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　　What are the causes of the onset of non-alcoholic fatty liver disease?

　　In addition to general symptoms, it can also cause other diseases, such as hyperlipidemia, hypercoagulability, liver fibrosis and cirrhosis, metabolic syndrome, and atherosclerosis. Therefore, once discovered, active treatment is needed, and preventive measures should also be taken in daily life.

　　Most patients have no symptoms and are discovered during routine physical examinations, with mild liver function abnormalities. NAFLD is divided into two major categories: primary and secondary. The former is related to insulin resistance and genetic susceptibility, while the latter is caused by certain special reasons.

　　Weight loss, blood sugar reduction, scientific diet, and moderate exercise are the key to prevention. The patient's diet should be light and easy to digest, with more fruits and vegetables, a reasonable diet combination, and attention to adequate nutrition. In addition, patients should also pay attention to avoiding spicy, greasy, and cold foods.

　　First, serological examination of enzymes

　　1. ALT, AST:Generally, there is a mild increase, reaching 2 to 3 times the normal upper limit. In non-alcoholic fatty liver, ALT/AST > 1. If ALT > 130U, it indicates significant lobular fat infiltration, and persistent increase in ALT suggests fatty granuloma.

　　2. γ-GT, ALP:Non-alcoholic fatty liver patients may have elevated γ-GT.

　　3. GST:Can reflect stress-induced liver injury and is more sensitive than ALT.

　　4. Glutamate dehydrogenase (GDH), ornithine carbamoyltransferase (DCT):GDH is a mitochondrial enzyme, mainly active in the liver acinar III zone, and DCT is a urea synthesis enzyme, participating in the transmethylation reaction. Both enzymes are elevated in fatty liver.

　　5. Cholinesterase (CHE), lecithin cholesterol acyltransferase (LCAT):80% of fatty liver serum CHE and LCAH are elevated. CHE has a certain significance in distinguishing fatty liver.

　　2. Changes in plasma proteins

　　1. β-Globulin:α1, α2, β lipoproteins are mostly elevated.

　　2. Albumin is mostly normal.

　　3. Fatty liver due to obesity:LDL-C is elevated, HDL-C is significantly reduced, and ApoB, ApoE, ApoCⅡ, and ApoCⅢ are elevated.

　　3. Plasma lipids:TG, FA, cholesterol, and phospholipids are often elevated, among which cholesterol is significantly elevated, often >13mmol/L.

　　4. Pigment excretion test:BSP and ICG excretion decrease. In fatty liver, because fat accumulation is mainly in the liver acinar III zone, and pigment processing also occurs in this area. Liver fat accumulation affects the liver cell excretion of pigment function. The degree of excretion reduction is related to the degree of liver fat infiltration.

　　5. Bilirubin:Serum bilirubin may increase in severe fatty liver, while bilirubin is mostly normal in mild to moderate fatty liver.

　　6. Prothrombin time (PT).

　　7. Blood insulin level:It shows a hyperresponsive delayed type, with the peak of the glucose tolerance curve rising and descending delayedly.

　　Occasional elevation of blood urea nitrogen and uric acid.

　　A diet low in salt, fat, high in vitamins, and moderate in protein, avoiding excessive calorie intake. Avoid eating or eating less animal fat and sweets (including sugary drinks). Eat more vegetables, fruits, and foods rich in fiber, do not eat snacks, and do not eat before bedtime.

　　1. Treatment strategies

　　1. Prevent and treat the primary disease or related risk factors.

　　2. Basic treatment:Establish reasonable energy intake, adjust dietary structure, moderate aerobic exercise, and correct bad lifestyle and behavior.

　　3. Avoid exacerbating liver damage:Prevent sudden weight loss, drug abuse, and other factors that may induce the deterioration of liver disease.

　　4. Weight loss:All patients with overweight, visceral obesity, and rapid weight gain in the short term with NAFLD need to control weight and reduce waist circumference through lifestyle changes. For those with a 6-month weight loss of 27kg/m2 per month and two or more abnormal indicators such as blood lipids, blood glucose, and blood pressure, it can be considered to add weight loss drugs such as sibutramine or orlistat, with weekly weight loss not exceeding 1.2Kg (not exceeding 0.5Kg per week for children); for those with BMI>40kg/m2 or BMI>35kg/m2 combined with sleep apnea syndrome and other obesity-related diseases, it can be considered to undergo proximal gastric bypass surgery for weight loss.

　　5. Insulin sensitizers:Combining metformin and thiazolidinedione drugs for patients with type 2 diabetes, impaired glucose tolerance, increased fasting blood glucose, and visceral obesity can be considered to improve insulin resistance and control blood glucose.

　　6. Hypolipidemic drugs:For patients with dyslipidemia who have been treated with basic treatment and/or weight loss and hypoglycemic drugs for more than 3-6 months, and still present with mixed hyperlipidemia or hyperlipidemia combined with two or more risk factors, it is necessary to consider adding bile acid sequestrants, statins, or probucol and other hypolipidemic drugs.

　　7. Liver disease drugs:For patients with NAFLD accompanied by liver dysfunction, metabolic syndrome, still ineffective after 3-6 months of basic treatment, and those confirmed as NASH by liver biopsy and showing chronic progressive course, adjuvant drug treatment for liver disease can be adopted to antioxidant, anti-inflammatory, and anti-fibrotic, which can be reasonably selected based on drug properties, disease activity, and stage, such as polyene phosphatidylcholine, vitamin E, silymarin, and ursodeoxycholic acid, but it is not advisable to use multiple drugs at the same time.

　　8. Liver Transplantation:主要用于NASH-related end-stage liver disease and some cryptogenic liver cirrhosis patients with decompensated liver function, metabolic screening should be performed before liver transplantation. BMI>40kg/m2 is a contraindication for liver transplantation.

　　Secondly, Treatment Monitoring

　　1. Self-evaluation and monitoring, setting up indicators that allow patients to monitor their diet, exercise, sleep, weight, and quality of life-related observations, such as simple graphical records, for evaluation.

　　2. Assessment of primary disease and clinical symptoms and signs related to liver disease, be alert to the possibility of subacute NASH and liver function failure caused by rapid weight loss (more than 5kg per month).

　　3. Practical objectives and treatment control targets for the components and degree of metabolic syndrome.

　　4. Evaluation of liver enzymes and liver function reserve, the latter can be assessed by Child-Pugh classification and/or MELD scoring system.

　　5. Imaging evaluation of the degree and distribution type of liver fat infiltration.

　　6. Dynamic observation of non-invasive indicators of liver inflammation and progressive fibrosis, including serum fibrosis markers and other relevant laboratory indicators.

　　7. Liver biopsy to evaluate the changes in liver steatosis, inflammation, and fibrosis, monitor the effectiveness, safety of treatment, and assess prognosis.

　　8. Clinical and laboratory related examinations for adverse reactions of basic treatment drugs.