Alcoholic cirrhosis of the liver

Chronic alcohol intoxication is the cause of 50% of all liver cirrhosis.

The disease develops in 10-30% of patients with liver cirrhosis 10-20 years after the onset of alcohol abuse.

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Symptoms alcoholic cirrhosis of the liver

Alcoholic cirrhosis of the liver is characterized by the following distinctive features:

• in the early stages, alcoholic liver cirrhosis is usually micronodular; histological examination of liver biopsies often reveals fatty hepatosis and signs of acute alcoholic hepatitis (hepatocyte necrosis, alcoholic hyaline, neutrophilic infiltration);
• in later stages, macronodular and mixed variants of liver cirrhosis develop, and the symptoms of fatty hepatosis decrease;
• symptoms of portal hypertension predominate in the clinical picture compared to symptoms of hepatocellular insufficiency;
• the basis for the exacerbation of liver cirrhosis, as a rule, are episodes of acute alcoholic hepatitis, which are renewed with continued alcohol abuse;
• an improvement in the general condition and clinical and laboratory remission after stopping alcohol consumption is extremely characteristic;
• significantly earlier than with viral cirrhosis of the liver, pronounced signs of protein and vitamin deficiency appear;
• there are systemic manifestations of chronic alcohol intoxication (peripheral polyneuropathy; muscle atrophy; cardiovascular system damage with hyperdynamic syndrome - tachycardia, shortness of breath; chronic pancreatitis; facial hyperemia with dilation of skin capillaries, especially in the nasal area, etc.).

Classic "alcoholic's cirrhosis" is micronodular. Normal zonal architecture cannot be detected in the liver and venules are difficult to detect in zone 3. Node formation is often slow, apparently due to the inhibitory effect of alcohol on liver regeneration. The liver may accumulate varying amounts of fat; acute alcoholic hepatitis may be observed in cirrhosis. With ongoing necrosis and fibrosis replacing it, cirrhosis may progress from micronodular to macronodular, but this is usually accompanied by a decrease in steatosis. In the terminal stage, it becomes difficult to confirm the alcoholic etiology of cirrhosis based on the histological picture.

Cirrhosis may develop against the background of pericellular fibrosis without obvious cell necrosis and inflammation. In the chain of events leading to the formation of alcoholic liver cirrhosis, the first visible changes may be myofibroblast proliferation and collagen deposition in zone 3.

Increased liver iron levels may be due to increased iron absorption, iron in beverages (especially wines), hemolysis, and portocaval shunting; however, iron levels in the body's depots increase only moderately.

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Treatment alcoholic cirrhosis of the liver

Liver cirrhosis is an irreversible condition, so treatment should be aimed at correcting complications. These include portal hypertension, encephalopathy, and ascites. There is a disturbance in the metabolism of drugs, especially sedatives, which requires increased caution. Diazepam appears to be the safest drug.

Oral supplementation with purified soybeans, polyunsaturated fatty acids, and lecithin extract containing 94-98% phosphatidylcholine (the main active ingredient of Essentiale) prevented the development of septal fibrosis and cirrhosis in baboons that had been exposed to alcohol for a long time. The mechanism of this effect is unknown, but it may be related to stimulation of lipocyte collagenase.

In patients with alcoholism, portocaval shunting, including transjugular intrahepatic shunting with stents, is associated with a reduction in variceal bleeding, but hepatic encephalopathy occurs in 30% of cases, and survival increases only slightly. The results obtained with selective splenorenal shunting are worse in patients with alcoholism than in patients who do not drink alcohol. In general, patients with alcoholism, especially if they continue to drink alcohol, do not tolerate any surgical intervention well.

Liver transplantation for alcoholic liver cirrhosis

In the United States, 20,000 patients die each year from liver failure as an end-stage of alcoholic liver disease. Early mortality in liver transplantation among patients with alcoholic liver disease is the same as among patients with other liver diseases. Selection of patients for transplantation is difficult.

Alcoholics themselves are to blame for the development of liver cirrhosis. After transplantation, the patient may start drinking again, which complicates immunosuppressive therapy. Should alcoholics compete with other patients if the number of donor organs is limited? Patients selected for liver transplantation should have a stable mental status and the necessary socioeconomic prerequisites, a job to which they can return after the operation, and they should not have extrahepatic, such as cerebral, alcoholic lesions. They should abstain from alcohol for at least 6 months, which is the most significant prognostic factor for post-transplant relapse. The patient should be consulted by a psychiatrist, sign an "anti-alcohol contract" in which he undertakes to abstain from alcohol and undergo a course of rehabilitation before and after the operation. The longer the follow-up, the more severe the relapses. Alcoholic hepatitis can quickly develop in the "new" liver. Of 23 liver transplant recipients who resumed alcohol abuse, 22 had liver biopsy findings of alcoholic hepatitis within 177-711 days, and 4 had cirrhosis.

Selection of patients is extremely important. Patients who are refused transplantation on the grounds that their condition is still good enough should be followed up, since they may subsequently deteriorate. Patients who are not transplanted because their condition is too severe or their mental status is unstable have a significantly shorter survival than transplant recipients. It is much more difficult to justify liver transplantation in a patient with acute alcoholic hepatitis, in whom a period of sobriety before surgery is less likely, than in a patient with terminal alcoholic cirrhosis who is compliant with treatment. Liver transplantation should not be performed in acute alcoholic hepatitis until reliable methods for predicting relapses and especially possible relapse into alcoholism are available. Study of these issues requires well-designed controlled trials.

Selection criteria for patients with alcoholic liver disease for liver transplantation

• Abstinence from alcohol consumption for 6 months
• Child Group C
• Stable socio-economic situation
• The work the patient will return to after surgery
• Absence of alcohol-induced damage to other organs

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Forecast

The prognosis for alcoholic cirrhosis is much better than for other forms of cirrhosis, and depends largely on whether the patient can overcome alcohol dependence. This in turn depends on family support, financial resources, and socioeconomic status. A large group of workers with alcoholic cirrhosis of the liver was studied in Boston, many of whom lived in slums. The average survival time in this group was 33 months from diagnosis, compared with 16 months for patients with nonalcoholic cirrhosis. A study at Yale involved patients from a higher socioeconomic group who suffered from cirrhosis complicated by ascites, jaundice, and gavage vomiting. Their survival time exceeded 60 months in more than 50% of cases. If patients continued to drink alcohol, this figure dropped to 40%, while if they stopped drinking alcohol, it rose to 60%. Similar data were obtained in England. Continued heavy alcohol consumption was associated with poor survival.

Women with alcoholic cirrhosis of the liver live shorter lives than men.

Liver biopsy findings are the best predictor of prognosis. Zone 3 fibrosis and perivenular sclerosis are extremely unfavorable prognostic features. At present, such changes can only be detected by liver biopsy with appropriate connective tissue staining.

In alcoholic hepatitis, the presence of histological signs of cholestasis serves as an unfavorable prognostic sign. In patients who have survived acute alcoholic hepatitis, liver biopsies reveal a greater number of hepatocyte proliferation factors, TGF-a, and hepatocyte growth factor.

One study found that 50% of patients with alcoholic hepatitis developed cirrhosis after 10 to 13 years. In another study, 23% of patients with alcoholic liver disease but without cirrhosis developed cirrhosis after an average of 8.1 years. Fatty liver probably does not contribute to cirrhosis.

Patients who have only fibrosis and nodules in the liver without signs of hepatitis have the same prognosis that is usually observed in patients with fatty liver without cirrhosis and hepatitis.

Independent poor prognostic features appear to include encephalopathy, low serum albumin, elevated PT, and low hemoglobin. Patients with persistent jaundice and azotemia who are precomatose are at high risk of developing hepatorenal syndrome.

In patients in a state of decompensation, improvement occurs slowly. Obvious jaundice and ascites for 3 months or more indicate a grave prognosis. At a late stage, one cannot expect that abstinence from alcohol can affect the prognosis. The damage is irreversible. The highest mortality rate among patients suffering from liver cirrhosis or alcoholic hepatitis, as well as their combination, is noted in the first year of observation.

The detection of giant mitochondria in liver biopsy indicates "mild" disease and higher survival.

Patients with alcoholic hepatitis often experience worsening symptoms during the first few weeks of hospitalization. Resolution of the inflammatory process may take 1-6 months, with 20-50% of patients dying. Patients whose PV is markedly increased and does not respond to intramuscular vitamin K and whose serum bilirubin level exceeds 340 μmol (20 mg%) have a particularly poor prognosis. Alcoholic hepatitis resolves slowly even in patients who abstain from alcohol.

A multicenter study conducted at a Veterans Affairs hospital showed that the worst prognosis was observed in patients with alcoholic hepatitis and cirrhosis. Prognostic factors for survival were age, amount of alcohol consumed, AST/ALT ratio, and severity of disease based on morphologic and clinical findings. A high mortality rate was observed in malnourished patients who had fasted shortly before admission. Serum bilirubin and PT were used to determine a discriminant function for assessing prognosis in alcoholic hepatitis.

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