Alcoholic liver disease

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Alcoholic liver disease is a term that includes liver manifestations of excessive consumption of alcohol, including fatty liver, alcoholic hepatitis, and chronic hepatitis with hepatic fibrosis or cirrhosis.

This is the leading cause of liver disease in Western countries. Although steatosis (fatty liver) will develop in any individual who consumes large amounts of alcoholic beverages over a long period of time, this process is temporary and can be recovered. Of all the chronic heavy drinkers, only 15-20% develop hepatitis or cirrhosis, which can occur simultaneously or sequentially.

The mechanism behind this is not fully understood. 80% of alcohol passes through the liver to be detoxified. Chronic alcohol consumption results in the secretion of proinflammatory cytokines (TNF-alpha, Interleukin 6 [IL6] and Interleukin 8 [IL8]), oxidative stress, lipid peroxidation, and acetaldehyde toxicity. These factors cause inflammation, apoptosis and eventually fibrosis of the liver cells. Why this happens to only a few individuals remains unclear. In addition, the liver has an amazing ability to regenerate and even when 75% of the hepatocytes die, it continues to function as usual.

Video Alcoholic liver disease

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The current known risk factors are:

• Number of alcohol taken : Consumption 60-80g per day (14g is considered as one standard drink in the US, 1.5 liters of liquor, 5 bottles of wine, 12 beers, drinking six packs of beer every day will be in the middle of the range) for 20 years or more in men, or 20g/day for women significantly increases the risk of hepatitis and fibrosis by 7% to 47%,
• Drinking pattern: Drinking outside the meal time increases up to 3 times the risk of alcoholic liver disease.
• Sex: Women are twice as susceptible to alcohol-related liver disease, and may develop alcoholic liver disease with shorter duration and chronic dose consumption. Lower amounts of alcohol dehydrogenase secreted in the intestine, higher body fat proportions in women, and changes in fat absorption due to the menstrual cycle can explain this phenomenon.
• Hepatitis C infection : Concurrent hepatitis C infection significantly speeds up the process of liver damage.
• Genetic factors: Genetic factors affect both alcoholism and alcoholic liver disease. Both monozygotic twins are more likely to become addicted to alcohol and develop liver cirrhosis than dizygotic twins. Polymorphisms in enzymes involved in alcohol metabolism, such as ADH, ALDH, CYP4502E1, mitochondrial dysfunction, and cytokine polymorphism can partially explain this genetic component. However, no specific polymorphisms are currently closely related to alcoholic liver disease.
• Excess iron (Hemochromatosis)
• Diet : Malnutrition, particularly vitamin A and E deficiency, can worsen liver damage due to alcohol by preventing hepatocyte regeneration. This is especially a concern because alcoholics are usually malnourished due to poor diet, anorexia, and encephalopathy.

Maps Alcoholic liver disease

Pathophysiology

Replace fat

Changes in fat, or steatosis is the accumulation of fatty acids in liver cells. This can be seen as a lump of fat under a microscope. Alcoholism causes the development of large fat clots (macro vesicular steatosis) throughout the liver and can begin to occur after several days of heavy drinking. Alcohol is metabolized by alcohol dehydrogenase (ADH) to acetaldehyde, then further metabolized by aldehydes dehydrogenase (ALDH) to acetic acid, which eventually oxidizes to carbon dioxide (CO ₂ ) and water ( H ₂ O). This process generates NADH, and increases the NADH/NAD ratio. A higher NADH concentration induces fatty acid synthesis while decreased NAD levels result in decreased fatty acid oxidation. Furthermore, higher levels of fatty acids signify the liver cells to join the glycerol to form triglycerides. These triglycerides accumulate, producing fatty liver.

Alcoholic hepatitis

Alcoholic hepatitis is characterized by hepatocyte inflammation. Between 10% and 35% of heavy drinkers develop alcoholic hepatitis (NIAAA, 1993). While the development of hepatitis is not directly related to the dose of alcohol, some people seem to be more susceptible to this reaction than others. This is called alcoholic steam necrosis and the inflammation seems to predispose to liver fibrosis. Inflammatory cytokines (TNF-alpha, IL6 and IL8) are considered essential in initiation and sequestration of liver damage by inducing apoptosis and necrosis. One possible mechanism for increased TNF- activity is an increase in bowel permeability due to liver disease. This facilitates the absorption of endotoxin produced by the intestine into the portal circulation. Kupffer cells from the liver then endotoxin phagocytosis, stimulate the release of TNF-. TNF-? then trigger the pathway of apoptosis through the activation of caspases, resulting in cell death.

Cirrhosis

Cirrhosis is a late stage of serious liver disease characterized by inflammation (swelling), fibrosis (hardening of cells) and the damaged membrane prevents the detoxification of chemicals in the body, ending in scar tissue and necrosis (cell death). Between 10% to 20% of heavy drinkers will develop liver cirrhosis (NIAAA, 1993). Acetaldehyde may be responsible for alcohol-induced fibrosis by stimulating the deposition of collagen by stellate liver cells. The production of oxidants derived from NADPH oxidase and/or cytochrome P-450 2E1 and the formation of acetyl- amin-protein adducts damage cell membranes. Symptoms include jaundice (yellowing), enlarged liver, and the pain and tenderness of structural changes in the damaged liver architecture. Without total restriction from alcohol use, cirrhosis will eventually lead to liver failure. Final complications of cirrhosis or liver failure include portal hypertension (high blood pressure in the portal vein due to increased flow of resistance through the damaged liver), coagulation disorders (due to impaired production of coagulation factors), ascites (severe stomach swelling due to fluid accumulation in the tissues) and complications others, including hepatic encephalopathy and hepatorenal syndrome. Cirrhosis can also be caused by other causes than alcohol abuse, such as viral hepatitis and exposure to heavy toxins other than alcohol. The final stage of cirrhosis may seem medically similar, regardless of the cause. This phenomenon is called the "final common pathway" for disease. Changes in fat and alcoholic hepatitis with abstinence can be reversible. The subsequent stages of fibrosis and cirrhosis tend to be irreversible, but can usually be retained by abstinence for long periods of time.

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Diagnosis

In the early stages, patients with ALD showed subtle and often abnormal physical findings. It is usually not until the progression of advanced liver disease that stigmata of chronic liver disease becomes apparent. Early ALD is usually found during routine health checks when the liver enzyme levels are found to increase. This usually reflects alcoholic liver steatosis. Microvesicular and makrovesicular stenosis with inflammation seen in liver biopsy specimens. This histologic picture of ALD can not be distinguished from nonalcoholic fatty liver disease. Steatosis usually disappears after discontinuation of alcohol use. Continued use of alcohol will result in a higher risk of liver disease progression and cirrhosis. In patients with acute alcoholic hepatitis, clinical manifestations include fever, jaundice, hepatomegaly, and possible liver decompensation with hepatic encephalopathy, varicose hemorrhage, and ascitic accumulation. Hepatomegaly hearing may be present, but abdominal pain is unusual. Occasionally, patients may be asymptomatic.

Laboratory findings

In people with alcoholic hepatitis, serum aspartate aminotransferase (AST) for alanine aminotransferase (ALT) ratio is greater than 2: 1. AST and ALT levels are almost always less than 500. Increased AST to ALT ratio is caused by pyridoxal phosphate deficiency, which is required in lane synthesis of ALT. Furthermore, metabolic alcohol-induced hepatic mitochondrial injury results in AST isoenzyme release. Other laboratory findings include red corpuscular volume (gt; 100) and increased serum gamma-glutamyl transferase (GGT), alkaline phosphatase (Alk Phos), and bilirubin levels. Folate levels are reduced in alcoholic patients due to decreased intestinal absorption, increased bone marrow demand for folate in the presence of alcohol, and increased urine loss. The magnitude of leukocytosis (white blood cell depletion) reflects the severity of liver injury. Histologic features include Mallory's body, giant mitochondria, hepatocyte necrosis, and neutrophil infiltration in the area around the vein. Mallory's body, also present in other liver diseases, is the condensation of the cytokeratin component in the hepatocyte cytoplasm and does not contribute to liver damage. Up to 70% of patients with moderate to severe hepatitis alcohol already have cirrhosis that can be identified at the biopsy examination at the time of diagnosis.

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Treatment

Not drinking any further alcohol is the most important part of the treatment. People with chronic HCV infection should distance themselves from alcohol intake, because of the risk of rapid acceleration of liver disease.

Drugs

A 2006 Cochrane review found no sufficient evidence for the use of androgenic anabolic steroids. Corticosteroids are sometimes used; However, this is recommended only when severe inflammation of the liver is present.

Sylimarin has been studied as a possible treatment, with ambiguous results. One review claimed benefits for S-adenosyl methionine in the disease model.

The effects of anti-tumor necrosis factor drugs such as infliximab and etanercept are unclear and may be dangerous. The evidence is unclear for pentoxifylline. Propylthiouracil may cause harm.

Evidence does not support additional nutrients in liver disease.

Transplant

Although in rare cases, cirrhosis of the liver is reversible, the disease process remains largely irreversible. Liver transplantation remains the only definitive treatment. Today, survival after liver transplant is similar for people with ALD and non-ALD. The requirement for transplant recording is the same as for other types of liver disease, except for a 6 month calm prerequisite along with psychiatric evaluation and rehabilitation assistance (ie, Alcoholics Anonymous). Special requirements vary among centers of transplantation. Return to alcohol use after transplant recording resulted in delisting. Re-listing is possible in many institutions, but only after 3-6 months of calm. There is limited data on transplant survival in patients transplanted for acute alcoholic hepatitis, but it is believed to be similar to that occurring in non-ALD ALD, non-ALD, and alcoholic hepatitis with less than 32 MDF.

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Prognosis

The prognosis for people with ALD depends on liver histology as well as cofactors, such as chronic viral hepatitis together. Among patients with alcoholic hepatitis, progression to liver cirrhosis occurs at 10-20% per year, and 70% will eventually develop cirrhosis. Despite the discontinuation of alcohol use, only 10% would have normalized histology and serum liver levels. As mentioned earlier, MDF has been used to predict short-term mortality (ie, MDF> = 32 associated with spontaneous survival of 50-65% without corticosteroid therapy, and MDF & 32, associated with spontaneous survival by 90%). Models for End-Stage Liver Disease (MELD) scores have also been found to have the same predictive accuracy in 30-day (MELD & gt; 11) and 90-day (MELD & gt; 21) deaths. Liver cirrhosis develops in 6-14% of those who consume more than 60-80 g of alcohol daily for men and more than 20 g daily for women. Even in those who drink more than 120 g per day, only 13.5% will suffer serious alcohol-related liver injury. However, alcohol-related deaths were the third cause of death in 2003 in the United States. Mortality worldwide is estimated at 150,000 per year.

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References

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External links

• "Alcoholic liver disease (per capita) (most recent) by country". NationMaster. Archived from the original on June 21, 2009 . Retrieved July 29 2009 .

Source of the article : Wikipedia