Alcoholic Liver Disease StatPearls NCBI Bookshelf

But you could develop alcohol-related cirrhosis without ever having alcohol-related hepatitis. According to the American College of Gastroenterology, females who consume more than two drinks per day and males who consume more than three drinks per day for more than 5 years are at an increased risk for alcoholic liver disease. This article explores the early signs and symptoms of alcoholic liver disease, its stages, causes, risk factors, treatments, and prevention. According to the Centers for Disease Control and Prevention (CDC), in 2020, the number of deaths from alcoholic liver disease in the U.S. was 29,505, while all causes of chronic liver disease and cirrhosis are estimated to lead to 12 fatalities per 100,000 people per year. This is called alcoholic fatty liver disease, and is the first stage of ARLD. Consuming too much alcohol can inhibit the breakdown of fats in the liver, causing fat accumulation.

While each of these imaging studies are useful for determining the presence of underlying liver disease, they cannot confirm alcohol use as the etiology of a patient’s liver disease. Nonetheless, imaging studies can be useful for excluding other causes of abnormal liver tests in patients who abuse alcohol such as infiltrative disease, obstructive biliary pathology and neoplastic diseases of the liver[120]. Imaging can also aid in the diagnosis of cirrhosis and can be used to screen for and identify hepatocellular carcinoma. The biochemical markers for chronic alcohol consumption that have been most commonly studied are serum GGT, AST, ALT, mean corpuscular volume (MCV) and carbohydrate-deficient transferrin (CDT)[82-84]. Specific IgA antibodies directed towards acetaldehyde-derived protein modifications are frequently seen alcoholics and thus IgA levels are increased in chronic ALD.

Interactions between alcohol consumption and metabolic syndrome

If excessive alcohol consumption continues, inflammation levels can begin to increase in the liver. This chemokine is released by hepatocytes, liver sinusoidal endothelial cells, Kupffer cells and hepatic stellate cells (HSCs) and promotes chemo-attraction and mononuclear cell infiltration130. In patients with alcohol-related hepatitis, ethanol can also promote the release of CXCL chemokines from liver sinusoidal endothelial cells and infiltrating immune cells in a process that is regulated by the TNF–nuclear factor-κB (NF-κB) signalling axis131.

In a meta-analysis of 10 randomized studies, pentoxifylline failed to show survival benefit at 1 month, but was effective in reducing the occurrence of hepatorenal syndrome by 53% (120). The exact mechanism of renal protection with pentoxifylline remains unclear. In a network meta-analysis of 22 studies including the STOPAH study, there was low-quality evidence for benefit of pentoxifylline in reducing the short-term mortality at 28 days by 30% (121).

Preterm and alcohol

As there is no specific biomarker for the diagnosis of ALD, diagnosis requires excluding other liver diseases in a patient with heavy alcohol use. When considering the intersection between NAFLD and ALD, there are several challenges and gaps in research and unmet clinical needs (Box 2). Promising biomarkers, such as extracellular vesicles, apoptotic products and cytokines, have not alcoholic liver disease been validated in overlapping NAFLD and ALD. Additionally, clinical trials should evaluate alcohol consumption more accurately and should consider patients with NAFLD and active alcohol consumption in a separate category. Therapies capable of attenuating disease progression in patients with dual-aetiology fatty liver disease should also be tested in randomized controlled trials.

Men who consume more than 4 standard drinks in any single day (or more than 14 drinks per week) and women who consume more than 3 in any single day (or more than 7 drinks per week) are at increased risk for alcohol-related problems[30]. Alcoholic liver disease is treatable if it is caught before it causes severe damage. The chances of getting liver disease go up the longer you have been drinking and more alcohol you consume. To minimize the risk of recidivism, most transplant centers require a minimum of 6 months of abstinence before considering LT for a patient with ALD.

MeSH terms

Figure 5 shows the postulated scheme of transcriptional control that contributes to enhanced lipogenesis in the liver. Patients can present with any or all complications of portal hypertension, including ascites, variceal bleeding, and hepatic encephalopathy. The histology of end-stage alcoholic cirrhosis, in the absence of acute alcoholic hepatitis, resembles that of advanced liver disease from many other causes, without any distinct pathologic findings (Figure 3).

Common hematological findings in patients with ALD include thrombocytopenia, macrocytic anemia, lymphopenia, elevated erythrocyte sedimentation rate and an elevated INR[70,71]. Macrocytosis suggests chronic disease and may be secondary to toxicity of alcohol on bone marrow, folate or vitamin B12 deficiency, or increased lipid deposition in erythrocyte membranes. Thrombocytopenia is present in about a third of alcoholics admitted to hospitals and with abstinence will tend to normalize within 1-3 wk[72].

Deficiencies in micronutrients (e.g., folate, vitamin B6, vitamin A, and thiamine) and minerals (e.g., selenium, zinc, copper, and magnesium) often occur in ALD and, in some instances, are thought to be involved in its pathogenesis (Halsted 2004). According to the current guidelines of the American Association for the Study of Liver https://ecosoberhouse.com/ Diseases, all patients with alcoholic hepatitis or advanced ALD should be assessed for nutritional deficiencies and treated aggressively with enteral nutritional therapy. A protein intake of 1.5 grams per kilogram bodyweight and 35 to 49 kcal per kilogram bodyweight per day is recommended for ALD patients (Frazier et al. 2011).

• Make an appointment with your doctor if you have any persistent signs or symptoms that worry you.
• Psychological care is needed to act on the causes of alcohol addiction, and this may require the help of the patient’s family.
• Treatment of the patient with alcoholic cirrhosis mirrors the care of patients with any other type of cirrhosis, and includes prevention and management of ascites, spontaneous bacterial peritonitis, variceal bleeding, encephalopathy, malnutrition, and hepatocellular carcinoma.

This tool has been shown to be 83% sensitive and 84% specific for alcohol abuse or dependence in the past year[54]. More information and support for people with alcoholic liver disease and their families can be found by joining support groups for alcoholism or liver disease. Alcoholic liver disease is damage to the liver and its function due to alcohol abuse. Additionally, the supplementation of nutritional substances helps to protect liver toxicity.

Risk factors

Survival of patients with recurrent cirrhosis is about 41 and 21% at 10 and 15 years after LT respectively, compared to similar survival rates of about 70 and 50% among abstainers (183). Immunosuppression should be maintained at the lowest safe levels as with all patients who undergo a liver transplant; it is unclear whether everolimus or sirolimus are superior to calcineurin inhibitors among patients transplanted for alcoholic cirrhosis (185). Oxidative stress is a major player in the pathogenesis of ALD and AH (129). Antioxidant cocktails and vitamin E examined earlier have not shown beneficial effects in the management of severe AH (88,130,131).

Previously unsuspected hepatomegaly is often the only clinical presentation. Occasionally, a patient with fatty liver is presented with right upper quadrant discomfort, tender hepatomegaly, nausea, and jaundice. Differentiation of alcohol-induced fatty liver and non-alcohol-induced fatty liver is difficult unless an accurate history of drinking habits, pattern, and quantity is obtained [68]. The initial and most common histologic response to hepatotoxic stimuli is fatty liver, and that includes excessive ingestion of alcohol.