Thrombocytopenia pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Direct myelosuppression
- Valproic acid
- Methotrexate
- Carboplatin
- Interferon
- Other chemotherapy drugs
Immunological platelet destruction
- Drug binds Fab portion of an antibody. The classic example of this mechanism is the quinidine group of drugs. The Fc portion of the antibody molecule is not involved in the binding process.
- Drug binds to Fc, and drug-antibody complex binds and activates platelets. Heparin induced thrombocytopenia (HIT) is the classic example of this phenomenon. In HIT, the heparin-antibody-platelet factor 4 (PF4) complex binds to Fc receptors on the surface of the platelet. Since Fc portion of the antibody is bound to the platelets, they are not available to the Fc receptors of the reticulo-endothelial cells, so therefore this system cannot destroy platelets as usual. This may explain why severe thrombocytopenia is not a common feature of HIT.
Heparin-induced thrombocytopenia
(HIT or white clot syndrome): this is a rare but serious condition that may occur in a hospitalized population. The most common clinical setting for HIT is in postoperative coronary artery bypass graft recipients, who may receive large quantities of heparin during surgery. HIT typically occurs about a week after exposure to heparin. The heparin-PF4 antibody complex will activate the platelets, and this can often lead to thrombosis. The term HITT, where the last T stands for thrombosis, denotes the concept that heparin-induced thrombocytopenia often is associated with thrombosis.