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Frequently Asked Questions
 

A: A hypercoagulable state is a condition in which the blood is more readily coagulated or clotted than is normal. The formation of a hemostatic clot requires the coordinated action of a number of factors. A balance exists between the formation and dissolution of a thrombus (clot) in the normal physiologic response. At times, congenital (hereditary) defects or acquired defects destroy this balance, which can result in abnormal bleeding or in abnormal thrombosis. In 80–90% of people with a thrombosis, a cause can be defined. In 50–80% of these, a hereditary or acquired defect is the cause. Most hypercoagulable states are associated with a spontaneous onset of deep venous thrombosis at an early age.

A:  Heparin-induced thrombocytopenia (HIT) is a decrease in the platelet count caused by heparin therapy. This may happen in up to 30% of people who have started heparin therapy. Only about 5% experience a significant decrease in platelets, which results in clotting or hemorrhage.

Type I HIT is the acute form, occurring early in heparin treatment. Platelet count improves as heparin therapy continues. Type II, the delayed form, occurs 5 to 10 days after the start of heparin in a patient’s first exposure to it and within 3 to 9 days in a patient who has had previous heparin therapy. Type II HIT reportedly has a 23–60% complication rate, and 12–18% of people die. Treatment consists in eliminating all sources of heparin, including heparin flushes and intravascular and heparin-coated catheters. Even very low doses of heparin can evoke a reaction. Alternative options for anticoagulant therapy in patients with HIT include hirudin or argatroban.

A: Factor V Leiden is a genetic change in factor V, which causes factor V to be resistant to protein C and which can result in clotting. Activated protein C cleaves (divides) and inactivates coagulation factors Va and VIIIa in the presence of protein S. This system allows blood to clot while maintaining fluidity. Diagnosis is by a blood test that measures the responsiveness of plasma to coagulation factor V Leiden or by direct assay for factor V molecule that is resistant to inactivation by factor V Leiden. Treatment is long-term warfarin.

A: Hyperhomocysteinemia is elevated homocysteine (an amino acid) blood levels, which have been found to increase the risk of venous thrombosis up to fourfold. According to one multicenter study, high blood levels of homocysteine are associated with early onset of vascular disease and venous thrombosis (10–25%) and with recurrence (19%) of deep venous thrombosis after 2 years.

High homocysteine levels in people who have no symptoms can be normalized with supplements of folic acid, B₆, and B₁₂ (although the benefit is not proved). Patients who have had deep venous thrombosis should have anticoagulation therapy with warfarin or low molecular weight heparin. The physician determines the duration of this treatment.

A: Protein C is a vitamin K-dependent proenzyme (enzyme precursor) involved in blood clotting and the destruction or decomposition of a blood clot (thrombolysis).  A deficiency of protein C leads to an increased risk of inappropriate clot formation. Age of onset of protein C deficiency is between 15 and 30 years. Persons with this inherited disorder have an 8 to 10 times risk of thrombosis compared with those who do not have the disorder.

Persons with protein C deficiency and no thrombosis are usually not given anticoagulants unless they are having major surgery or are immobilized for a prolonged period of time. Persons with protein C-related thrombosis are usually treated with the anticoagulant heparin. Since there is a risk of recurrence, long-term therapy with warfarin or low molecular weight heparin is prescribed.