Thrombophilia is defined as a disorder of hemostasis, which leads to hypercoagulability of the blood and subsequent thrombosis. The final clot solidifies with a fibrous mesh.
What is Hemostasis?
Hemostasis is a defense function of the body, which has as its main mission the preservation of the integrity of the vessels and the fluidity of the blood inside the blood vessels, so that there is neither thrombosis nor bleeding.
In addition, hemostasis is actively involved in the implantation of the fertilized egg in the uterus, in the metastases of malignant cells, etc. Impaired hemostasis is involved in coronary heart disease, retinopathy of diabetes mellitus, preeclampsia, pulmonary hypertension, vascular occlusive disease of sickle cell disease, thrombotic microangiopathy, etc. Hemostasis works with the harmonious cooperation and balance of two opposing mechanisms, the coagulation mechanism (normally in vascular injury, acts locally and explosively and occludes the vessel) and the fibrinolysis mechanism (restores after thrombosis, patency and vascular integrity by dissolving the fibrin).
The hemostasis system includes soluble agents (coagulation agents, coagulation inhibitors, fibrinolytic and anti-fibrinolytic agents) and cellular components (platelets and endothelial cells). The coordinator of hemostasis is the endothelium (occupies an area of 3,000 sq.m., weighing only 100g.), As long as the endothelial cells (which line the inner wall of blood and lymph vessels) have a friend / coagulant and anticoagulant factors, explains Mr. Nikolaos Anagnostopoulos, Hematologist Director of the Metropolitan General Hematology Clinic.
When do we have thrombosis and when do we bleed?
When the mechanism of blood coagulation is overactive or when the mechanism of fibrinolysis is underactive, then thrombosis is produced. Conversely, when the coagulation mechanism is underactive or the fibrinolysis mechanism is overactive, then bleeding is produced.
What are the causes of Thrombophilia?
The causes are either hereditary / genetic or acquired. Is there coagulation and an increased risk of thrombosis in COVID-19? Of course, because COVID-19 is not just a lung disease, but also a vascular and thrombophilic disease. Indeed, pathologically there is a diffuse inflammation of the endothelial cells, i.e. endothelitis, which is caused by the coronavirus spike. COVID-19 is a high risk factor for thrombosis (even in abnormal sites, including arterial and venous cerebral thrombosis) and coagulation disorders in hospitalized patients including severe thrombocytopenia, especially in patients (especially patients).
At autopsies, 80% of patients who died had thrombosis in the microcirculation. Hypercoagulability is detected in the blood by: increased fibrinogen, increased δ-dimers (small proteins produced by thrombus degradation by fibrinolysis), overstimulated platelets, increased coagulation factors (FVIII, vF) coagulation and pathological thromboelastography. In particular, an increase in D-Dimers (> 0.5mg / L) is the most common (detected in approximately 50% of patients), while very high values are a particularly aggravating prognostic factor.
Does the COVID-19 vaccine cause blood clots?
In February 2021 a friend / prothrombotic syndrome was observed in a small number of people vaccinated with the ASTRAZeneca vaccine and then similarly with Johnson & Johnson. This syndrome is called Vaccine-Induced Immune Thrombotic Thrombocytopenia (VITT). It has also been called the syndrome of thrombosis and thrombocytopenia (TTS). The exact frequency of VITT remains unknown. Indicatively, the US CDC initially identified fifteen (15) cases in a total of eight (8) million people vaccinated with ASTRAZeneca, while in Norway after vaccination with ASTRAZeneca 1 case is reported in 26,000 vaccinations. VITT has not been described after mRNA vaccines, (Up To Date Aug 20,2021).
Predisposing factors [εκτός της υπεροχής των γυναικών (9/11 ασθενείς), έναντι των ανδρών και της υπεροχής σε ηλικίες <60 ετών] remain unknown. Cerebral vein thrombosis, which can also occur as cerebral hemorrhage, is considered the most common location. Thrombosis can be either venous or arterial or as a sudden death (necropsy diagnosis). Low platelets (10,000 / μL -100,000 / μL) may be accompanied by bleeding or non-bleeding events.
How is the VITT diagnosis confirmed?
Typically with the detection of antibodies against platelets (PF4 / ELISA) which are also responsible for platelet activation, coagulation overstimulation and finally thromboembolic complications.
What is the treatment for thrombophilia in COVID-19 and which in VITT?
In COVID-19, immediate Thromboprophylaxis is performed with Low Molecular Heparin (HXMB), while in VITT complete anticoagulant therapy (but not HXMB) is administered and in persistent cases, Plasmapheresis and high doses of γ-Globin.
The Metropolitan General Hospital, equipped with state-of-the-art medical technology and staffed with experienced staff, provides full clinical and laboratory support in the complete investigation of Thrombophilia and personalized treatment (Thromboprophylaxis or Anticoagulant treatment or Medical Monitoring) by an experienced specialist.
The Hellenic Healthcare Group is also a pioneer in the Excellence of Clinical Hematology. To this end, it adopted our accepted proposal from the Medical Society of Athens for the institutionalization and subsidization of the Award by the Metropolitan “| Hematopoiesis-Hematotherapy” at each Annual Panhellenic Medical Conference from May 2018.
Writes Mr. Nikolaos Anagnostopoulos, Hematologist Director of the 2nd Metropolitan General Hematology Clinic.
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