Interpretation of liver function indicators I

  Summary of liver function-related items
  I. Liver synthesis function
  (I) Albumin (Alb) 
  The liver is the only place where albumin is synthesized, and serum albumin level is one of the good indicators of chronic liver injury. Decreased serum albumin level is seen in: insufficient nutritional intake, impaired synthesis, excessive consumption and increased loss. The serum albumin level in patients with chronic liver disease can reflect the ability of the liver to synthesize albumin and changes in the volumetric distribution of albumin, and if the serum albumin level is reduced and not easily recovered, the prognosis is often poor.
  (ii) Prothrombin time
  In hepatic impairment, the associated impaired synthesis of coagulation factors can lead to prolonged PT, which is one of the early predictors of abnormal liver function. prolonged PT and uncorrectable vitamin K predicts extremely poor liver function. In fulminant liver failure, PT is an important early diagnostic indicator.
  (iii) Lipids and lipoproteins
  Lipids and lipoproteins are not sensitive indicators of liver damage, but serum cholesterol ester levels decrease in response to hepatocellular damage and are proportional to the degree of liver damage. In chronic liver disease, lipoproteins are reduced and their levels are negatively correlated with transaminases and bilirubin.
  Liver excretion function
  Bilirubin
  Bilirubin is one of the important indicators of liver function. The normal level of total bilirubin TBIL is <1.1mg/dl (17.1μmol/l), 70% of which is indirect bilirubin and cannot be filtered from the kidney. Only direct bilirubin can be excreted from the urine. Note: 1. In hemolytic jaundice with normal liver function, TBIL is << span="">5 times normal (85 μmol/l). 2. In jaundice of any cause with normal renal function, TBIL is <500 μmol/l. 3. The presence of jaundice, but negative urinary bilirubin, indicates elevated indirect bilirubin. 4. Many jaundices with predominantly elevated indirect bilirubin alone are Gilbert syndrome, this syndrome has no pathological tissue changes in the liver tissue, has no significant effect on the organism, and generally requires no special treatment.
  III. Serum enzymatic levels
  (I) ALT, AST
  The specificity of ALT is better than AST.
  1.When ALT>10 times normal, there is definitely liver damage (such as chronic hepatitis B)
  2, ALT and AST are elevated in biliary tract disease, but << span="">8 times normal
  3, AST/ALT ratio: (1) estimate the degree of liver damage: the greater, the more serious the damage; (2) identify liver disease: alcoholic liver > 2, slow hepatitis B > 1 may have liver fibrosis or cirrhosis
  (B) Alkaline phosphatase ALP
  1, ALP>4 times normal: cholestasis syndrome
  2, ALP>2.5 times normal, ALT, AST<< span="">8 times normal: 90% cholestasis
  3.ALP>2.5 times normal, ALT, AST>8 times normal: 90% for viral hepatitis
  (C) Glutamyl transpeptidase GGT
  90% of patients with hepatobiliary disease have elevated GGT, GGT>10 times normal, mostly due to alcoholic liver, intrahepatic and extrahepatic biliary sludge, primary liver cancer
  Four, the evaluation of liver enzymatic indicators
  1, a large sample of healthy people in the UK survey found that: 6% of asymptomatic normal people have elevated ALT and AST, and 5% of normal people have all test results outside the “normal value” range. Therefore, some abnormal liver test results are not really abnormal.
  2.The treatment of elevated single transaminase level is: check again, if the elevation is more than 2 times normal, further examination is needed.
  V. Interpretation of hepatitis B two pairs of half
  Major triple-positive HBsAg (+) HBeAg (+) HBcAb (+)
  Minor triplet HBsAg (+) HBeAb (+) HBcAb (+)
  Single HBsAg (+) is a hepatitis B carrier
  Hepatitis B two pairs of half results and clinical significance
  HBsAg (surface antigen) HBsAb (surface antibody) HBeAg (E antigen) HBeAb (E antibody) HBcAb (core antibody) Clinical significance
  1 + – – – + (major triple positive) acute and chronic hepatitis, HBV replication phase
  2 + – – – + Acute HBV infection, chronic HBsAg carriers, weakly infectious
  3 + – – – + + Acute HBV tends to recover, chronic HBsAg, long-term persistent susceptible to cancer (small triplet)
  4 – – – – – Not infected with HBV
  5 – + – – + Pre-existing infection with immunity Atypical recovery, acute HBV infection
  6 – – – + + Previous HBV infection, acute HBV recovery, few still infectious
  7 – – – – + Pre-existing HBV infection, acute HBV window
  8 – + – – – Passive or active HBV immunization, recovered from infection
  9 – + – + + – Previous HBV infection, acute HBV recovery
  10 + – – – – Chronic HBV carrier, acute HBV infection
  11 + – – + – Chronic carrier, acute HBV infection tending to recover
  12 + – + – – Chronic carriers, tend to turn negative; acute infection tends to recover; acute early infectious, should be treated while it is still possible to turn negative or control recurrent disease.
  13 + – + + + – Acute HBV infection tends to recover, chronic HBsAg carriers
  14 + + – – – -/+ Early stage of subclinical HBV infection, secondary infection with different subtypes of HBV
  15 + + + + – + Subclinical type or atypical infection

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