Alcoholic hepatitis

Alcoholic hepatitis

    * Introduction
    * Causes
    * Signs and symptoms
    * Diagnosis
    * Treatment
Hepatitis is an inflammation of the liver caused by liver cell damage associated with prolonged consumption of alcohol. It is a serious disease, a precursor of cirrhosis. Severely affected patients present with subacute fever, hepatomegaly, leukocytosis, jaundice, coagulopathy and manifestations of portal hypertension: variceal hemorrhage. However, mild forms of alcoholic hepatitis does not cause symptoms.
Alcoholic hepatitis often progresses to cirrhosis, alcohol continues fall, if it is stopped, the condition resolves within a few months, with or without residual sequelae of liver cirrhosis. Although not shown any genetic component, it seems that women are more succeptibile, than men to the adverse effects of alcohol. They develop alcoholic hepatitis after short periods of alcohol abuse, and the progression is faster. Minimum daily dose of ethanol that leads to the initiation of liver injury in men is 40g and 20g for women. For patients who continue to drink alcohol after being diagnosed with alcoholic hepatitis, 5-year survival rate is 30% for women compared with 70% for men. Alcoholic hepatitis can develop at any age, though the top of incidence is between 20 and 60 years. The complications of this disease are very severe, they include: portal hypertension, variceal bleeding, retention of fluid in the abdominal cavity, ascites, bleeding disorders, jaundice, hepatic encephalopathy and cirrhosis. Abstinence is the main treatment. General treatment includes proper diet and vitamin supplementation, especially in group B. There are few drugs that can be used successfully in the treatment of alcoholic liver disease is controversial still use corticosteroids may be used to reduce fibrosis drugs: colchicine, pentoxifylline. Propilthiouracilul gave some results in improving metabolic dysfunction, but are not yet fully accepted. Remedies antioxidant silymarin, vitamin A and E, are not proven yet. Liver transplant survival rates can make it five years the value of non-alcoholic liver disease: 80% in the absence of acute liver disease and 50% for acute alcoholic hepatitis. Because over 50% of patients continue drinking after transplantation, most programs require abstinence for at least 6 months prior to its performance. The only form of prevention is abstinence alcohol.
Pathogenesis
Most body tissues possess enzymes to metabolize ethanol, but most of the plant is the liver. It uses three enzyme systems: ADH and NAD, the microsomal ethanol oxidation system and catalase and NADPH peroxisomala. The product of these three reactions is acetaldehyde, which is further metabolized to acetate by ALDH. Acetaldehyde is a metabolite that produces lesions by numerous mechanisms. Genetics Although not demonstrated a predominant gene, it is clear that there are certain factors that determine the quantity and severity of injuries that occur by gender. Women are more succeptibile to develop alcoholic liver disease with rapid progression, than in men. Malnutrition Many patients with alcoholic hepatitis nutritional deficiencies are present. Toxic effects on cellular membranel Ethanol and its metabolite acetaldehyde, alters the function of membrane transport and mitochondrial gigantism detremina. Hypermetabolic status of hepatocytes Injuries caused by alcohol perivenulara prevailing in the area, and causes hypoxia. Generation of oxygen free radicals Superoxide and hydroperoxide are the byproduct of metabolism and peoxisomal ethanol by microsomal enzyme mechanism. Acetaldehyde reacts with glutathione and decreases hepatocyte protective barrier against the radicals. Other antioxidant systems, such as selenium, zinc, vitamin E, are low in alcoholic persons. Membrane lipid peroxidation associated with alcoholic liver damage is involved in cell death and inflammation. Steatosis Require conversion to ethanol oxidation NAD reduced form NADH. Because NAD is required to fat oxidation, they inhibit the oxidation of fatty acid deficiency, causing their accumulation in hepatocytes. Excessive NADH can be converted into pyruvate to lactate reoxidat. Fat accumulation in hepatocytes may occur in a few days of alcohol abuse, along with abstinence, normal redox status is restored, lipids are mobilized, and steatosis resolves. Although steatosis was considered a reversible condition, prperea hepatocytes filled with fat can lead to local inflammation, granuloma formation and fibrosis, contributing to liver damage. The role of immune system Active alcoholic hepatitis usually persists for months after cessation of ethanol. In fact, may worsen during the first weeks of abstinence. This observation indicates that an immunologic mechanism is involved to perpetuate the damage. The levels of immunoglobulins, especially IgG A, are increased in these cases. Some people have set forth Ac anti-acetaldehyde, antinuclear, and anti anticitoscheletali DNA double helix. In periportal areas were observed in B and T lymphocytes, and killer lymphocytes. Immunosuppressive therapy with corticosteroids appears to improve survival and accelerate recovery in patients with alcoholic hepatitis.