Acute alcoholic hepatitis

Acute alcoholic hepatitis is an acute progressive inflammatory-dystrophic liver damage that develops at any stage of alcoholic liver disease with prolonged (from 3 days to 12 weeks), frequent (possibly daily) use of toxic (for a given patient) doses of ethanol, as a rule, background pathological addiction to it, and characterized by a high frequency of fatal complications – progressive hepatocellular insufficiency, hepatic encephalopathy, hepato-renal syndrome, etc. In 4% acute alcohol hepatitis relatively quickly transformed into alcoholic cirrhosis of the liver.

Clinical picture . The course and prognosis of acute alcoholic hepatitis depend on the severity of liver dysfunction. The most severe course of acute alcoholic hepatitis develops after alcoholic excesses against the background of formed alcoholic cirrhosis of the liver. Clinical variants of acute alcoholic hepatitis usually develop in young patients between the ages of 25-35 (however, the age range can vary from 25 to 70 years) after severe binge drinking in patients with pre-existing cirrhosis of the liver, which causes the summation of symptoms and significantly worsens the prognosis.

The acute onset of alcoholic hepatitis with a sudden onset of pain and dyspeptic syndromes and the rapid development of jaundice is characteristic, but hepatitis can develop gradually. With the gradual development of syndromes, the initial stage is poor in symptoms: dyspeptic disorders usually do not encourage patients to see a doctor. Clinically acute alcoholic hepatitis can be represented by four variants of the course: latent, icteric, cholestatic, fulminant.

The latent variant of acute alcoholic hepatitis, as its name implies, does not provide an independent clinical picture or manifests itself as blurred dyspeptic disorders, without jaundice and pronounced deviations of hepatic function and is diagnosed by detecting hepatomegaly, as well as by increasing transaminase, the presence of anemia or persistent leukocytosis (in a patient alcohol abuser). Liver biopsy is required to confirm the diagnosis. Most often the reason for a thorough examination of the liver and functional studies are polyneuritis, cardiomyopathy, pancreatitis.

The icteric variant of acute alcoholic hepatitis is most common. Patients have marked weakness, anorexia, dull pain in the right hypochondrium, nausea, vomiting, diarrhea, weight loss, jaundice; the latter is not accompanied by pruritus. Approximately half of the patients have remittent or persistent fever, often reaching febrile numbers. The liver is enlarged in almost all cases, compacted, with a smooth surface (with cirrhosis nodular), painful. Detection of severe splenomegaly, ascites, telangiectasia, palmar erythema, asterixis indicate the presence of background cirrhosis. Associated bacterial infections often develop : pneumonia, urinary infection, spontaneous bacterial peritonitis, septicemia. The latter, along with the hepatorenal syndrome, often act as the immediate cause of death.

The cholestatic variant of acute alcoholic hepatitis is observed in 5–13% of cases and is accompanied by severe itching, jaundice, stool discoloration, darkening of the urine and an increase in temperature. There is a sharp increase in the content of bilirubin, cholesterol, alkaline phosphatase, gammaglutamyltranspeptidase, along with a slight increase in the activity of serum aminotransferases. In the presence of fever and pain in the right hypochondrium, the clinical picture is difficult to distinguish from acute cholangitis. Cholestatic acute alcoholic hepatitis is characterized by a protracted course.

Fulminant variant of acute alcoholic hepatitis is characterized by rapid progression of symptoms: jaundice, hemorrhagic syndrome, hepatic encephalopathy, renal failure. Patients are in serious condition, in most cases, icteric, the content of bilirubin in the blood serum is constantly increasing, the prothrombin time is prolonged, the content of albumin in serum is reduced. Hepatorenal syndrome or hepatic coma usually leads to death. The risk of developing severe (fulminant) acute alcoholic hepatitis occurs when taking paracetamol.

The diagnosis of acute alcoholic hepatitis can be assumed on the basis of clinical data, but it can be reliably established according to biopsy data. Systematic use of alcohol by patients is often necessary to establish by questioning his family and friends. Essential are the appearance, behavioral, neurological and visceral changes, which are considered characteristic of alcoholism. The most common are tremor of the hands, eyelids, tongue, fades alcoholica (rhinophyma), venous congestion of the eyeball, polyneuropathy, Dupuytren’s contracture. The presence of patients with jaundice, fever, painful enlarged liver, leukocytosis makes it possible to suspect acute alcoholic hepatitis

Laboratory indicators. Neutrophilic leukocytosis is characteristic, reaching 20–40 x 10 * 9 / l, increasing the ESR to 40–50 mm / h. Red blood cell change is usually characterized by macrocytosis. An increase in bilirubin is noted mainly due to the direct fraction, reaching especially high rates in the cholestatic form. The activity of transaminases can increase both severalfold and tenfold, while the AST / ALT ratio exceeds 2. The activity of g – glutamyl transpeptidase increases many times, with a cholestatic form, along with alkaline phosphatase. IgA concentration is usually elevated. Often there is hypercholesterolemia and b-lipoproteidemia. In the presence of cirrhosis and severe course of acute alcoholic hepatitis, biochemical signs of liver failure increase: an increase in prothrombin time (decrease in prothrombin index), a decrease in serum albumin concentration, hyperammonemia.

To determine the severity of alcoholic hepatitis and predict its course, the Maddrey coefficient is used, which is calculated on the basis of biochemical parameters using the formula: 4.6 x (the difference between the patient’s prothrombin time and control) + serum bilirubin in μmol / l / 17. For its value more than 32 the probability of death in the current hospitalization exceeds 50%, and values ​​close to and exceeding this value are an indirect indication for the use of glucocorticosteroids.

Histology. At the advanced stage of acute alcoholic hepatitis, as a rule, there are contraindications for needle biopsy of the liver. If the latter is still performed, then, regardless of the previous liver damage, acute alcoholic hepatitis has certain histological manifestations. Structural changes in the liver are divided into mandatory and optional for alcoholic hepatitis (Mansurov XX, Mirodzhov GK, 1988). Mandatory morphological features include perivenular lesion of hepatocytes, manifested by balloon dystrophy and necrosis, by the onset of the onset of the onset of Mallory corpuscles (bodies consisting of condensed intermediate cytoskeleton microfilaments, which, when stained with hematoxylin-eosin, are visualized as purple-red cytoplasmatic inclusions, and the appendix, an appendix, and appendix. Necessary for the diagnosis of alcoholic hepatitis should be considered symptoms such as liver obesity, identification of giant mitochondria, acidophilic bodies, oxyphilic hepatocytes, hepatic vein fibrosis, proliferation of the bile ducts and cholestasis.

Treatment. The main components of the treatment of acute alcoholic hepatitis, in addition to eliminating alcohol, include a regimen and a balanced diet, the elimination of hepatotoxic drugs, the correction of metabolic disorders, and the prevention of hepatic encephalopathy and hepato-renal syndrome. Taking into account the pathogenesis of the disease, effects on the hyperimmune response, cytokine level and oxidative stress are foreseen.

Correction of hyperimmune response: glucocorticosteroids are the drugs of choice, and their use is advisable at Maddrey coefficient values ​​in patients with acute alcoholic hepatitis more than 32 in the absence of gastrointestinal bleeding and infectious complications. The criterion for the effectiveness of treatment is the dynamics of reducing the level of bilirubin by 25-50% or more after the first week of therapy, which avoids undesirable complications and changes the treatment regimen with its ineffectiveness. Prednisolone is recommended to be used in the minimum effective individual dose (40-60 mg daily for 30 days or more). If on the 7th day the level of bilirubin does not decrease, you should stop taking glucocorticosteroids and add pentoxifylline (1200 mg / day) to treatment.

Anticytokine therapy (with a significant increase in the content of cytokines, especially TNF-a). It is recommended to administer pentoxifylline (400 mg 3 times a day), which, being a non-selective phosphodiesterase inhibitor, inhibits cytokine synthesis, increasing the intracellular content of cAMP, reduces the activity of neutrophils, and inhibits the proliferation of monocytes and lymphocytes.

Oxidative stress therapy: Ursodeoxycholic and lipoic acids, essential phospholipids, ademetionine and other hepatoprotectors are used. In addition to these agents, the artichoke juice extract has a powerful antioxidant effect, which is used in the form of the drug “Hofitol”.

Forecast. Acute alcoholic hepatitis has a variable but serious prognosis, which depends on the degree of hepatitis activity and the presence of background cirrhosis of the liver. Mortality ranges from 10 to 30%. Prognostically unfavorable symptoms associated with high mortality are encephalopathy, renal failure, and prolongation of the prothrombin time by more than 50% of the control figures. The prognosis is much better with the latent form of acute alcoholic hepatitis. A poor long-term prognosis of acute alcoholic hepatitis is associated with its frequent transition to cirrhosis. According to a large number of authors, in 38% of patients, the transition of hepatitis to cirrhosis was observed for 5 years or less; 52% had an outcome in chronic hepatitis and liver fibrosis, and only 10% of patients had alcohol hepatitis completely resolved.

In terms of the survival of patients with acute alcoholic hepatitis, the prognosis for the development of severe complications, in particular the hepato-renal syndrome (renal failure associated with severe liver damage), is important. Recovery is possible only in case of cessation of alcohol use, but in some cases withdrawal does not guarantee against the development of cirrhosis. In the case of the outcome of alcoholic hepatitis in progressive liver fibrosis, portal hypertension and ascites develop early.

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