Liver hepatosis
What is liver hepatosis?
Hepatosis is a common name that combines several liver pathologies at once, occurring with dystrophic changes in parenchymal tissue without an obvious mesenchymal cell reaction. There are acute and chronic forms of the disease.
Causes of liver hepatosis
Acute hepatosis occurs with toxic damage to the organ. It can be poisoning with fluoride, arsenic, the characteristic symptoms of acute hepatosis also appear after taking high doses of alcohol, with an overdose of drugs, the use of poisonous mushrooms. Sometimes acute liver dystrophy becomes a complication of viral hepatitis or sepsis.
Chronic hepatosis in most cases is a consequence of prolonged intake of alcoholic beverages; the cause of liver hepatosis can also be a deficiency of protein or vitamins, the action of bacterial toxins, carbon tetrachloride, organophosphorus compounds and a number of other agents with hepatotropic action.
Violation of metabolic processes in the body entails metabolic disorders in the liver. In this case, the pathogenesis of the disease consists in a violation of lipid metabolism and is reflected in the formation of lipoproteins in liver cells.
A number of exogenous substances, including medicines (chlorpromazine, testosterone preparations, gestagens), with prolonged uncontrolled use, can cause cholestatic hepatosis.
With liver damage, in this case, there is a violation of the metabolism of cholesterol and bile acids in the liver cells, and the process of bile formation, its outflow through the ducts, is also disturbed. With the progression of the symptoms of the disease, not only the effect of the harmful factor on hepatocytes, but also the toxic-allergic factor is of great importance.
Symptoms of liver hepatosis
Symptoms of acute liver hepatosis develop rapidly. Pathology manifests itself in the form of dyspepsia and is accompanied by signs of severe intoxication, jaundice. At the initial stage of the disease, the liver slightly increases in size, when palpated, it is soft, over time, the percussion size of the organ becomes smaller, and palpation is impossible.
When conducting a laboratory study of blood tests, there is a high concentration of aminotransferases, in particular alanine aminotransferase, fructose-1-phosphataldolase, urocaninase. In a severe course of the disease, there is a low level of potassium in the blood, an increase in ESR. The change in liver function tests does not always occur and is not natural.
Chronic fatty hepatosis is accompanied by dyspeptic disorders, loss of strength, dull pain in the right hypochondrium. The liver is slightly enlarged, its surface is smooth, on palpation, the patient notes pain; unlike cirrhosis, the liver does not have a dense consistency and sharp edges.
A frequent companion of hepatitis and cirrhosis - splenomegaly - is not typical for fatty hepatosis. The concentration of aminotransferases in the blood in this disease is slightly higher than normal, often there may be high levels of cholesterol and B-lipoproteins. The results of bromsulfalein and vafaverdin tests have their own specifics. There is often a delay in liver clearance of these drugs. When making a diagnosis, a puncture biopsy of the liver plays a decisive role.
Cholestatic hepatosis of the liver can be acute or chronic. The main symptoms of liver hepatosis in this case include cholestasis syndrome. It is characterized by jaundice, itching, dark staining of urine, discoloration of feces, increased body temperature. During laboratory tests, bilirubinemia, high activity of alkaline phosphatase and leucine aminopeptidase in the blood, high cholesterol levels and high ESR values are noted.
Acute fatty hepatosis occurs with symptoms of hepatic failure in severe form and can cause the patient's death from hepatic coma or secondary hemorrhagic events. With a more favorable outcome, the pathology becomes chronic if the etiological factor that caused the disease continues to act on the human body.
The course of chronic fatty hepatosis is more favorable. Very often, recovery occurs, especially if the effect of the damaging agent is eliminated and the therapy is carried out in a timely manner. Fatty liver hepatosis under unfavorable circumstances can turn into chronic hepatitis and liver cirrhosis. Cholestatic hepatosis relatively quickly transforms into hepatitis due to the appearance of a reaction of the reticulohistiocytic stroma of the liver and the development of secondary cholangitis.
Treatment of liver hepatosis
Patients with symptoms of acute toxic hepatosis of the liver are urgently hospitalized. In case of poisoning, the patient needs to carry out a set of measures as soon as possible aimed at stopping the intake of toxins into the body and accelerating their elimination. These procedures can be carried out by the victim independently, as part of the provision of first aid or in a hospital setting.
Also, the goal of emergency measures to help the patient becomes in this case the fight against hemorrhagic syndrome, general intoxication, and low levels of potassium in the blood. In a severe course of the disease, it is necessary to prescribe corticosteroids, treatment of liver failure.
In chronic hepatosis of the liver, it is also important to prevent the harmful effects of the etiological factor; alcohol is strictly prohibited. The patient is prescribed a diet high in animal protein and low in fat, especially animal origin.
Lipotropic factors such as choline chloride, lipoic acid, folic acid are recommended. In addition, vitamin B12 and a preparation with liver hydrolyzate extract - "Sirepar" are prescribed. Treatment of chronic liver hepatosis requires the use of corticosteroids.
Patients suffering from chronic hepatosis require dispensary observation, they are not recommended to be treated in a sanatorium and in resorts.
Disease prevention measures include timely therapy of gastrointestinal diseases, balanced nutrition.
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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".
