Alkolik sirozu

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Devedikeni tohumu özütü, yaygın olarak karaciğer bozukluklarının tedavisinde de belirtilen geleneksel tıp flavonoid silymarin karaciğer koruyucu özelliklerini içerdiği bilinmektedir şifalı bitki.

Alcoholic liver disease(Alc

oholic cirrhosis)

Alcoholic liver disease is a term that encompasses the hepatic manifestations of alcohol over consumption, including fatty liver, alcoholic hepatitis, and chronic hepatitis with hepatic fibrosis or
cirrhosis It is the major cause of liver disease in Western countries. Although steatosis (fatty liver) will develop in any individual who consumes a large quantity of alcoholic beverages over a long period of time, this process is transient and reversible. Of all chronic heavy drinkers, only 15–20% develop hepatitis or cirrhosis, which can occur concomitantly or in succession.

How alcohol damages the liver is not completely understood. 80% of alcohol passes through the liver to be detoxified. Chronic consumption of alcohol results in the secretion of pro-inflammatory cytokines (TNF-alpha, IL6 and IL8), oxidative stress, lipid peroxidation, and acetaldehyde toxicity. These factors cause inflammation, apoptosis and eventually fibrosis of liver cells. Why this occurs in only a few individuals is still unclear. Additionally, the liver has tremendous capacity to regenerate and even when 75% of hepatocytes are dead, it continues to function as normal

Alcoholic hepatitis

Main article: Alcoholic hepatitis

Alcoholic hepatitis is characterized by the inflammation of hepatocytes. Between 10% and 35% of heavy drinkers develop alcoholic hepatitis (NIAAA, 1993). While development of hepatitis is not directly related to the dose of alcohol, some people seem more prone to this reaction than others[citation needed]. This is called alcoholic steato necrosis and the inflammation appears to predispose to liver fibrosis. Inflammatory cytokines (TNF-alpha, IL6 and IL8) are thought to be essential in the initiation and perpetuation of liver injury by inducing apoptosis and necrosis. One possible mechanism for the increased activity of TNF-α is the increased intestinal permeability due to liver disease. This facilitates the absorption of the gut-produced endotoxin into the portal circulation. The Kupffer cells of the liver then phagocytose endotoxin, stimulating the release of TNF-α. TNF-α then triggers apoptotic pathways through the activation of caspases, resulting in cell death.

Thistle seed extract, medicinal plant, which is known to contain flavonoid silymarin liver protective properties in traditional medicine widely prescribed in the treatment of liver disorders.

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