Alcoholic fatty liver diseasesK70.0
Synonym(s)
DefinitionThis section has been translated automatically.
Diseases belonging to the chronic alcoholic liver diseases, which develop in patients with chronic alcohol abuse (the low-risk amount of pure alcohol is 24g/day in men, 12g/day in women), and are characterized by liver cell damage, which cannot be separated histologically from the non-alcoholic fatty liver diseases (fatty liver, non-alcoholic steatohepatitis NASH; micronodular liver cirrhosis).
ClassificationThis section has been translated automatically.
The alcoholic fatty liver diseases can be divided (depending on the extent of toxic damage) into:
- Alcoholic fatty liver (light microscopically visible, diffuse, coarse-dropped fatty deposits of >50% of the liver parenchyma)
- Alcoholic fatty liver hepatitis (can appear as symptomatic acute or as mostly asymptomatic, possibly cholestatic hepatitis)
- Alcoholic micronodular cirrhosis of the liver (risk of cirrhosis increases several times over for amounts >60g(m) and >40g(w).
Occurrence/EpidemiologyThis section has been translated automatically.
Prevalence: 5-10% of the Western European population. About 1/3 of all liver diseases are alcohol-induced. The reason for this is probably, apart from toxic alcohol consumption, the simultaneous increase in metabolic risk factors, also in connection with the increasing ageing of the population. The prevalence of obesity (whether alcoholic or non-alcoholic) in fatty liver patients is between 30 and 100%.
EtiopathogenesisThis section has been translated automatically.
In women who consume > 40g and men who consume > 60g 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 influenced by alcohol metabolism as well as oxidative stress and endotoxins. Alcohol induces the cytochrome P450-dependent microsomal ethanol oxidizing system (MEOS) with increased oxygen consumption in the liver parenchyma. The consequence is a lobular central hypoxia of the hepatocytes. In addition to ethanol, its degradation product, 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 an inflammatory reaction (fatty liver hepatitis - alcoholic steatohepatitis - ASH).
ImagingThis section has been translated automatically.
Sonography: enlarged liver, echo pattern homogeneously condensed (so-called light liver), rounding of the lower edge of the liver.
LaboratoryThis section has been translated automatically.
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)
DiagnosisThis section has been translated automatically.
Clinic, anamnesis (alcohol consumption), nutrition, underlying diseases, laboratory, sonography (condensed internal reflex pattern of the liver)
Differential diagnosisThis section has been translated automatically.
Non-alcoholic fatty liver, non-alcoholic fatty liver hepatitis, non-alcoholic micronodular liver cirrhosis
General therapyThis section has been translated automatically.
The primary therapeutic goal is an alcohol withdrawal combined with nutritional therapy. An intake of 2000 kcal / day should be aimed for.