Alcoholic fatty liver alcoholic liver disease is short for alcoholic liver disease. It is estimated that there are about 15-20 million alcoholics worldwide, and 10%-20% of these people (1.5-4 million) have varying degrees of alcoholic liver disease. Alcoholic liver disease can be asymptomatic in its early stages, but by this time the internal tissues of the liver have already undergone pathological changes. Alcoholic liver disease can be divided into three main categories, namely alcoholic fatty liver, alcoholic hepatitis and alcoholic cirrhosis. These three forms can exist separately or mixed.
1.Clinical manifestations
Before the onset of alcoholic hepatitis, there is often a history of heavy drinking within a short period of time, and patients have obvious symptoms such as weight loss, loss of appetite, nausea and vomiting, general weakness, abdominal pain and diarrhea. According to statistics, 77% of patients showed loss of appetite, 55% had nausea and vomiting, 46% had abdominal pain, and 43% had weight loss. Jaundice, hepatomegaly and pressure pain are common signs in patients with alcoholic hepatitis. Hepatomegaly was present in 81% of patients and jaundice was present in 77% of patients. Transaminases are moderately increased.
The clinical manifestations of alcoholic fatty liver are proportional to the degree of fatty infiltration of the liver and the symptoms may disappear after the excess fat is removed from the liver. Hepatomegaly is the most common clinical sign, followed by hepatic pain and pressure pain. A few patients may have mild jaundice, and laboratory tests suggest an association with obstruction of the biliary system. In severe cases, ascites and lower limb edema may be present, and splenomegaly is occasionally seen. Some patients may present with vitamin deficiency manifestations such as peripheral neuritis, tongue inflammation, stomatitis, and skin petechiae. In conclusion, alcoholic fatty liver lacks specific clinical symptoms.
2.Examination
1.Plasma protein
Total plasma protein changes and inversion of the ratio of albumin are the most common biochemical abnormalities, and some patients show increased α1, α2 and β globulins by plasma protein electrophoresis. After recovery from fatty liver, the recovery of plasma protein abnormalities is later than other indicators, and it takes 3-6 months to return to normal.
2.Serum glutamic aminotransferase (ALT) and glutamic oxalacetic aminotransferase (AST)
The former increase is not obvious, AST/ALT>2 has diagnostic significance, ALT elevation is not sensitive because acetaldehyde makes the enzyme’s active cofactor B6 decrease. ALT is more significantly inhibited than AST activity in liver tissue.
3.γ-Glutamyl transpeptidase (γ-GT)
It is more sensitive to increase when the microsomes of hepatocytes are damaged by alcohol. It is a more sensitive indicator for the diagnosis of alcoholic liver disease.
4.Alcohol oral method load test
To detect the changes of glycoprotein, prealbumin, α2HS glycoprotein and haptoglobin, which are reduced in alcoholic fatty liver.
5.B ultrasound examination
Diffuse fatty liver under B ultrasound can be divided into three kinds.
① Mild fatty liver: it shows enhanced near-field echogenicity and insignificant far-field echogenicity attenuation, and intrahepatic tubular structures are visible.
②Moderate fatty liver: anterior field echogenic enhancement, posterior field echogenic attenuation, and blurred tubular structures.
③Severe fatty liver: significant enhancement of near-field echogenicity, significant attenuation of far-field echogenicity, indistinct and indistinguishable tubular structures. The ultrasound changes of restricted fatty liver are non-uniformly distributed, and the acoustic image shows multiple strong echogenic nodules, but there is no mass effect, and liver biopsy is feasible if necessary.
6.CT examination
Accuracy is better than ultrasound, mainly showing generalized or focal decrease of liver parenchyma density.
3.Diagnosis
1.History of long-term heavy alcohol consumption or short-term binge drinking.
2.There are clinical manifestations of alcoholic fatty liver and corresponding abnormal experimental examination and imaging changes.
3.Exclude fatty liver caused by virus, drugs or other reasons.
According to the above three points, clinical diagnosis can be made, and if there are histological changes in the liver, further diagnosis can be confirmed.
4.Treatment
Most patients with alcoholic fatty liver have a good prognosis. Generally, after abstaining from alcohol and treatment for about one month, the fat in the liver will be reduced and disappear after a few months in mild cases and one to two years in severe cases. The prognosis for alcoholic hepatitis is poor, but most can recover with a mortality rate of only 1.5% to 8% if alcohol is abstained and hospitalized in a timely manner. The prognosis of alcoholic cirrhosis is poor, according to statistics, about 50% of patients with alcoholic cirrhosis die within 5 years.
Five percent of patients can be transformed into liver cancer. And it has been reported that patients with alcoholic fatty liver may turn into cirrhosis in 10 to 15 years without good treatment. Therefore, experts emphasize that alcoholic liver disease should be prevented and treated early, and alcoholic fatty liver should be quitted and treated in time after suffering from alcoholic fatty liver in order to stop its development in a bad direction. In most patients, alcoholic fatty liver is completely reversible, and generally the fatty liver gradually disappears after quitting alcohol.
However, if excessive drinking occurs for a long time, it can cause repeated fatty degeneration and necrosis of liver cells and eventually develop into alcoholic hepatitis and alcoholic cirrhosis, which can endanger people’s lives in serious cases. Sudden death can occasionally occur in patients with fatty liver as a result of polyencephalopathy and pulmonary fat embolism.