2024 Author: Josephine Shorter | [email protected]. Last modified: 2023-12-16 21:43
Symptoms and treatment of alcoholic hepatosis
60–70% of patients with chronic alcoholism suffer from fatty hepatosis. The cause of alcoholic fatty hepatosis is the violation of ethanol metabolism, which proceeds with the use of a large amount of NAD (a compound necessary for the final stage of fatty acid oxidation). The resulting NAD deficiency causes the accumulation of fatty acids in the liver, which are converted over time into neutral fats (triglycerides).
Ethanol causes the release of catecholamines, which promote the release of fat from the depot, which also leads to an increase in the amount of fatty acids entering the liver. In addition, ethanol interferes with the processing of free fatty acids and triglycerides in the muscles.
Symptoms of alcoholic hepatosis
Alcoholic fatty hepatosis is characterized by complaints of pain, a feeling of heaviness and distention in the right hypochondrium and in the epigastric region. Patients do not tolerate fatty foods, they also note general weakness, loss of strength, low efficiency, rapid excitability, flatulence. Half of the patients have no subjective manifestations of pathology.
The main symptom of alcoholic hepatosis is a moderate increase in the size of the liver, rounded at the edges. At the same time, the consistency of the organ is tightly elastic; upon palpation, the patient may feel moderately severe pain.
Functional liver tests differ slightly from the norm. In 20-30% of cases, there is a moderate increase in the activity of aminotransferases (ALT, ASAT), as well as alkaline phosphatase in the blood, the level of bilirubin in the blood and γ-glutamyl transpeptidase increases slightly, and the level of triglycerides, free fatty acids, and lipoproteins may also increase.
According to the results of ultrasound, one can judge an increase in the size of the liver. In the framework of the examination, a number of characteristic features are revealed: the echogenicity of the organ is uniformly high, the contours are indistinct, the structure is homogeneous. In its structure, the liver becomes more tender, it consists of numerous small, equal-sized dots, resembling semolina.
With radioisotope hepatography, changes in the secretory-excretory function of the liver are determined.
Puncture biopsy of the liver is of decisive importance in the diagnosis of the disease. The diagnosis of fatty alcoholic hepatosis is considered definitive if 50% or more of the liver cells contain drops of fat, pushing the nucleus and other organelles to the periphery of the cell - such changes are most noticeable in the centrilobular zone. When you stop taking alcoholic beverages, fatty hepatosis undergoes a reverse development.
Quite rare forms of fatty alcoholic hepatosis include Tsive's syndrome, which may accompany chronic alcoholism. A distinctive symptom of pathology is a pronounced fatty degeneration of the organ, accompanied by an increased content of bilirubin, cholesterol, triglycerides in the blood, as well as hemolytic anemia. Hemolysis of erythrocytes is associated with a decrease in the concentration of tocopherol in the blood and erythrocytes, which is a strong antioxidant. With a decrease in antioxidant activity, the activity of free radical lipid oxidation and hemolysis of red blood cells sharply increase. The clinic of Zive's syndrome resembles acute alcoholic hepatitis with obvious jaundice, pain in the liver, high fever and cholestasis.
AF Bluger and IN Novitsky in 1984 described alcoholic hepatosis with "massive fatty liver". The pathology is accompanied by overt hepatomegaly, severe hepatocellular failure and cholestasis. The outcome of the disease can be fatal.
When diagnosing alcoholic fatty hepatosis, it is important to remember that the disease can develop against the background of diabetes mellitus or protein deficiency. Also, the symptoms of the disease can be triggered by taking certain medications.
Treatment of alcoholic hepatosis
The most effective drug for the prevention and treatment of alcoholic hepatosis are the amino acids arginine and betaine (special amino acid compounds that accelerate the synthesis of phospholipids and take part in fat metabolism). Arginine promotes the elimination of toxins from the liver, its main feature is its participation in the neutralization of acetaldehyde - the product of the breakdown of ethyl alcohol, the most dangerous substance formed as a result of the decomposition of alcohol in the liver. In addition to neutralizing toxins, arginine accelerates their excretion from the body, improving blood circulation in the liver.
It is also important that the amino acid promotes the accumulation of energy in liver cells, making them more resistant to hypoxia in the treatment of alcoholic hepatosis. At the same time, arginine reduces the severity of inflammatory processes.
Alcoholic hepatosis also requires the normalization of fat metabolism in the liver to stop the process of fatty degeneration of the organ. Betaine helps to reduce the amount of fat in the liver, since it is from it that phosphatidylcholine is formed, which is necessary for this process to proceed, as well as for the restoration of cell membranes.
Betaine in the human body is produced in small quantities, in contrast to the body of most animals. A person receives this compound exclusively from food, therefore a stable supply of betaine is the main factor in the treatment of alcoholic hepatosis.
The intake of arginine and betaine from food, as well as taking medications such as Citrarginine, help to restore hepatocytes from the inside. The drug contains the required concentration of arginine and betaine in an easily absorbed form and serves as the most effective means for the prevention and treatment of alcoholic hepatosis.
Article author: Mochalov Pavel Alexandrovich | d. m. n. therapist
Education: Moscow Medical Institute. IM Sechenov, specialty - "General Medicine" in 1991, in 1993 "Occupational Diseases", in 1996 "Therapy".
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