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Hypoprothrombinemia can be the result of a genetic defect, may be acquired as the result of another disease process, or may be an adverse effect of medication.For example, 5-10% of patients with systemic lupus erythematosus exhibit acquired hypoprothrombinemia due to the presence of autoantibodies which bind to prothrombin and remove it from the bloodstream (lupus anticoagulant ...
The incorrectly glycosalated fibrinogen is dysfunctional and may cause pathological episodes of bleeding and/or blood clotting. [5] Congenital hypodysfibrinogenemia, an inherited disorder in which low levels of fibrinogen composed at least in part of a dysfunctional fibrinogen may cause pathological episodes of bleeding or blood clotting. [6]
The haemostatic (blood clotting) system involves the interaction of proteins in the blood, the blood vessel wall and the flow of blood to control bleeding and blood clotting. Developmental Haemostasis is a term that represents the maturation of the haemostatic system from birth to adulthood. There are differences in the concentration, structure ...
Although it is a recombinant protein, rFXIII subunit A is identical in structure and function to the A subunit of factor XIII naturally produced in the body by healthy individuals. [5] These patients need exogenous subunit A of factor XIII since they have a mutation which prevents production of the A subunit.
Antithrombin III deficiency (abbreviated ATIII deficiency) is a deficiency of antithrombin III.This deficiency may be inherited or acquired. [1] It is a rare hereditary disorder that generally comes to light when a patient suffers recurrent venous thrombosis and pulmonary embolism, and repetitive intrauterine fetal death (IUFD). [2]
The assembled protein is passes to the Golgi apparatus where it is glycosylated, hydroxylated, sulfated, and phosphorylated to form the mature fibrinogen glycoprotein that is secreted into the blood. Congenital hypofibrinogenemia results from inherited mutations in one of the three fibrinogen chains that results in the disruption of fibrinogen ...
Sickle cell disease is a group of inherited blood disorders, caused by a genetic abnormality in the oxygen-carrying protein haemoglobin found in red blood cells. [57] Under certain circumstances, this leads to the red blood cells adopting an abnormal sickle -like shape; with this shape, they are unable to deform as they pass through capillaries ...
The normal clotting process depends on the interplay of various proteins in the blood. Coagulopathy may be caused by reduced levels or absence of blood-clotting proteins, known as clotting factors or coagulation factors. Genetic disorders, such as hemophilia and Von Willebrand disease, can cause a reduction in clotting factors. [2]