slopes 

Alcoholism and neurological complications. Alcohol withdrawal, delirium tremens, alcoholic dementia, etc. A complete approach in the treatment of alcoholic liver dystrophy Peripheral nervous system lesions

Movement disorders. These can be paralysis (complete or almost complete loss of muscle strength), paresis (partial decrease in muscle strength). Paralyzed muscles become relaxed and soft, their resistance during passive movements is weakly expressed or absent, an atrophic process also develops in these muscles (within 3-4 months, the normal muscle volume decreases by 70-80%), tendon reflexes will be absent - this is peripheral paralysis . Central paralysis will be characterized by an increase in muscle tone, an increase in tendon reflexes, the appearance of pathological reflexes, and no muscle degeneration. The second group of movement disorders, in which there is no decrease in muscle strength, include lesions of movement and posture disorders due to damage to the basal ganglia. In this case, the following symptoms occur: akinesia, characterized by the inability to make quick movements in the limbs, muscle rigidity, tremor (trembling in the fingers, upper limbs, chin), chorea (arrhythmic involuntary rapid movements involving the fingers, hand, entire limb or other parts body), athetosis (relatively slow worm-like involuntary movements, replacing one another), dystonia (manifested by the occurrence of pathological postures). Disturbances in coordination of movements and other disorders of the function of the cerebellum. In this case, there is a violation of the coordination of voluntary movements (ataxia), dysarthria (slowing or fuzzy speech), hypotension of the limbs. Other movement disorders include tremor (trembling), asterixis (fast, large-scale, arrhythmic movements), clonus (rhythmic unidirectional contractions and relaxation of a muscle group), myoclonus (arrhythmic, jerky contractions of individual muscle groups), polymyoclonus (common lightning-fast, arrhythmic contractions muscles in many parts of the body), tics (periodic sharp twitches in certain muscle groups, apparently allowing patients to reduce the feeling of internal tension), motor stereotypy, akathisia (a state of extreme motor restlessness), startle. Impaired stability and walking are cerebellar gait (legs wide apart, unsteadiness while standing and sitting), sensory atactic gait (pronounced difficulty standing and walking despite maintaining muscle strength), and many others. Often there are disorders of tactile sensitivity. Other symptoms include pain. Here, it is especially necessary to highlight headache (simple migraine, classic migraine, cluster migraine, chronic tension headache, pain with brain tumors, pain with temporal arteritis), pain in the lower back and limbs (sprain in the lumbosacral region, herniated discs located between the vertebrae, spondylolisthesis, spondylosis, tumors of the spinal cord and spine), pain in the neck and upper limb (intervertebral hernia, degenerative diseases of the cervical spine). Changes in the function of other types of sensitivity, impaired sense of smell: anosmia (loss of smell), dysosmia (perversion of the perception of olfactory sensations), olfactory hallucinations, taste disturbances. Of the other types of sensitivity, these are visual impairments, eye movements and pupillary function, auditory analyzer disorders, dizziness and changes in the balance system - may be signs of pathological processes in the nervous system. Other manifestations of the pathology of the nervous system can be epileptic seizures, hysterical seizures, impaired consciousness (coma, fainting), sleep disorders (insomia - a chronic inability to fall asleep, hypersomnia - excessive sleep, sleepwalking, and others), in addition to mental disorders, changes in behavior, speech disorders, severe anxiety, fatigue, mood swings and pathology of drives.

Alcoholism is a global problem

The consumption of alcoholic (ethanol-containing) beverages is a worldwide cause of alcoholic liver disease and can also contribute to the progression of other liver diseases such as hepatitis C. Alcohol consumption is a significant cause of death worldwide, affecting men more than women.

A Danish study of patients with alcoholic hepatitis found a 5-year mortality rate of 47% and an increase to 69% for those with alcoholic hepatitis and concomitant cirrhosis. Because of the high level of associated risk, patients with evidence of alcoholic liver disease should also be screened for hepatitis C virus and hepatitis B virus.

Screening for excessive alcohol consumption is an important preventive measure and should be the standard of care during the clinical evaluation of older children and adults. The AUDIT (Alcoholic Drink Consumption Test) is a questionnaire containing 10 questions regarding excessive alcohol consumption and the presence of alcohol dependence. Patients with positive test results should be referred for treatment.

For those patients who present with signs of liver damage, abstinence from further alcohol consumption is the most important component of the treatment of this disease, which can improve their long-term outcomes. Baclofen has been included in the treatment of certain patients to reduce the likelihood of relapse.

Pathophysiology of alcoholic liver dystrophy

Due to the influence of alcohol, symptoms of multiple liver diseases can develop. Fatty liver, alcoholic hepatitis, cirrhosis, acute or chronic liver failure, and hepatocellular carcinoma - all these diseases are the result of excessive consumption of alcoholic beverages. Fatty liver disease is the most common histological manifestation of regular alcohol consumption. Hepatocellular carcinoma usually develops in patients with end-stage alcoholic cirrhosis, but in some cases it can be detected in alcohol-dependent patients without signs of cirrhosis.

The pathophysiological mechanism leading to the development of alcoholic hepatitis and end-stage cirrhosis remains unclear. Only 10%-20% of chronic alcoholics are at risk of developing cirrhosis, despite the fact that the degree of alcohol consumption is generally the same. Concomitant factors such as nutritional deficiencies, genetic predisposition, immune system characteristics, differences in ethanol metabolism, and exposure to circulating endotoxins also play a significant role. Ethanol increases the permeability of the intestinal wall, and recent studies indicate that changes in the intestinal and endogenous microflora may play a role in the development of major alcoholic liver diseases.

The development of alcoholic liver disease also appears to depend on the amount and duration of ethanol consumption, ethnicity, and genetic predisposition. Despite higher alcohol-related death rates among men, women who consume the same daily amount of ethanol as men are at even greater individual risk of developing severe liver disease and progressing to end-stage liver disease. Hispanic men and Native Americans are also at an increased risk of developing alcoholic liver disease.

The development of alcoholic liver disease may be associated with associated obesity or malnutrition. Metabolic syndrome in patients who consume alcoholic beverages may increase the risk of developing various liver diseases. Type 2 diabetes mellitus increases mortality and hospitalization rates in individuals with alcoholic liver disease. Patients who regularly consume alcohol and who have coexisting obesity have a greater risk of developing alcoholic hepatitis and cirrhosis. An analysis of data from patients participating in Scottish cohort studies found that obesity significantly increases the severity of the negative effects of excessive alcohol consumption. Obesity can also increase the risk of developing hepatocellular carcinoma.

The most common diseases

Alcoholic degeneration of the liver

Fatty liver disease is a common manifestation of excessive alcohol consumption, which occurs in most chronic alcoholics; it is often a disease that can be stopped by abstaining from ethanol consumption. Alcohol consumption can accelerate the development of fibrosis and damage to liver cells in the presence of other liver pathologies. In patients with non-alcoholic fatty liver disease, excessive alcohol consumption also accelerates the progression of the disease, moreover, it may be associated with the subsequent development of hepatocellular carcinoma.

Alcoholic hepatitis

The mechanism that leads to the transition of alcoholic liver disease to alcoholic hepatitis remains unclear. In some patients, a sharp increase in the amount of alcohol consumed precedes the clinical development of alcoholic hepatitis.

In the case when obesity is combined with excessive alcohol consumption, the differential diagnosis of alcoholic hepatitis and progressive non-alcoholic fatty liver becomes difficult. Patients with alcoholic hepatitis may present with symptoms such as associated fever, right upper quadrant pain, liver tenderness, systemic inflammatory response syndrome, and signs of portal hypertension with ascites, encephalopathy, and splenomegaly. Alcoholic hepatitis has several degrees of severity. Mortality within 30 days, detected in patients with a severe degree of this disease, is 30%. When alcoholic hepatitis develops in the setting of alcoholic cirrhosis, subsequent acute and chronic liver failure also results in increased mortality. Co-existing bacterial infection may occur in patients with severe alcoholic liver disease, which greatly increases the risk of multiple organ failure.

A liver biopsy is no longer a routine procedure for making a diagnosis when there are signs of alcoholic liver disease. The diagnosis of this disease should be questioned as often as possible and differential diagnosis should be carried out regularly. A recent histological study has shown that the severity of degeneration of affected hepatocytes and the density of Mallory-Denk bodies may indicate a possible clinical response to corticosteroid treatment. The Maddray Discriminant Function Scores and End Stage Liver Disease (MELD) Templates are commonly used to assess the clinical severity of alcoholic hepatitis. The severity of alcoholic hepatitis is considered severe with a Maddrey discriminant function score greater than 32, or a MELD value greater than 20, although a MELD score may be a more accurate indicator of outcome. The combination of a pre-treatment MELD pre-treatment assessment with a Lille assessment performed at the end of the first week of corticosteroid treatment is best predictive of disease severity and clinical outcome. Alcoholic hepatitis can be cured up to a return to normal liver histology, but despite this, most patients develop cirrhosis.

The clinical severity of alcoholic hepatitis can be progressive and also associated with the spread of sepsis and symptoms of end-stage liver disease, including encephalopathy, gastrointestinal bleeding, and hepatorenal syndrome. The systemic inflammatory response syndrome in patients with alcoholic hepatitis indicates a high risk of developing multiple organ failure.

Alcoholic cirrhosis

Up to 20% of patients suffering from excessive alcohol consumption are at risk of developing cirrhosis of the liver. Patients with alcoholic cirrhosis may develop portal hypertension and hepatocellular carcinoma and should be regularly screened for esophageal varices, moreover, they should undergo liver ultrasound every six months to screen for carcinoma. People with cirrhosis who resume alcohol consumption are at risk of developing recurrent alcoholic hepatitis, which in turn can lead to acute or chronic liver failure and multiple organ failure.

The American College of Gastroenterology, the American Gastroenterological Association and the European Hepatology Association have published the latest guidelines for the evaluation and management of alcoholic liver disease.

Principles of treatment

For patients with alcoholic liver disease, the most important element of treatment is immediate and prolonged abstinence from alcohol consumption. Any comprehensive treatment of such conditions should be carried out by multidisciplinary teams that include drug and alcohol addiction specialists, as well as psychosocial and behavioral therapy.

Resumption of alcohol consumption after recovery from alcoholic hepatitis is associated with an increased risk of subsequent mortality. Patients with severe forms of alcoholic liver disease should be screened for infections because infectious diseases along with alcoholic hepatitis increase the risk of death and/or failure to respond to treatment.

Since protein and calorie deficiencies are common among patients with alcoholic hepatitis, they should be given appropriate nutritional supplements. Sufficient is the consumption of 1-1.5 g of protein per kg of body weight and 30-40 kcal per kg of body weight per day.

In terms of drug therapy, early studies have shown that taking Pentoxifylline may improve survival in patients with advanced alcoholic hepatitis. This drug is effective in the absence of hepatorenal syndrome, since no improvement in survival has been found in individuals with elevated creatinine levels taking Pentoxifylline. A randomized study of the effectiveness of Penoxifylline in severe alcoholic hepatitis did not demonstrate a significant positive effect. Although pentoxifylline may reduce the risk of hepatorenal syndrome, current evidence does not support this drug as the only treatment for severe alcoholic hepatitis.

Several randomized clinical trials have been conducted on the use of corticosteroids as a treatment for alcoholic hepatitis. A meta-analysis of these studies demonstrated that such treatment leads to improved mortality rates, including a reduction in the risk of developing hepatorenal syndrome with the combined use of corticosteroids and Pentoxifylline. The STOPAH study evaluated the clinical response to treatment with corticosteroids, pentoxifylline, or both simultaneously for 28 days, compared with placebo, in 1053 patients. None of the treatments resulted in a statistically significant reduction in mortality, although corticosteroid treatments have a greater reduction in mortality at 28 days than the other groups. At 90 days after the start of treatment, there was no difference in long-term treatment outcomes.

Based on these numerous studies, the current treatment recommendations are that patients with severe alcoholic hepatitis (Maddrey discriminant function score greater than 32 or MELD score greater than 20) should receive corticosteroid treatment that includes methylprednisolone 32 mg daily for 28 days. The Lille score uses data on the patient's age, degree of renal insufficiency, albumin, prothrombin time, bilirubin, and bilirubin levels at day 4 and day 7 to calculate a preliminary outcome of 28 days of corticosteroid therapy.

Corticosteroids may increase the risk of infection during treatment for alcoholic hepatitis. An increase in the level of bacterial DNA circulating in the blood is a sign of the presence of an infection in the body, as well as a high likelihood of developing sepsis.

Transplantation

Liver transplantation is considered the last resort for patients with end-stage alcoholic liver disease. The number of liver transplants performed annually in the United States of America for alcoholic liver disease is increasing. In the presence of liver cirrhosis complicated by portal hypertension, preparation for transplantation should be especially thorough.

Six months of abstinence from alcohol consumption is the main condition for the inclusion of patients with alcohol dependence in the queue for liver transplantation. This recommendation is used to determine whether alcoholic hepatitis will have sufficient clinical improvement to avoid transplantation, to allow treatment of complications and prevention of relapse after transplantation, and possibly in response to public perceptions of a lack of donor livers.

Recent studies show that patients with alcoholic hepatitis are suitable candidates for liver transplantation. Short-term and long-term survival rates in patients with alcoholic hepatitis after liver transplantation are similar to those in patients with end-stage alcoholic cirrhosis after transplantation. The frequency of relapses of alcoholism is also the same in both groups. This has led to strict requirements for selection for liver transplantation in patients with severe alcoholic hepatitis. When treating individuals with severe alcoholic hepatitis with corticosteroids, if a positive response to treatment is not observed within 7 days (as assessed by the Lille scale), such patients can be considered as candidates for immediate liver transplantation.

Patients who suffered from alcoholic hepatitis before liver transplantation are not at higher risk of relapse of alcoholism after the operation. A meta-analysis of 11 studies of liver transplantation for alcoholic hepatitis showed that the risk of recurrence after such operations does not differ from the same risk for patients who suffered from alcoholic cirrhosis before the operation. This analysis also demonstrated that survival rates at 6 months after transplantation were similar in both groups. All liver transplant patients should be regularly screened for recurrence, as recurrent alcoholic hepatitis and cirrhosis may be at increased risk of mortality. Also, people with alcoholism have a significant risk of developing cardiovascular disease and carcinoma after liver transplantation. Moreover, smoking patients should stop smoking to reduce the risk of developing carcinoma and heart disease associated with smoking.

One of the consequences of alcoholism is the alcoholic degradation of the personality, which is expressed in the moral and ethical decline and coarsening of the person's personality. The term “degradation” itself comes from the Latin word “degradatio”, which means “reverse development”, “decline”. An alcoholic loses his old life values ​​and replaces them with new ones, while the desire to drink becomes the main thing in his life.

In people with low intelligence, with a weak will and character, who do not have clearly defined life values, degradation occurs many times faster than those with high intelligence and clear goals. The latter may not be degraded for a very long time, even in the last stages of alcoholism.

An example can be a lot of well-known creative people who continued their successful activities even with severe alcoholism.

Alcoholic degradation of personality is manifested by a number of signs. The dependent is changing the hierarchy of values:

The degradation of personal qualities manifests itself in the appearance of such character traits:

  • Boastfulness.
  • Deceit.
  • Justifying your alcoholism (trouble at work or in the family, health problems, and so on).
  • Tactlessness.
  • Exaggerated self-esteem.
  • Familiarity.
  • Sloppiness.
  • Annoyance.
  • Commercialism.

There are disturbances in the process of thinking:

  • Passivity and lethargy.
  • Decreased productivity of thinking.
  • Inability to see cause and effect relationships.
  • Progressive deterioration of memory, especially for recent events.

The first signs of degradation begin to appear after 7-8 years of regular drinking, after another 2 years they become obvious to everyone. When degradation occurs much faster.

Alcohol has an extremely negative effect on all organs and systems of the human body, but the brain suffers most from it. Getting into the human blood, alcohol destroys the cerebral cortex. It consists of neurons (nerve cells), of which there are 15 billion. Each of them receives power from its own microcapillary. It is very thin, so red blood cells can only pass through it in one row. Under the influence of alcohol, red blood cells stick together, clogging the microcapillary, which leads to the death of the neuron.

Oxygen ceases to enter the brain in the required amount, which, in turn, causes hypoxia (oxygen starvation). A drinking person feels relaxed and euphoric at this time, not knowing that alcohol blocks unpleasant information, contributing to the death of neurons, as a result of which the brain overflows with blood, the vessels of the meninges and convolutions rupture.

Thus, alcohol disrupts the normal functioning of the brain, which is the cause of personality degradation.

Further abuse of alcohol leads to changes in the functions of the entire nervous system, and the spinal cord and medulla oblongata are also affected. The result of this can be a coma or death of an alcoholic.

Types of alcohol degradation

Alcoholism in patients can manifest itself in different ways. It is customary to distinguish four main types of alcoholic degradation of the personality according to:

  • Astheno-neurosis-like type.
  • Alcohol type.
  • Alcohol-organic type.
  • Psychopathic type.

With this type of degradation, irritability and asthenia become the main signs. They lead to a permanent sleep disturbance (the patient sleeps from 2 to 5 hours a day). To sleep, alcoholics drink large amounts of alcohol at night.

The following clinical manifestations of the disease appear:

  • Excessive excitability and emotionality.
  • Irritability.
  • Decline of mental and physical strength.
  • Memory deterioration.
  • Decreased performance.
  • Absent-mindedness.
  • Problems with concentration.
  • Suspiciousness, a tendency to obsessive thoughts.
  • Unstable mood (low or dysphoric).
  • Decreased sexual function, which is aggravated by alcohol intake.
  • Problems with cardiac activity.
  • Headache, pain in different parts of the body.

A feature of patients with alcoholism with a personality change according to the astheno-neurosis-like type is the desire to be treated. They go to the doctor with pleasure, go to sanatoriums and fulfill the prescribed appointments. They demand that doctors give them many prescriptions. They always ask the doctor if they have any serious health problems.

With appropriate treatment and sobriety for a long time, astheno-neurosis-like syndrome gradually disappears.

Degradation of personality by alcohol type

With personality degradation according to the alcoholic type, patients develop various emotional disorders due to a decrease in the regulation, adequacy and determinism of emotions. Such people are characterized by duplicity: they always support the interlocutor, but show disdain behind their backs.

With the degradation of the personality according to the alcoholic type, we can talk about the following features of human behavior:

  • Increased suggestibility.
  • Weakening of the volitional sphere.
  • Narrowing the circle of interests.
  • Loss of responsibility to the team and family.
  • Ignoring your safety.
  • Irresponsible attitude towards one's own health.
  • Rough behavior.
  • Cynicism.
  • Decrease in shame and disgust.
  • Surface judgment.
  • The mood is usually carefree, with elements of euphoria.
  • Decreased self-criticism.
  • Hypocrisy.
  • Deterioration of attention and memory.
  • Loss of desire to work.

Such patients may be aware of their behavior, but do not have the will to change their behavior.

Degradation of this type in most cases occurs in people with such diseases:

  • Alcoholic encephalopathy.
  • Atherosclerosis of cerebral vessels.
  • Residual effects of traumatic brain injury and so on.

This type of degradation is characterized by the following features:

  • Affective-volitional personality disorder.
  • Gross violation of memory and ingenuity.
  • Sluggishness of thought.
  • Excessive talkativeness.
  • Propensity to rationalize.
  • Progressive lack of will (such people are ready to drink at any suitable opportunity).
  • Loss of human dignity.
  • Increased sentimentality.
  • Finding the patient in a passive-inert state, in which he escapes from life's problems, plunging into the world of fantasy.

Some alcoholics, losing the line between real and fictional, like to talk about their extraordinary exploits or acquaintances with famous people. Others understand their situation, due to unrestrained drunkenness, and promise to stop drinking, but their words always diverge from their deeds.

Patients with personality degradation according to the psychopathic type are usually prone to mood swings and excessive irritability. Most often, the disease begins in adolescence. The adoption of alcohol makes patients inferior, unadapted to life in society. In alcohol, they see a sedative that allows them to level their inferiority.

In most cases, alcohol addiction occurs against the background of the pampered and connivance of parents, communication in "bad" companies, where alcohol is first taken periodically, and then constantly.

The process of moral and intellectual degradation of such patients lasts quite a long time. They are characterized by long binges, during which some alcoholics commit immoral acts.

Often, patients are distinguished by isolation, severity and indifference to loved ones. Their mood is usually gloomy. They prefer to drink alone, hiding alcohol in various places of the apartment.

In a number of patients with degradation of this type, alcohol provokes a violent reaction: scandal, hysteria, banging their heads against the wall, throwing various objects. Such people do not tolerate when they are contradicted, trying to frighten their relatives or threaten them. They often run away from home.

Some alcoholics become insecure and timid, as they say, "flies will not offend", however, after taking alcohol, their behavior changes: they become arrogant, picky and vicious.

Alcohol has a destructive effect on the human body. It not only strikes at all organs and systems, but also leads to the degradation of the individual, the loss of moral and social norms. That is why addiction to alcohol must be treated, and the sooner this process is started, the more effective it will be.

This term refers to a common, clinically similar, non-hereditary form of cerebellar ataxia that develops against the background of prolonged alcohol use. Symptoms usually develop subacutely over several weeks or months, sometimes faster. In some patients, the condition may be stable and the symptoms are mild, but they increase after an exacerbation of pneumonia or delirium tremens.

There are symptoms of cerebellar dysfunction, primarily balance and walking disorders. The lower limbs are affected more than the upper limbs, while nystagmus and speech changes are relatively rare. Once having arisen, these symptoms undergo insignificant dynamics, but in the case of stopping alcohol consumption, some recovery of gait is possible, due, apparently, to an improvement in general nutrition and regression of concomitant polyneuropathy.

The pathoanatomical picture is characterized by varying degrees of degeneration of the neurocellular elements of the cerebellar cortex, especially Purkinje cells, with a pronounced restriction of the topography of the lesion to the anterior superior sections of the vermis and the adjacent parts of the anterior cerebellar lobes. Balance and gait disorders are associated with the involvement of the vermis, and ataxia of the extremities - the anterior lobes of the cerebellar hemispheres. A similar clinicopathological syndrome is sometimes observed with alimentary exhaustion in patients who do not suffer from alcoholism.

Alimentary polyneuropathy (see also chapters 76 and 355)

In the United States, only alcoholics suffer from alimentary polyneuropathy. As already noted, in 80% of patients this condition accompanies Wernicke-Korsakoff syndrome, but often also serves as the only manifestation of deficiency disease. Peripheral neuropathy of alcoholics (alcoholic polyneuropathy) does not have any significant differences from that of beriberi. The clinical signs of alimentary polyneuropathy and its identity with beriberi are discussed in Chapters 76 and 355. It has been shown that some cases of alimentary polyneuropathy are caused by a deficiency of thiamine chloride, pyridoxine, pantothenic acid, vitamin b12 and, possibly, folic acid. In alcoholics, it is usually not possible to associate polyneuropathy with a deficiency of any one of these vitamins.

The toxic effect of alcohol on the central nervous system, not associated with vitamin deficiency. By now, the existence of alcohol-related brain lesions unrelated to nutritional deficiency or trauma has been recognized. Among patients with alcoholism, the incidence of arterial hypertension and, possibly, strokes, ischemic infarction and spontaneous subarachnoid hemorrhage is increased. Compared with the control groups in patients with alcoholism, CT scan reveals the expansion of the lateral ventricles and sulci of the brain. The origin of these changes is unclear. They do not serve as signs of cerebral atrophy, since they are partially and sometimes completely reversible with prolonged abstinence from alcohol. The notion that alcohol can cause intellectual impairment without regard to the alimentary insufficiency provoked by it is constantly repeated in medical publications, but the existence of alcoholic dementia as a nosological form has never been established on the basis of clinical and neuropathological studies. The syndrome of progressive myelopathy in those suffering from alcoholism has been clinically described. Such patients do not show signs of alimentary deficiency (Biz or folic acid) and liver damage. The nature of the spinal cord injury is unclear, and its causal relationship to the toxic effects of alcohol needs to be investigated.

Alcoholic fatty liver, alcoholic fatty liver, alcoholic steatosis

Version: Directory of Diseases MedElement

Alcoholic fatty liver [fatty liver] (K70.0)

Gastroenterology

general information

Short description


Steatosis of the liver(fatty hepatosis, fatty infiltration of the liver) - the most common hepatosis Hepatosis is the common name for a number of liver diseases characterized by degenerative changes in the hepatic parenchyma in the absence or slight severity of signs of inflammation.
in which fat accumulates in the liver cells. The accumulation of fat can occur as a reaction of the liver to various toxic effects or in connection with certain diseases and pathological conditions of the body.

Alcoholic liver steatosis(fatty degeneration) - the initial stage of structural changes in the liver due to chronic alcohol intoxication. It is one of the forms of alcoholic liver disease and can act both as its initial stage and proceed in parallel with its other forms (stages). In the latter case, the diagnosis is made on the basis of the predominance of morphological signs of a particular process, according to the most severe identified process (for example, when foci of fibrosis are detected against the background of alcoholic liver steatosis, it is more appropriate to code the disease as "Alcoholic fibrosis and sclerosis of the liver" - K70.2).

Classification

Alcoholic fatty liver (liver steatosis), according to the general classification of alcoholic liver lesions (Loginov A.S., Dzhalalov K.D., Blok Yu.E.), is divided into the following forms:

1. Without fibrosis.
2. With fibrosis.
3. In combination with acute alcoholic hepatitis.
4. With intrahepatic cholestasis.
5. With hyperlipemia and hemolysis (Ziwe's syndrome).

Etiology and pathogenesis


Etiology
The risk of developing alcoholic liver disease occurs with the use of more than 40 g of pure ethanol per day for men and 20 g for women. 1 ml of strong alcohol contains approximately 0.79 g of ethanol. Previously, long-term alcohol consumption was thought to be a prerequisite for the onset of the disease, but it is now noted that alcoholic liver steatosis occurs after drinking moderate or large amounts of alcohol, even for a short period of time.

The question of a direct correlation between the degree of liver damage and the amount of alcohol taken is considered controversial by some authors: according to some studies, less than 50% of people who drink alcohol in dangerous doses have severe forms of liver damage (hepatitis and cirrhosis). Apparently, many other factors also play a role (see the section "Factors and Risk Groups").

Alcohol acts as a direct hepatotoxic agent. Its metabolism involves a number of enzymatic systems that convert ethanol to acetaldehyde, and further, acetaldehyde dehydrogenase Acetaldehyde dehydrogenase is an enzyme found in the human liver and is responsible for the breakdown of acetaldehyde (converts acetaldehyde to acetic acid).
(ALDH) metabolizes to its acetate. The main factor in the development of alcoholic liver disease is the high content of acetaldehyde in the blood and liver cells. This causes most of the toxic effects of ethanol, including through increased lipid peroxidation, the formation of stable complexes with proteins, impaired mitochondrial function, and stimulation of fibrogenesis.

Pathomorphology
On external examination, the liver is large, yellow with a greasy sheen; hepatocytes are loaded with fat, signs of inflammation or fibrosis are not detected. Fatty degeneration of the liver is diagnosed when the fat content in the liver exceeds 10% of its wet mass, while more than 50% of the liver cells contain fat droplets, the size of which reaches the size of the nucleus of the liver cell or exceeds it. Fatty degeneration is often accompanied by moderate siderosis of stellate reticuloendotheliocytes.

Epidemiology

Prevalence sign: Common

Sex ratio (m/f): 0.5



The true prevalence of alcoholic fatty liver disease is unknown. It is believed that this disease is present in 90-100% of alcohol abusers.
In intravital liver biopsies performed for other reasons, the disease is detected in 3-9% (USA and Canada). At autopsy, liver damage is determined in 65-70% of people who abuse alcohol at a dose of more than 60 g of ethanol per day.
Naturally, the incidence of alcoholic hepatic steatosis correlates with the prevalence of alcoholism itself and can vary significantly in countries with a greater or lesser prevalence. Therefore, international morbidity statistics are estimated at 3-10%.

Age: mostly 20-60 years old.
Race: Whites have a statistically lower rate of all forms of alcoholic liver disease.
Gender: Women are thought to be more at risk for the disease. There are several hypotheses in this regard (hormonal background, low levels of alcohol dehydrogenase in the gastric mucosa, high levels of autoantibodies to the gastric mucosa in drinking women), but none of them has been confirmed.

Factors and risk groups


Risk factors for the development and progression of alcoholic fatty liver disease:
1. Reception from 40 grams of ethanol per day (for women - more than 20 g) for 10-12 years.
2. Genetically determined phenotypes of enzymes that provide a high rate of ethanol metabolism and accumulation of acetaldehyde; genetic polymorphism of enzymes involved in ethanol metabolism.
Alcohol dehydrogenase (ADH) is encoded by five loci on the fourth chromosome. With the predominance of a more active isoenzyme (ADH2), there is an increased formation of toxic acetaldehyde (most characteristic of the Mongoloid race).
Acetaldehyde dehydrogenase (ADH) is encoded by four loci on four different chromosomes. The presence of the abnormal AlDH2 × 2 allele also leads to excessive accumulation of acetaldehyde.
3. Infection with hepatotropic viruses.
4. Overweight.
5. Non-Caucasian race.
6. Dyslipidemia Dyslipidemia is a metabolic disorder of cholesterol and other lipids (fats), which consists in a change in their ratio in the blood
.
7. Diabetes.
8. Metabolic syndrome.
9. Female.


Clinical picture

Clinical Criteria for Diagnosis

Anorexia, nausea, abdominal discomfort, dull pain in the right hypochondrium, epigastric pain, hepatomegaly, jaundice, palmar erythema, alcohol abuse.

Symptoms, course

Alcoholic steatosis is usually asymptomatic in outpatients.

Possible manifestations of severe fatty infiltration of the liver:
- symptoms of malaise, weakness, loss of appetite, nausea and abdominal discomfort;
- jaundice (present in 15% of patients with alcoholic steatosis admitted to the hospital);
- weakness of skeletal muscles;
- dilated cardiomyopathy Dilated cardiomyopathy (DCM) is a condition in which the heart's ability to pump blood is reduced due to enlargement and weakening of the left ventricle (the main pumping chamber of the heart), which reduces the ejection fraction (the amount of blood the heart pumps out with each beat)
;
- pancreatitis Pancreatitis - inflammation of the pancreas
;
- peripheral neuropathy;
- gynecomastia, hypogonadism are often detected Hypogonadism is a pathological condition caused by reduced secretion of sex hormones and characterized by poor development of the genital organs and secondary sexual characteristics.
, Dupuytren's contracture, white nails, spider veins, palmar erythema.
On palpation, the liver is moderately enlarged in 70% of patients, smooth with a rounded edge.

A careful history, especially regarding the amount of alcohol consumption, is essential in determining the role of alcohol in the etiology of abnormal liver test results. Questioning family members can reveal alcohol-related problems in the past.
The American Association for the Study of Liver Diseases (AASLD) in its 2010 guidelines emphasizes the importance of using special questionnaires to clarify the anamnesis in patients for whom the anamnesis data collected by conventional methods seems unreliable. Also, the use of the questionnaire is recommended in cases of suspected (clinically, laboratory, instrumental) alcoholic liver steatosis.


Diagnostics


The criterion for the diagnosis of alcoholic fatty degeneration of the liver is the presence of an alcohol history and histological examination of the biopsy. The diagnosis is considered reasonable if at least 50% of hepatocytes contain large lipid vacuoles that push the cell nucleus to the periphery of the cytoplasm (see the section "Etiology and pathogenesis"). However, in practice, biopsy is rarely used, and imaging methods are the leading methods for confirming the diagnosis.

1.Ultrasound:
- different echogenicity of the structure of the liver parenchyma (with non-alcoholic steatosis, as a rule, only bright hyperechoic changes are noted);
- for alcoholic steatosis of the liver, a sonographic picture of both focal and diffuse lesions is characteristic (at the stage of alcoholic hepatitis, only diffuse lesions are noted).
Alcoholic hepatic steatosis, like any other steatosis, is identified by ultrasound only in the presence of more than 30% liver tissue damage. The sensitivity of the method is about 75%.


2. Computed tomography, magnetic resonance imaging are sensitive methods, but do not testify in favor of the alcoholic etiology of steatosis.

3. Laparoscopy Laparoscopy (peritoneoscopy) is a study of the abdominal organs by examining them with the help of medical endoscopes inserted into the peritoneal cavity through a puncture of the abdominal wall.
with liver biopsy allow to describe the surface of the liver and morphologically confirm the diagnosis. These studies are carried out only in the absence of contraindications to them. For example, percutaneous puncture liver biopsy is often not feasible due to contraindications (primarily coagulopathy) and is associated with a large number of diagnostic errors.

3.Radioisotope study of liver function with I 31- at present, this diagnosis is practically not carried out.


Laboratory diagnostics


Signs of alcohol abuse:


1. A sharp increase in the level of gamma-glutamyl transferase (GGT) in the blood serum and its sharp decrease against the background of withdrawal. The test has low specificity and sensitivity. Approximately 70% of people who abuse alcohol have normal GGT values ​​(against the background of withdrawal Withdrawal is a condition that occurs as a result of a sudden cessation of the intake (introduction) of substances that caused substance abuse, or after the introduction of their antagonists.
). However, against the background of alcohol excess, the sensitivity of the test is characterized in the region of 70%.


2. An increase in the concentration of non-carbohydrate transferrin (desialized transferrin, asialotransferrin, CDT) is a specific (80-100%) and sensitive (75-100%) test for patients with alcohol consumption exceeding 60 g per day.
A decrease in total transferrin is present in approximately 28% of alcohol abusers. Therefore, to narrow down the diagnosis, transferrin testing can be done initially rather than the costly multi-wavelength liquid chromatography test for CDT.

3. Blood and urine amylase can be increased only during the period of acute alcohol intoxication and only indicates the fact of alcohol intake up to 36 hours before the analysis.


4. Macrocytosis. The test has low sensitivity (27-52%) and high specificity (85-91%).


Signs of liver damage:
1. Increasing the level of aminotransferases by more than 2 times. The absolute values ​​of AST and ALT are almost always less than 500 IU / l and the ratio of AST / ALT > 2. An increase in transaminases is often the only laboratory sign of alcoholic liver steatosis.

2. An increase in the level of alkaline phosphatase is possible (about 20-40% of patients) in the range of 200-300%.
3. Hyperbilirubinemia (detected in 30-35% of patients), apparently associated with alcoholic hemolysis or concomitant cholestasis.

Notes

1. Ziwe's syndrome is a rare clinical form of fatty hepatosis in chronic alcoholism. With a pronounced fatty degeneration of the liver, the following are noted:
- an increase in serum lipids (hypertriglyceridemia, hypercholesterolemia, hyperphospholipidemia);
- hemolysis (the development of hemolysis in Zieve syndrome is associated with an increase in the sensitivity of erythrocytes to peroxidases due to a decrease in the level of vitamin E in blood serum and erythrocytes);
- an increase in the amount of bilirubin.

2. Changes in fasting insulin and glucose levels should alert the clinician to the potential for impaired glucose tolerance that often accompanies steatosis.

3. In most patients, there is a mild decrease in the absorption-excretory function of the liver according to the bromsulfalein test (currently rarely used).

Differential Diagnosis


Alcoholic liver steatosis is differentiated from non-alcoholic fatty liver disease, anicteric forms of viral hepatitis, hemochromatosis, obstruction of the biliary tract.
Of particular difficulty is the differential diagnosis between various forms of alcoholic liver disease and non-alcoholic steatohepatosis.

Complications


In alcoholic liver steatosis, continued drinking can lead to the development of alcoholic hepatitis or cirrhosis.
A fatty liver without signs of fibrosis is not a pre-cirrhotic disease, since the structure of the liver can be restored when alcohol is stopped.
Identification of perivenular and pericellular fibrosis in liver biopsy specimens of patients with fatty hepatosis Fibrosis is the growth of fibrous connective tissue, which occurs, for example, as a result of inflammation.
(40% of patients) indicates the possibility of developing cirrhosis. Although perivenular fibrosis may be considered as a marker of an increased risk of cirrhosis, there is no evidence of progression of the disease when alcohol is stopped.
In one population-based study, there was an increase in mortality and an increase in the risk of cancer (especially liver cancer) among patients discharged with a diagnosis of alcoholic fatty liver disease.

Pathology associated with alcoholism (alcoholic stigmas detected during examination) should be distinguished from complications:
- expansion of the vessels of the nose and sclera;
- enlargement of the parotid glands;
- atrophy of the muscles of the shoulder girdle;
- bright spider veins;
- gynecomastia Gynecomastia - an increase in the mammary glands in men
;
- Dupuytren's contracture Dupuytren's contracture (synonymous with palmar fibromatosis) - painless cicatricial degeneration and shortening of the palmar tendons; It is manifested by a violation of the ability to unbend the fingers, a nodular thickening of the skin on the palms.
;
- testicular atrophy;
- the presence of lesions of other organs and systems (pancreatitis, dilated cardiomyopathy, peripheral neuropathy).

Treatment abroad