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Many of these liver diseases can cause devastating long-term health effects, potentially culminating in liver failure and death.2 Understanding the impact of alcohol and liver damage can help people make healthy life choices. Approximately 90% of deaths attributed to cirrhosis are estimated to be preventable since excessive alcohol use is the most common cause of cirrhosis. However, it is also estimated that 40% of chronic https://ecosoberhouse.com/article/alcoholic-liver-disease-symptom-and-treatment/ liver disease is related to hepatitis c virus (HCV) infection, the most chronic bloodborne infection in the United States, with approximately 4 million people infected. About 20% of the HCV infected individuals develop chronic liver disease and cirrhosis. Chronic liver disease often shows no symptoms and many patients are found to have the disease during the course of physical examination for an unrelated illness.
What are the three stages of alcoholic liver disease?
Alcoholic liver disease is defined by three stages of liver damage following chronic heavy alcohol consumption: fatty liver, alcoholic hepatitis, and fibrosis/cirrhosis (Figure 5).
Alcoholic hepatitis can be confused with other causes of hepatitis, such as viral, drug-induced, or autoimmune hepatitis. Clinical context and serum tests are fundamental to distinguish these entities. For the optimal assessment of liver fibrosis, it must be appreciated by specific stains, as Masson Trichrome or Sirius Red.
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Acute alcoholic hepatitis can develop after as few as four drinks for women and five drinks for men. The major risk factor for alcoholic hepatitis is the amount of alcohol you consume. How much alcohol it takes to put you at risk of alcoholic hepatitis isn’t known. But most people with the condition have a history of drinking more than 3.5 ounces (100 grams) — equivalent to seven glasses of wine, seven beers or seven shots of spirits — daily for at least 20 years. On average, 1 in 3 people with the most advanced stage of liver disease and cirrhosis are still alive after 2 years.
According to the National Institute on Alcohol Abuse and Alcoholism, the amount of beverage containing approximately 14 g of pure ethanol is defined as a standard drink. The percent of pure alcohol, expressed as alcohol by volume (alc/vol), varies by beverage. Thus, 12 ounces (360 mL) of beer at 6 percent alc/vol, 5 ounces (150 mL) of wine at 12 percent alc/vol, or 1.5 ounces (45 mL) of distilled spirits at 40 percent alc/vol each are equivalent to a standard drink.
Is cirrhosis different from alcoholic hepatitis?
Years of alcohol abuse can cause the liver to become inflamed and swollen. If you’re diagnosed with alcoholic hepatitis, you must stop drinking alcohol. People who continue to drink alcohol face a high risk of serious liver damage and death. Alcohol-related liver disease may be suspected based on a person’s history of alcohol abuse, laboratory or radiologic abnormalities or medical conditions related to alcohol abuse.
The metabolism of alcohol increases the production of NADH by reducing NAD in the body. This shifting of metabolic balance toward the production of NADH leads to the formation of glycerol phosphate, which combines with the fatty acids and becomes triglycerides, which accumulate within the liver. When lipid oxidation (lipolysis) stops due to alcohol consumption, fats accumulate in the liver and lead to “fatty liver disease.” Continued alcohol consumption brings the immune system into play. Interleukins with the help of neutrophils attack the hepatocytes, and swelling of the hepatocytes known as the “alcoholic hepatitis” takes place. Ongoing liver injury leads to irreversible liver damage, the cirrhosis of the liver.
Specific treatment
If cirrhosis develops, you will need to manage the problems it can cause. 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). 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). Micronutrient supplementation should be considered if deficiencies are detected. Supplementation with one such micronutrient, zinc, has been shown to be therapeutic in animal models of alcoholic liver injury.
Zinc deficiency disrupts the epithelial barrier function by disassembling tight junction proteins in addition to its direct detrimental effects on the liver, whereas dietary zinc supplementation protects against ALD. In summary, both human and animal studies suggest that zinc intervention might be an attractive therapy for ALD and that the protection by zinc against ALD includes both hepatic and extrahepatic actions. Acetaldehyde may be the principal mediator of alcoholic liver injury. The deleterious effects of acetaldehyde include impairment of the mitochondrial beta-oxidation of fatty acids, formation of oxygen-derived free radicals, and depletion of mitochondrial glutathione. In addition, acetaldehyde may bind covalently with several hepatic macromolecules, such as amines and thiols, in cell membranes, enzymes, and microtubules to form acetaldehyde adducts.
Alcoholic hepatitis
Egr-1 controls the expression of genes that respond to cellular stress. It binds to gene promoter regions that are relevant to alcohol-induced liver injury and steatosis. The most notable of these is tumor necrosis factor alpha (TNFα), a lipogenic cytokine. Additionally, because Egr-1 is activated very early after ethanol administration (Donohue et al. 2012), it also regulates the expression of the SREBP-1c gene (Thomes et al. 2013).
Characteristic ultrasonographic findings include a hyperechoic liver with or without hepatomegaly. Computed tomography (CT) and magnetic resonance imaging (MRI) can readily detect cirrhosis. On MRI, special features may be present with ALD including increased size of the caudate lobe, more frequent visualize of the right hepatic notch, and larger regenerative nodules.
Is alcoholic hepatitis dangerous?
The literature proposes several interventions that have been designed to improve the care delivered to the patient in terms of rapid recovery, the stability of health patient safety (compensated cirrhosis), and the performance of the patient. Those with cirrhosis often develop kidney problems, intestinal bleeding, fluid in the belly, confusion, liver cancer, and severe infections. Alcohol liver disease (ALD) is either alone or in association with other comorbidities such as obesity or viral hepatitis, the leading cause of liver disease. Liver cirrhosis is ranked as the 5th to 7th leading cause of death among adults years old. It is responsible for approximately 25,000 deaths per year in the United States, a mortality rate which is roughly equivalent to that caused by stroke, HIV or type 1diabetes. At Stanford, our team includes a dedicated group of specialists who treat all aspects of your disease.