Malnutrition-related liver cirrhosis

　　Malnutrition-related liver cirrhosis is caused by long-term nutritional deficiency. The mechanism by which malnutrition leads to liver cirrhosis may be that when proteins containing cysteine are lacking, the source of cysteine and glutathione is reduced, affecting the production and activity of enzymes in liver cells, causing the liver cells to be damaged by various factors and undergo变性坏死. Choline is a lipotropic substance that can synthesize phospholipids with neutral fats in the liver, making it easy for liver fat to be oxidized and utilized. If choline or the essential amino acids required for the synthesis of choline are seriously lacking, fat will accumulate in liver cells and become fatty liver. Fatty degeneration of liver cells can reduce the resistance of liver cells to various harmful factors, and can also cause compression and pressure on the liver sinusoids due to the increase in cell volume, gradually leading to ischemia, necrosis, fibrous tissue proliferation, and eventually liver cirrhosis.

　　The causes of malnutrition-related liver cirrhosis, in addition to individual patients due to insufficient intake, are mainly due to other diseases that limit the intake and absorption of food. Similar to other types of liver cirrhosis, malnutrition-related liver cirrhosis is preceded by liver cell injury such as fatty degeneration, accompanied by inflammatory cell infiltration in the portal area and liver lobules and granuloma formation, which later develops into liver fibrosis. Similar to alcoholic liver injury, perivenous liver fibrosis is a sign of the development of liver cirrhosis. Long-term repeated damage to the liver eventually leads to liver cirrhosis, and the entire pathological process and characteristics of liver lesions in each stage are similar to those of alcoholic liver injury.

　　Fatty degeneration of liver cells can reduce the resistance of liver cells to various harmful factors, and can also cause compression and pressure on the liver sinusoids due to the increase in cell volume, gradually leading to ischemia and necrosis, fibrous tissue proliferation, and eventually liver cirrhosis. Malnutrition-related liver cirrhosis often leads to death due to complications, and the diseases it may cause mainly include hepatic encephalopathy, massive upper gastrointestinal bleeding, infection, hepatorenal syndrome, ascites, and primary liver cancer.

　　The causes of malnutrition, in addition to individual patients due to insufficient intake, are mainly due to other diseases that limit the intake and absorption of food, and some postoperative patients may also suffer from malnutrition. Liver cirrhosis due to malnutrition is caused by long-term nutritional deficiency, and clinical symptoms include loss of appetite, weakness, abdominal pain, nausea, and vomiting. The formation process of liver cirrhosis is hidden, and some patients have atypical clinical manifestations.

　　Prevention is very important for malnutrition-related liver cirrhosis, and the main measures include the following aspects:

　　1. For those with high blood ammonia or extremely poor liver function, protein intake should be restricted to prevent hepatic coma. Those with ascites should consume low-sodium or salt-free diet.

　　2. In terms of diet, provide sufficient nutrition, diversify food, supply high-priced proteins containing amino acids, various vitamins, low-fat, and low-fiber diet, and prevent rough and fibrous foods from damaging esophageal varices, causing massive bleeding.

　　3. Pay attention to changes in bleeding, purpura, fever, and changes in mental and neurological symptoms, and promptly contact a doctor.

　　4. Measure abdominal circumference and determine urine output daily. Abdominal obesity can be a method for self-discrimination of fatty liver.

　　Regarding the prevention of early malnutrition-related liver cirrhosis, regular check-ups are an important measure for preventing early liver cirrhosis, thus allowing for early intervention.

　　The clinical examination methods for malnutrition-related liver cirrhosis mainly include laboratory examination and imaging examination, as follows:

　　First, Laboratory examination

　　1. Complete blood count: In cases of splenic hyperfunction, the total blood cell count is reduced. Leukopenia is common, often below 4.0×109/L (4000). Platelets are usually below 50×109/L (50000). Most cases present with normal cellular anemia, while a few cases may be macrocytic anemia.

　　2. Urinalysis: In cases of jaundice, uric bilirubin/uric acid is positive.

　　3. Routine examination of ascites: Ascites is an exudate, with a density below 1.018, negative Lee's test, cell count below 100/mm3, and protein quantification less than 25g/L.

　　4. Liver function tests.

　　Second, Imaging examination

　　1. Ultrasound examination: During liver cirrhosis, due to fibrous tissue proliferation, ultrasound shows uniform, diffuse dense punctate echoes, with increased echoes in the late stage. The liver volume may decrease. If portal hypertension is present, the portal vein may dilate, and the spleen may thicken.

　　2. Liver biopsy: This method can determine the diagnosis and understand the histological type of liver cirrhosis and the extent of liver cell damage and connective tissue formation. However, if the sample is too small, there may be a false-negative result. Currently, rapid needle biopsy is widely used due to its simplicity, fewer complications, and safety.

　　3. Laparoscopic examination: It is one of the reliable methods for diagnosing liver cirrhosis and can directly observe the liver surface. Typical cases show nodular liver surface, varices on the abdominal wall, and splenomegaly. Liver biopsy can also be performed under direct vision. For cases that cannot be diagnosed clinically, this examination can confirm the diagnosis and detect early lesions.

　　4. Esophageal X-ray barium meal examination: When esophageal varices are present, the varices are higher than the mucosa, and the barium appears unevenly distributed on the mucosa, resulting in worm-eaten or earthworm-like defects. In cases of gastric fundus varices, the barium appears in a daisy-like filling defect.

　　5. Esophagogastroduodenoscopy or gastroscopy: It can directly observe the esophagus and stomach for varices and understand the degree and extent of varices, which is helpful for differential diagnosis of upper gastrointestinal bleeding. The accuracy of varix detection through gastroscopy is higher than that of esophageal X-ray barium meal examination.

　　6. Radioisotope scanning: Use colloidal 198 gold or other radionuclides for liver scanning. In patients with liver cirrhosis, the liver area can be seen to have a sparse, uneven, or spotted reduction in radioactive areas. Scanning with 99mTc and 113mIn can show the size and shape of the spleen. During liver cirrhosis, the liver shadow may increase during the compensatory period, while it may decrease in the late stage, and the spleen shadow may increase.

　　Patients with malnutrition-induced liver cirrhosis should pay attention to the following aspects in their diet:

　　1. Ensure sufficient calorie intake. Adequate calories can reduce protein consumption, alleviate the burden on the liver, and be beneficial to the synthesis of tissue proteins. For patients with liver cirrhosis, the daily food calorie intake of 2500-2800 kcal is more appropriate. Based on body weight, about 35-40 kcal per kilogram of body weight is needed per day.

　　2. Pay attention to the supplement of fiber. Vegetables should mainly be leafy, melon, and solanaceous vegetables, and they should be chopped and cooked when eaten. Fruits should be made into purees or juices for consumption.

　　3. Pay attention to the supplement of vitamins and minerals. Liver cirrhosis is often due to a lack of various trace elements and vitamins, which often participate in the repair function of liver cells. Pay attention to the intake of foods rich in zinc, such as lean pork, beef, eggs, fish, and foods rich in magnesium such as green leafy vegetables, dairy products, and grains, etc.

　　4. Limit the intake of salt. The daily salt intake should not exceed 6 grams, and if edema and mild ascites occur, the salt intake should not exceed 2 grams.

　　There is currently no effective drug for the treatment of malnutrition-induced liver cirrhosis. It is not advisable to misuse drugs, as this may increase the burden on the liver and have the opposite effect. The current treatment methods for malnutrition-induced liver cirrhosis are as follows:

　　1. Supplement various vitamins. Vitamin C, E, and B-group vitamins can improve liver cell metabolism, prevent fatty degeneration, and protect liver cells. Yeast tablets can also be taken. Considerably supplement vitamin K, B12, and folic acid as needed.

　　2. Medications to protect liver cells, such as Gan Tai Le, Wei Bing Gan, Gan Ning, Yi Gan Ling (Silymarin Tablets), inosine, etc., can be added with vitamin C, B6, potassium chloride, and soluble insulin to 10% glucose solution.

　　3. Traditional Chinese medicine has unique insights into the diagnosis and treatment of chronic liver diseases. The integration of traditional Chinese and Western medicine often achieves good results.