What are they and how do they work?
Fibrin and fibrinogen degradation products (FDPs) are part of the secondary anticoagulant system. They are formed during fibrinolysis, specifically during the lysis of microthrombi.
FDPs are potent anticoagulants that:
- Inhibit thrombin;
- Inhibit fibrin formation: fibrin monomers lose their polymerization capacity and become resistant to thrombin;
- Prevent platelet aggregation.
How is blood FDP level regulated?
Under normal conditions, the reticuloendothelial system (RES) removes intermediate clotting products.
- When the RES is blocked, for example in amniotic fluid embolism, the amount of FDPs in the circulating blood increases.
- In newborns, especially premature infants, the ability to clear activated clotting factors and FDPs is reduced. This is due to immature phagocytosis and fibrinolysis, as well as immaturity of the protein-synthesizing function of the liver. Mortality in such newborns reaches 75–90%.
Role in the pathogenesis of DIC
In disseminated intravascular coagulation (DIC syndrome), there is a progressive increase in FDP levels. This is due to significant platelet consumption and recurrent intensive fibrinolysis resulting from activation of the kallikrein-kinin system.
- Stage of profound hypocoagulation, Stage III: usually develops 2–8 hours after the onset of the syndrome. Against the background of hyperplasminemia, easily soluble fibrin-containing complexes and FDPs appear.
- The accumulation of FDPs enhances the anticoagulant and antiplatelet effect. As a result, blood completely loses its clotting ability, leading to severe profuse bleeding, hemorrhages into undamaged tissues, and microangiopathic hemolytic anemia.
Clinical and diagnostic significance
- Laboratory diagnostics: high levels of FDPs, including high- and low-molecular-weight fragments, are detected in intravascular coagulation. An increase in FDPs is also noted in the active phase of rheumatic diseases alongside elevated circulating immune complexes (CICs) and inflammatory markers.
- Obstetric hemorrhage: when DIC syndrome develops, FDPs block receptors responsible for actomyosin formation, causing massive bleeding.
- Internal bleeding: autologous blood shed into the abdominal cavity contains fibrinogen degradation products. Such blood is also characterized by reduced platelet and fibrinogen counts, as well as high levels of free hemoglobin.
- Therapy: plasmapheresis is the method of choice for detoxification and elimination of FDPs, immune complexes, and bacterial toxins.
Class and exam questions
Why do massive hemorrhages occur in DIC syndrome?
Bleeding develops due to the depletion of clotting factors, consumption coagulopathy, and elevated FDP levels. The action of FDPs enhances the anticoagulant effect and can lead to a complete loss of blood clotting ability.
How does the body normally get rid of intermediate clotting products?
Under normal conditions, intermediate clotting products are removed from the blood by the reticuloendothelial system (RES).
What blood purification method is effective for removing excess FDPs?
Plasmapheresis is the method of choice for detoxification and elimination of FDPs, circulating immune complexes, and bacterial toxins.
What else to study on this topic
- DIC syndrome (Disseminated intravascular coagulation syndrome)
- Fibrinolysis and the plasmin system
- Secondary anticoagulants
- Reticuloendothelial system (RES)
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