Clinical significance of commonly used coagulation tests

Commonly used coagulation tests

Commonly used coagulation tests:

1,Activated partial thromboplastin time (APTT)

2,Prothrombin time (PT)

3,Thrombin time (TT)

4,Fibrinogen (FIB)

5,D-Dimer (D-Dimer)

6,Fibrin degradation products (FDP)

7,Antithrombin III (AT III)

1,APTT

Reference range: 20-40 seconds

Principle and clinical application: APTT is the most sensitive and most commonly used screening experiment in endogenous coagulation system. It is used to reflect the defects of congenital or acquired coagulation factors VIII, IX, XI or whether there are corresponding inhibitors. At the same time, APTT can also reflect whether coagulation factor XII, kallikreinogen and high molecular weight kallikreinogen are deficient.

Extension: > 10 seconds is clinically meaningful

1,Coagulation factor VIII, XI, XII deficiency

2,Hemophilia A (VIII), hemophilia B (IX) and some patients with vascular pseudohemophilia

3,Severe prothrombin and coagulation factor V, X reduction and fibrinogen deficiency: liver disease, obstructive jaundice, neonatal hemorrhage and low (no) fibrinemia, etc.

4,The presence of anticoagulant drugs in the blood circulation: such as antibodies to factor VIII or factor IX

5,Systemic lupus erythematosus and some immune diseases

Shorten:

1,Coagulation factor VIII, X activity increased

2,Thrombocytosis

3,Hypercoagulable state: such as procoagulant substances into the blood and the activity of coagulation factors increased, DIC hypercoagulability, unstable angina, cerebral infarction, etc.

4,Pregnancy hypertension syndrome and nephritis syndrome, intravenous puncture does not smoothly mix into the tissue fluid.

5,Prethrombotic status and thrombotic diseases: such as diabetes with vascular lesions, myocardial infarction, deep vein thrombosis, pulmonary infarction, cerebrovascular disease, etc.

2,PT

Reference range: 10-14 seconds

Clinical principle and clinical application: PT is a sensitive and most commonly used screening experiment for exogenous coagulation system. It is used to reflect the presence of defects or inhibitors of congenital or acquired fibrinogen, prothrombin, and coagulation factors V, VII, X. It is also the preferred indicator for monitoring oral anticoagulants; and it can also be used as a detection of liver synthetic protein function.

Extension: > 3 seconds is clinically meaningful

1,Extensive and severe liver substantial damage, such as acute severe hepatitis and cirrhosis

2,Congenital exogenous coagulation factors II, V, VII, X decreased and fibrinogen deficiency

3,Acquired coagulation factor deficiency, such as acute DIC consumable hypocoagulation period, primary hyperfibrinolysis, obstructive jaundice, vitamin K deficiency, etc.

4,There are anticoagulants in the blood circulation: oral anticoagulants, taking anticoagulants such as heparin, FDP and coumarin, etc.

Shorten:

1,Early hypercoagulable state of DIC

2,Thromboembolic disease and other prethrombotic states such as increased coagulation factors and platelet activity, vascular damage, etc.

3,Oral contraceptives

4,Congenital coagulation factor V hyperplasia

3,TT

Reference range: 10-14 seconds

Principle and clinical application: TT mainly reflects the activity and concentration of fibrinogen in plasma, and the concentration of heparin-like substances in plasma.

Extension: > 3 seconds clinical significance

1,The presence of heparin or heparin anticoagulant substances in the blood

2,Fibrinogen degradants (FDP) increased

3,Fibrinogen reduction, dysfunction, molecular abnormalities, etc.

Shorten: no clinical significance

4,FIB

Reference range: 2-4 g/L

Principle and clinical application: FIB is coagulation factor I, the main protein substance in the coagulation process. Taking the Clauss method as an example, a certain amount of thrombin is added to the plasma to be tested, which converts the fibrinogen in the plasma into fibrin, and the content of FIB is calculated by the rate of blood clotting.

Elevate:

1,Body infection: toxemia, hepatitis, mild hepatitis, cholecystitis and long-term local inflammation

2,Aseptic inflammation: diabetes, nephrotic syndrome, uremia, rheumatic fever, malignant tumors, rheumatoid arthritis

3,Cardiovascular diseases: arteriosclerosis, cerebral thrombosis, thrombophlebitis, myocardial infarction, radiation therapy

4,Third trimester, pregnancy, menstruation and after strenuous exercise

5,After radiation therapy, burns, shock, after major surgical operations, malignant tumors, diabetic acidosis, etc.

Decrease:

1,Liver disease: chronic hepatitis, cirrhosis, acute liver atrophy

2,Arsenic, chloroform, carbon tetrachloride poisoning can reduce fibrinogen

3,DIC: due to fibrinogen consumption and secondary fibrinolytic hyperactivity of fibrinogen showed a progressive decline

4,Primary fibrinogen deficiency

5,Primary fibrinolytic hyperactivity

6,Pernicious anemia and lung, thyroid, prostate surgery

5,D-Dimer

Reference interval: 0-0.50 mg/L FEU

Principle and background knowledge:

1,D-Dimer is one of the specific markers of fibrin degradation by plasmin after crosslinking, and are indicators to determine whether there is thrombosis and secondary hyperfibrinolysis in vivo. Changes in their content can be used as evaluation markers of hypercoagulability and hyperfibrinolysis in vivo.

2,The average age increases by ten years, D-Dimer increased by 0.1mg/L

Clinical Use:

1,Exclude pulmonary embolism (PE)

The sensitivity and negative expected value of D-Dimer to PE are both 100% for the mass quantitative detection of D-Dimers, and PE can be excluded when the D-Dimer detection value < 0.50 mg/L FEU.

2,One of the most valuable indicators for diagnosing DIC

The content of D-Dimer was positively correlated with the fibrinolytic status of the patient, and the content of D-Dimer gradually increased with the progression of the disease course, and the content of D-Dimer gradually decreased after effective treatment. If the D-Dimer content > 0.50 mg/L FEU, it has a high warning value for high-risk patients with DIC.

3,Screening for deep vein thrombosis (DVT)

D-Dimer detection is an effective means of DVT screening. Patients with clinical suspicion of DVT can rule out the diagnosis of DVT if the D-Dimer content is normal.

4,The value of cerebral infarction diagnosis and prognosis judgment

In the acute phase of cerebral infarction, there were statistically significant differences in D-Dimer levels from the normal control group. Decreasing D-Dimer levels in the convalescent phase indicate a good prognosis compared to the acute phase, while those who rise in the more acute phase indicate a poor prognosis.

5,Monitoring and evaluation of thrombolysis

In the process of thrombolysis, the D-Dimer content is first increased and then decreased, indicating that the thrombolysis has reached a therapeutic effect; if it is maintained at a high level after elevation, it indicates insufficient dosage. Changes in D-Dimer contribute to the observation of thrombolytic efficacy and guide the concentration of medications.

6,FDP

Reference interval: 0-5 mg/L

Principle and clinical application: FDP is the general term for the various degradation products produced by fibrin / fibrinogen under the action of plasmin, FDP includes fibrinogen (Fg) and fibrin monomer (FM) products (FgDPs), as well as crosslinked fibrin degradation products (FbDPs), where FbDPs include D-Dimers and other fragments. FDP mainly reflects the lytic function of fibrin (fibrinogen) and is a sensitive indicator of hyperfibrinolysis in the body, and its content can be increased in both primary and secondary hyperfibrinolysis.

Increase:

1,Primary hyperfibrinolysis

2,Secondary hyperfibrinolytic: such as DIC, malignant tumors, acute promyelocytic leukemia, pulmonary embolism, deep vein thrombosis, rejection after transplantation, thrombolytic therapy, etc.

7,AT Ⅲ

Reference range: 80%-120%

Principle and clinical application:

1,AT III is the most important anticoagulant factor in the coagulation pathway, it controls the coagulation of blood and the dissolution of fibrin.

2,The level of AT III in the blood is reduced, which may cause the effect of heparin therapy to be unable to be presented.

Increase:

Common in hemophilia A and hemophilia B, oral anticoagulants, and progesterones.

Reduce:

1,Hereditary AT III deficiency, divided into two types:

(1)CRM- type: decreased antigen, decreased activity.

(2)CRM+ type: normal antigen, decreased activity.

2,Acquired AT III deficiency:

(1)Decreased AT III synthesis: seen in liver disease, liver dysfunction, often associated with disease severity, may be accompanied by thrombosis.

(2)Increased loss of AT III: seen in nephrotic syndrome

(3)Increased consumption of AT III: seen in prethrombotic and thrombotic diseases.