Selection and evaluation of laboratory tests for liver disease in children

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Liver injury is often encountered in pediatric clinical practice. The liver function has a great reserve, many liver diseases often in the d


Liver injury is often encountered in pediatric clinical practice. The liver function has a great reserve, many liver diseases often in the development of late to have clinical symptoms, the laboratory examination to determine whether liver damage and damage the existing types of treatment and management of liver disease in children is very important. If there is no jaundice viral hepatitis, some liver cirrhosis (such as Wilson 's disease) and drug hepatotoxicity can be no clinical symptoms. Viral infection is the most common cause of liver injury worldwide, and serological and nucleic acid testing techniques are often required to detect the presence of the virus and to monitor the response to treatment. In the past 10 years, due to the application of hepatitis A, hepatitis B vaccine and blood screening for hepatitis C virus (HCV), the incidence of acute viral hepatitis was significantly decreased, liver damage caused by many other reasons, especially congenital or acquired metabolic defects of autoimmune disorders and liver injury caused by a rising trend. Laboratory tests are especially critical in identifying these causes, particularly in patients with no evidence of viral infection. Of course, the use of certain drugs can also cause liver damage, in this case to determine the possible causes of liver injury, clinical information is the most reliable.

Because the liver is a complex, interconnected with the metabolism, secretion and defense organs, no single or simple laboratory tests can cover all the test items on liver function, liver function variety. However, excessive inspection items often cause serious economic burden and the limited medical resources for domestic waste, sometimes more than one project to obtain the information often overlap, so how to reasonably select the project and explain the significance of the project is especially important. The purpose of this paper is to review the comrades and related theoretical knowledge, correct choice in pediatric patients and explain relevant indicators.

Laboratory indicators of liver function and injury

We often use laboratory tests to diagnose and detect liver disease and to determine the prognosis of liver disease. In some cases, the type of laboratory abnormalities contribute to the diagnosis, such as liver function tests show that the damage is mainly to liver cells, or depressed biliary or biliary obstruction; some liver function index, especially a series of follow-up, can reflect the degree of liver damage, and prognosis. At the same time, the change of laboratory parameters over time is helpful to follow up the course of liver disease and the response of patients to treatment. Although most of these tests are called liver function tests, most of the trials used routinely do not really reflect liver function. Many of the trials are indirect reactions to liver injury, which can also occur in many other cases, and are not specific.

Experimental evaluation of liver disease can be divided into 6 categories: 1) biochemical activity test, also known as the enzymatic test, divided into test reflect liver injury (such as ALT, AST, LDH) and depression (GGT, AP, bile test (total bilirubin, non binding, binding, d), urobilinogen, blood and urinary bile acid); 2) test of liver synthesis function include albumin and other serum protein, prothrombin time and other coagulation indexes, NH3, plasma and urinary amino acids, lipid and lipoprotein, triglyceride and cholesterol; 3) quantitative function test; 4) imaging studies; 5) histology 6); serum specific tests, such as A1AT, ceruloplasmin, AFP, autoantibodies, pathogen indicators etc.. Some content has a specific introduction, which introduces some commonly used enzymology check, synthesis function and specific serological marker.

1 biochemical activity test (enzymatic test)

1) hepatocyte injury index

The most commonly used transaminase. Aspartate aminotransferase (AST, SGOT) and alanine aminotransferase (ALT, SGPT) are sensitive markers of liver injury and hepatocyte necrosis. AST is found in the liver, myocardium, skeletal muscle, kidney, pancreas and red blood cells. AST levels were elevated in any cause (trauma, ischemia, drugs, etc.) that caused the damage to the tissues. Because this kind of examination is nonspecific, alone with AST height to diagnose liver disease must pay special attention to. Virus infection caused by rhabdomyolysis and hemolysis can be AST significantly increased (with elevated ALT). It has been reported that in our clinical practice, we have also encountered a case of ALT with a significant increase in AST and / or an initial diagnosis of liver disease, followed by a finding that the liver is normal and has a chronic subclinical myopathy. Then check the LDH isozyme can help differentiate hemolysis or myopathy, or muscle enzyme inosine monophosphate (CPK) or aldolase helps to distinguish whether to muscle.

ALT mainly in the cytoplasm of liver cells, liver enzyme activity in serum was 100 times higher, as long as there are 1% necrosis of liver cells, serum enzyme activity can be increased 1 times. Other tissues, such as muscle, are significantly lower, and thus have a high specificity for liver disease. Multiple and AST increased simultaneously, but also increased independently. The normal values of ALT and AST vary with age (see figure below), so it is best to have normal values of different ages and genders. For convenience, we usually use 25U/L as the normal upper limit of ALT in children.

Some of the factors that may affect the detection of transaminase, the clinical value should be noted (see table below). Because AST and ALT are vitamin B6 coenzyme, so in the absence of vitamin B6, its value was significantly lower (especially ALT). Uremia can also cause AST false reduction. Giant AST (macro-AST, AST combined with IgG) can reduce the clearance of AST, which can cause the false elevation of blood AST. The reference range of AST was slightly higher in men, obesity and non whites.

The change of transaminase has a limited effect on speculation. The magnitude of the increase in AST is usually less than ALT, but in alcoholic liver injury 90% of cases AST/ALT > 2 is an exception. In addition, the development of chronic hepatitis to cirrhosis, AST/ALT often > 1.

There are few studies on AST/ALT in children. However, it is reported that in the 13 months follow-up of children with liver disease, the ratio of AST/ALT was found to be increased in the case of poor prognosis, and the ratio of AST/ALT was decreased in the patients with good prognosis.

Although the increase of AST and ALT may be the laboratory evidence of liver disease first appeared (such as viral hepatitis jaundice appears before) or the only evidence (such as jaundice hepatitis), but must keep in mind that even severe liver disease when AST and ALT can also be normal. For example, in the case of static necrosis after inflammatory disease and fulminant hepatitis cirrhosis cases.

It is of great value to detect the transaminase in serum to detect the damage of liver cells and monitor the clinical course. However, some very high levels (up to 200 times normal) are found in acute viral hepatitis, drug-induced hepatotoxicity and ischemia. The extent of the increase was not related to clinical outcome, and was not related to the extent of liver necrosis in liver biopsy, and therefore had no prognostic value.

However, the trend of transaminase change is valuable in judging prognosis. Transaminase levels decreased rapidly, but elevated levels of bilirubin, especially PT, may be indicative of massive hepatic necrosis and poor prognosis. A study in Austria found that gluten enteropathy patients often have elevated transaminase, in the use of a gluten free diet after return to normal.

2) the experimental index of Yu Yu

Including AP, GGT, 5 '-NT and bilirubin and bile acid test. Serum alkaline phosphatase (AP) from the liver, bone and placenta during pregnancy, some tumors (such as bronchial lung cancer) when the value is increased. In childhood, due to bone growth and is dependent on age (see table), which was often difficult to distinguish liver disease or disease is caused by the application, so some limitations in children.

Gamma glutamyl transpeptidase (GGT) and gamma glutamyl transferase, is a transfer of the gamma glutamyl peptide from one group to another L- peptide or amino acid enzyme. The enzyme is widely distributed in the body, and its elevation does not necessarily mean liver disease.

GGT activity may be inhibited by female hormones, female hormones interfere with GGT release from hepatocytes. In addition, there are also hyperbilirubinemia can make the GGT value decreased in vitro.

Neonatal GGT levels can be very high, up to 5-8 times the upper limit of normal adults. The first few days of the premature infant GGT levels higher than full-term infants. At approximately 6-9 months of age up to adult level. Large changes in children after the. GGT is a useful indicator when there is a suspected biliary disease.

Compared with other serum markers, GGT was the most sensitive indicator of hepatobiliary disease. Because there is an increase in GGT of up to 90% of primary liver disease, the value of differential diagnosis is not very large. The highest level of GGT is seen in biliary obstruction, but particularly high GGT is also seen in intrahepatic biliary disorders such as Alagille syndrome.

GGT levels are associated with the prognosis of idiopathic infantile hepatitis syndrome. Infants with normal GGT have poor prognosis. It is now clear that some of these cases are due to defects in bile salt synthesis, and some cases are familial. It is clear that there is a progressive familial intrahepatic cholestasis syndrome of type two (PFIC) patients of GGT is not high. PFIC-1 and 2 in the neonatal period onset, blood cholesterol and GGT normal, serum bile acid concentration, severe itching, no bile duct proliferation studies. Extrahepatic factors affecting GGT are shown in the table. Different from the alkaline phosphatase in the active period of bone or bone growth in children and its serum level is not increased, at the same time as the children less medication, medication history often even clear that children drink less alcohol, so the influence factors of GGT in children than in adults significantly less, in the detection of pediatric liver biliary disease when compared to AP more meaningful.

Because of increased production of hyperbilirubinemia bilirubin, liver uptake and / or combined to reduce or reduce the secretion of bile. An increase in bilirubin production (such as hemolysis) or an impairment of hepatic uptake or binding, such as Gilbert disease, causes an increase in serum unconjugated bilirubin (or free bilirubin). The formation and secretion of bile (such as cholecystitis), the increase in serum bilirubin, and even bilirubin in urine.

Serum bilirubin may not be a particularly sensitive indicator of liver disease or its prognosis, but it is still necessary to examine. The total bilirubin level was 1mg/L (17.1 mol/L). The total bilirubin and the direct reaction should be separated when there is an increase in isolated bilirubin (other normal liver function tests are normal) or neonatal jaundice. It is worth noting that the infant liver function is in the process of maturation, combined with bilirubin secretion from the liver cells into the bile duct function is not perfect, the excretion of bilirubin formed its metabolic rate limiting step. The serum bilirubin in patients with hepatitis infants was mainly direct bilirubin, were similar to those of obstructive jaundice and bilirubin; some liver factors such as hemolysis caused by increased production can be expressed as two phase reaction. Now some of the hospital can determine d bilirubin, its change and prognosis have a certain relationship, but the data is still small, do not have clinical as routine.

Urine Bilirubin (normal negative) can be used at the bedside of the commercialization of urine test paper test, it indicates that the liver and gallbladder diseases. Unconjugated bilirubin and albumin are closely linked, not through the glomeruli, even if very high levels of plasma bilirubin in urine was negative, but the positive plasma total bilirubin (direct bilirubin). Bilirubin can be an early sign of liver and gallbladder disease, can occur before the onset of acute viral hepatitis. Due to poor concentration of urine in infants, normal urine should be colorless, urine is yellow that prompted the existence of hepatobiliary disease, there is little black urine. In other cases, however, the level of plasma bilirubin increases and the urine bilirubin is negative. This may be related to the presence of urine samples for too long, or the presence of ascorbic acid (vitamin C) from the food or the presence of nitrate (from the presence of urinary sepsis), and bilirubin is oxidized and the urine bilirubin is false negative.

When the urine is normal, it appears in a small amount (10mg/L = 17 mol/L). The intestinal metabolite of bile pigment by hemolysis (more than the amount of pigment synthesis) or moderate hepatic uptake and secretion of damage increased (i.e. the amount of the enterohepatic circulation of the pigment than liver clear and excretion of its capacity). When the biliary tract completely blocked, secreted into the small intestine for reducing bilirubin urobilinogen ability is very low, there may be the absence of urobilinogen. However, due to the influence of the external factors, such as renal function, urinary PH, intestinal flora and diarrhea, and so on, it is very difficult to explain the results, so it is of little significance in clinical practice.

The detection of serum bile acids in adults has been proposed as a sensitive indicator of liver disease detection, but its application in children with liver disease has been questioned. The increased complexity of the interpretation of bile acids in neonates and early childhood liver disease is complicated by a high level of baseline in newborn infants and early infants. Attempts to use the serum bile acid levels to distinguish between biliary atresia and other non obstructive neonatal bile stasis have also failed. Similarly, in patients with A1AT deficiency, serum bile acid testing is not valuable for prognosis.

Now, the new technique can be used to analyze the precursors and derivatives of bile acids in body fluid, so as to detect the birth defects of bile acid metabolism. Screening was performed using fast atom bombardment mass spectrometry, and abnormal cases were then analyzed using expensive and time-consuming GC/MS (gas chromatography-mass spectrometry). A number of birth defects have been detected by this method, but only in some large liver disease centers abroad.

2 liver function test

Most of the proteins in serum proteins are synthesized in the liver, such as alpha, beta globulin, albumin and coagulation factors. Serum albumin is the major factor, determine the plasma colloid osmotic pressure of 28-44g/L at 1 weeks of age, adult level 37-50g/L, to 6 years of age up to 45-54g/L and maintain this concentration to the adult stage, then decreased to the level of a typical adult. No significant difference between men and women. Only in the rough endoplasmic reticulum albumin synthesis in hepatic cells. Normal liver synthesis 150mg/kg daily, its biological half-life of about 19-21 days. A carrier of a variety of substances, such as unconjugated bilirubin.

Significant changes in the liver parenchyma can affect the synthesis of albumin so as to reduce the level of serum albumin, so serum albumin concentration is a major indicator of the residual liver function. Because albumin has a long half-life, it is often reduced as a sign of chronic liver disease rather than acute liver disease. However, compensated chronic liver disease may show a sudden decrease in serum albumin concentrations due to acute disease such as sepsis or only mild disease. The decrease of serum albumin may be mainly due to the increase of the distribution capacity. Other causes of non liver include malnutrition or loss of the kidney (nephrotic syndrome), intestinal (loss of protein gastrointestinal disease) and loss of skin (burns), which can also lead to hypoproteinemia. The decrease of albumin in liver disease may also be due to the increase of degradation rate.

Serum globulin is usually obtained by subtracting albumin from total protein. By electrophoresis can be further divided into A1, A2, B and G components. The A1 group is mainly composed of 1 alpha - antitrypsin (it is absent in the A1AT deficiency), ceruloplasmin (decrease in Wilson disease) and mucin (A1 acid glycoprotein), belong to the acute phase protein, increase in liver disease and many other inflammatory diseases, resulting in acute reaction can produce false normal or elevated values.. Haptoglobin accounted for the majority of A2, also belong to the acute phase reaction material. Transferrin and B lipoproteins are mainly composed of B components. The G component is mainly immunoglobulin in the reticuloendothelial system by plasma cell synthesis.

A variety of patients with liver disease can show abnormal plasma protein electrophoresis. Many non involvement of the liver disease may have hypoalbuminemia and / or hypergammaglobulinemia. Therefore, the specificity of protein electrophoresis is of limited diagnostic value. There are, however, exceptions: chronic liver disease, including cirrhosis of the liver caused by any cause, especially in patients with chronic active hepatitis, especially autoimmune liver disease. The typical manifestation is that in the absence of albumin, Polyclonal (broadband) gamma globulin increases. Acute viral hepatitis may also have an acute increase in serum gamma globulin and usually return to normal within a few weeks. A1 antitrypsin deficiency can be a A1 component of intravascular hemolysis can cause the decrease of a2. It has recently been suggested that there may be cold globulin in patients with hepatitis C.

Coagulation function

The liver has three role in blood coagulation mechanism: a) in addition to VIII factors other than all other coagulation factors are partly or entirely synthesized by the liver; b) and fibrinolytic factors involved in the degradation process such as plasminogen activator and plasminogen activator; c) the removal of activated coagulation factors from the circulation. The synthesis of coagulation factor II, VII, IX and X requires the participation of vitamin K, which is called vitamin K dependent factor. Due to the limited storage of vitamin K in the liver, the liver disease in the gallbladder, vitamin K absorption barriers, and soon caused a lack of vitamin K, causing coagulation disorders.

Commonly used indicators of prothrombin time (PT) and partial thromboplastin time (APTT). PT is involved in liver protein synthesis of the original fiber (I), prothrombin (II), V, VII and X interaction factor, the lack of any single factor is not sensitive to prolonged PT only until 10% below normal; blood coagulation factor APTT involves more factors, including IX and VIII. But does not include factor VII. PT can be expressed in absolute time (seconds), and can also be compared with the normal control, which is called INR. Except in the vitamin K deficiency (1mg/ years after slow intramuscularly or intravenously at least after 4-6hr), coagulation function test is suitable for detection of liver function index.

Because of the short half-life of several coagulation factors (such as the VII factor of only 3-5hrs), PT can reflect the changes of liver function in a timely manner, such as in the case of acute liver failure can occur, is a good indicator of prognosis. It has also been suggested that the determination of individual coagulation factors may help to determine the prognosis of acute liver failure. The level of VII factor was higher than 8%, indicating survival. PT prolongation in chronic liver disease is also associated with a poor prognosis, and a reduction in serum albumin is the most important indicator of liver transplantation. Any late hepatic parenchymal disease can be prolonged by PT. In some neonatal inherited metabolic diseases, PT can be significantly prolonged, and other indicators of liver dysfunction disproportionately.

In addition to vitamin K deficiency, it should be noted that in patients with liver disease can also be caused by other extrahepatic factors caused by PT or APTT extension, such as DIC caused by consumption of coagulation factors. Because of the VIII factor in the synthesis of the liver, such as the consumption of the coagulation factor, VIII factor is normal or elevated in all kinds of liver diseases, so its level can be used as an indicator to distinguish the severity of liver disease with DIC. Chronic liver disease caused by infection and explosive increase the chances are more prone to DIC. Some drugs and congenital coagulation factor deficiency also affect PT.

Fibrinogen is synthesized both in the liver and also in the liver, although it can be increased, but the level of liver disease is more normal. DIC in patients with liver disease was accompanied by the consumption of other coagulation factors. Because it belongs to the acute phase protein, can increase in liver disease. Cholestatic liver disease is often elevated.

Almost all of the information comes from adults. The study of coagulation function in term or preterm infants and young children lagged significantly. Recent attention has been paid to their differences in the concentration of thrombin, the ability to produce thrombin and the ability to inhibit thrombin once it is formed. In term or preterm neonates, many of the clotting factors, including vitamin K, are less than 70% of the adult level. It is now clear that the coagulation system in the newborn is changing and will soon reach the adult level. Therefore, PT evaluation of liver function based on infants, must be used for age Youying normal gestational age and after birth (left). Despite prolonged PT and APTT, there is no clinical evidence of an increased risk of bleeding in healthy infants.

Blood ammonia: ammonia is amino acid metabolites, mainly through the urea cycle. Elevated blood ammonia is a typical manifestation of liver failure in liver disease. Serum s levels were significantly higher in the urea cycle, as well as in the Reye deficiency syndrome and acute and chronic hepatic encephalopathy. When the blood ammonia is measured, the arterial blood is collected, because only the blood ammonia level of the artery is related to the liver function. In order to correctly measure the blood ammonia, the plasma must be separated in time (15min) to prevent false elevation. Table 2 extrahepatic factors affecting blood ammonia.

3 specific serological markers

1) hepatitis markers

Viral antigens and antibodies are associated with viral hepatitis. The most reliable method for diagnosis of acute HAV infection is the detection of anti -HAV IgM-, which can reflect the immune state of hepatitis A virus total anti hav antibody. The significance of hepatitis B indicators are as follows


incubation period

Acute infection

past infection

Chronic infection

Vaccine immunization



















Anti -HBc













Anti -HBe






Anti -HBs






Note: a - PCR method, B - 10-15% patients can be reactivated infection, C - chronic infection often HBeAg or anti -HBe positive.

In the high incidence area, EIA detection of anti HCV in the diagnosis of HCV infection or previous is enough to determine whether active infection of HCV-RNA detection. The specimens used for HCV-RNA detection were better with EDTA plasma, or serum samples were separated in time so as to avoid false negative. HDV infection occurs on the basis of HBV infection, and it is generally recognized that the detection of total anti - HDV, usually after the virus cleared 1-5 years disappear. Epidemiological and clinical manifestations are very important for the diagnosis of HEV infection and EIA detection of anti HEV poor specificity, high false positive rate, for reference only.

Although the state of HCV and HBV markers detection reagent inspection strictly, because of the use of domestic reagent manual operation, possibility of testing error is still large. It has been used to compare different kits, hepatitis B two pairs of semi HBsAg and anti -HBs with the rate of good, anti -HBc and anti -HBe HbeAg is acceptable, and the coincidence rate of only 50-70%. Therefore, the test results should be repeated in doubt. The test results should be repeated inspection: HBsAg positive / -HBc negative resistance; HBsAg, anti -HBs and anti -HBc positive alone; anti -HBc positive; the unvaccinated alone positive anti -HBs; HBsAg negative and HBeAg positive; HBeAg and anti -HBe positive; the total anti -HBc negative and anti -HBc positive IgM.

In addition, special attention should be paid to the following questions:

A.HBsAg false positive: poor serum separation or heparin anticoagulation often lead to false positive HBsAg.

B.HBsAg false negative: a) 5% of patients with acute infection in the presence of symptoms of hepatitis is still negative, then need to detect anti -HBc-IgM and HBV-DNA. S (B) gene mutation. (C) latency of some chronic low level carriers (latent HBV infection) or HBV infection.

C. detection of anti -HBs and HBsAg:a) of acute HBV infection when used, the two concentration is very low, then the only blood detection of anti -HBs; b) before and after infection in different subtypes of HBV or at the same time, HBsAg can be used to exist or exist for a long time, the two can also be long-term coexistence of high titer C); HBV S gene mutation in vaccine breakthrough vaccine for the treatment of infection or chronic HBV infection. D (anti -HBs) false positive.

D. negative -HBc:a positive is generally false positive; b) anti -HBc negative and HBsAg positive rare, usually occurs in cases of immune deficiency, there are other indicators of HBV replication, such as HBeAg and / or HBV-DNA positive. C) alone should double anti -HBc positive review, to eliminate false positives, should consider the recovery after acute infection early (window period, the anti -HBc-IgM positive), long-term infection with anti -HBs disappeared, long-term infection with low levels of HBsAg (occult HBV infection) or HDV/HCV infection causes HBsAg less overlap.

Mother to child transmission of E. virus infection index: HBsAg cannot pass through the placenta, but the delivery can be a trace of maternal blood to the fetus, can cause very low titer of HBsAg positive, high low HBsAg shows that the intrauterine infection has occurred. HbeAg may pass through the placenta, but the titer is significantly lower than that of the mother, often disappear before the age of April. Anti -HBs, anti -HBe and anti -HBc are free to pass through the placenta and maternal anti -HBs protection of infants at the age of 1, anti -HBe often disappeared within 18 months, anti -HBc positive to sustainable after birth, at the age of 2. Anti -HCV antibodies can also be transmitted from mother to child, most of which disappeared 18 months ago. Therefore, 18 months after the detection of anti -HBc or anti -HCV positive more active infection or infection.

Detection of autoantibodies in autoimmune liver disease (2)

The incidence of autoimmune liver disease is also on the rise, at home and abroad have been reported in recent years. Autoimmune hepatitis (AIH) often insidious onset, but also acute onset, acute hepatitis and even liver failure. Laboratory examination of gamma globulin increased significantly, circulating autoantibodies and histological characteristics of interface hepatitis. According to the characteristics of autoantibodies in autoimmune hepatitis is mainly divided into two types: type 1 showed anti smooth muscle antibody or anti nuclear antibody positive, 2 anti liver kidney microsomal antibody or anti liver cytosolic type 1 antibody positive characteristic. 40% of the cases of type 1 and type 2 autoimmune hepatitis in our country are diagnosed in childhood, so autoimmune hepatitis is a major disease in children. Indirect immunofluorescence method was used to detect autoantibodies in our hospital. Commonly used antibodies:

The titer of ANA antibody in the serum of anti nuclear antibody AIH was 1: 320, only about 16% of the patients had a titer of 1: 40, but the positive rate of SMA was positive in 87% of them. The results showed that the ANA titer was more significant when the titer of was above 1. Generally, ANA is homogeneous (34%) or spot type (accounting for about 38%), while the central type, peripheral type and mixed type are very rare. The fluorescence pattern of ANA is of little significance in prognosis evaluation.

Anti smooth muscle antibody (SMA) is a basic marker of type AIH, which is usually present with ANA, but only about 26% of cases are SMA only. SMA and ANA are rarely seen in patients with viral hepatitis, so both of them appear to be more useful in the diagnosis of AIH.

Anti liver kidney microsomal antibody (LKM1) is a class of antibodies against microsomal antigens. The antibody is a type II AIH antibody and its target antigen is cytochrome oxidase P450 II D6.

Anti soluble liver antigen antibody (SLA) - this antibody is only seen in patients with AIH, so that SLA is a marker of AIH. This type of AIH often has some characteristics of type AIH, but the patients with serum ANA, LKM1 antibody and anti thyroid antibody negative, and SMA, anti liver cytoplasmic 1 antibody and anti mitochondrial antibody positive. Some people think that this type of AIH is only a special form of type I AIH, rather than an independent subtype.

Anti liver cytoplasmic 1 (LC1) antibody was found only in non HCV infected individuals, and the antibody was used to identify the presence of HCV infection in patients with positive anti LKM1 antibody. The positive rate of anti LC1 in anti LKM1 positive but not associated with HCV was 32%, so it should be used as a supplementary marker of AIH. In addition to about 14% of AIH patients, the antibody was the only positive marker.

Anti mitochondrial antibody (AMA) is a marker of primary biliary cirrhosis (PBC), almost 100% of PBC patients are positive for AMA, and the antibody titer is higher. However, about 20% of patients with AIH can also be detected in serum AMA, but the antibody titer is low (about 88% patients less than 1: 160). There was no difference between the target antigens of AMA and AMA in the serum of patients with E2, AIH and PBC. It is worth noting that AIH positive patients with serum AMA have better effect on glucocorticoid treatment. The mitochondrial antibody has direct antagonism to the mitochondrial inner membrane antigens of several tissues. M2 antigen was most associated with primary biliary cirrhosis, and was positive in 95% of patients with primary biliary cirrhosis. These antibodies were also found in 30% of autoimmune chronic active hepatitis and some of the drug induced hepatitis and connective tissue disease. Mechanical biliary obstruction and primary sclerosing cholangitis, the antibody negative.

Two, laboratory indicators of liver disease in children

When there is a known or suspected liver disease should be carried out at least a group of checks, including ALT/AST, TB/DB, ALP/GGT, TP/Alb, ALT exceeds the normal limit of 10 times, while ALP is lower than the normal limit of 3 times the diagnosis of acute liver injury. Check DB for jaundice except for hemolysis. However, it should be noted that, due to the development of the liver in the infant, bilirubin excretion from the liver is the rate limiting step of bilirubin metabolism, jaundice caused by pre liver factors can also be manifested as a combination of elevated bilirubin. TB> (257umol/L), or PT (15mg/dl) or 4S exceeding the normal upper limit for severe liver injury, if not affected by other factors. In acetaminophen poisoning, PT prolongation continued for more than 4 days after the onset of severe liver injury.

Children with liver disease has its particularity, the infection and metabolic is particularly important, so the children have liver disease inspection should be carried out including: INR/APTT, blood glucose, blood cell count & smear; & reticulocytes, liver and kidney function, blood lipid (ALT/TB/DB/AKP/GGT/Ca/P/Cr/BuN), HIV, E, VitA& antibody; urine electrolytes and osmotic pressure, blood and urine culture and drug sensitivity, liver and spleen ultrasound. In addition, due to the different manifestations of liver disease in different periods, it is necessary to consider different causes, so the need for different auxiliary examination. For more than 6 months of children with chronic liver disease and / or hepatomegaly should consider the infection factors, metabolic factors and autoimmune factors, so there should be screened for hepatitis B antigen, hepatitis C antibody, CMV/EBV serological indexes, Ig/C3/C4/ antibody and VMA/HVA/AFP, /CK, NH3/, uric acid salt of amino acid Cu/Zn/ ceruloplasmin, penicillamine challenge test, eye KF ring ring, bone, and young liver biopsy; for acute liver failure still should check the blood glucose test (4hr) and poison screening (especially paracetamol, copper) HAV-IgM/HBc-IgM/ anti HBc/HCV-RNA, fibrinogen, autoantibodies and immunoglobulins, NH3, CK/, AFP, CMV/EBV/HSV/, serum amylase adenovirus virus blood gas analysis / lactate / pyruvate and 24 hours urine copper and penicillamine challenge test, urine organic acid, ophthalmologic examination and liver biopsy; infant hepatitis One of the most common type of liver disease in pediatrics at present with intrauterine or perinatal infection, endocrine and metabolic abnormalities are most common in children under the age of June so we called the cases of liver disease, in addition to the basic examination items of infant hepatitis syndrome and other inspection items and significance shown in the table below:



Iron and transferrin

Neonatal Hemoehromatosis

TSH, free T4


Morning Cortisol (4hr after fasting)

Hypopituitarism (short Synacthen test*)

Amino acids (postprandial 2hr)


-1- urine galactose phosphate anhydride transferase

Classical galactose

IRT and sweat test, the CF allele was *


Plasma very long chain fatty acids *

Zellweger 's syndrome

Uric acid *

Bile salt metabolic defect screening

Urine succinic acid acetone / organic acid

Tyrosine viremia

Blood and urine culture

Sepsis and urinary tract infection

Toxoplasma /CMV/ rubella / herpes simplex / adenovirus / syphilis

Congenital infection

HAV IgM, anti-HBc IgM*

Rare congenital infection

Complement, ds-DNA, anti -Rho, anti -lambda

Congenital lupus (simultaneous examination of mother)

X ray

Metabolic bone disease or congenital infection, Alagille

Ophthalmic examination

Congenital infection, Alagille, cataract, storage diseases

Bone penetration

Niemann Pick/Gaucher 's/HLH

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