出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/11/26 16:55:30」(JST)
| Liver function tests | |
|---|---|
| Intervention | |
| ICD-10-PCS | K-70 to K-77 |
| MeSH | D008111 |
| MedlinePlus | 003436 |
Liver function tests (LFTs or LFs) are groups of blood tests that give information about the state of a patient's liver.[1] These tests include prothrombin time (PT/INR), aPTT, albumin, bilirubin (direct and indirect), and others. Liver transaminases (AST or SGOT and ALT or SGPT) are useful biomarkers of liver injury in a patient with some degree of intact liver function.[2][3][4] Most liver diseases cause only mild symptoms initially, but these diseases must be detected early. Hepatic (liver) involvement in some diseases can be of crucial importance. This testing is performed on a patient's blood sample. Some tests are associated with functionality (e.g., albumin), some with cellular integrity (e.g., transaminase), and some with conditions linked to the biliary tract (gamma-glutamyl transferase and alkaline phosphatase). Several biochemical tests are useful in the evaluation and management of patients with hepatic dysfunction. These tests can be used to detect the presence of liver disease, distinguish among different types of liver disorders, gauge the extent of known liver damage, and follow the response to treatment. Some or all of these measurements are also carried out (usually about twice a year for routine cases) on those individuals taking certain medications, such as anticonvulsants, to ensure the medications are not damaging the person's liver.
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Although example reference ranges are given, these will vary depending on age, gender, ethnicity, method of analysis, and units of measurement. Individual results should always be interpreted using the reference range provided by the laboratory that performed the test.
| Reference range |
| 3.5 to 5.3 g/dL |
Albumin is a protein made specifically by the liver, and can be measured cheaply and easily. It is the main constituent of total protein (the remaining from globulins). Albumin levels are decreased in chronic liver disease, such as cirrhosis. It is also decreased in nephrotic syndrome, where it is lost through the urine. The consequence of low albumin can be edema since the intravascular oncotic pressure becomes lower than the extravascular space. An alternative to albumin measurement is prealbumin, which is better at detecting acute changes (half-life of albumin and prealbumin is about 2 weeks and about 2 days, respectively).
| Reference range |
| 6-40 IU/L[5] |
AST, also called serum glutamic oxaloacetic transaminase or aspartate aminotransferase, is similar to ALT in that it is another enzyme associated with liver parenchymal cells. It is raised in acute liver damage, but is also present in red blood cells, and cardiac and skeletal muscle, so is not specific to the liver. The ratio of AST to ALT is sometimes useful in differentiating between causes of liver damage.[6][7] Elevated AST levels are not specific for liver damage, and AST has also been used as a cardiac marker.
AST/ALT elevations instead of ALP elevations favor liver cell necrosis as a mechanism over cholestasis. When AST and ALT are both over 1000 IU/L, the differential can include acetaminophen toxicity, shock, or fulminant liver failure. When AST and ALT are greater than three times normal but not greater than 1000 IU/L, the differential can include alcohol toxicity, viral hepatitis, drug-induced level, liver cancer, sepsis, Wilson's disease, post-transplant rejection of liver, autoimmune hepatitis, and steatohepatitis (nonalcoholic). AST/ALT levels elevated minorly may be due to rhabdomyolysis, among many possibilities.
| Reference range |
| 30 to 120 IU/L[8] |
Alkaline phosphatase (ALP) is an enzyme in the cells lining the biliary ducts of the liver. ALP levels in plasma rise with large bile duct obstruction, intrahepatic cholestasis, or infiltrative diseases of the liver. ALP is also present in bone and placental tissue, so it is higher in growing children (as their bones are being remodelled) and elderly patients with Paget's disease. In the third trimester of pregnancy, ALP is about two to three times higher.
| Reference range |
| 0.1–1.0 mg/dL |
Measurement of total bilirubin includes both unconjugated and conjugated bilirubin. Unconjugated bilirubin is a breakdown product of heme (a part of hemoglobin in red blood cells). It is very hydrophobic and is mainly transported bound to albumin circulating in the blood. Addition of high-concentration hydrophobic drugs (certain antibiotics, diuretics) and high free fatty acids can cause elevated unconjugated bilirubin. Heme can also come from myoglobin, found mostly in muscle, cytochromes, found mostly in mitochondria, catalase, peroxidase, and nitric oxide synthase. The liver is responsible for clearing the blood of unconjugated bilirubin, and about 30% of it is taken up by a normal liver on each pass of the blood through the liver by the following mechanism: bilirubin is taken up into hepatocytes, 'conjugated' (modified to make it water-soluble) by UDP-glucuronyl-transferase, and secreted into the bile by CMOAT (MRP2), which is excreted into the intestine. In the intestine, conjugated bilirubin may be metabolized by colonic bacteria, eliminated, or reabsorbed. Metabolism of bilirubin into urobilinogen followed by reabsorption of urobilinogen accounts for the yellow color of urine, as urine contains a downstream product of urobilinogen. Further metabolism of urobilinogen into stercobilin while in the bowels accounts for the brown color of stool. Thus, having white or clay-colored stool is an indicator for a blockage in bilirubin processing and thus potential liver dysfunction or cholestasis.
Increased total bilirubin (TBIL) causes jaundice, and can indicate a number of problems:
| Reference range |
| 0.1–0.4 mg/dL |
The diagnosis is narrowed down further by evaluating the levels of direct bilirubin.
About 5% of the population has Gilbert's syndrome, a mutation (or variation) in the UDP-glucuronyl-transferase promotor that manifests itself as jaundice when the individual is stressed (i.e. starves). Autosomal recessive knockouts of UDP-glucuronyl-transferase can lead to Crigler-Najjar syndrome and elevations of unconjugated bilirubin. Defects in CMOAT (MRP2) results in Dubin-Johnson syndrome and elevations of conjugated bilirubin.
Neonates are especially vulnerable to high bilirubin levels due to an immature blood-brain barrier that predisposes them to kernicterus/bilirubin encephalopathy, which can result in permanent neurological damage. Neonates also have a low amount of functional UDP-glucuronyl-transferase and can have elevated unconjugated bilirubin, since conjugation is limited. So, newborns are often treated with UV light to turn the hydrophobic, albumin-binding unconjugated bilirubin into a form that is more hydrophilic and able to be secreted in urine, sparing the neonate's brain.
| Reference range |
| 0 to 42 IU/L[8] |
Although reasonably specific to the liver and a more sensitive marker for cholestatic damage than ALP, gamma glutamyl transpeptidase (GGT) may be elevated with even minor, subclinical levels of liver dysfunction. It can also be helpful in identifying the cause of an isolated elevation in ALP (GGT is raised in chronic alcohol toxicity).
Prothrombin time (PT) and its derived measures of prothrombin ratio (PR) and international normalized ratio (INR) are measures of the extrinsic pathway of coagulation. This test is also called "ProTime INR" and "INR PT". They are used to determine the clotting tendency of blood, in the measure of warfarin dosage, liver damage, and vitamin K status.
5' Nucleotidase (5'NTD) is another test specific for cholestasis or damage to the intra- or extrahepatic biliary system, and in some laboratories, is used as a substitute for GGT for ascertaining whether an elevated ALP is of biliary or extrabiliary origin.
The liver is responsible for the production of coagulation factors. INR measures the speed of a particular pathway of coagulation, comparing it to normal. Increased levels of INR means blood is taking more time than usual to clot. The INR increases only if the liver is so damaged that synthesis of vitamin K-dependent coagulation factors has been impaired; it is not a sensitive measure of liver function.
It is very important to normalize the INR before operating on people with liver problems (usually by transfusion with blood plasma containing the deficient factors), as they could bleed excessively.
The serum glucose test, abbreviated as "BG" or "Glu", measures the liver's ability to produce glucose (gluconeogenesis); it is usually the last function to be lost in the setting of fulminant liver failure.
Lactate dehydrogenase (LDH) is found in many body tissues, including the liver. Elevated levels of LDH may indicate liver damage.[citation needed] LDH isotype-1 (or cardiac) is used for estimating damage to cardiac tissue, although troponin and creatine kinase tests are more preferred.[9]
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| リンク元 | 「肝機能検査」 |
| 関連記事 | 「function」「testing」「live」「test」「liver」 |
| AST | 逸脱酵素 - 肝細胞の変性・壊死 |
| ALT | |
| LDH | |
| ALP | 胆管系の障害 |
| γ-GTP | |
| 総ビリルビン | ビリルビン負荷増大、ビリルビン抱合障害、胆汁の流出障害 - 黄疸 |
| 総コレステロール | 肝細胞のタンパク質合成脳障害 - 浮腫、腹水 |
| アルブミン | |
| コリンエステラーゼ | |
| プロトロンビン時間 | 肝細胞のタンパク質合成脳障害 - 出血傾向 |
| アンモニア | 解毒能低下 - 肝性脳症 |
| ICG試験 | |
| γ-グロブリン | 間葉系の反応 - 免疫反応持続、慢性炎症、自己免疫性疾患 |
| TTT | |
| ZTT | |
| IgG | |
| IgM | |
| IgA | |
| IgE | |
| ANA | |
| AMA | |
| ヒアルロン酸 | 間葉系の反応 - 線維化マーカー |
| IV型コラーゲン7S | |
| AFP | 肝細胞の癌化 |
| AFP-L3 | |
| PIVKA-II |