Alcoholic steatohepatitis is a liver disease characterized by fibrosis and necrosis of the liver tissue induced by excessive alcohol consumption.
Excessive consumption of alcohol has various effects on the body. From unknown causes one third of chronic alcohol consumers, do not develop alcoholic staetohepatitis . Others develop fatty liver or cirrhosis and chronic pancreatitis, dilating cardiomyopathy and neuro-psychiatric disorders.
There are several risk factors for alcoholic staetohepatitis:
- Duration of alcohol consumption and alcohol consumption itself: it is considered toxic, a dose of 60 -80 ml ??of pure alcohol / day in men and 40-50 ml of pure alcohol / day in women. Is also important is the duration of alcohol consumption, because there is a higher risk for the development of alcoholic steatohepatitis if the length of this behavior is more than 5 years. Daily consumption of alcohol is more dangerous than occasional use. Changes occurring in the liver does not depend on the type of alcoholic beverage, but its alcohol content.
- Gender: women are more likely to develop alcoholic steatohepatitis than men. For men to develop the disease, they must consume a higher quantity of alcohol in function than women and the metabolism of alcohol in stomach and liver is slower in women than in men.
- Genetics: Although not demonstrated a clear genetic markers that have a clear susceptibility to alcoholism, it seems that exist some inherited behavioral patterns related to alcohol consumption.
- The existence of a chronic hepatitis B or chronic hepatitis C;
- Nutritional factors. Protein malabsorption favors the development of alcoholic steatohepatitis and was noticed that protein malabsorption is very common in alcoholics. It was demonstrated that a balanced diet can protect the individual who consume alcohol, at least for a while.
There are three histological types of alcoholic steatohepatitis:
- Alcoholic fatty liver;
- Alcoholic hepatitis;
- Alcoholic cirrhosis, which is the last stage of alcoholic statohepatitis, in which the fibosis affects the entire liver.
Alcoholic fatty liver:
It is characterized pathologically by lipid loading with more than 5% of hepatocytes. Macroscopic liver is enlarged, firm, pale yellow.
Clinically is observed asymptomatic hepatomegaly and sometimes signs of chronic liver disease such as Dupuytren’s contracture, testicular atrophy, palmar erythema, gynecomastia and vascular asterisks. Later physical fatigue can occur, cachexia, fever, anorexia, nausea, vomiting, jaundice, painful hepatomegaly, splenomegaly andascites. A complication of alcoholic fatty liver can be Zieve syndrome, characterized by hyperlipidemia, hemolytic anemia, jaundice and abdominal pain.
Paraclinical, can be observed an increase in transaminases, with a AST / ALT report greater or equal to 2, and 80% of cases there is an increase in gamma-glutamyl-transpeptidase.
Alcoholic fatty liver positive diagnosis is on account of symptoms, clinical history, due to laboratory and ultrasound liver steatosis highlighting.
A particular form of alcoholic fatty liver is represented by focal steatosis, which often pose problems of diagnosis with liver tumors.
Complications that can occur are the sudden death due to fatty embolism, alcohol withdrawal and hypoglycemia.
Treatment involves permanent stop of alcohol consumption, correction of protein deficiencies and administration of hepatoprotective drugs.
Unlike the alcoholic fatty liver, in alcoholic hepatitis occur in necrosis, inflammation and fibrosis of the liver.
Clinically, patients may be asymptomatic, or may have the usual events like anorexia, nausea, asthenia, physical fatigue, abdominal pain, jaundice, fever, weight loss or may have symptoms that arise during complications: encephalopathy, upper gastrointestinal bleeding and ascites, complications that progress rapidly to death.
Clinical examination reveals hepatomegaly, liver tenderness, signs of portal hypertension (splenomegaly, ascites), signs of alcoholism (palmar erythema, bruising, vascular asterisks, gynecomastia).
Paraclinical may reveal anemia due to vitamin B12 deficiency or folic acid deficency, leukocytosis or leukopenia and thrombocytopenia. Always transaminases are increase over the amount of 300 U / l, report AST / ALT is 2 / 1, increase in gamma-glutamyl-transpeptidase and alkaline phosphatase. Sometimes may occur a increases in bilirubin occur.
Alcoholic hepatitis may be complicated by: portal hypertension, which may be reversible after stopping the alcohol consumption or irreversible if the liver presents fibrosis. Cirrhosis is another complication which can lead to death.
Ascites is another complication of alcoholic hepatitis, which is being difficult to control.
Hepatic encephalopathy may appear in advanced forms of the disease.
Mortality in alcoholic hepatitis is between 20% and 80%, patients with the worse prognosis are those who have associated severe jaundice, hepatic encephalopathy, renal failure and gastrointestinal bleeding.
Treatment consists of permanently interruption of alcohol consumption and correcting protein deficiencies by administering amino acid, because was observed that the degree of protein deficiency is associated with mortality. Corticosteroids may also be administered, because have imunosupersor and anti-inflammatory role and can inhibit the fibrosis.
Despite medication, mortality remains high in alcoholic hepatitis.