Alcoholic liver cirrhosis

　　Long-term excessive drinking can cause liver cells to repeatedly undergo fatty degeneration, necrosis, and regeneration, eventually leading to liver fibrosis and cirrhosis. Alcoholic liver disease is pathologically manifested as a trilogy: alcoholic fatty liver → alcoholic hepatitis → alcoholic cirrhosis, and the three often coexist. The pathogenesis of alcoholic cirrhosis includes:

　　I. Liver Injury

　　In the past, it was believed that alcoholic liver injury was caused by nutritional deficiency, leading to malnutrition. However, current research has confirmed that even without nutritional deficiencies, and even under the premise of consuming a diet rich in protein, vitamins, and minerals, drinking can still lead to liver ultrastructure damage, liver fibrosis, and liver cirrhosis.

　　II. Immune Response Disorders

　　1. Ethanol can activate lymphocytes.

　　2. Ethanol can enhance the pathogenicity of hepatitis B and C viruses.

　　3. Ethanol enhances the hepatotoxicity of endotoxins.

　　4. During alcoholic hepatitis, cytokines increase, such as tumor necrosis factor (TNF) and leukocyte lysate (TL). These cytokines mainly come from lymphocytes, monocytes, fibroblasts, and increased collagen, leading to liver fibrosis. TGF-β is currently the most important cytokine found to cause fibrosis.

　　5. Ethanol and its metabolites have a direct impact on immune regulation, causing changes in immune markers.

　　III. Collagen Metabolism Disorders and the Formation of Liver Cirrhosis

　　1. Lipid peroxidation promotes collagen formation.

　　2. The key enzyme prolyl hydroxylase in collagen synthesis of alcoholic liver disease patients is activated.

　　3. Alcohol can transform adipocytes into myofibroblasts, synthesize laminin, and increase the mRNA content of collagen, leading to the synthesis of various collagens.

　　4. Alcohol contains iron, and drinking increases intake and absorption, causing iron particles to accumulate in liver cells. Iron can stimulate fibrosis, aggravating liver cirrhosis.

　　Patients with alcoholic liver cirrhosis may develop complications such as infection, upper gastrointestinal bleeding, and hepatic encephalopathy in the late stage.

　　1. Infection

　　The most common complication in alcoholic cirrhosis patients is primary peritonitis. The incidence is about 3-10%, with abdominal tenderness, rebound pain, and ascites as exudative fluid, and increased peripheral blood count.

　　2. Upper gastrointestinal bleeding

　　Bleeding from varices of the esophageal and gastric fundus and bleeding from hepatogenic gastrointestinal mucosal ulcers.

　　3. Hepatic encephalopathy

　　On the basis of cirrhosis, excessive protein intake, gastrointestinal bleeding, infection, and electrolyte imbalance can all induce hepatic encephalopathy.

　　4. Hepatorenal syndrome

　　Hepatorenal syndrome manifests as oliguria, anuria, azotemia, low sodium, high potassium, hepatic coma, and hypotensive shock.

　　The clinical manifestations of alcoholic cirrhosis are divided into compensated and decompensated stages.

　　1. Compensation period

　　During the compensation period, patients may have clinical manifestations of hepatitis, or the onset may be insidious. There may be mild fatigue, abdominal distension, mild enlargement of the liver and spleen, mild jaundice, palmar erythema, and spider angiomas. Imaging, biochemical, or hematological tests may show evidence of liver cell synthetic dysfunction or portal hypertension syndrome (such as hyperfunction of the spleen and varices of the esophagus and gastric fundus), or histology is consistent with the diagnosis of cirrhosis, but without severe complications such as variceal bleeding, ascites, or hepatic encephalopathy.

　　2. Decompensation period

　　1. General symptoms: fatigue, weight loss, dark complexion, oliguria, edema of the lower extremities.

　　2. Gastrointestinal symptoms: loss of appetite, abdominal distension, disturbed gastrointestinal function, even malabsorption syndrome, hepatogenic diabetes, which may appear polyuria, polyphagia, and other symptoms.

　　3. Bleeding tendency and anemia: gingival bleeding, epistaxis, purpura, anemia.

　　4. Endocrine disorders: spider angiomas, palmar erythema, hyperpigmentation of the skin, menstrual disorders in women, gynecomastia in men, and parotid swelling.

　　5. Hypoproteinemia: edema of the lower extremities, oliguria, ascites, hepatogenic pleural effusion.

　　6. Portal hypertension: ascites, pleural effusion, splenomegaly, hyperfunction of the spleen, establishment of portal collateral circulation, varices of the esophageal and gastric fundus, varices of the abdominal wall.

　　Alcoholic cirrhosis patients can be diagnosed by laboratory tests, imaging examinations, endoscopic examinations, and other methods.

　　1. Laboratory examination

　　1. Blood routine: Decreased hemoglobin, platelets, and white blood cells.

　　2. Liver function tests: Mild abnormalities during compensation period, decreased serum protein, increased globulin, and inverted A/G ratio. Prolonged prothrombin time and decreased prothrombin activity. Elevated transaminases and bilirubin. Decreased total cholesterol and cholesterol esters, potentially increased blood ammonia. Disordered amino acid metabolism, imbalance of branched-chain to aromatic ratio. Increased blood urea nitrogen and creatinine. Electrolyte imbalance: low sodium and potassium.

　　3. Pathogenic examination: Negative for HBV-M or HCV-M or HDV-M.

　　4. Fibrosis examination: PⅢP values rise, prolyl hydroxylase (PHO) rises, monoamine oxidase (MAO) rises, and serum laminin (LM) rises.

　　5. Ascites examination: For patients with newly appeared ascites or those with rapid increase of ascites of unknown cause, abdominal puncture should be performed to draw ascites for routine examination, adenosine deaminase (ADA) measurement, bacterial culture, and cytological examination. To improve the positive rate of culture, ascites culture should be performed at the bedside using blood culture bottles, and both aerobic and anaerobic bacterial cultures should be performed separately.

　　Second, Imaging examination

　　1. X-ray examination: Barium esophagogram, showing erosion-like or earthworm-like varices in the esophageal and gastroesophageal fundus.

　　2. B-type and color Doppler ultrasound examination: In the early stage of alcoholic liver cirrhosis, the regenerative nodules formed by pseudo-liver lobules are small, and the surrounding fibrous bundles are narrow and regular. The B-ultrasound measurement values are often increased, the liver echo is dense and enhanced, slightly thicker, and it is not easy to distinguish from other chronic liver diseases. With the progression of the disease, a large number of liver cells are destroyed, liver cell regeneration and a large amount of fibrous tissue proliferation, and the ultrasound cross-sectional images can show numerous circular or oval hyperechoic nodules, diffusely distributed throughout the liver. The nodules are finer and more uniform than those in post-hepatitis cirrhosis, and the size is mostly between 0.2-0.5cm. The nodules are surrounded by fibrous tissue and present as a grid-like hyperechoic pattern. The liver capsule thickens and the echo is enhanced, but there is no saw-toothed change commonly seen in post-hepatitis cirrhosis, and the liver volume is often reduced.

　　3. CT examination: Abnormal proportions of liver lobes, reduced density, nodular changes, widened porta hepatis, enlarged spleen, and ascites.

　　Third, Endoscopy

　　It can determine whether there is esophageal varices and gastroesophageal varices, with a higher positive rate than barium meal X-ray examination. It can also understand the degree of varices and assess the risk of bleeding. Esophageal varices and gastroesophageal varices are the most reliable indicators for diagnosing portal hypertension. In cases of upper gastrointestinal bleeding, emergency gastroscopy can determine the bleeding site and cause, and carry out hemostatic treatment.

　　Fourth, Liver biopsy examination

　　Liver biopsy can confirm the diagnosis.

　　Fifth, Laparoscopic examination

　　It can directly observe the abdominal cavity organs and tissues such as liver and spleen, and can take biopsies under direct vision, which is valuable for diagnosis when it is difficult to diagnose.

　　Sixth, Portal vein pressure measurement

　　The hepatic venous wedge pressure (HVPG) and free pressure are measured by inserting a catheter through the jugular vein, and the difference between the two is the hepatic venous pressure gradient (HVPG), reflecting the portal vein pressure. The normal value is usually less than 5mmHg, and greater than 10mmHg is considered portal hypertension.

　　The onset of alcoholic liver cirrhosis is mostly related to poor living and dietary habits. Patients should ensure a scientific and reasonable dietary structure and avoid drinking and other foods that are harmful to health. In food selection, it is important to consume a certain amount of expensive protein foods containing essential amino acids such as fish, lean meat, eggs, and dairy products to meet the needs of recovery. The diet for alcoholic liver cirrhosis should also be varied. Since the appetite and digestive ability of patients with liver cirrhosis are poor, the diet should be as varied as possible, fresh, and delicious to stimulate appetite and improve digestion.

　　According to information, liver injury in alcoholic liver disease is related to the content of lipids in the diet. Those with high lipid content in the diet are more prone to develop fatty liver and liver fibrosis. At the same time, a diet rich in saturated fatty acids can alleviate or prevent the occurrence of fatty liver and liver fibrosis, while a diet rich in unsaturated fatty acids can induce and exacerbate fatty liver and liver fibrosis. The diet for alcoholic liver cirrhosis tells us that if patients with alcoholic liver disease are given a diet rich in saturated fatty acids, it can alleviate or disappear fatty liver and liver fibrosis, while a diet rich in unsaturated fatty acids has not been improved.

　　There is no effective treatment for alcoholic liver cirrhosis, the key is early diagnosis, treatment for the cause, and strengthening general treatment, so that the condition is alleviated and the compensatory period is prolonged. For patients in the decompensated phase, symptomatic treatment is mainly used to improve liver function and rescue complications; for patients with portal hypertension, various effective measures to prevent upper gastrointestinal bleeding should be taken, including choosing good indications and timing for surgery.

　　First, General Treatment

　　1. Rest: Patients in the compensated phase should reduce their activities appropriately and pay attention to the combination of work and rest. Patients in the decompensated phase should rest in bed mainly.

　　2. Diet: It is advisable to eat high-calorie, high-protein, and easily digestible foods rich in vitamins. When there are signs of hepatic encephalopathy, protein intake should be restricted or prohibited; when there is ascites, the diet should be low in salt or salt-free. Alcohol should be avoided, and rough or hard foods should be avoided; drugs that damage the liver should not be used.

　　3. Supportive treatment: Patients in the decompensated phase have a lack of appetite and eat less, and it is advisable to infuse glucose, vitamin C, insulin, potassium chloride, and other substances intravenously. It is especially important to maintain water, electrolyte, and acid-base balance. In severe cases, amino acids, albumin, or blood should be used.

　　Second, Western Medicine Treatment

　　At present, there is no effective medicine for Western medicine treatment, and it is not advisable to abuse a variety of hepatoprotective drugs. The principle should be to use fewer drugs and necessary drugs. Vitamins and digestive enzymes can be used daily. Abdominal fluid treatment requires limiting the intake of sodium and water; commonly used diuretics include potassium-sparing diuretics such as Spironolactone 20-60mg, three times a day. If the effect is not significant, dihydrochlorothiazide or Lasix can be used; if diuretics are ineffective, or in the presence of hepatic-renal syndrome, hyponatremia, 20g of mannitol can be taken 1-2 times a day.