There are a lot of patients to the clinic after seeing the transaminases elevated very scared, there is a huge error in the understanding of transaminases, especially some bad hospitals artificially raise the value of transaminases, intimidate patients, more sales of drugs, really hateful, which I put the basic situation with the majority of patients to say. In fact, we put the transaminase elevation, not by adding or subtracting to determine how much elevation, but by the number of times to determine how much liver cell damage. For example, ALT 62, which is 22 times higher than normal, is less than 2 times the normal value (calculated at 40), meaning that the overall liver cell damage is no more than 2%, which is different from a fever of 37.5! It is possible that rest will be fine and no medication is needed at all (of course a long-term low level of ALT increase (more than six months) requires a specific analysis of the cause). Here I put several indicators of liver function analysis, I hope that the majority of sufferers will help. The half-life of plasma ALT is 37-57 h. GPT is mainly present in the hepatocyte plasma, and its intracellular concentration is 1000-3000 times higher than that in serum. Having 1% of hepatocytes necrotic can double the serum enzyme. Therefore, we consider ALT below 120 as mild liver damage; 120-400 as moderate damage; and if it exceeds 400, it indicates that the hepatocyte count destruction is more than 10% or more, which is called severe and requires active hospitalization. We often see mildly elevated transaminases in liver function test, especially single ALT elevation, in fact, there is not much clinical meaning, the number of damaged liver cells is also very limited, there is no need to deal with drugs, most of the rest can automatically return, there is no need to use drugs (three points of treatment, seven points of nutrition). Because ALT can accurately respond to the amount of liver cell damage, ALT is recommended by the World Health Organization as the most sensitive indicator of liver function damage. Clinical significance of lowering transaminases: 1, reduction to end of hepatocyte destruction (but inflammation in the liver does not subside) 2.Improve liver reserve function and reduce inflammation within the liver. 3, Determine the effect of liver protection treatment. Disadvantages: Can not accurately liver inflammation subsides and liver reserve function is established. II. Glutathione aminotransferase (AST,GOT) There are 2 isoenzymes of glutathione aminotransferase in the liver, which are present in the mitochondria (mAST) and intracytoplasm (sAST) of liver glutathione aminotransferase cells. Under normal conditions, glutathione is present in tissue cells, with the highest levels in cardiac myocytes, followed by the liver, and very little in serum. Glutathione is mainly found in the mitochondria of hepatocytes and can only cause high glutathione concentrations in serum when severe necrosis or destruction of the liver occurs, it is not as sensitive as ALT and the basic clinical meaning can be referred to elevated ALT. The clinical significance of high glutamic transaminase (need to combine with the actual situation of clinical patients): 1, high glutamic transaminase can indicate myocardial infarction or myocarditis. 2, high glutamic oxalacetic transaminase can reflect serious liver cell damage, especially after the inversion of the two indicates that the patient may have reached the degree of cirrhosis, of course, the prerequisite here is that the transaminases are repeatedly abnormal for a long time. 3.High glutathione aminotransferase can reflect the severity of liver cell damage, which has spread to the organelle damage, or the damage starts from the organelle inside the liver cell (such as drug hepatitis, alcoholic hepatitis, etc.). Alkaline phosphatase (ALP) is widely distributed in all organs of the body, with the liver being the most abundant, followed by the kidneys, bones, intestines, and placenta, etc. The ALP in serum mainly comes from the epithelial cells of the liver bile ducts and bones. Most of the serum in growing children comes from osteoblasts and growing osteochondrocytes, with a small amount coming from the liver. 1.Physiological reasons: children’s skeletal development, pregnant women, fracture healing period, in these cases the alkaline phosphatase in bone tissue is very active, so the value will be high when tested. 2, pathological reasons: when the human body suffers from obstructive jaundice, primary liver cancer, secondary liver cancer, cholestatic hepatitis, bile duct cell carcinoma, drug-related liver injury, etc., the bile duct epithelial cells overproduce ALP, which enters the blood through the lymphatic tract and liver sinusoids, and at the same time, due to the obstruction of bile excretion, backflow into the blood, causing high alkaline phosphatase in the serum; when the bones have diseases, such as rickets, tumors on the bone, chondromalacia Other not very common diseases, such as kidney disease, severe anemia, thyroid insufficiency, leukemia, etc. Fourth, γ-glutamyl transpeptidase (γ-GT) is widely distributed in human tissues, the most in the kidney, followed by the pancreas and liver, and the most in the liver during the embryonic stage, mainly in the hepatocyte pulp and microsomes in the intrahepatic bile duct epithelium, which is an important indicator of the synthesis ability of hepatocytes, including, of course, the enhanced abnormal synthesis ability of hepatocytes. However, most of the enhanced abnormal synthesis ability is more than 500-600, and there are many patients with repeated hepatocyte damage, such as patients with alcoholic liver, PBC or AIH, who have repeatedly elevated γ-GT by several hundred. It is generally believed that after the destruction of hepatocytes, they must be regenerated, and the size of the regenerative capacity depends on this index; if it is elevated for a long time, it also indicates that the destruction is longer, and the destruction and regeneration of hepatocytes are intertwined. Clinical significance: 1. In primary or metastatic liver cancer, GGT in blood is significantly elevated. The reason is that the increase of GGT produced by cancer cells and the inflammatory stimulating effect of cancer tissue itself or its surrounding increase the permeability of hepatocyte membrane, resulting in the increase of GGT in blood (its sensitivity is much less than AFP and ultrasound, MRI and CT, so patients should review ultrasound every 3-6 months and AFP is important, not only including liver function). 2, obstructive jaundice, acute hepatitis, active chronic hepatitis, biliary tract infection, cirrhosis and drug metabolic diseases can increase GGT. 3, other diseases such as myocardial infarction, acute pancreatitis and certain drugs can raise the GGT in the blood. V. Jaundice (T-BIL) It is the main pigment in human bile, orange-yellow in color, including direct bilirubin and indirect bilirubin. Generally, bilirubin should be interpreted separately, where direct bilirubin mostly indicates intrahepatic bile duct stasis and bile duct obstruction is common. Indirect bilirubin mostly indicates increased bilirubin production, such as hemolysis. Of course, different intracellular energy metabolism also causes different mechanisms of bilirubin metabolism. Pathologically, it is the main metabolite of iron porphyrin compounds in the body, which is toxic and can cause irreversible damage to the brain and nervous system, but it also functions as an antioxidant and can inhibit the oxidation of linoleic acid and phospholipids. Bilirubin is an important clinical basis for determining jaundice and is an important indicator of liver function. It is generally considered that elevated jaundice is a sign of loss of liver function, indicating that the destruction of liver cells produces jaundice, which has exceeded the body’s metabolic capacity and is caused by the accumulation of jaundice, where the prerequisite is mostly accompanied by elevated ALT or other enzymatic levels. Of course, this also requires specific analysis, if the bilirubin disorder itself, manifested as a single bilirubin elevation (50Umol or less) (such as D-BIL alone or I-BIL), in fact, indicates a mild metabolic disorder of bilirubin, and does not require special medication treatment, regular observation can be. Clinical significance: 1. Prehepatocellular jaundice: mainly refers to increased jaundice production, including hemolysis, etc. 2, hepatocellular jaundice: including hepatocyte destruction, increased hepatocyte load (endotoxin, toxin levels, ammonia, etc.), synthetic dysfunction (indirect bilirubin cannot be synthesized into direct bilirubin), excretory dysfunction (elevated direct bilirubin), genetic and inherited metabolic defects, etc. 3, post-hepatocellular jaundice: bile duct obstruction, often combined with an increase in ALP or GGT. Protein (PRO, ALB+GLO) mainly includes albumin and globulin: albumin is the main factor to maintain plasma osmolality, and is also one of the energy providers in the body, also involved in the metabolism of jaundice, the only organ of albumin synthesis is the liver, so the destruction of liver cells and reduced synthesis capacity can cause a decrease in albumin, long-term decrease in albumin (below 30Umol) the most common effect The most common effect of a long-term decrease in albumin (below 30Umol) is tissue edema, commonly in the lower extremities and eyelids, and after a long period of time, the formation of ascites. Of course, the precursor of albumin is pre-albumin, so pre-albumin is more sensitive than albumin to the synthesis capacity of liver cells. Globulin is the sum of all inflammation in the body, i.e., the body’s overall humoral immunity, and is secreted by plasma cells in the body. Long-term elevation of globulin indicates the presence of chronic inflammation in the body, including all inflammatory conditions in the body, including pneumonia, nephritis, rheumatism, etc., and of course, hepatitis is also one of them.