Alcoholic cirrhosis

Chronic alcohol intoxication causes 50% of all cirrhosis of the liver.

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

[1], [2]

Symptoms of the alcoholic cirrhosis

Alcoholic cirrhosis is characterized by the following distinguishing features:

• In the early stages, alcoholic cirrhosis, as a rule, micronodular, histological examination of liver biopsy specimens often reveals fatty hepatosis and signs of acute alcoholic hepatitis (hepatocyte necrosis, alcoholic hyaline, neutrophilic infiltration);
• in later stages, macronodular and mixed variants of cirrhosis develop, the effects of fatty hepatosis are reduced;
• symptoms of portal hypertension predominate in the clinical picture compared with the symptoms of hepatocellular insufficiency;
• episodes of acute alcoholic hepatitis, which are renewed with continued alcohol abuse, are usually the basis of exacerbation of cirrhosis of the liver;
• improvement of the general condition and clinical laboratory remission after stopping alcohol intake are extremely characteristic;
• much earlier than with viral cirrhosis there are pronounced signs of protein and vitamin deficiency;
• there are systemic manifestations of chronic alcohol intoxication (peripheral polyneuropathy; muscle atrophy; cardiovascular lesions with hyperdynamic syndrome — tachycardia, shortness of breath; chronic pancreatitis; flushing of the face with dilated skin capillaries, especially in the nasal area, etc.).

The classic "alcoholic cirrhosis" is a small node. At the same time, it is impossible to identify normal zonal architecture in the liver and in zone 3 it is difficult to detect venules. The formation of nodes is often delayed, apparently due to the inhibitory effect of alcohol on the regeneration of the liver. Different amounts of fat can be deposited in the liver; in case of liver cirrhosis, acute alcoholic hepatitis can be observed. With continued necrosis and fibrosis replacing it, cirrhosis can progress from small to large node, however, as a rule, this is accompanied by a decrease in steatosis. In the terminal stage, on the basis of the histological picture, it becomes difficult to confirm the alcoholic etiology of cirrhosis.

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

Increased iron content in the liver may be due to increased iron absorption, the presence of iron in beverages (especially in wines), hemolysis, and portocaval shunting; while in the body, the iron content in the depot increases only moderately.

[3], [4], [5], [6]

Treatment of the alcoholic cirrhosis

Cirrhosis is an irreversible condition, so treatment should be aimed at correcting complications. These include portal hypertension, encephalopathy and ascites. There is a violation of the metabolism of drugs, especially sedative drugs, which requires increased caution. Apparently, the safest drug is diazepam.

Oral addition of purified soybeans, polyunsaturated fatty acids, lecithin extract, containing 94-98% phosphatidylcholine (the main active ingredient of the drug Essentiale), prevented the development of septal fibrosis and cirrhosis in baboons who received alcohol for a long time. The mechanism of this effect is unknown; however, it is possible that it is associated with the stimulation of lipogen collagenase.

In patients with alcoholism, portocaval shunting, including transjugular intrahepatic shunting with stents, is accompanied by a decrease in bleeding from varicose veins, however, in 30% of cases, hepatic encephalopathy develops, and survival increases slightly. The results obtained in selective splenorenal bypass surgery are worse in patients with alcoholism than in patients who do not drink alcohol. In general, patients with alcoholism, especially if they continue to consume alcohol, do not tolerate any surgical intervention.

Liver transplantation in alcoholic cirrhosis

In the United States, 20,000 patients die from liver failure as the terminal stage of alcoholic liver disease every year. Early mortality in liver transplantation in patients with alcoholic liver disease is the same as in patients with other liver diseases. Patient selection for transplantation is difficult.

Patients with alcoholism themselves are guilty of the development of liver cirrhosis. After transplantation, the patient may again begin to consume alcohol, which complicates the conduct of immunosuppressive therapy. Should alcohol patients 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 socio-economic prerequisites, work to which they can return after the operation, and they should not have extrahepatic, for example, cerebral, alcoholic lesions. For at least 6 months, they should refrain from drinking alcohol, which is the most significant predictor of post-transplant recurrence. The patient must be advised by a psychiatrist, sign an "anti-alcohol contract", in which he undertakes to give up alcohol consumption and undergo a rehabilitation course before and after surgery. The longer the catamnesis, the harder the relapses. Alcoholic hepatitis can quickly develop in the “new” liver. Of the 23 patients who underwent liver transplantation, who resumed alcohol abuse, 22 showed signs of alcoholic hepatitis in liver biopsy in 22 within 177-711 days, and cirrhosis in 4 patients.

Patient selection is extremely important. Patients who were denied transplants should continue to be monitored on the basis that their condition is still quite good, as they may worsen later. Patients to whom liver transplantation was not performed due to a too severe condition or an unstable mental status, live significantly less than patients after transplantation. It is much more difficult to justify a liver transplant in a patient with acute alcoholic hepatitis, in which the period of sobriety before the operation is less likely than in a patient in the terminal stage of alcoholic cirrhosis who is committed to treatment. In acute alcoholic hepatitis, liver transplantation should not be carried out until reliable methods are available to predict the recurrence, and especially the possible resumption of alcoholism. The study of these issues requires well-designed controlled studies.

Selection criteria for patients with alcoholic liver disease for liver transplantation

• Abstinence from alcohol for 6 months
• Group C by Child
• Stable socio-economic situation
• Work to which the patient will return after surgery
• Lack of alcohol damage to other organs

[7], [8], [9], [10], [11], [12], [13], [14], [15], [16]

Forecast

With alcoholic cirrhosis, the prognosis is much better than with other forms of cirrhosis, and depends largely on whether the patient is able to overcome alcohol dependence. In turn, this depends on family support, financial opportunities and socio-economic status. A large group of workers suffering from alcoholic cirrhosis of the liver, many of whom lived in slums, were studied in Boston. The average life expectancy in this group was 33 months from the time of diagnosis, in contrast to the group of patients with non-alcoholic cirrhosis, in which it was 16 months. The study, conducted at Yale, involved patients from a higher socioeconomic group who suffered from cirrhosis, complicated ascites, jaundice, and vomiting. Their life expectancy exceeded 60 months in more than 50% of cases. If patients continued to consume alcohol, then this indicator decreased to 4 0%, while at refusal from alcohol consumption it increased to 60%. Similar data were obtained in England. Continuing heavy drinking combined with poor survival.

Women suffering from alcoholic cirrhosis of the liver, live less than men.

The data obtained from liver biopsy best indicate the prognosis of the disease. Fibrosis of zone 3 and perivenular sclerosis are extremely unfavorable prognostic signs. At present, such changes can only be detected with a liver biopsy with a corresponding staining of the connective tissue.

In alcoholic hepatitis, the presence of histological signs of cholestasis is an unfavorable prognostic sign. In patients who have experienced acute alcoholic hepatitis, a greater number of hepatocyte proliferation factors, TGF-a and hepatocyte growth factor are detected in liver biopsy specimens.

According to one study, 50% of patients with alcoholic hepatitis develop cirrhosis after 10-13 years. In another study, 23% of patients with alcoholic liver disease, but without cirrhosis, on average, after 8.1 years developed cirrhosis. Fatty liver is probably not a risk factor for liver cirrhosis.

Patients in whom only fibrosis and nodes are detected in the liver in the absence of signs of hepatitis have the same prognosis that is usually observed in patients with fatty liver without cirrhosis and hepatitis.

Independently poor prognostic signs seem to include encephalopathy, a low serum albumin level, an increase in PV and a low hemoglobin level. In patients with persistent jaundice and azotemia, who are in a pre-comatose state, the likelihood of developing hepatorenal syndrome is very high.

In patients with decompensation, improvement is slow. Obvious jaundice and ascites for 3 months and more indicate a severe prognosis. At a late stage it is impossible to expect that a refusal to use alcohol may affect the prognosis. Defeat is irreversible. The highest mortality rate among patients suffering from cirrhosis of the liver or alcoholic hepatitis, as well as their combination, is noted in the first year of observation.

Detection of giant mitochondria in the liver biopsy indicates a "mild" disease and a higher survival rate.

Patients with alcoholic hepatitis often worsen in the first few weeks of their stay in the hospital. The resolution of the inflammatory process can last 1-6 months, while 20-50% of patients die. Patients in whom PV is significantly increased and does not respond to the intramuscular administration of vitamin K, and the serum bilirubin level exceeds 340 µmol (20 mg%), have a particularly poor prognosis. Alcoholic hepatitis is resolved slowly even in those patients who abstain from alcohol.

According to a multicenter study undertaken by the Hospital for Veterans, the worst prognosis was observed with a combination of alcoholic hepatitis and cirrhosis of the liver. Prognostic factors determining survival were age, amount of alcohol consumed, the ratio of AST / ALT, and the severity of the disease according to morphological and clinical data. A high probability of death was observed in patients with reduced nutrition who were starving shortly before admission to the hospital. Serum bilirubin and PV levels were used to determine the discriminant function, which was used to evaluate the prognosis of alcoholic hepatitis.

[17], [18], [19], [20],