Why this test?
- For the diagnosis of acquired dysfibrinogenemia (for liver diseases, autoimmune diseases).
- For the diagnosis of hereditary dysfibrinogenemias.
- To find out the reason for habitual miscarriage.
- To assess the risk of developing DVZ-syndrome, diagnose it and monitor its treatment.
- To assess the risk of arterial thrombosis.
In what cases is it prescribed?
- With liver diseases: cirrhosis, chronic active hepatitis, obstructive liver diseases, hepatomas.
- With symptoms of hypo (a) fibrinogenemia and dysfibrinogenemia: increased bleeding (metro-, menorrhagia, epistaxis, soft tissue hematomas, bleeding in the postpartum or postoperative period) or a tendency to thrombosis (phlebothrombosis, thromboembolism of pulmonary artery branches, arterial thrombosis), as well as when combining both states.
- With two or more involuntary terminations of pregnancy within 22 weeks.
- In diseases accompanied by a high risk of developing DIC syndrome: severe infectious diseases, acute and chronic leukemias, complications of pregnancy and childbirth, autoimmune diseases that are difficult to develop. If there are risk factors for arterial thrombosis: high concentration of homocysteine and C-reactive protein.
Thrombin time is the time required for the formation of a fibrin clot when thrombin is added to the plasma - an enzyme (factor IIa), which appears as a result of the interaction of blood coagulation factors when a vessel is damaged.
Thrombin is necessary for the final stage of the coagulation cascade - the transformation of the fibrinogen molecule into insoluble fibrin, which is able to polymerize and form a stable fibrin clot, which ensures the stopping of bleeding in case of damage to small and medium vessels and contains, in addition to fibrin polymers, cellular elements - platelets and erythrocytes.
Qualitative or quantitative changes in fibrinogen lead to insufficient / excessive production of fibrin, which is manifested by increased bleeding or tendency to thrombosis. In laboratory conditions, the final stage of the coagulation cascade is reproduced by adding ready-made thrombin to plasma, and changes in the structure or concentration of fibrinogen are reflected in an increase or decrease in thrombin time. Fibrinogen is a glycoprotein secreted by hepatocytes into the blood. In addition to being a blood coagulation factor (factor I), it also provides some reactions of fibrinolysis, the process of dissolving blood clots, - it binds excess thrombin (that is why fibrinogen is also called antithrombin I) and activates plasminogen. In this regard, diseases with a change in the structure or concentration of fibrinogen can be manifested by bleeding and thrombosis, as well as in some cases their combination.
Pathologies accompanied by a deficiency of fibrinogen are called hypo- and afibrinogenemia, and pathologies in which the structure and function of fibrinogen are disturbed are called dysfibrinogenemia. They can be hereditary or acquired. Acquired include liver disease, disseminated intravascular coagulation syndrome (DIC), primary fibrinolysis, and drug-induced reactions (eg, thrombolytic agents and L-asparaginase).
The most common cause of acquired dysfibrinogenemia is liver disease. In cirrhosis, chronic active hepatitis, acute liver failure, obstructive liver diseases and hepatoma, too much sialic acid is added to the secreted fibrinogen. Such modified fibrinogen has a greater negative charge, which prevents the polymerization of fibrin molecules.
Patients with liver diseases have numerous coagulation disorders, which are manifested by increased bleeding. Determination of thrombin time is the main screening test that allows you to suspect dysfibrinogenemia as one of the causes of bleeding. Abnormal fibrinogen is also synthesized by some tumors (cervical squamous cell carcinoma, breast adenocarcinoma, hypernephroma, hepatoma). In certain diseases accompanied by the synthesis of antibodies that interact with fibrinogen (systemic lupus erythematosus, multiple myeloma), its activity decreases, which is manifested by an increase in thrombin time.
The most frequent cause of acquired hypofibrinogenemia is DVZ-syndrome - a systemic thrombohemorrhagic disorder in which there is excessive formation of fibrin microthrombi and consumption of blood coagulation factors and platelets. DIC syndrome always develops secondarily as a complication of some disease.
A distinction is made between acute and chronic DVZ-syndrome. The causes of acute DVZ-syndrome are infectious diseases (E. coli - sepsis, HIV, cytomegalovirus infection, malaria), acute myeloblastic leukemias, complications of pregnancy and childbirth (premature detachment of the placenta, eclampsia, amniotic fluid embolism), large burns, massive blood transfusions and others . Causes of chronic CVD syndrome: solid tumors, chronic leukemias, complications of pregnancy (intrauterine fetal death), myeloproliferative diseases, rheumatoid arthritis and Raynaud's disease, myocardial infarction, nonspecific ulcerative colitis and Crohn's disease, etc. It «triggers» the development of DVZ-syndrome in all the listed conditions of the entry of a large amount of thromboplastin (tissue factor, factor III) into the blood.
At the same time, multiple microthrombi are formed in the vessels of the kidneys, brain, liver, and lungs, which determine the clinical picture of the syndrome in the form of multiple organ failure. As a result of massive consumption of fibrinogen and other blood coagulation factors, their secondary insufficiency develops and hypercoagulation is replaced by hypocoagulation and disseminated bleeding. It should be noted that hypercoagulation and hypocoagulation are often present at the same time in the same patient, therefore, the selection of consecutive periods of DVZ-syndrome is very conditional.