The non-cirrhotic HCC group showed significantly better survival because of absence of non-cancerous liver failure. Comparison between non-cirrhotic NAFLD patients with or without HCC (n = 612) revealed the following risk factors for HCC: male gender (OR: 7.774, 95%CI: 2.176-27.775), light drinker (OR: 4.893, 95%CI: 1.923-12.449), and high FIB4 index (OR 2.634, 95%CI: 1.787-3.884). Conclusion: In patients with non-cirrhotic NAFLD, important risk factors for HCC were male gender, alcohol consumption, and the FIB4 index. HCC recurrence and survival were only influenced by the tumor stage. We should be aware of alcohol consumption as a modifiable risk factor for HCC.

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Nonheavy Drinking and Worsening of Noninvasive Fibrosis Markers in Nonalcoholic Fatty Liver Disease: A Cohort Study

Cited by 121 publications

References 41 publications

What's in a name? Renaming ‘NAFLD’ to ‘MAFLD’

What's in a name? Renaming ‘NAFLD’ to ‘MAFLD’

Interaction Between Alcohol Use and Metabolic Risk Factors for Liver Disease: A Critical Review of Epidemiological Studies

The characteristics and risk factors of hepatocellular carcinoma in nonalcoholic fatty liver disease without cirrhosis

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