The most common cause of thrombocytopenia is increased destruction of platelets. Platelets are eliminated from peripheral circulation faster than the bone marrow can produce new platelets.
Increased platelet destruction may be the result of immune or nonimmune mechanisms. Immune platelet destruction begins when antibodies coat platelets. These sensitized platelets are then destroyed by macrophages, mostly from the spleen but also from the liver. Disorders that are associated with immune mechanisms of destruction include:
- Idiopathic (or immune) thrombocytopenic purpura (ITP)
- Heparin-induced thrombocytopenia (HIT)
- Neonatal alloimmune thrombocytopenia (NAIT)
Increased destruction of platelets is not always caused by the immune system. Platelet destruction can occur as a result of abnormal platelet aggregation or endothelial cell injury. Both of these occurrences can cause fibrin to form in arterioles and capillaries. This leads to platelet activation and consumption. Conditions associated with nonimmune destruction and consumptive thrombocytopenia include:
- Thrombotic thrombocytopenic purpura (TTP)
- Hemolytic uremic syndrome (HUS)
- Disseminated intravascular coagulation (DIC)
All of these conditions are associated with significantly decreased platelet counts that may become life threatening. Restoration of platelet numbers is essential to promote clotting and vascular patency.
