Alcoholic fatty cirrhosisK70.0; K74.6

Alcoholic cirrhosis of the liver (from Greek kirros - yellow-orange, lemon yellow) is a chronic, alcohol-induced, progressive and irreversible destruction of the lobular and vascular structure of the liver parenchyma with fibrotic bridging and the formation of regenerative nodes. The functional consequences are liver failure, portal hypertension and the formation of intrahepatic porto-systemic shunts.

Prevalence: About 1/3 of all liver diseases are alcohol-induced. In addition, the increase in metabolic risk factors, also associated with 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). This chronic inflammatory reaction ultimately leads to a destructive remodelling of the organ structure with parenchyma necroses, formation of regenerative nodes (pseudolobuli) and connective tissue septums with a profound disturbance of the functionality of the liver.

The consequences are signs of decompensation (icterus, bleeding tendency, malnutrition, cachexia, hepatic encephalopathy, hepatic coma), portal hypertension with venous collateralization (esophageal varices, hypertensive gastropathy, hypersplenism, ascites).

Clinical symptoms of alcoholic fatty cirrhosis are reduced performance, lack of concentration and fatigue. In addition, there is a feeling of pressure and fullness in the upper abdomen, meteorism.

Further dermatological signs (hepatic skin signs) such as palmar and plantar erythema, jaundice, spidernaevi, varnished lips, varnished tongue, corner of the mouth rhagades, pruritus, leukonychia (white nails), skin atrophy (banknote skin with telangiectasia), Dupuytren's contracture.

Hormonal disorders (reduced testosterone, increased oestrogen in men), in women menstrual disorders.

Signs of decompensation: jaundice, bleeding tendency, malnutrition, cachexia, hepatic encephalopathy, hepatic coma, hepatopulmonary syndrome (arterial hypoxaemia in advanced cirrhosis due to functional disturbance of pulmonary circulation without primary lung disease).

A characteristic feature of alcoholic cirrhosis is the appearance of portal hypertension resulting in venous collateralization (esophageal varices, hepatic gastropathy), edema, splenomegaly, hypersplenimus.

Late effects: Hepatocellular carcinoma

Ultrasound shows that the liver is inhomogeneous. The edge of the liver is wavy, the internal vessels are rare. The lobus caudatus may be enlarged. The ultrasound can very well detect ascites and splenomegaly.

Transient Elastography: This method can be used to determine the extent of fibrosis of the liver by means of the strength of the tissue. Colour duplex sonography can be used to measure reduced elasticity of the liver in the hepatic veins, reduced flow in the portal vein and increased peripheral resistance in the hepatic artery.

The definitive diagnosis is made by a liver biopsy.

Anemia, hyperchromia due to folic acid deficiency, thrombocytopenia, hyperbilirubinemia, thrombocytopenia; furthermore, reduced synthesis capacity of the liver with reduced values for cholinesterase, albumin and some coagulation factors (reduced Quick value). The liver enzymes GOT, GPT and γ-GT, bilirubin and ammonia may be elevated.

Examination often reveals icterus, increased abdominal girth (ascites-related), edema, gynecomastia, skin hemorrhages, and flapping tremor and impaired consciousness in hepatic encephalopathy. Typical, but appearing late, are the so-called hepatic skin signs: spidernaevi (vascular spider), leuconychia (milk glass nails), pruritus, lacquer tongue, skin atrophy ("bill skin"), and palmar or plantar erythema. Other clinical signs of alcoholic cirrhosis include caput medusae (rare), Dupuytren contractures, and lack of abdominal hair in males (abdominal baldness, "belly baldness").

Goat syndrome (alcohol toxic liver damage + hemolytic anemia + hyperlipidemia).

Fully developed liver cirrhosis with hepatic insufficiency, portal hypertension and its vascular consequences.

Tendency to hypoglycemia (inhibition of gluconeogenesis by alcohol).

Further extrahepatic alcohol damage (neuropsychiatric disorders, alcohol withdrawal syndromes, gastrointestinal disorders such as nausea and diarrhoea, circulatory disorders such as tachycardia and hypertension, pancreatitis, etc.).

An effective drug therapy is not known. The only effective treatment is abstinence from alcohol.

Nutritional therapeutic general measures as well as the elimination of vitamin deficiencies (e.g. vitamin B1, vitamin K) and a sufficient energy supply are important components of a therapy. Vitamin K substitution is indicated in cases of increased bleeding risk and low quick values. As half of the alcoholic patients have a vitamin B1 deficiency, this must be remedied (prophylaxis of Wernicke's encephalopathy).

Malnourished patients have both an increased mortality in the spontaneous course of the disease and an increased rate of complications. Care must be taken to ensure an adequate energy supply.

Protein intake: A daily protein intake of 1.2-1.5 g protein per kg body weight is recommended. Protein restriction may only be applied in patients with refractory chronic hepatic encephalopathy.

Osteoporosis prophylaxis: Osteoporosis prophylaxis should be started early in all patients with alcoholic liver cirrhosis. This is done by calcium substitution (1200-1500 mg/day). In patients with cholestatic liver disease, vitamin D3 is additionally substituted (400-800 IU/day).

Regular examinations are important for the early detection of liver carcinoma.

A last resort in many cases is liver transplantation.

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