gepatoze

Steatosis - liver disease characterized by degenerative changes in its parenchyma without the expressed mesenchymal cell response. There are acute and chronic gepatozy, among the last fat and cholest-matic.

Steatosis acute (toxic degeneration of the liver, acute yellow atrophy of the liver, and others.).

Etiology and pathogenesis. Acute steatosis develops in toxic liver damage - severe poisoning, phosphorus, arsenic, high doses of alcohol, certain medications (tetracyclines, an extract of the fern, etc..), Inedible mushrooms -. Morels, pale toadstool, etc. Sometimes, acute liver degeneration complicated by hepatitis and sepsis.

Symptoms within. Acute steatosis develops rapidly, manifested dyspeptic disorders, signs of intoxication, jaundice. Liver initially increased slightly, soft, in the future - is not palpable, percussion its dimensions are reduced. The significant increase in blood content of aminotransferases, particularly ALT, fructose-1 -fosfataldolazy, urokinase. In severe cases, hypokalemia occurs may increase the ESR. Changes in liver samples of other irregularities. The liver biopsy specimens reveal fatty degeneration of hepatocytes up to necrosis.

Differential diagnosis. In contrast to viral hepatitis at gepatozah no typical prodromal period. It should also take into account the data of the anamnesis (the systematic abuse of alcohol, intake of hepatotoxic drugs, consumption of mushrooms is not known to the patient, and so on. D.), Epidemiological data. In acute gepatozah spleen usually does not increase, acute hepatitis, increased.

Acute steatosis may be accompanied by severe renal failure and lead to death of the patient by hepatic coma, secondary hemorrhagic phenomena. In milder cases, the morphology and function of the liver can recover or disease becomes chronic.

Treatment. Patients admitted to the hospital, take urgent measures to stop the intake of toxic factors and removing it from the body (gastric lavage, saline laxatives, enemas siphon). Carry out the struggle with hemorrhagic syndrome (transfusion of fresh frozen plasma - 1.5-2 liters or more, the introduction of vikasola - 1-3 ml of 1% solution 3-4 times a day, a routine), general toxicity, hypokalaemia (drop in / in a panangina 5% glucose solution with vitamins C, group B, gemodeza et al.). At first priznakah- plasmapheresis (see. Acute Hepatitis). In acute viral gepatoze patient is admitted to the infectious diseases hospital (treatment of the underlying disease, liver failure).

Prevention - the sanitary-epidemic measures aimed at combating viral hepatitis, prevention of toxic industrial and household intoxications hepatotropic poisons.

Chronic steatosis fat (fatty degeneration, fatty infiltration, hepatic steatosis, and others.) Is characterized by fat (sometimes with elements of the protein), hepatitis-totsitov dystrophy and chronic course.

The etiology, pathogenesis, most often, alcoholism, -endogenny less (with severe pancreatitis, enteritis) vitamins and protein deficiency, chronic intoxication with carbon tetrachloride, organophosphorus compounds and other toxic substances having hepatotropic activity, bacterial toxins, and various metabolic disorders in the body (hypovitaminosis general obesity, diabetes, hyperthyroidism, etc.). The pathogenesis of liver damage in these cases is largely confined to a violation of lipid metabolism in hepatocytes and formation of lipoproteins. The progression of degenerative changes and necrobiotic are important not only to the direct effect of damaging factors in the liver cells, but also toxic and allergic processes.

Symptoms within. Can malosimptomno form, in which the clinic is masked manifestations of the underlying disease (hyperthyroidism, diabetes, and others.), Toxic damage to other organs or concomitant diseases of the gastrointestinal tract. In other cases, there are marked dyspepsia, fatigue, dull pain in the right upper quadrant; sometimes-mild jaundice. The liver is moderately enlarged, with a smooth surface, painful on palpation. Splenomegaly is not typical. content in serum aminotransferases moderately or slightly increased, as is often elevated cholesterol, beta-lipoproteins. Characteristic of bromsulfaleinovoy and vofaverdinovoy samples: delay release of these drugs by the liver is observed in most cases. Other laboratory tests maloharakter HN. Crucial in the diagnosis data are biopsy of the liver (fatty degeneration of hepatocytes).

The current relatively favorable, in many cases, especially the exclusion of the damaging agent and timely treatment, recovery is possible. However, steatosis in some cases, can be transformed into chronic hepatitis and cirrhosis.

Differential diagnosis. The absence of splenomegaly allows a certain degree of confidence to differentiate chronic gepatozy with hepatitis and cirrhosis. In cirrhosis of the liver are usually liver stigmata (liver -teleangiektazii stars, bright red or crimson language "pearl" nails and so on. D.), Signs of portal hypertension, which is not the case with gepatozah. It should be borne in mind also hepatolenticular degeneration (cm.), Hemochromatosis (see.). It is very important for the differential diagnosis with other gepatoza liver disease is percutaneous liver biopsy.

Treatment. It is necessary to seek the termination of the etiological factor. Strictly prohibits alcoholic beverages. Assign a diet number 5 with a high content of proteins of animal origin (100-120 g / day) and lipotropic factors (cottage cheese, boiled cod, yeast, products from buckwheat, oatmeal and so on. D.). Restrict the intake of fat, particularly refractory, animal origin. Assign lipotropic: choline chloride, lipoic, folic acid, vitamin B12 preparations containing liver extracts and hydrolysates (5ml Syrepar intramuscularly daily Essentiale et al.).

Cholestatic steatosis is characterized by cholestasis and gall pigment accumulation in hepatocytes, degenerative changes in them (mostly protein dystrophy).

Etiology: toxic and toxic and allergenic effects of some substances, such as medicines (chlorpromazine, testosterone analogues, progestogens, some antibiotics, and others.).

Pathogenesis: violation metabolism in hepatocytes, mainly of cholesterol and bile acids, bile and violation of the outflow of bile by the gall Lobular tubules.

Symptoms within. Jaundice, itching, discoloration of feces, dark urine, fever, often occurs. The liver is usually enlarged. Laboratory studies reveal hyperbilirubinemia, increased activity of alkaline phosphatase and leucine aminopeptidase in the blood serum, hypercholesterolemia, often - increased ESR. Bowel movements are more or less discolored due to the reduced content of stercobilin.

Diagnostic value of the data have biopsy: when gepatoze cholestatic bile pigment accumulates in hepatocytes and in retikuloendoteliotsitah intralobular bile tubules are determined degenerative changes of hepatocytes (mostly protein degeneration), in advanced cases, the phenomenon of cholangitis.

The disease can be acute or chronic course be prolonged. Chronic cholestatic hepatotoxicity relatively quickly transformed into hepatitis due to reactions occurring retikulogistiotsitarnoy stroma liver and secondary cholangitis.

Treatment is the same as in chronic fatty gepatoze. Additionally often prescribe corticosteroid hormones. Spa treatment is not recommended.

Preventing chronic steatosis is to eliminate the causes of these diseases (the fight against alcoholism, careful medical supervision of the application of the sick and the influence of various drugs have side hepatotropic effect), providing balanced nutrition, timely treatment of digestive system diseases, detection and treatment of diseases, which can be complicated by FH (diabetes, thyrotoxicosis). Patients with chronic hepatosis should be under medical supervision with periodic (1 to 2 times per year or more) courses of treatment and prevention of exacerbations.