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What is the mechanism of type II Heparin Induced Thrombocytopenia ?
a) Antibodies against platelet one factor
b) Antibodies against platelet two factor
c) Antibodies against platelet three factor
d) Antibodies against platelet four factor
e) Antibodies against platelet five factor
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Correct answer is "d"
Heparin-induced thrombocytopenia (HIT) may develop in two distinct forms, type I and type II (See Table 1). Type I HIT, also known as heparin-associated thrombocytopenia (HAT), is a non-immunologic response to heparin therapy, while type II HIT is an immunologic response to heparin therapy. Type I is more common than type II, occurring in 10 to 20% of patients given heparin, while type II occurs in 1 to 3% of patients receiving heparin.
The cause of type I HIT may be mediated by a direct interaction between heparin and circulating platelets causing platelet clumping or sequestration. This type of thrombocytopenia may exist in patients receiving heparin in the presence of other comorbid factors, such as other medications or sepsis, which may complicate the diagnosis. Type I HIT usually occurs within the first 48 to 72 hours after initiation of heparin therapy and the platelet count usually does not fall below 100 X 103/mm3, often returning to normal within 4 days despite continued heparin use. No laboratory tests are required to diagnose type I HIT, and it is not associated with an increased risk of thrombosis.
Type II HIT occurs in approximately 1 to 3% of patients receiving heparin and can occur at any dose or route of administration. Clinically, type II HIT displays thrombocytopenia after 5 to 10 days of heparin therapy, and the platelet count decreases approximately 30 to 50%, decreasing to less than 100 X 103/mm3, but usually not falling below 10 to 20 X 103/mm3.
Type II Heparin-Induced Thrombocytopenia:
New Treatment Options
by Robert Barcelona, Pharm.D.
Introduction: Heparin-induced thrombocytopenia (HIT) may develop in two distinct forms, type I and type II (See Table 1). Type I HIT, also known as heparin-associated thrombocytopenia (HAT), is a non-immunologic response to heparin therapy, while type II HIT is an immunologic response to heparin therapy. Type I is more common than type II, occurring in 10 to 20% of patients given heparin, while type II occurs in 1 to 3% of patients receiving heparin.
The cause of type I HIT may be mediated by a direct interaction between heparin and circulating platelets causing platelet clumping or sequestration. This type of thrombocytopenia may exist in patients receiving heparin in the presence of other comorbid factors, such as other medications or sepsis, which may complicate the diagnosis. Type I HIT usually occurs within the first 48 to 72 hours after initiation of heparin therapy and the platelet count usually does not fall below 100 X 103/mm3, often returning to normal within 4 days despite continued heparin use. No laboratory tests are required to diagnose type I HIT, and it is not associated with an increased risk of thrombosis.
Type II HIT occurs in approximately 1 to 3% of patients receiving heparin and can occur at any dose or route of administration. Clinically, type II HIT displays thrombocytopenia after 5 to 10 days of heparin therapy, and the platelet count decreases approximately 30 to 50%, decreasing to less than 100 X 103/mm3, but usually not falling below 10 to 20 X 103/mm3. Type II HIT is more severe because of the increased risk of thrombotic events, occurring in 30 to 80% of patients. Thrombotic events may occur in both the arterial and venous systems. These events occur primarily in the venous system and may lead to deep venous thrombosis (DVT), pulmonary embolism (PE), acute myocardial infarction, skin necrosis, venous limb gangrene, and possibly death.
Type II HIT is caused by the formation of antibodies that activate platelets following heparin administration. This leads to an interaction with platelet factor 4 (PF4), which is normally found on endothelial cells and platelets, and formation of immunogenic heparin-PF4 complexes which cause an immunologic response. Antibodies are generated resulting in a complex forming between antibodies, heparin, and PF4 (mediated through the FcyIIa portion of the platelet). This complex leads to further platelet activation resulting in formation of microparticles and thrombin generation. Antibodies also recognize PF4 bound to heparin on the endothelial surface and this surface becomes activated leading to another route of thrombin production. These pathways of thrombin generation may ultimately lead to thrombus formation and possible thromboembolic sequelae. The antibodies that are formed may persist for weeks to months following heparin administration; therefore, if a patient develops type II HIT and is administered heparin at a later date when circulating antibodies are still present, platelet levels may decrease within hours.
