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Reactive thrombocythemia is the most common cause of a high platelet count. It accounts for 88% to 97% of thrombocythemia cases in adults, and near 100% in children. In adults, acute infection, tissue damage, chronic inflammation and malignancy are the common causes of reactive thrombocythemia. Usually, one or more of these conditions is ...
Factor V is produced by megakaryocytes, which produce platelets and platelet-derived factor V, and hepatocytes, which produce plasma-derived factor V. [9] The molecule circulates in plasma as a single-chain molecule with a plasma half-life of 12–36 hours. [10] Factor V is able to bind to activated platelets and is activated by thrombin.
Factor V Leiden is an autosomal dominant genetic condition that exhibits incomplete penetrance, i.e. not every person who has the mutation develops the disease. The condition results in a factor V variant that cannot be as easily degraded by activated protein C. The gene that codes the protein is referred to as F5.
Coagulopathy (also called a bleeding disorder) is a condition in which the blood's ability to coagulate (form clots) is impaired. [1] This condition can cause a tendency toward prolonged or excessive bleeding (bleeding diathesis), which may occur spontaneously or following an injury or medical and dental procedures.
Up to 8% of patients receiving heparin are at risk to develop HIT antibodies, but only 1–5% on heparin will progress to develop HIT with thrombocytopenia and subsequently one-third of them may develop arterial or venous thrombosis. [1] After vascular surgery, 34% of patients receiving heparin developed HIT antibodies without clinical symptoms ...
Budd–Chiari syndrome is a very rare condition, affecting one in a million adults. [1] [2] The condition is caused by occlusion of the hepatic veins (usually due to a blood clot) that drain the liver. The symptoms are non-specific and vary widely, but it may present with the classical triad of: abdominal pain, ascites, and; liver enlargement.
Many cases of congenital dysfibrinogenemia are asymptomatic. Since manifestations of the disorder generally occur in early adulthood or middle-age, younger individuals with a gene mutation causing it may not have had time to develop symptoms while previously asymptomatic individuals of advanced age with such a mutation are unlikely to develop symptoms.
Low-dose low molecular weight heparin (e.g. enoxaparin) may be used. [20] For life-threatening complications, the platelet count can be reduced rapidly using plateletpheresis, a procedure that removes platelets from the blood and returns the remainder to the patient. [20]
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