Alcoholic fatty liver hepatitisK70.0

A clinical picture belonging to the chronic alcoholic liver diseases, which develops in patients with chronic alcohol abuse, with liver cell damage that cannot be separated histologically from the non-alcoholic fatty liver diseases.

Prevalence: 5-10% of the Western European population. About 1/3 of all liver diseases are alcohol-induced. In addition, the increase in metabolic risk factors, also related to the aging of the population may be. In fatty liver patients, the prevalence of obesity (whether alcoholic or non-alcoholic) is between 30% and 100%, and that of type 2 diabetes mellitus is between 10% and 75%.

In women who consume > 40g and men who consume > 60 grams of pure alcohol per day, consumption is considered problematic. With this amount, long-term consequences of various organ damage are to be expected. The pathophysiology of alcoholic steatohepatitis (ASH) is not yet understood in detail. It is known that alcohol metabolism as well as oxidative stress and endotoxins play a role. Alcohol induces the cytochrome P450-dependent microsomal ethanol-oxidizing system (MEOS) with increased oxygen consumption in the liver parenchyma. (Note: in chronic alcohol consumption MEOS is induced and breaks down alcohol in addition to the original alcohol dehydrogenase. This "additional enzyme" is responsible for the tolerance development towards alcohol. The organism responds to a constant and strong alcohol stimulus with an increased production of MEOS).

The consequence is a lobular central hypoxia of the hepatocytes. Furthermore, the degradation product of ethanol, acetaldehyde, has a liver-toxic effect. The fatty acid degradation is disturbed. Fat storage in the liver cells occurs. Furthermore, cytokines are released from the damaged liver cells. These induce fatty liver hepatitis (alcoholic steatohepatitis - ASH)

Sonography: enlarged liver, echo pattern homogeneously condensed (so-called light liver), rounding of the lower edge of the liver.

In pure fatty liver gamma-GT increased; IgA increased. In fatty liver hepatitis additional increase of transaminases. With increasing liver insufficiency, reduced synthesis performance of the liver (cholesterol esterase, albumin, coagulation factors of the prothrombin complex)

In the mildest form, the diagnosis is made randomly. Severe episodes of alcoholic hepatitis typically occur after a period of intensive alcohol abuse with nausea, vomiting, jaundice, fever, abdominal pain. The diagnosis can be made on the basis of clinical symptoms, medical history (alcohol consumption, diet, underlying diseases), laboratory, sonography (condensed internal reflex pattern of the liver). A biopsy is recommended to confirm the diagnosis (see also under Mallory body).

Non-alcoholic fatty liver, non-alcoholic fatty liver hepatitis, non-alcoholic cirrhosis of the liver

The primary therapeutic goal is an alcohol withdrawal combined with nutritional therapy. An intake of 2000 kcal / day should be aimed for. There is no additional convincing drug therapy approach.

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