Nutrition and Alcoholic Liver Disease

Dasarathy, Srinivasan

doi:10.1016/j.cld.2016.02.010

Cited by 66 publications

(26 citation statements)

References 86 publications

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“…We chose patients with alcoholic cirrhosis because previous studies reported that chronic alcohol consumption induced expression of myostatin in animal models and in patients with hypertensive heart disease [ 40 , 41 ]. Although many studies suggested that chronic alcohol drinking was associated with elevated serum myostatin levels, there were no concrete data regarding prognostic performance of serum myostatin and HCC development in patients with alcoholic cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

Serum Myostatin Predicts the Risk of Hepatocellular Carcinoma in Patients with Alcoholic Cirrhosis: A Multicenter Study

Kim

Kang

Lee

et al. 2020

Cancers

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Background and Aim: Previous studies reported that serum myostatin is associated with sarcopenia. We aimed to elucidate the association between serum myostatin levels and hepatocellular carcinoma (HCC) development in patients with alcoholic liver cirrhosis (ALC). Methods: This retrospective, multicenter study assessed 1077 Asian ALC patients enrolled from 2007 to 2017. The primary endpoint was the development of HCC within 5 years. Cox proportional hazards model analyses were used to assess the association of serum myostatin levels and HCC development. The time-dependent areas under the receiver operating characteristic curve (AUROC) of serum myostatin for 5-year HCC development were calculated. Serum myostatin levels were measured using an enzyme-linked immunosorbent assay with samples collected on the index date. Results: During a median follow-up of 2.5 years, 5-year cumulative HCC incidence rates were 6.7% in the total population. The median level of serum myostatin was 3.3 ng/mL (interquartile, 2.1–5.2 ng/mL). The AUROC of serum myostatin for 5-year HCC development was 0.78 (95% confidence interval [CI], 0.76–0.81). In Cox proportional hazards model analyses, age, gender, platelet counts, and serum myostatin levels were independent risk factors for HCC development (adjusted hazard ratios [HRs] of age, male gender, platelet counts, and serum myostatin: 1.03, 2.79, 0.996, 1.18, respectively; all p < 0.05). Patients with high myostatin levels had a significantly higher risk of 5-year HCC development than those with low myostatin levels (HR 7.53, p < 0.001). Conclusion: Higher serum myostatin levels were significantly associated with a higher risk of developing HCC in ALC patients, which could identify high-risk patients who need stringent surveillance.

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Section: Discussionmentioning

confidence: 99%

Serum Myostatin Predicts the Risk of Hepatocellular Carcinoma in Patients with Alcoholic Cirrhosis: A Multicenter Study

Kim

Kang

Lee

et al. 2020

Cancers

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“…The main outcome is loss of muscle mass and fat, which is associated with the etiology of liver disease[ 80 - 83 ]. In ALD, there is marked loss of weight and muscle mass, with deficiencies of macronutrients and micronutrients, which can adversely affect the body composition of AC patients[ 84 , 85 ].…”

Section: Nutritional Evaluation In Aldmentioning

confidence: 99%

Liver transplantation and alcoholic liver disease: History, controversies, and considerations

Ca¹,

Am²,

Sa³

et al. 2018

WJG

115

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Alcohol consumption accounts for 3.8% of annual global mortality worldwide, and the majority of these deaths are due to alcoholic liver disease (ALD), mainly alcoholic cirrhosis. ALD is one of the most common indications for liver transplantation (LT). However, it remains a complicated topic on both medical and ethical grounds, as it is seen by many as a “self-inflicted disease”. One of the strongest ethical arguments against LT for ALD is the probability of relapse. However, ALD remains a common indication for LT worldwide. For a patient to be placed on an LT waiting list, 6 mo of abstinence must have been achieved for most LT centers. However, this “6-mo rule” is an arbitrary threshold and has never been shown to affect survival, sobriety, or other outcomes. Recent studies have shown similar survival rates among individuals who undergo LT for ALD and those who undergo LT for other chronic causes of end-stage liver disease. There are specific factors that should be addressed when evaluating LT patients with ALD because these patients commonly have a high prevalence of multisystem alcohol-related changes. Risk factors for relapse include the presence of anxiety or depressive disorders, short pre-LT duration of sobriety, and lack of social support. Identification of risk factors and strengthening of the social support system may decrease relapse among these patients. Family counseling for LT candidates is highly encouraged to prevent alcohol consumption relapse. Relapse has been associated with unique histopathological changes, graft damage, graft loss, and even decreased survival in some studies. Research has demonstrated the importance of a multidisciplinary evaluation of LT candidates. Complete abstinence should be attempted to overcome addiction issues and to allow spontaneous liver recovery. Abstinence is the cornerstone of ALD therapy. Psychotherapies, including 12-step facilitation therapy, cognitive-behavioral therapy, and motivational enhancement therapy, help support abstinence. Nutritional therapy helps to reverse muscle wasting, weight loss, vitamin deficiencies, and trace element deficiencies associated with ALD. For muscular recovery, supervised physical activity has been shown to lead to a gain in muscle mass and improvement of functional activity. Early LT for acute alcoholic hepatitis has been the subject of recent clinical studies, with encouraging results in highly selected patients. The survival rates after LT for ALD are comparable to those of patients who underwent LT for other indications. Patients that undergo LT for ALD and survive over 5 years have a higher risk of cardiorespiratory disease, cerebrovascular events, and de novo malignancy.

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“…Specific emphasis is necessary for zinc, vitamin D, thiamine, folate, cyanocobalamin, and selenium. Oral supplementation may not be effective due to poor intake and compliance due to anorexia, dysguesia, impaired absorption, and continued hypermetabolic states [63].…”

Section: Stagementioning

confidence: 99%

Alcohol Induced Fatty Liver: A Tragic Inception of Wrong Turn

2019

ARC Journal of Nursing and Healthcare

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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 cirrhosis. 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 60-80g every day (14g 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 20g/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.

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Nutrition and Alcoholic Liver Disease

Cited by 66 publications

References 86 publications

Serum Myostatin Predicts the Risk of Hepatocellular Carcinoma in Patients with Alcoholic Cirrhosis: A Multicenter Study

Serum Myostatin Predicts the Risk of Hepatocellular Carcinoma in Patients with Alcoholic Cirrhosis: A Multicenter Study

Liver transplantation and alcoholic liver disease: History, controversies, and considerations

Alcohol Induced Fatty Liver: A Tragic Inception of Wrong Turn

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