Alcoholic liver damage

The term "alcoholic liver disease" appeared in the international statistical classification of diseases of the tenth revision in 1995.It is quite large, because it includes not one but several diseases that are accompanied by a violation of the structure and function of the liver cells and are united by a single cause - a prolonged use of alcohol by the patient. Some narcologists consider them stages.

The defeat of the liver with alcoholism is well enough studied. Conclusions of scientists are unanimous: the main role is played not by the high cost and variety of drinks, but by the regular use of the limiting dosage in recalculation on pure alcohol.

All forms of alcoholic liver disease( abbreviated ABP) have one pathogenetic origin - the entry of alcohol into the stomach, and from it into the small intestine and blood. The specific damaging effect on the hepatic cells develops in different ways and is determined by the individual capabilities of the organism. Data from pathological anatomical studies indicate that 30% of alcoholics have no changes in the liver.

Who is more sensitive to alcohol?

It is established that men suffer from alcoholic liver disease 3 times more often than women. The disease is common among people of young and middle age( from 20 to 60 years) and has a tendency to seize adolescents.

For men, a critical dose of ethanol is about 80 ml daily. Women are 20-40 grams per day, and in adolescence, alcoholic liver damage occurs when 15 grams of alcohol are consumed. It should be noted that the advertised non-alcoholic beer contains at least 5% pure alcohol. Therefore, with enthusiasm for this drink, young people "get" a dose of drunk volume.

The risk factors are:

• alcoholic "experience" for more than 8 years;
• regular use of ethanol, for people taking breaks in 2 weeks, the duration of liver damage is extended to 10-15 years;
• sex - women have the characteristics of producing enzymes that break down ethanol, starting with gastric juice;
• malnutrition, lack of protein and vitamin nutrition;
• obesity caused by impaired metabolism of lipid metabolism;
• incidental poisoning of the liver with toxic substances of alcohol substitute;
• transferred viral hepatitis( in ¼ of patients with alcoholic disease, antibodies indicating viral chronic hepatitis C were detected);
• a hereditary predisposition caused by a certain genetic mutation tied to a disruption in the production of enzyme systems that cleave ethyl alcohol, for the same reason, the residents of Southeast Asia, China, are more likely to alcoholism;
• liver overload with iron due to increased absorption of this electrolyte in the intestine, hemolysis process, increased concentration in some alcohol-containing beverages.

Characteristics of forms by development mechanism

The biochemical process of ethanol breakdown in the body begins with its entry into the stomach. Here, the fourth part of the dose is converted to acetaldehyde, due to the presence of alcohol dehydrogenase in the gastric juice. It is because of its low activity in women and persons of the Mongoloid race that the sensitivity to the relatively low volume of alcohol taken has been increased.

Absorbing through the intestinal wall into the bloodstream, alcohol enters all body fluids( blood, cerebrospinal fluid, urine, semen).The venous system from the abdominal cavity organs delivers ethanol to the hepatic cells( hepatocytes).

Here the "work" of the hepatic fraction of alcohol dehydrogenase begins. Its outcome is the formation of acetaldehyde. The reaction is controlled by powerful coenzymes. Subsequent transformation of acetaldehyde occurs under the influence of microsomal oxidation systems in the cytoplasm of hepatocytes and catalase enzyme, acetic acid is formed.

The easiest stage is fatty degeneration or steatosis. It is found in 100% of people who abuse alcohol, especially if at the same time there is excess weight and impaired fat metabolism. There is an increase in triglycerides in cells and the deposition of fatty inclusions in the form of macro- or microbubbles.

It is important that this violation in the liver can pass without a trace a month after the complete refusal of alcohol. No symptoms appear. Continuation of the process leads to fatty degeneration( replacement of the cell with fat tissue).

Alcoholic hepatitis - a more severe liver damage, is inflammatory. Occurs in acute or chronic form. In the center of the hepatic lobules, under the influence of acetaldehyde, leukocyte infiltration appears, the cells swell, they are distinguished by giant mitochondria, hyaline protein inclusions( Mallory's bodies) are formed in the cytoplasm.

It is established that hyaline is formed by the cell from the epithelium with a broken synthesis process and is a composition of cytokeratin. Pathological protein accumulates near the nucleus of the cell and is accompanied by irreversible changes. Fibrosis in the form of collagen fibers is localized in the center and in the region of the sinuses. Inside the cells is a pronounced picture of fatty degeneration. In the bile ducts of the liver - stagnation.

In the support of the inflammatory process and further aggravation of hepatic parenchyma violations, an important role is played by:

• autoimmune type of reactions, development of antibodies and anti-inflammatory cytokines on cell nuclei, "alcoholic hyaline" with the deposition of immunoglobulin complexes in liver structures;
• hypoxia( oxygen starvation of hepatocytes) due to compression of the leading arterial vessels with edematous tissue.

It is important to note in the diagnosis that alcoholic hepatitis affects individual parts of the hepatic tissue. They, in the final analysis, are fibrotic. But the other part is able to perform its functions. Therefore, with acute course, there is hope for positive results of treatment against substitution therapy. Chronic inflammation leads to continuously progressive replacement of hepatocytes with connective tissue, loss of all basic functions by the body.

Alcoholic fibrosis of the liver - connective tissue proliferating does not disturb the structure of the hepatic lobules, therefore some functions are preserved. In the process of scarring, the significance of:

• is increased production of cytokines, which promotes the growth of fibroblast cells and collagen;
• increased production of angiotensinogen II;
• changes in the intestinal microflora, excess bacteria synthesize a specific endotoxin, which affects the process of fibrosis.

Alcoholic cirrhosis differs from diffuse liver damage, gradual death of hepatocytes and replacement of tissue with scars. The structure of the liver is broken, the lobules are replaced by dense knots from the connective tissue. At first they are small in size, then large formations are formed. With the exclusion of more than 50-70% of hepatocytes from functioning, signs of hepatic insufficiency appear.

Symptoms and manifestations of

Symptoms of alcoholic liver disease appear gradually. Steatosis in patients occurs most often asymptomatically, is detected by chance. In rare cases, patients feel:

• blunt pain in the hypochondrium right;
• nausea;
• general malaise.

15% have jaundice of the skin.

When alcoholic hepatitis the clinic depends on the form of the flow. Acute hepatitis is possible in four variants. Latent - has no symptoms, it is detected only with liver biopsy. Jaundice is the most frequent, accompanied by:

• weakness;
• lack of appetite;
• pain in the hypochondrium right;
• with vomiting and nausea;
• by diarrhea;
• weight loss;
• yellowing of the skin and sclera;
• in half the cases the temperature rises to low figures.

Cholestatic - differs from icteric form:

• with severe itching;
• severe jaundice;
• with bursting pain;
• the possibility of raising the temperature.

Fulminant is a severe rapidly progressing form of alcoholic hepatitis. To pain and jaundice are joined:

• manifestations of hemorrhagic syndrome( hemorrhage);
• toxic effect on the brain;
• kidney damage;
• progressive hepatic failure.

Chronic form of alcoholic hepatitis is present in 1/3 of persons suffering from alcoholism. It can take place in a light, medium-heavy, severe variant. They are explained by persistent current( gradual) or actively progressing development of the disease.

The persistent form is usually manifested:

• by low intensity pain in the hypochondrium on the right;
• loss of appetite;
• change of diarrhea and constipation;
• belching;
• bloating.

With progressive form, the symptoms are brighter, the clinic is growing rapidly, accompanied by jaundice, fever, significant weight loss, increased liver and spleen, complications.

Asthenia manifests itself:

• with a constant sense of fatigue, fatigue;
• marked weakness;
• with a depressed mood;
• disturbed sleep( insomnia at night and drowsiness during the day);
• lack of appetite.

Dyspeptic syndrome is expressed by:

• in a decrease or total absence of appetite;
• attacks of nausea and vomiting;
• flatulence and rumbling in the abdomen;
• unstable stool( diarrhea is replaced by constipation).
• tenderness along the bowel.

In the clinic of alcoholic liver disease, the beginning symptoms of hepatic insufficiency are distinguished according to the syndrome of "small" symptoms, which include:

• vascular dots and "asterisks" on the skin of the face and other areas of the body( telangiectasia);
• reddening of the skin on the palmar and plantar surfaces of the limbs( palmar and plantar erythema);
• bruises on the skin from slight depression;
• swelling of the salivary glands in the parotid region;
• increased end phalanx on the fingers, flattening and widening of the nails( "drumsticks");
• may shorten the tendons of the palmar muscles, disrupting the brush function( Dupuytren's contracture), while painless pain is palpated under the skin.

Because of the decrease in synthesis in the liver of sex hormones, the appearance of men changes, it is called "feminization", since typical female symptoms appear:

• fat is deposited on the abdomen and hips;
• arms and legs become thin;
• decreased hair in the armpit and pubic;
• possible enlargement of the mammary glands( gynecomastia);
• testes atrophy, the man is not able to have offspring, becomes impotent.

Syndrome of portal hypertension - on its symptoms indicate:

• appearance and growth of ascites( enlarged abdomen due to effusion of fluid in the abdominal cavity);
• a symptom of the "jellyfish head" - is formed by a characteristic expansion of the subcutaneous veins around the navel;
• significantly enlarged spleen;
• enlarged veins of the esophagus and stomach due to stagnation in the zone included in the portal portal system.

Symptoms that indicate the damage to other organs and systems:

• toxic effects of acetaldehyde on the nerve trunks lead to peripheral polyneuropathy, the patient has a sensitivity in the limbs, limited movement;
• muscle atrophy is accompanied by their thinning, weakness at work;
• cardiovascular system responds with tachycardia, a tendency to arrhythmias, shortness of breath, stabbing pain in the heart area, hypotension due to lowering of the upper pressure;
• brain damage leads to encephalopathy, clinically it manifests itself as a violation of consciousness( from inhibition to coma), behavioral changes, memory loss, irritability;
• adherence of renal failure is accompanied by edema of the face and body, violation of urination, dysuric phenomena.

What complications occur at different stages?

With the continued use of alcohol in patients, alcoholic steatosis necessarily goes to the following stages: hepatitis, fibrosis, cirrhosis. Consequences of alcoholic hepatitis can become:

• brain damage( encephalopathy);
• manifestations of hemorrhagic syndrome with hemorrhages in internal organs;
• hepatorenal syndrome, accompanied by blocking the filtration function of the kidneys with renal insufficiency;
• hypoglycemia;
• bacterial peritonitis due to infection;
• in chronic course - hypertension in the portal portal system, ascites.

The development of complications indicates an unfavorable prognosis. The fibrosis stage passes into cirrhosis of the liver and is accompanied by:

• hypertension in the portal venous area with bleeding from the esophagus and stomach;
• development of renal and hepatic insufficiency;
• anemia;
• marked ascites and edema on the legs;
• cardiac decompensation, arrhythmias;
• high risk of degeneration into cancer.

Diagnosis

To correctly diagnose alcoholic liver damage means not only to reveal the characteristic signs, but also to connect them with an alcoholic anamnesis. After all, the patient always has to differentiate the condition with various diseases, including:

• viral hepatitis;
• liver cancer;
• parasitic lesions;
• drug and toxic hepatitis occur with long-term treatment with valproic acid( Depakin drug), tetracycline antibiotics, Zidovudine;
• inflammatory diseases of the biliary tract;
• cirrhosis in heart failure;
• non-alcoholic fatty disease.

Patient questioning helps to clarify the risk factors and causes of liver damage:

• presence of bad habits, doses and regularity of alcohol consumption;
• previous illnesses( viral hepatitis);
• prescription of symptoms;
• hereditary predisposition;
• power features;
• availability of occupational hazards.

In the general blood test:

• , the decrease in erythrocytes and hemoglobin indicates anemia;
• platelet loss - reduced coagulation;
• the growth of leukocytes with a shift of the formula to the left and a high index of ESR - on the current inflammation, possibly joining the infection;
• eosinophilia - on the expressed autoimmune processes.

The study of plasma proteins shows a moderate increase in the fraction of gamma globulins with a decrease in albumins. The activity of the enzyme systems of the hepatic cells is reflected by:

• increase in the level of gamma-glutamyltranspeptidase in plasma;
• increase in alkaline phosphatase;
• increased the content of transferrin, carrying iron;
• the change in the ratio of aspartic and alanine aminotransferases towards alanine aminotransferase activity( ALT, ALT), normally the coefficient determining this proportion is equal to unity, the content of both enzymes is approximately the same, against the background of hepatocyte death, it becomes lower.

The markers of fibrosis are:

• level of hyaluronic acid;
• procollagen III type and type IV collagen;
• laminin;
• matrix metalloproteinases and their inhibitors.

These blood tests are not performed in polyclinic laboratories, but only in specialized clinics. They show any fibrosis of the internal organs, so they can not be considered specific for alcoholic liver disease. More specific is the increased level of proline and hydroxyproline.

In the general analysis of urine, growth is important:

• bilirubin;
• proteinuria and erythrocyturia( associated with hepatorenal syndrome);
• leukocytes and bacteria if the disease is complicated by infection of the urinary tract.

Stool analysis shows changes in the coprogram towards the appearance of undigested food fragments, growth of fats, coarse dietary fiber.

Instrumental types of the

study Among the instrumental methods of confirming the liver lesion, the following are most often used:

• ultrasound examination - shows the structure and dimensions of the liver, spleen;
• esophagogastroduodenoscopy - gives a visual picture of stagnation in the veins of the stomach and esophagus;
• magnetic resonance imaging and computed tomography is performed to more accurately elucidate the structure of the liver parenchyma;
• elastography is a kind of ultrasound, evaluates the ability of tissues to contract, reveals scars, fibrosis sites;
• cholangiography - a contrast medium is injected intravenously, which is released through the bile ducts, the cause of congestion of bile is identified using X-rays, it is performed only for patients with suspicion of cholelithiasis.

Complete confirmation of the diagnosis and the stage of alcoholic illness gives the result of a puncture liver biopsy.

Differential diagnosis with non-alcoholic fatty lesions

Non-alcoholic steatohepatitis or fatty liver disease( NAWA) refers to fairly common types of pathology. In different countries it affects from ¼ to half the population.

It is observed more often in women aged 40-60 years, in children with metabolic disorders accompanying:

• obesity;
• hypertension;
• diabetes mellitus;
• hormonal disorders;
• reception of corticosteroid drugs, contraceptives;
• improper nutrition( both prevalence of easily assimilated carbohydrates and fats, and rapid weight loss in fasting).

Acute fatty hepatosis can be provoked by pregnancy. Factors of disease activation include:

• chronic pancreatitis;
• gastric or duodenal ulcer:
• gout;
• lung disease;
• psoriasis;
• systemic pathology of connective tissue.

. Normally triglycerides break down with release of energy. In conditions of pathology, their excessive amount is capable of:

• deposited within the cytoplasm of cells;
• violate the integrity of cell membranes;
• activate the processes of fibrosis.

Patients complaining about:

• for weakness, fatigue;
• severity and abdominal pain;
• headaches;
• disorder of stool.

In advanced cases, the enlarged liver and spleen is determined. An important difference are:

• lack of a prolonged alcoholic history;
• increased patient weight;
• significant growth in the analysis of blood triglycerides;
• hyperglycemia;
• in 40% of patients has skin pigmentation in the neck, armpits.

Among the clinical manifestations of jaundice indicates concomitant hepatitis, it is rare.

Treatment of

Treatment of alcoholic liver disease is impossible without the patient stopping drinking alcohol. Necessarily observance of dietary recommendations for nutrition:

• prohibits sharp, fatty, fried and smoked products( meat, sausages, sauces, pickles);
• is limited to salt;
• protein is replenished with dairy products, cereals( with encephalopathy is reduced);
• increases the proportion of vegetables, fruits;
• shows boiled fish.

Medical aid

At the initial stages of alcoholic illness in treatment is enough:

• application of hepatoprotectors;
• complex of vitamins;
• drugs from the adenomethionine group;
• components of bile( ursocholic acid).

They provide:

• protection of cell membranes of the liver and brain cells;
• improve the outflow of bile;
• bind toxic substances;
• activate the processes of regeneration of damaged tissue sites;
• normalizes some mental disorders.

Glucocorticoids are used to suppress autoimmune inflammatory components, obstructed scar scar tissue regeneration. A group of drugs related to ACE inhibitors( angiotensin converting enzyme) not only lowers blood pressure, but also has anti-inflammatory effect, delaying the spread of connective tissue. The blockers of tissue proteases help to stop scarring.

In the presence of portal hypertension apply:

• nitrates - dilate the peripheral vessels and reduce pressure in the portal vein;
• β-adrenoblockers - used at sufficient arterial pressure;
• preparations-analogues of somatostatin - suppress the hormonal effect on the vessels of the abdominal cavity;
• diuretics are necessary for removing excess fluid.

If necessary, antibiotics are prescribed to suppress pathogenic flora and associated infection. In ascites, if diuretics do not help, paracentesis is performed - puncturing the abdominal wall with a trocar and removing the fluid.

Surgical methods

Surgical treatment is used to eliminate complications of liver cirrhosis:

• portocaval bypass provides an additional way of discharging blood into the lower vena cava;
• installation of a shunt between the splenic and renal veins;
• ligation of the arteries and veins of the esophagus and stomach with bleeding.

Radical treatment for severe alcoholic illness is liver transplantation. But it is practically not produced.

Forecast

The outcome of alcoholic liver disease is determined by the stage in which the patient stopped drinking alcohol.

. In case of alcoholic illness, there is a significant improvement in the patient's condition during periods of refusal to drink alcohol. This creates a false sense of self-ability to improve health and hope for a cure.

Unfortunately, the comprehension of the harmful effects of alcohol in most people comes too late, when a part of the liver is already destroyed and can not be restored. In such conditions, even with complete renunciation of alcohol, the patient can live 5-7 years. In women, the change in stages of the disease occurs more quickly. Alcoholic liver disease is a vivid example of the harmful relationship of a person to the gift of nature, to his own health.